Med-Surg.

Final Study Guide

Med Surg Final

Altered LOC Head Injuries Cerebral Vascular Disease Seizure Disorders Brain Tumors Brain Surgery Diabetes Mellitus Oxygen Therapy Pneumonia Tuberculosis ? Asthma/COPD (Bronchitis, Emphysema) Fractures Hip Fractures Amputations Osteoarthritis Orthopedic Surgery Cancer Womens Health Osteoporosis STDs PUD Gastritis Intestinal Obstruction Diverticulosis Diverticulitis CAD MI Angina Pectoris EKG Hypertension PVD CHF Systemic Lupus Erythematosus (Not Included) Rheumatoid Arthritis (Not Included) Precautions Contact, Airborn, Droplet (Not included)

Med-Surg Neurological System Head Injuries Pathophysiology Primary injury Initial damage to the brain from a traumatic event Contusion bruising of the brain surface, an injury that doesnt disrupt the integrity of the skin, caused by a blow to the body and characterized by swelling, discoloration, and pain. Laceration a torn, jagged wound Torn blood vessels Aneurism leading to hemorrhage Acceleration & Deceleration an increase in the speed or velocity of an object or reaction Closed blunt brain injury occurs when the head accelerates and then rapidly decelerates or collides with another object and brain tissue is damaged but there is no opening through the skull or dura. Foreign body penetration Depressed skull fracture with bone fragments embedded in the brain, penetrating head wounds require surgical debridement to remove foreign bodies and devitalized brain tissue and to control hemorrhage. IV antibiotic treatment is instituted immediately, particularly for dural lacerations, and blood component therapy is administered if indicated. Secondary injury Hrs and days after the initial injury Brain swelling (edema), ischemia, and chemical changes associated with direct trauma to the brain Ongoing bleeding Increased ICP

It can cause lateral displacement of the brain against the rigid structures of the skull. Restriction of blood flow to the brain tissue decreasing O2 delivery and waste removal. Cells within the brain become anoxic and cannot metabolize properly, producing ischemia, infarction, irreversible
brain damage, brain death. Classifications

Scalp Injury: (Minor head injury)

ABRASION (brush wound) CONTUSION (bruising of the brain surface, an injury that doesnt disrupt the integrity of the skin, caused by a

blow to the body and characterized by swelling, discoloration, and pain. LACERATION (avulsion or tearing away of the scalp) HEMATOMA UNDER THE SCALP TISSUE (Subgaleal hematoma - collection of blood) Skull Fractures: (Break in the continuity of the skull by forceful trauma) Open (laceration or tear in the dura, ie. Bullet) Closed (intact dura) Simple (linear) fracture is a break in the continuity of the bone. Comminuted refers to a splintered or multiple fracture line Depressed fracture refers to bone fragments are embedded in the brain tissue Basilar refers to a fracture at the base of skull resulting in CSF loss at ears, nose, eyes S&S Persistent & localized pain: fracture Fractures of the base of the skull: Hemorrhage from the nose, pharynx, or ears. Blood under the conjunctiva Battle sign (Ecchymosis over the mastoid) CSF drainage from the ears & nose ( otorrhea, rhinorrhea) Bloody CSF suggest brain laceration or contusion Diagnostic tools & Assessment Ct scan Computed Tomography uses high-speed xray scanning to detect less apparent abnormalities. It is fast, accurate, and safe diagnostic procedure that shows the presence, nature, location, and extent of acute lesions. Cerebral edema, contusion, hematomas, subrachnoid & intraventricular hemorrhage, (infarction) hydrocephalus, abd.

MRI Magnetic Resonance Imagery is used to evaluate patients with head injury when a more accurate picture
of anatomic nature of the injury is warranted and when the Pt is stable enough to undergo this longer diagnostic procedure. Cerebral angiography identifies supratentorial, extracerebral, and intracerebral hematomas and cerebral contusions. Lateral and anteroposterior views of the skull are obtained. Management Scalp injury Basilar Skull Fractures HOB 30 degree to reduce ICP and promote spontaneous closure of the leak. Instruct patient to avoid blowing the nose & sneezing. Depressed Skull Fractures ABTs (antibiotics) therapy Scalp is shaved and cleanse with copious amount of saline to remove the debris. Surgical repair (non-depressed skull Fx usually do not required surgical TX) Brain Injury (injury that is severe enough to interfere with normal functioning) Closed (blunt) injury Head rapidly accelerates and decelerates or collides with another object. Brain tissue damage with no opening through the skull and dura. Open injury Object penetrates the skull and damages the soft brain tissue. Penetrating injury Concussion Temporally loss of neurologic function (from dizziness to complete loss of consciousness) after a head trauma with no apparent structural damage Last from seconds to minutes Frontal lobe: bizarre irrational behavior Temporal lobe: amnesia and/or disorientation Contusion More severe than concussion Bleeding Loss of consciousness for more than few minutes S&S depend on the extend of the cerebral edema Residual vertigo and headaches are common Diffuse axonal injury Widespread damage to the axons in the cerebral hemispheres, corpus callosum, and brain stem. Severe injury leads to coma with decorticate and decerebrate posturing Intracranial Hemorrhage Intracranial hemorrhage Collection of blood that develops within the cranial vault Most serious brain injury epidural, subdural, or intracerebral hematoma P. 1914 Epidural hematoma: Blood collects between the dura and the skull Classic sign: Lucid interval Emergency with poss. obvious neurologic deficit and Resp. arrest within min. TX: burr holes to decreased ICP immediately, craniotomy, both with drain Subdural hematoma Collection of blood between the dura and the brain Cause: Trauma, coagulopathies, ruptured aneurysm but most common is venous in origin and is caused by a rupture of small vessels that bridge the subdural space. Acute: S&S within 24-48 hrs. AMS (altered mental status), pupillary signs, hemiparesis. Sub-acute: S&S within 48hrs-2wks. S&S similar to Acute Subdural Hematoma Chronic: repetitive minor head injuries. S&S appear wks-months. On-and-off severe headaches, mental deterioration, seizures, and personality changes TX: burr holes, craniotomy Intracerebral hemorrhage Bleeding into the brain tissue

Causes: HTN, ruptured vein/aneurysm, vascular anomalies, tumor, leukemia, hemophilia, aplastic anemia, thrombocytopenia, and anticoagulant therapy. S&S: Headache and neurologic deficits TX: craniotomy, cranietomy (? Surgery depends on location and containment of blood) Management includes supportive care, control of ICP, and careful administration of fluids, electrolytes, and antihypertensives

Brain Injury Management Every pt with head injury is presumed to have a cervical spine injury until proven otherwise. Cervical collar and cervical X-Rays Neurological assessment CT scan & MRI PET Scan Positron emission tomography is a method of scanning that examines brain function rather than structure Prevention of ICP Prevention of further neurological deterioration Treatments to prevent secondary injury include stabilization of cardiovascular and respiratory function to maintain adequate cerebral perfusion, control of hemorrhage and hypovolemia, and maintenance of optimal blood gas values Brain Injury NSG Assessment Glasgow Coma Scale a tool for assessing a patients response to stimuli. Scores range from 3 (deep coma) to 15 (normal) (<8 indicates severe head injury) Eye opening response Spontaneous 4, To Voice 3, To Pain 2, None 1 Best Verbal Response oriented 5, Confused 4, Inappropriate words 3, Incomprehensible sounds 2, none 1 Best Motor Response Obeys command 6, localizes pain 5, Withdraws 4, Flexion 3, Extension 2, none 1 LOC Vital signs Neurological assessments (**Pupil response) Maintaining the airway Monitor fluid and electrolyte balance

Promote adequate nutrition Preventing injury Maintain skin integrity

Med-Surg Neurological System Altered level of consciousness The patient is: Not oriented Does not follow commands Needs persistent stimuli to achieve a state of alertness (LOC sensitive indicator of neurological function). Coma A clinical state of unconsciousness in which the patient is unaware of self or the environment for prolonged periods. A clinical state of un-arouseable unresponsiveness in which there are no purposeful responses to internal or external stimuli. Akinetic Mutism A state of unresponsiveness to the environment in which the patient makes no movement or sound but sometimes open the eyes. Eye movement is measured for responsiveness Altered LOC Pathophysiology Symptom of multiple pathologies: Neurologic, toxicologic, and/or metabolic. Neurologic: Head injury or stroke Toxicologic: Drug overdose, ETOH intoxication Metabolic: Hepatic and/or renal failure, and DKA (Diabetic Ketoacidosis diabetic coma, an acute lifethreatening complication of uncontrolled DM. S&S urinary loss of water, K, Ammonium, and sodium results in hypovolemia, electrolyte imbalance, extremely high blood glucose levels, and breakdown of free fatty acids, causing acidosis, often with coma.) Disruption in the anatomic structure is cause by head trauma, edema, pressure from tumors, increased/decreased blood or CSF circulation. Altered LOC S&S Decreased state of alertness and consciousness Behavioral changes (restlessness & anxiety) are initial changes which are subtle Sluggish pupillary response (as the Pt becomes comatose, the pupils become fixed) Change in verbal and motor response If Pt is comatose but with pupillary light reflexes preserved, a toxic or metabolic disorder is suspected. If Pt is comatose and has localized signs such as abnormal papillary and motor responses, it is assumed that neurologic disease is present until proven otherwise Diagnostic tools Lab tests: Glucose Test whether Pt is hyperglycemic or hypoglycemic (glucose blood levels which help to indicate liver function (metabolism of glucogon) and indicate the need for insulin because if Plasma levels are to high that could indicate pancreas function problems, as well as insulin receptor functionality and glucose metabolism at the cellular level. Electrolytes critical for cellular functions, provide inorganic chemicals for a variety of cellular functions (e.g., nerve impulse transmission, muscular contraction, water balance). Concentrations of cations. Na, K, Ca, Mg is higher in the plasma than in the interstitial fluid. Na The most abundant cation (90% of the electrolyte fluid) and the chief base of the blood. Primary function in the body is maintain osmotic pressure and acid-base balance chemically and to transmit nerve impulses. Determinations of plasma sodium levels detect changes in water balance rather than sodium balance. Sodium levels are used to determine electrolytes, acid-base balance, water balance, water intoxication, and dehydration. K Potassium is the principal cation of intracellular fluid and the primary buffer within the cell itself. 90% of K is concentrated within the cell; only small amounts are contained in bone and blood. Damaged cells release K into the blood. 80% to 90% of cells K is excreted in the urine by the glomeruli of the kidneys; the remainder is excreted in sweat and stool. Even when no K is taken into the body 40 to 50 mEq is still excreted daily in the urine. The Kidneys do not conserve K, and when an adequate amount of K is not ingested, a severe deficiency

will occur. K plays an important role in nerve conduction, muscle function, acid-base balance, and osmotic pressure. Along with Ca and Mg, K controls the rate and force of contraction of the heart and thus cardiac output. Evidence of a K deficit can be noted on an ECG by the presence of a U wave. Ca The bulk of the bodies calcium (99%) is stored in the skeleton and teeth which act as huge reservoirs for maintaining blood levels of calcium. About 50% of the blood Ca is ionized; the rest is protein bound. Only ionized Ca can be used by the body in such vital processes as muscular contraction, cardiac function, transmission of nerve impulses, and blood clotting. The amount of protein in the blood also affects calcium levels because 50% is protein bound. Thus, a decrease is serum albumin will result in a decrease in total serum Ca. Mg Mg in the body is concentrated (40-60%) in the bone, 20% muscle, 30% within the cell itself, and 1% in the serum, and is required for use of ADP as a source of energy. It is necessary for the action of numerous enzyme systems such as carbohydrate metabolism, protein synthesis, nucleic acid synthesis, and contraction of muscular tissue. Mg also regulates neuromuscular irritability and the clotting mechanism. Mg deficiency will result in the drift of calcium out of the bones, possible resulting in abnormal calcification in the aorta and the kidney. When there is decreased kidney function, greater amounts of magnesium are retained, resulting in increased blood serum levels. Magnesium measurement is used to evaluate renal function, electrolyte status, and evaluate magnesium metabolism. Cl Chloride, a blood electrolyte, is the major anion that exists predominantly in the extracellular spaces as part of sodium chloride or hydrochloric acid. Cl maintains cellular integrity through its influence on osmotic pressure and acid-base and water balance. In an emergency, chloride is the least important electrolyte to measure. However, it is especially important in the correction of hypokalemic alkalosis. Ammonia NH3, an end product of protein metabolism, is formed by bacteria acting on intestinal proteins together with glutamine hydrolysis in the kidneys. The liver normally removes most of this ammonia via the portal vein circulation and converts the ammonia to urea. Because any appreciable level of ammonia in the blood affects the bodys acid-base balance and brain function, its removal from the body is essential. The liver accomplishes this by synthesizing urea so that it can be excreted by the kidneys. BUN Blood Urea Nitrogen test which measures the nitrogen portion of urea, is used as an index of glomerular function in the production and excretion of urea. Rapid protein catabolism and impairment of kidney function will result in an elevated BUN level. The rate at which the BUN level rises is influenced by the degree of tissue necrosis, protein catabolism, and the rate at which the kidneys excrete the urea nitrogen. A markedly increased BUN is conclusive evidence of sever impaired glomerular function. In chronic renal disease, the BUN level correlates better with symptoms of uremia than does the serum creatinine. Serum osmolarity PT Prothrombin Time normal range 11.0 to 13.0 seconds. Prothrombin is a protein produced by the liver for clotting of the blood. Prothrombin production depends on adequate vitamin K intake and absorption. During the clotting process, prothrombin is converted to thrombin. The prothrombin content of the blood is reduced in patients with liver disease. PT directly measures a potential defect in stage II of the clotting mechanism (extrinsic coagulation system) through analysis of the clotting ability of five plasma coagulation factors (prothrombin, fibrinogen, factor V, factor VII, and factor X). The PT is used also to evaluate disfibrinogenemia, evaluate the heparin effect and coumarin effect, liver failure, and vitamin K deficiency. PTT Partial Thromboplastin Time normal range 21-35 seconds, one stage clotting test, screens for coagulation disorders. Specifically, it can detect deficiencies of the intrinsic thromboplastin system and also reveals defects in the extrinsic coagulation mechanism pathway. Prolonged PTT occurs in congenital deficiencies, Heparin therapy, Warfarin (Coumadin) therapy, Vitamin K deficiency, liver disease, DIC (disseminated intravascular coagulation) fibrin breakdown products. Shortened PTT occurs in: extensive cancer, except when the liver is involved, Immediately after acute hemorrhage, very early stages of DIC. Serum ketones Level of concentration of ketones. Ketoacidosis vs Ketoalcolosis ETOH level Ethanol is absorbed rapidly from the GI tract, with peak blood levels usually occurring within 40 to 70 minutes of ingestion on an empty stomach.Quantitation of alcohol level may be performed for medical or legal purposes, to diagnose alcohol intoxication, and to determine appropriate therapy. Alcohol level must be tested as a possible cause of unknown coma because alcohol intoxication mimics diabetic coma, cerebral trauma, and drug overdose. This test is also used to screen for alcoholism and to monitor ethanol treatment for methanol intoxication. Toxicology the scientific study of poisons, their detection, their effects, and methods of treatment for conditions they produce. Urine drug screen. Common Urine Drug Tests include Alcohol, Amphetamines, Analgesics, Barbiturates, Benzodiazepines, Cocaine crack, Cyanide, LSD, Major tranquilizers, Marijuana, Opiates, PCP, Sedatives Stimulants, Sympathomimetics. ABGs Arterial Blood Gases measurement are obtained to assess adequacy of oxygenation and ventilation, to evaluate acid-base status by measuring the respiratory and nonrespiratory components, and to monitor effectiveness of therapy. They are also used to monitor critically ill patients, to establish baseline values in the

perioperative and postoperative periods, to detect and treat electrolyte imbalances, to titrate appropriate oxygen flow rates, to qualify a patient for use of oxygen at home, and in conjuction with pulmonary function testing. Glasgow coma scale is a tool for assessing a patients response to stimuli. Scores range from 3 (deep coma) to 15 (normal). Eye opening response Spontaneous 4, To Voice 3, To Pain 2, None 1 Best Verbal Response oriented 5, Confused 4, Inappropriate words 3, Incomprehensible sounds 2, none 1 Best Motor Response Obeys command 6, localizes pain 5, Withdraws 4, Flexion 3, Extension 2, none 1 Ct scan Computed Tomography uses high-speed xray scanning to detect less apparent abnormalities. It is fast, accurate, and safe diagnostic procedure that shows the presence, nature, location, and extent of acute lesions. Cerebral edema, contusion, hematomas, subrachnoid & intraventricular hemorrhage, (infarction) hydrocephalus, abd. Can Identify bleeding without contrast. MRI Magnetic Resonance Imagery is used to evaluate patients with head injury when a more accurate picture of anatomic nature of the injury is warranted and when the Pt is stable enough to undergo this longer diagnostic procedure. EEG Electroencephalography, an instrument used for receiving an recording the electric potential produced by the brain cells. Electroencephalogram, a graphic chart on which is traced the electric potential produced by the brain cells, as detected by electrodes placed on the scalp. The resulting brain waves are called alpha, beta, delta, and theta rhythms, according to the frequencies they produce. Variations in brain wave activity are correlated with neurologic conditions, psychologic states, and level of consciousness. Altered LOC Assessment Mental status the degree of competence shown by a person in intellectual, emotional, psychologic, and personality functioning as measured by psychologic testing with reference to a statistical norm. Alertness is measured by the patients ability to open the eyes spontaneously or in response to a vocal or noxious stimulus. Pts with severe neurologic dysfunction cannot do this. Cranial nerves 12 pairs of nerves emerging from the cranial cavity through various openings in the skull. Beginning with the most anterior, they are designated by Roman numerals and named: Cranial Nerve I Cranial Nerve II Cranial Nerve III Cranial Nerve VI Cranial Nerve V Cranial Nerve VI Cranial Nerve VII Cranial Nerve VIII Cranial Nerve IX Cranial Nerve X Cranial Nerve XI Cranial Nerve XII Olfactory Optic Oculomotor Trochlear Trigeminal Abducens Facial Vestibulocochlear Glossopharyngeal Vagal Accessory Hypoglossal Smell Visual acuity and visual fields Muscles that move the eye and lid, papillary constriction, lens accomodation Muscles that move the eye Facial sensation, corneal reflex, mastication Muscles that move the eye Facial expression and muscle movement, salivation, and tearing, taste, sensation in the ear Hearing and equilibrium Taste, sensation in pharynx and tongue, pharyngeal muscles, swallowing Muscles of pharynx, larynx, and soft palate; sensation in external ear, pharynx, larynx, thoracic and abdominal viscera; parasympathetic innervation of thoracic and abdominal organs Sternocleidomastoid and trapezius muscles Movement of the tongue

Cerebellar function (balance & coordination) Reflexes Deep tendon reflexes & pathologic reflexes e.g., Babinskis sign Sensory and motor function applying a painful stimulus (firm but gentle pressure to the nailbed or by squeezing
the muscle. If the patient attempts to push away or withdraw, the response is recorded as purposeful or appropriate (patient withdraws with painful stimuli) Altered LOC Complications

Respiratory failure

Pneumonia hospital aquired

Pressure ulcers from lack of mobility and being in one position for too long Aspiration Venous stasis Deep vein thrombosis Musculoskeletal deterioration loss of muscle tone an mass resulting from inactivity Disturbed GI function Constipation, peristalsis
Medical Management

Maintain a patent airway (mechanical ventilation if needed) Maintain adequate perfusion to the brain and the body (B/P & Heart Rate) IV access Nutritional intake
NSG Assessment Alertness (pts ability to open eyes spontaneously or with stimulation) Determine patient orientation to person, place, and time (AAOx3) Verbal response (clear vs. slurred speech, aphasia & incoherent speech) Motor response: Spontaneous, response to stimulus (light touch vs. deep pain), and posturing decerebrate involving extension and outward rotation of upper extremities and plantar flexion of the feet decorticate involving adduction and flexion of the upper extremities, internal rotation of the lower extremties, and plantar flexion of the feet Posture Decorticate: (towards the body) Severe brain injury Flexion of upper extremities and extension of lower extremities Internal rotation of lower extremities Decerebrate: (away from the body)

Continuous assessment (q15 min-q1hr) V/S, Respiratory Status, Pupils, (PERRLA) Reflexes Neurological exam Indicates deeper and more severe dysfunction than does decorticate posturing; implies brain pathology; poor prognostic sign Altered LOC Nursing Interventions Maintain a patent airway: Administer O2 as ordered HOB 30 degree Frequent suctioning and mouth care (for deep suction get order from physician after initial suction) Turn patient from side to side Chest physiotherapy and postural drainage as ordered Lungs auscultation NSG: Maintain a patent airway Suctioning: the pt lacks pharyngeal reflexes Mouth care HOB 30 degree: Prevents aspiration Chest physiotherapy & postural drainage (promotes removal of secretions) Chest auscultation (to ID adventitious breath sounds) NSG: Mouth care

Extension of upper extremities Outward rotation of upper extremities

Assess for dryness (dehydration), inflammation and crusting (infection) Keep membranes moist Provide mouth care (remove crust, excess saliva, maintain moisture & dental integrity) Apply moisturizing sol. to the lips.
NSG: Preserve corneal integrity Clean with NS with sterile gauze to prevent dryness Use of artificial tears Q2hrs, as ordered (saline ampules) Eye patches to prevent corneal damage and blindness NSG: Thermoregulation Causes of fever: Infection Drug reaction Damage to the hypothalamus (if neurological then the fever will never go down! Mortality rate is high, maybe 100%) (low grade) dehydration Use minimum amount of bedding to increase surface cooling.

Minimum amount of bedding Antipyretics as prescribed most common acetaminophen (no Tylenol if liver problem, renal no motrin) Give a cool vs. tap H2O sponge bath Use of hypothermia blanket Elderly dont regulate the body temperature as well
NSG: Provide sensory stimulation Talk and touch the pt while performing nursing care. Encourage the family to communicate with the pt. Orient the patient to time and place Q shift. Coma: Use of T.V. and radio Arousing from coma: Minimize stimulation, quiet environment and limit visitors to avoid agitation and anxiety (good sign) Fluids & nutritional needs Assess mucous membrane and skin turgor for hydration status Accurate I&O Report any abnormal lab results: BUN, Creatinin, Albumin level (aids in movement of fluids / protein which shows the nutritional status of patient), RBC, Hemoglobin & Hematocrit (H&H) IV access for hydration and Parenteral feeding NGT placement Maintain skin & joint integrity Order low-air-loss mattress (protocol) Follow a regular schedule of turning & repositioning Q2hrs. (prone for 15 minutes a day) Avoid dragging the pt up in bed (use drop/pull sheet) dragging creates a shearing force and friction on the skin surface PROM (encourage family to participate) Passive Range of Motion gets the family involved and also helps prevent contractures Prevent contractures and foot drop PROM exercises and the use of splints or foam boots aids in the prevention of foot drop and eliminates the pressure of bedding on the toes. The use of traochanter rolls to support the hip joints keeps the legs in proper alignment. The arms ar in abduction, the fingers lightly flexed, and the hands in slight supination. The heels of the feet are assessed for pressure areas. Specialty beds, such as fluidized or lowair-loss beds, may be used to decrease pressure on bony prominences. Benefits of turning Kinesthetic stimulation (sensation of movement) Propioception stimulation (awareness of position)(Im on my right side, Im on my left side) Vestibular stimulation (equilibrium)

NSG: Promote Bladder function (Bladder & Bowel or B&B) Palpate pelvic area for bladder distention the bladder is palpated or scanned at intervals to determine whether urinary retention is present, because a full bladder may be an overlooked cause of overflow incontinence. If urine retention: insert indwelling catheter, as ordered Accurate I&O If Catheter is in place, monitor for S&S of infection e.g., fever and cloudy urine, the area around the urethral orifice is inspected for drainage. Bladder training protocol (when you have a foley the patient has no sense of full bladder and lose bladder tone, train the bladder by clamping the foley for 30 minutes at a time so the patient gets full bladder sensation) The incontinent patient is monitored frequently for skin irritation and skin breakdown. Appropriate skin care is implemented to prevent these complications NSG: Promote bowel function

Auscultate ABD (abdomen) for bowel sounds Palpate ABD for distention, tenderness &/or mass Institute a regular pattern (promote walking for peristalsis, normal daily schedule) Provide privacy Presence of diarrhea - infection (antibiotics kill the normal flora leading to infection), ABTs (antibiotics), and
hyperosmolar fluids (osmotic pressure the pressure exerted on a differentially permeable membrane by a solution containing one or more solutes that cannot penetrate the membrane, which is permeable only by the solvent surrounding it. Prevent Fecal impaction increase fiber intake to prevent Prevent Constipation: (due to lack of activity & dietary fiber) Fiber, stool softener, and enemas ,as ordered NSG: Provide safety

Side rails up (x2 or X4) Padded side rails Call light within easy reach Bed in the lowest position Keep belongings within easy reach Keep room clutter free Provide privacy Explain every procedure to the pt
References: Bare. B. & Smeltzer. S. (2004). Altered level of consciousness. Textbook of Medical-Surgical Nursing. 18501856

Med-Surg Neurological System Cerebrovascular Disease Two things to remember: Ischemic no blood supply to brain due to blockage therefore the tissue dies / able to reperfuse the area using anticoagulants Hemorrhagic bleeding into the brain (too much blood) / increased intercranial pressure due to edema / takes longer for recuperartion CVA

Leading cause of serious, long term disabilities in USA Divided into 2 major categories:
Ischemic Hemorrhagic
Ischemic stroke

Vascular occlusion and significant hypo-perfusion occur (due to thrombosis) 85% of CVA cases Sudden loss of function resulting from disruption of the blood supply to a part of the brain. 8% result in death within 30 days
Types of ischemic attacks

Large artery Thrombotic stroke-caused by atherosclerosis plaques of large vessels of the brain. Thrombus formation and occlusion at the site of the atherosclerosis result in ischemia and infarction (a localized area of necrosis in a tissue resulting from anoxia) (deprivation of blood supply) Small artery Thrombotic stroke most common type of ischemic stroke.
with valvular heart disease and thrombi in the left ventricle.

Cardiogenic emboli - R/T cardiac dysrhythmias, usually atrial fibrillation, embolic strokes can also be associated Cryptogenic - No known cause Other causes strokes from other causes such as illicit drug use, coagulopathies, migraine, and spontaneous Watch for this is the worst headache of my life! this could definitely be ruptured anurism
CVA: Hemorrhagic

Affects one or more vessels, also called lacunar strokes because infarcted (a localized area of necrosis in a tissue resulting from anoxia) brain tissue disintegrates creating a cavity

dissection of the carotid or vertebral arteries

Account for 15% to 20% of cerebrovascular disorders and are primarily caused by intracranial or subarachnoid
hemorrhage

Extravasation of blood into the brain, ventricles, or subrachnoid space. Intracranial or subrachnoid hemorrhage. More severe with longer recovery. Causes: Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for 80% of
hemorrhagic strokes chiefly by uncontrolled hypertension.

Subarachnoid hemorrhage results from a ruptured intracranial aneurysm (a weakening in the arterial wall) in about half the cases. Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVMs), intracranial aneurysms, intracranial neoplasms, or certain medications.

Intracerebral hemorrhage in the elderly is cerebral amyloid angiopathy, which involves damage cause by the deposit of beta-amyloid protein in the small and medium-sized blood vessels of the brain.

AVM (arteriovenous malformation, birth defect) Anticoagulants (toxicity) Amphetamines, cocaine, crack (vasoconstriction and rupture)
CVA: Pathophysiology Ischemic Blood flow obstruction - due to thrombosis resulting in deprivation of blood supply Ischemic cascade Begins when cerebral blood flow decreases to less than 25 mL per 100 g per minute. At this point, neurons are no longer able to maintain aerobic respiration. The mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in the pH level. This switch to the less efficient anaerobic respiration also renders the neuron incapable of producing sufficient quantities of ATP to fuel the depolarization processes. The membrane pumps that maintain electrolyte balances begin to fail, and the cells cease to function. Each step in the ischemic cascade represents an opportunity for intervention to limit the extent of secondary brain damage caused by a stroke. Penumbra region - (saveable region) Early in the ischemic cascade, an area of low cerebral blood flow referred to as the penumbra region, exists around the area of infarction. The penumbra region is eschemic brain tissue that may be salvaged with timely intervention. The ischemic cascade threatens cells in the penumbra because membrane depolarization of the cell wall leads to an increase in intracellular calcium and the release of glutamate. The influx of calcium and the release of glutamate, if continued, activate a number of damaging pathways that result in the destruction of the cell membrane, the release of more calcium and glutamate, vasoconstriction, and the generation of free radicals. These processes enlarge the area of infarction into the penumbra, extending the stroke. TIA (transient ischemic attack) same as stroke but only lasts 10 -30 minutes CVA: Pathophysiology Hemorrhagic

Symptoms are produced when a primary hemorrhage, aneurysm, or AVM presses on nearby cranial nerves or brain tissue or, more dramatically, when an aneurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space) Normal brain metabolism is disrupted by the brains: Being exposed to blood Increased ICP by sudden bleeding into the brain (entry of blood into the subarachnoid space, which Secondary ischemia of brain tissue is caused by reduced perfusion and vasospasms that frequently
accompany subarachnoid hemorrhage CVA: Risk factors Non-modifiable (there is nothing you can do about it) compresses and injures brain tissue)

Age >65 years Male > women Blacks higher incidence (less medical care as well)
Modifiable (preventable)

HTN (80%) Diabetes High cholesterol Atherosclerosis Obesity

Smoking
(P. 1892 chart 62-2)
CVA: Risk factors

Phenylpropanolamine:

Chemical substance found in appetite suppressant drugs and in cold & cough agents related to the incidence of hemorrhagic strokes.
CVA: Diagnostic tools Plain CT scan of the brain (ischemic vs. hemorrhagic) (without contrast) any Pt with suspected stroke should undergo a CT scan to determine the type of stroke, the size and location of the hematoma, and the presence or absence of ventricular blood and hydrocephalus (blood in the subarachnoid space or ventricles impedes the circulation of CSF. This test and the cerebral angiography provide information about the affected arteries, veins, adjoining vessels, and vascular branches. 12 lead EKG: cardiac arrhythmias (study of the electrical conduction of the heart) Carotid U/S: stenosis (an abnormal condition characterized by the constriction or narrowing of an opening or passageway in a body structure) & atherosclerosis (a common disorder characterized by yellowish plaques of cholesterol, other lipids, and cellular debris in the inner layers of the walls of arteries. MRI Magnetic Resonance Imagery is used to evaluate patients with head injury when a more accurate picture of anatomic nature of the injury is warranted and when the Pt is stable enough to undergo this longer diagnostic procedure. MRA the use of special MR imaging pulses to visualize the vascular sysem and identify regions of non-flowing blood. It may be performed with or without contrast. Cerebral angiography identifies supratentorial, extracerebral, and intracerebral hematomas and cerebral contusions. Lateral and anteroposterior views of the skull are obtained. Carotid angiography identify abnormalities or blockages pertaining to the arteries that supply the head and neck Toxicology screen When diagnosing a hemorrhagic stroke in a patient younger than 40 years of age, some clinicians obtain a toxicology screen for illicit drug use. Lumbar puncture is performed if there is no evidence of increased ICP, the CT is negative, and subarachnoid hemorrhage must be confirmed. Note: Lumbar puncture in the presence of increased ICP could result in brain stem herniation or rebleeding. Diagnostic tools Initial nursing assessment

Respiratory status and airway patency Cardiovascular status ID gross Neurologic deficits: Altered LOC Sluggish papillary reaction Motor and sensory dysfunction Cranial nerve deficits (extraocular eye movements, facial droop, presence of ptosis) Speech difficulties and visual disturbance Headache and nuchal rigidity or other neurologic deficits

Respiratory failure Pneumonia Pressure ulcers Aspiration Venous stasis Musculoskeletal deterioration Disturbed GI function

CVA: Complications

CVA: Complications Hemorrhagic

Acute hydrocephalus: accumulation of fluid in the brain Cerebral hypoxia: lack of oxygen to the brain Vasospasm: spasm in a blood vessel (narrowing of the lumen of the involved cranial blood vessel)
Hemorrhagic complications Management

Cerebral hypoxia:
1. 2. 3. 4.

Administer supplemental O2 Maintain H&H at acceptable levels Hydration to blood viscosity and improve cerebral blood flow Seizure Tx, prophylaxis

Vasospasm:
1. 2. 3. 4.

R/T amount of blood in the subarachnoid cisterns and cerebral fissures Causes vascular resistance, brain ischemia, and infraction. Caused by influx of calcium into the cells. Administration of Ca channel blockers IV, and fluid expanders

Acute hydrocephalus: 1. Management of ICP with Mannitol 2. CSF drainage by lumbar puncture or ventricular catheter drainage Systemic hypertension
1. Antihypertensive meds (avoid sudden drop pf BP to prevent brain tissue ischemia) 2. Administration of stool softeners to avoid straining

Craniotomy any surgical opening into the skull, performed to relieve intracranial pressure, to control bleeding, or
to remove a tumor

Worst headache of my life Arteriovenous Malformations (AVM) is caused by an abnormality in embryonal development that leads to a tangle
of arteries and veins in the brain that lacks a capillary bed. The absence of a capillary bed leads to dilation of the arteries and veins and eventual rupture. AVM is a common cause of hemorrhagic stroke in young people

CVA: S&S Hemorrhagic

Rupture of an aneurysm or AVM often produces a loss of consciousness for a variable period of time Nuchal rigidity (pain and rigidity in the back of the neck) and back pain due to meningeal irritability. Visual disturbances (visual loss, diplopia [double vision caused by defective function of the extraocular muscles or
a disorder of the nerves that innervate the muscles], ptosis [one or both eyelids droops because of an acquired weakness of the levator] CVA: Ischemic & Hemorrhage S&S

Neurologic deficits depends on the affected region of the brain Chief complaint:

Numbness &/or weakness of face, arm, or leg, especially on one side of the body Confusion or change in mental status Changes of LOC, dizziness, headache Aphasia -trouble speaking or understanding speech Visual disturbances Ambulatory difficulties difficulty walking, dizziness, or loss of balance or coordination

CVA: Ischemic S&S Motor loss

Lesion of the upper motor neurons results in lost of voluntary control over motor movements. 1st flaccid paralysis and loss/decreased deep tendon reflexes Hemiplegia - paralysis of one side of body caused by a lesion (stroke) of the opposite side of the brain (most common dysfunction) Hemiparesis - weakness of one side of the body Spasticity - Abnormal increase in muscle tone, 48hrs after when deep tendon reflexes re-appear Ataxia - An impaired ability to coordinate movement, an unsteady gait. Apraxia - inability to perform a previously learned action, as may be seen when a patient makes verbal substitutions for desired syllables or words. CVA: S&S Communication loss Stroke is the most common cause of aphasia

Dysarthria difficulty in speaking, caused by paralysis of the muscles responsible for producing speech Dysphasia - impaired speech Aphasia - loss of speech (expressive, receptive, global) Apraxia - inability to perform a previously learned action, as may be seen when a patient makes verbal
substitutions for desired syllables or words. CVA:S&S Ischemic & Hemorrhage Stroke Perceptual disturbance: Perception is the ability to interpret sensation Homonymous Hemianopsia - loss of the visual field (visual perceptual dysfunction) which may occur from stroke and may be temporary or permanent. The affected side of vision corresponds to the paralyzed side of the body. Sensory loss: The sensory loss from stroke may take the form of slight impairment of touch, or it may be severe, with loss of proprioception as well as difficulty in interpreting visual, tactile, and auditory stimuli. Propioception - ability to perceive the position and motion of body parts. Difficult interpretation of visual, tactile, and auditory stimuli Agnosias are deficits in the ability to recognize previously familiar objects perceived by one or more of the senses Paresthesia any subjective sensation, experienced as numbness, tingling, or a pins and needles feeling. CVA: S&S Ischemic & Hemorrhage Stroke Cognitive impairment Frontal lobe: (impaired intellectual function, memory & learning)

Memory loss Decreased attention span Impaired ability to concentrate Altered judgment
CVA:S&S Ischemic & Hemorrhage Stroke Psychological effect:

Emotional lability (mood swings) Hostility Frustration Resentment Lack of cooperation Depression

TIA: Medical management Carotid Endarterectomy

Peripheral vascular procedure. Removal of atherosclerotic plaque or thrombus from the carotid artery (surgical excision of stheromatous
Brain Aneurysm

segments of the endothelium and tunica media of the carotid artery, leaving a smooth tissue lining and facilitating blood flow through the vessel. Surgery is done to prevent stroke)

Stroke Animation CVA: Medical management ischemic Thrombolytic therapy

Dx. Made within 3 hrs of onset of symptoms. Stimulates fibrinolysis of the atherosclerotic plaque. Dissolves blood clot that blocks blood flow to the affected area of the brain. TPA (Tissue Plasminogen activator) ( no anticoagulants for 24hrs), follow protocol for contraindications.
CVA: Medical management ischemic Anticoagulant therapy

Heparin and low-molecular weight heparin (Lovenox, Agrastat, etc) Continuous homodynamic monitoring Maintain BP within set parameter to avoid further bleeding or ischemic damage. Neurologic assessment Patent airway and respiratory support with supplemental O2 administration.
CVA: NSG care and goals CVA: Medical management

Discharge planning and rehab begins the admission day. Improve mobility Avoid should dislocation and pain Relief sensory deprivation Improve self care Continence of Bowel & Bladder

Maintain skin integrity Absence of complications Restore family function

CVA: Nursing management

Acute phase may last for 1-3 days. Assessment:

LOC, (baseline and monitor for changes) Sensory-Motor (baseline and monitor for changes) Respiratory status Homodynamic status (report any abnormal BP levels) Presence of bleeding Recent surgeries (within the last 6mo) Recent head trauma/ falls TPA Presence of S&S of GI bleed (Melena)

CVA: NSG interventions

Turn and reposition Q2hrs (15-30 min ad-lib, prone position aids prevention of knee, hip, shoulder contractures, aids in the removal of
bronchial secretions) OOB, ASAP Assist with ambulation PROM 4-5xday to maintain joint mobility Prevention of shoulder pain Enhance self care

CVA: NSG interventions Dysphagia Monitor pt for cough, food dribbling or pooling at one side of the mouth, food retained for long periods, and nasal regurgitation.(also Tears) Consult with speech pathologist Instruct pt to tuck the chin toward the chest as he swallows Thickened fluids (avoid thin liquids) Complications: Aspiration, dehydration, and malnutrition. CVA: NSG interventions Aphasia

Brocas area: Comprehension and formulation of language Right sided paralysis- speech disorders vs. the left sided one. Supportive role
P. 1900 chart 62-5
CVA: NSG interventions Implementing aneurysm precautions: Provide quiet, non-stressful environment Restrict visitors Elevate HOB (semi fowler's position) Dim lighting of the room Avoid coffee and tea caffeine will cause increased blood pressure which could burst an existing aneurism. Caffeine stimulates the CNS.

Prevent any exertion by assisting the patient with bathing, and dressing including toileting and the Valsalva
maneuver. No enemas, however stool softeners are allowed No TV, Radio, or reading CVA: NSG interventions Monitor for S&S of vasospasm:

Assess for HA (headache), decreased level of responsiveness Altered LOC responsiveness (confusion, lethargy, disorientation) A new focal neurological deficit (aphasia, hemiparesis, hemiplegia) Avoid injury and maintain tissue perfusion (airway patency) Medication therapy - phenytoin (Dilantin)
CVA: NSG interventions Implement seizure precautions:

Maintain skin integrity B&B training Assist family with emotional support and referring to community resources.
CVA: NSG Interventions Team work

Med-Surg Neurological System Seizure Disorders Seizures

Episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) resulting from
sudden excessive discharge from cerebral neurons.

Epilepsy: chronic unprovoked recurrent seizures Aura: Peculiar sensation preceding the onset of a generalized seizure that may take the form of gustatory, visual,
or auditory experience. Funny feeling

Prodromal pertaining to early symptoms that may mark the onset of a disease.
hrs to days before a seizure. Seizures: Classifications Seizures: Etiology

Early manifestation that occurs

known and the epilepsy is a symptom of another underlying condition, such as a brain tumor)

Seizure: A symptom of an underlying disorder Epilepsy: Cause is unknown for most of them. Can be Primary (idiopathic) or secondary (when the cause is Occurs in areas with lesions (stroke)
Seizures: Etiology

Metabolic and toxic conditions (renal failure, hyponatremia, hypocalcemia, hypoclycemia, pesticides) Congenital malformations Genetic predisposition Perinatal injury Postnatal trauma Brain tumor, infection Vascular disease (hypoxemia) Drug or/and alcohol abuse Alcohol withdrawal Fever (childhood) Allergies Head trauma
Seizures: Triggering Factors

Stress Sleep deprivation Menses Drug and alcohol ingestion or withdrawal Change of seizure meds Missed meds
Seizures: diagnostic tests

cerebral degenerative changes.

Metabolic panel Drug toxicology MRI is used to detect structural lesions such as focal abnormalities, cerebrovascular abnormalities, and SPECT (Brain CT, Single Proton Emission Computed Tomography) EEG (electroencephalogram) helps to classify the type of seizure

Seizures: NSG Interventions

Seizure precaution:

Keep bed to the lowest position 2 to 3 side rails padded & up Call light within easy reach Clutter free environment Protect the patients head

Post-seizure:

Place pt on the side lying position to facilitate drainage of oral secretions (prevent aspirations). Maintain a patent airway The patient, on awakening, should be reoriented to the environment If the patient becomes agitated after a seizure, use calm persuasion and gentle restraint The patient may want to sleep for a while after the seizure so thats ok.

Seizures: NSG Interventions (Epilepsy in woman)

Bone loss R/T long term use of anti-seizure Meds Assess for low bone mass and osteoporosis Risk for long bone fractures
Seizures: NSG Teaching

Advise about state driving regulations Advice about swimming alone or operating dangerous equipment Patient should not to discontinue meds abruptly Wear medic alert bracelet R/T birth defects The risk for congenital fetal anomaly is two to three times higher in mothers with epilepsy.

The effects of maternal seizures, antiseizure medications, and genetic predisposition are all mechanisms that contribute to possible malformation. antiseizure medications.

Valproic acid alters the effectiveness of birth control pills. The effectiveness of contraceptives is decreased by
Seizures: Status Epilepticus (acute prolonged seizure activity)

A series of generalized seizures that occur without full recovery of consciousness between attacks and lasting
over 30 minutes

Medical Emergency Cumulative effects Vigorous muscular contractions impose a heavy metabolic demand and can interfere with Precipitating factors withdrawal of antiseizure medication, fever, and concurrent infection
Seizures: Status Epilepticus TX: the goals of treatment are to stop the seizures as quickly as possible, to ensure adequate cerebral oxygenation, and to maintain the patient in a seizure-free state.

respirations. Some respiratory arrest at the height of each seizure produces venous congestion and hypoxia of the brain. Repeated episodes of cerebral anoxia and edema may lead to irreversible and fetal brain damage.

Valium (intravenous diazepam) Ativan (lorazapam) Cerebyx - (fosphenytoin) , Dilantin

O2 supplemental therapyMed-Surg Neurological System

Med-Surg Neurological System Brain tumors Description

Primary brain tumors:

Abnormal cells growth from tissue within the cranium Normally grows as spherical mass, but it also can grow diffusely and infiltrate tissue. Named by origin (gliomas, meningiomas, acoustic neuroma, etc.) May be malignant or benign

Secondary brain tumors:

Etiology

Metastasize from the lung, breast, kidney, or GI tract.

Unknown Gliomas: 46% of all CNS tumors (Glial tissue) Grades 1-4. 3&4 more invasive, faster growing and with poor prognosis. Meningiomas: rarely malignant, cure with complete excision.
incidence

Gliomas: Most common in men Meningiomas & pituitary adenomas: most common in women Meningiomas increased with age Primary cerebral lymphomas R/T AIDS.
Diagnostic tools

CT scan MRI Angiography Hormone profile Neurological exam (focal cranial nerve or motor deficits)
S&S Headaches Dull and aching Increase intensity over wks nd 2 to hydrocephalus or pressure over sensitive structures New onset of seizures in adulthood Hx of nausea & vomiting with headaches Neurological S&S depending on the affected area of the brain. Management

Neurosurgical referral for excision Oncology referral Radiation & chemotherapy Dexamethasone for cerebral edema Anticonvulsant therapy
NSG

Self care deficit R/T impairment of motor/sensory functions.

Keep the patient as independent as possible Assist patient with self care

Referral for home care Develop an individualized exercise program. NSG

Imbalance nutrition less than body requirement R/T cachexia

Reposition patient for comfort during meals Provide attractive trays and food plates to enhance appetite Provide enough fluids Increased opportunities for socialization during meals Referral to dietitian

NSG

Anxiety R/T fear of dying

Spend time with patient to allow him/her to express fears and concerns Referral to spiritual advisors, social workers, and mental health professional. Referral to support groups and hospice care as needed

Med-Surg Neurological System Brain surgery Pre-op care Diagnostic studies include Ct scan, MRI, and cerebral angiography, etc. Meds: anti-seizure (Dilantin most common) Corticosteroids (Decadron most common) Hyper osmotic agent: Mannitol (to prevent & TX ICP Diuretic (Lasix) Pre-op Nursing Care Obtain a baseline (LOC, neuro-deficits, V/S) Obtain consent Prepare medical record with MD orders, labs, radiology results, consent, & nurses admission notes Keep pt NPO, as ordered Types of brain surgeries Craniotomy: Opening of the skull. Bony flap can be repositioned after surgery. Transsphenoidal: Approach through the mouth and nasal sinuses to the pituitary gland. Burr holes Circular openings made in the skull Cranietomy: Excision of a portion of the skull Cranioplasty: Repair of a cranial deflect using a plastic or metal plate. Post-op management Reduce cerebral edema (Mannitol and Decadron) Relieve pain (Acetaminophen, codeine, and Morphine sulfate) Prevention and treatment of seizures (Dilantin, and diazepam)

Monitor ICP (Monitor draining system)

Complications:

Increase ICP Infections Seizures Neurological deterioration (nerve damage) Bleeding Fluid and electrolyte disturbances
Post-op management Monitor ventricular drainage system (JPs) Vital signs (Maintain temp >99.6) Anti-seizure meds prescribed such as Dilantin and valium Meds to reduce cerebral edema such as mannitol and Decadron Post-op management NSG Assess Resp. function: (small degree of hypoxia increases cerebral ischemia) Resp. rate and pattern ABGs Assess for hyperthermia (2nd to hypothalamus damage0 Neurologic assessment (a change in LOC or response to stimuli is the 1st sign of increased ICP) Assess for seizure activity (record and report) NSG: Post-op management Maintain cerebral tissue perfusion

Assess Vital signs and neurological status every 15 min Avoid extreme head rotation (raises ICP) Monitor Resp. Rate, depth, and rhythm Provide O2 as ordered Place pt. In fowlers position (according to surgeons choice) Change patients position every 2 hrs Provide skin care frequently
NSG: Post-op management Regulating Temperature Monitor temp (V/S) Fever Remove blankets, apply ice bags to axilla and groin areas Use hypothermia blanket Give prescribed meds to reduce fever Hypothermia Re-warming should occur slowly to prevent shivering (increases O2 demand) NSG: Post-op management Improve gas exchange Assess for signs of Pulmonary infections temp, pulse, changes in Resp. Auscultate lungs ( decreased breath sounds/adventitious sounds) Re-position the pt every 2 hrs (mobilization of pulmonary secretions and prevent stasis) Teach pt to deep breathing & coughing, and the use of incentive spirometry Suction of oropharynx and trachea O2 humidifier NSG: Post-op management Preventing infection Monitor incision site for redness, tenderness, bulging, separation, and foul odor. Use of aseptic technique when handling dressing Monitor for S&S of infections NSG: Post-op management Seizure activity Keep bed to its lower position Side rails up (padded) Call light within easy reach Keep room clutter free O2 available with suction tubing Never force the patient into a position Never attempt to insert anything into the pts mouth Document eventMed-Surg Lecture Notes

Med-Surg Neurological System Diabetes Mellitus Objectives: MDC, Nursing Curriculum, P 110. Outline: Diabetes Mellitus: Etiology characterized by increased levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both. The cells stop responding to insulin or the pancreas may stop producing insulin entirely. This hyperglycemia can result in acute metabolic complications such as DKA and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Pathophysiology(type1 & type2) Insulin a hormone secreted by the beta cells of the islets of langerhans of the pancreas, (that is necessary for metabolism of carbohydrates, proteins, and fats, controlling the level of glucose in the blood. Classifications of Diabetes Risk factors Incidence S&S Diagnostic findings Complications Management Education Nutrition Exercise Pharmacology DKA HHNKS Foot care Nursing diagnosis Diabetes Mellitus Definition: Metabolic disease Hyperglycemia Defects in insulin secretion, insulin action, or both. Insulin Controls the level of glucose in the blood by regulating the production and storage of glucose. Inhibits glycogenolysis (breakdown of stored gulcose) Inhibits gluconeogenesis (production of new glucose from aminoacids) Classification of Diabetes Type 1 Diabetes Type 2 Diabetes Gestational Diabetes Mellitus Diabetes Mellitus related to other conditions Impaired glucose tolerance test (140-200 mg/dL) Impaired fasting glucose test (110-126 mg/dL) Risk Factors for Diabetes Family history of diabetes Low high-density lipoprotein (HDL) cholesterol High triglycerides High blood pressure History of gestational diabetes High-risk racial or ethnic background (African American, American Indian, Asian American, Pacific Islander, or Hispanic American/Latino). Diabetes
20.8 million Americans have diabetes, although 6.2 million of those are undiagnosed. Each day, approximately 2,200 people are diagnosed with diabetes.

Type 2 diabetes accounts for up to 95 percent of all diabetes cases, affecting 8 percent of the population age 20 and older. The prevalence of type 2 diabetes has tripled in the last 30 years, much of it due to an upsurge in obesity. Diabetes afflicts 120 million people worldwide, and the World Health Organization estimates that number to skyrocket to 300 million by 2025.

Mortality Diabetes is the 5th leading cause of death in America. Overall, the risk of death for people with diabetes is about 2 times that for people without diabetes.
Type 1 Diabetes Acute onset, usually before 30 5-10 % of cases Destruction of beta cell Genetic predisposition, infections (virus), and autoimmune response Production of little or no insulin Insulin injections requirement Type 1 Diabetes Pathophysiology Decreased or no production of insulin Unchecked glucose production by the liver Glucogenolysis & gluconeogenesis Increased renal threshold for glucose (180-200 mg/dL). Glucosuria Osmotic diuresis (loss of fluid and electrolytes with glucosuria) Increased production of ketones (fat breakdown) Type 2 Diabetes Most common in obese people over 30 May go undetected for many years Can be prevented or delayed with weight reduction and exercise 90-95% of cases Controlled with oral agents, insulin, or a combination of both Type 2 Diabetes Pathophysiology Insulin resistance Less effective insulin to stimulate glucose uptake by the tissue Less effective insulin to regulate glucose release from the liver Impaired insulin secretion Beta cells cannot keep up with the production of ineffective insulin, glucose levels rises Gestational Diabetes Any degree of glucose intolerance with its onset during pregnancy Secretion of placental hormones causes insulin resistance Occurs in up to 14% of pregnancies After delivery blood sugar returns to normal, but with a risk of type 2 diabetes later in life. Diabetes S&S Three Ps Polyuria, polydipsia, and polyphagia Fatigue and weakness Sudden vision changes Tingling and numbness in the hands/feet Dry skin Skin lesions that take long to heal Recurrent infections

Diagnostic findings Criteria to Dx Diabetes Fasting plasma glucose > 126 mg/dL Random plasma glucose > 200mg/dL on more than one occasion Symptoms of diabetes Diagnostic tests Hemoglobin A1C 4 6 average glucose levels over lifetime of rbcs 120 days (Glycosylated hemoglobin) Long term measure of glucose control Glucose attaching to the hemoglobin for the life of the RBC (5-7 % good control) Urinalysis for protein, glucose, and ketones BUN, Creat, urinalysis Serum cholesterol and lipid profile EKG and chest X-Ray for pulmonary and coronary pathology Complications Type 1 Diabetes DKA Type 2 Diabetes HHNS a metabolic disorder of type 2 diabetes resulting from a relative insulin deficiency initiated by an intercurrent illness that raises the demand for insulin; associated with polyuria and severe dehydration. Complications (target organ damage) Retinopathy (eyes) Peripheral neuropathy Nephropathy and renal failure Cardiovascular disease with lipid abnormalities Erectile dysfunction Infections Foot and skin ulcerations
Preventable

Prevention of Diabetes complications kidney failure: 50% (with better control of blood pressure and blood glucose levels) up to 90% (with proper screening and care)

Blindness:

Amputation:

up to 85% (with implementation of foot care programs that include regular examinations and patient education) due to heart disease or stroke: up to 30% (with improved control of blood pressure, blood glucose and lipid levels)

Death

Heart disease and stroke: up to 50% (with improved control of blood pressure and cholesterol and lipid levels) Nerve

disease: 40% (with a 1% reduction in hemoglobin A1c test)

Management Nutritional Exercise Monitoring

Pharmacologic therapy Education

Nutritional management Primary treatment for type 2 is weight reduction Priority for a young patient with type1 is to meet the caloric requirements to enhance growth and development Nutrition 3 meals with 3 snacks per day Avoid simple sugars, and refined CHO Caloric intake as follow: 30% protein, 20%fats, 50% CHO Cholesterol 300 mg/day Fiber 25 g/1000 calories Food Pyramid

Diabetes Dietary intake for small-frame woman Choose these servings from each food groups to have 1,200 to 1,600 calories a day: 6 starches 2 milk and yogurt 3 vegetables 2 meat or meat substitute 2 fruit up to 3 fats Diabetes: Exercise Lower blood sugar levels by: glucose uptake by muscles Improves insulin utilization Snack before or might suffer a hypoglycemic event Snack should be low carb and sugar free Controls lipids levels by: high density lipoprotein total cholesterol & triglycerides levels Diabetes: Exercise Teaching Eat a snack before and after exercising to prevent hypoglycemia Closely monitor blood sugar levels Use proper foot wear Inspect feet daily after exercise Avoid exercise during periods of uncontrolled sugar levels Diabetes Education Eat about the same amount of food each day. Eat your meals and snacks at about the same times each day. Do not skip meals or snacks. Take your medicines at the same times each day. Exercise at about the same times each day. Diabetes ABCs A1C Blood pressure monitoring Cholesterol

The target LDL cholesterol for most people with diabetes is less than 100 Diabetes Pharmacologic therapy Insulin Oral anti-diabetic agents Diabetes Management
Oral antidiabetic agents (Cannot use during pregnancy) (p. 1170) (only insulin)

Sulfonylureas Biguanides Alpha glucosides inhibitors Thiazolidinediones Meglitinides

Oral anti-diabetic agents Sulfonylureas (stimulates pancreas to release insulin) improves insulin action Biguanides (facilitates insulin action on peripheral receptor sites) Alpha-glucosidase inhibitors (delays absorption of glucose in the GI system) Thiazolidinediones (enhance insulin action, for pts with insulin therapy) Meglitinides (stimulates insulin release, has fast action with short duration) Diabetes Insulin therapy: Human insulin has a shorter duration of action that animal derived insulin. Humalog and Novolog produce a more rapid effect than Regular insulin. (onset 10-15min) (p. 1164) Insulin dose is based on the serum glucose level Give it Subcutaneous only. If given IM then it takes longer to react. Insulin time-course Agent Onset Peak Duration

Complications of Insulin Therapy Local allergic reaction Systemic allergic reaction (rare) Insulin lipodystrophy (loss of subcutaneous fat) Insulin resistance Morning hyperglycemia (dawn phenomenon & somogyi effect) Inhale insulin Approved January 27th, 2006 by the FDA. Treatment of type 1 and type 2 diabetes It is the first new insulin delivery option since the discovery of insulin in the 1920s EXUBERA Powder form of medication inhale through the mouth. Has a peak level from 30-90 minutes. SE: hypoglycemia Cough SOB sore throat dry mouth EXUBERA (new inhalant insulin) Contraindications: Smoking, recently stop smoking (within the last 6 months). Patients with asthma, bronchitis, or emphysema.

 Baseline tests for lung function are recommended after the first 6 months of treatment and every year thereafter, even if there are no pulmonary symptoms. Peak of 30 to 90 minutes
DKA Caused by NO insulin production (or small amounts) Hyperglycemia Dehydration with electrolyte loss Acidosis Diabetes DKA Markedly inadequate amounts of insulin. (without insulin there is no glucose uptake by the cells therefore the liver produces more glucose) Excessive production of ketones bodies (p. 1180) insulin= lipolysis= free fatty acids + glycerol Fatty acids convert to ketones DKA No insulin glucose uptake release of fatty acids Gluconeogenesis & Ketogenesis (Extremely elevated blood sugar levels) Metabolic acidosis DKA S&S Hyperglycemia = Polyuria & dehydration Deficits of Na, PO4, Mg levels Marked hypokalemia (serum level may appear normal due to hypovolemia and shift from the cell due to metabolic acidosis) Kussmaul Resp. (to compensate the metabolic acidosis) CNS depression Nausea, polyurea, thirst ketonuria DKA Treatment Continuous administration of insulin IV Fluids and electrolytes replacement HHNKS (Hyperglycemic hyperosmolar Nonketotic Syndrome) Insulin resistance (poor quality) Hyperglycemia & hyperosmolarity Altered level consciousness Minimal/absent ketosis Electrolyte imbalance (Na) Dehydration HHNKS S&S Profound dehydration Hypotension & tachycardia AMS (from sensory deficits to seizures)

Mortality rate is 10-40 %

Diabetes: Patient Education Recognition of S&S Self-glucose monitoring Nutritional counseling follow the American Diabetes Association (ADA) guidelines Avoid alcohol and smoking (inhibits the release or breakdown of glucose or sugar from the liver) Exercise, reduces insulin resistance Use of proper fitting shoes at all times Medi-alert ID bracelet or necklace Annual influenza vaccine (every year and pneumococcal vaccine every 5 years Diabetes Geriatric considerations: Elderly pts may not identify S&S of hypo/hyperglycemia If renal insufficiency: oral hypoglycemic agents take longer to be excreted. Deficiency nutritional intake R/T decreased appetite, poor dentition, and/or financial limitations. (p.1179) Foot Care (p.1194) General guidelines: (Assess your feet regularly) (use of mirror to inspect the bottom of the feet) Careful daily assessment of the feet Assess for redness, blisters, fissures, calluses, ulcerations, skin temp changes, and new deformities Assess interior surface of the shoes Assessment of feet during every health care visit. Once a year podiatrist evaluation Neuropathy: Monofilament study. Proper cleaning, drying, and foot lubrication. Avoid excess moisture between toes. Wearing closed-toe shoes that feet well. Trimming toenails straight across, mainly by a podiatrist. Avoid:Walking barefoot, open-toed shoes, soaking the feet, shaving calluses, and using heating pads. Blood glucose control. Nursing Diagnosis Imbalanced nutrition Risk for impaired skin integrity Deficient knowledge about diabetes and self care Risk for infection

RESPIRATORY DISORDERS
Class notes: The % of the atmosphere is 21% atelectisis: lung collapse; there is not expansion of the lungs they collapse COPD has problem with air traveling When the hemoglobin decrease pt has problem with respirations and carrying of oxygen Treatment of carbon monoxide toxicity is administration of 100% of O2 People living at high altitudes have increased hemoglobin and when coming to the city they get short of breath, respirations problem. Increased metabolic rate you get tachycardia Person with fever administer O2 because O2 increase with increased metabolic rate Hyperventilate when anxious. CO2 is blown out and become alkaline. Respiratory alkalosis. Hypoventilation happens with overdose or sedation Cyanosis: bluish color on the thorax, lips The most reliable test is ABGs (to test for oxygen) Higher than 2 Liters administer humidifier CPT: tapping over the chest 50% of pneumonia is caused by viruses treat pneumonia with antibiotics before doing a sputum collection but it create a resistance. First you need to get sputum then treat it. 23% are prevented with a simple vaccine immobility: staying of the secretions at the lungs viral: low grade fever CO2 is a waste product Lungs are responsible for gas exchange Dyspnea: difficulty breathing Cough: assess the sputum (amount, odor, color, consistency) If the pt has a non productive cough do not administer spectorants Wheezing: the air is trying to pass through the inflammated alveoli Clubbing of the finger: COPD, years of hypoxia Hemoptysis: coughing blood Pt with hemoptysis needs to put in isolation. Contact: wounds, CDEF Airbone: TB Droplet: bacterial pneumonia, MRSA 6 ft from the pt bed you are not expose to the virus hemoptysis patient need to be in negative pressure room cyanosis: central bluish color, not just the finger nail beds treatment of pulmonary edema: administer diuretics (lasix)

250 ml in the lungs to put you in CHF pulmonary edema: profuse, frothy pink sputum infection: foul smelling sputum liquify the sputum to remove it wash the mouth with water before getting a sputum sample. Teach the patient to dispose sputum correctly Vancomysin used to treat MRSA Walking pneumonia very common in nurses Consolidation: black lungs COPD is irreversible. Happens through the years. Takes time to get to this point. Asthma is reversible because you are able to treat it but is always there Chronic bronchitis is like asthma Polycythemia: because there is impaired gas exchange and pt needs to produce more RBCs Steroids: to reduce inflammation (prednisome, solumetrol) Low flow oxygen in pts with COPD because they have an increased CO2 levels and more than 2 liters of O2 would make the pt stop breathing Emphysema: end of the lugs being exposed to contaminators Lungs remain inflated, dont recoil back and interfere with gas exchange. Has barrel chest. A lot of air tap in the lungs. Looks black No levels of oxygen. Increased CO2 in the lungs High levels of CO2 lungs not able to recoil back. The gas exchange is impaired. There is more blood flow to the lungs to bring O2 but CO2 goes to the arterial blood and the CO2 levels remain high in the blood. There is more pressure.

Pt learns to breath in low levels of O2 and high levels of CO2 You should administer low levels of O2 because if you give high levels of O2 pt stops breathing Kidneys try to compensate from acidosis retaining HCO3. has to be good kidneys. Body try to compensate by reataining HCO3. Emphysema mainly in patient in their 60s A lot of impaired activity tolerance Pt with short of breath loose weight Pt at the end of the stage barrel chest Low level of oxygen but high hemoglobin Risk factor #1 is smoking cigarettes. Emphysema get a lot of antibiotics profilactive because of the accumulation of secretions Antibiotics: put them at risk for superinfections Carboxyhemoglobin: is the combination of carbon monoxide with hemoglobing and is hard to break the bonds 25 time more harder Emphysema is an end stage condition. A lot of complications Rescue medications: albuterol

Corticosteriods: reduce inflammation Flu shot every year; munoccocal vaccine every year Bulluctony: one piece vs a big piece Administer low level of oxygen Nurses need to teach patients and encourage to stop smoking

OXYGEN THERAPY
Oxygen: the cardiac and respiratory systems supply the body with oxygen demands Oxygenation: 3 steps in the process of oxygenation Ventilation: is the process of moving air into and out of the lungs. A major muscle is the diaphragm, innervated by the phrenic nerve with exits the spinal cord at the 4th cervical vertebra. Any process that changes the bronchial diameter or width affects airway resistance and alters the rate of airflow for a given pressure gradient during respiration. Factors that determine the lungs compliance are the surface tension of the alveoli, and the connective tissue of the lungs. Compliance is determined by examining the volume pressure relationship in the lungs and the thorax. Increased compliance occurs if the lungs have lost their elasticity and the thorax is over distended. Low compliance if the lungs are stiff. Inspiration: the diaphragm and external intercostals muscles contract to create a negative pressure that increases the size of the thorax. It is an active process, stimulated by chemical receptors in the aorta Expiration: it is a passive process that depends on the elastic recoil properties of the lungs. Clients with COPD lose elastic recoil of the lungs and the thorax. Perfusion: Respiratory gases are exchange in the alveoli and the capillaries of the body tissues. (Blood flow to the lungs and tissue). Most oxygen is transported by hemoglobin in the form of oxyhemoglobin. The pulmonary circulation is considered a low pressure system because the systolic blood pressure in the pulmonary artery is 20 to 30 mm Hg and the diastolic pressure is 5 to 15 mm Hg. Perfusion also is influenced by alveolar pressure. Pulmonary artery pressure, gravity, and alveolar pressure determine the patterns of perfusion. Diffusion: it occurs at the alveolocapillary membrane where molecules move from areas of higher concentration to an area of lower concentration. Increased thickness of the membrane impedes diffusion because gases take longer to transfer across seen in pulmonary edema, infiltrates, and effusions, emphysema, pneumothorax, and lobectomy. Is the process by which oxygen and carbon dioxide are exchanged at the air blood interface. Oxygen Therapy - Factors affecting oxygenation Anemia: decrease O2 carrying capacity of blood. Toxic inhalants: reduces the amount of available hemoglobin to transport oxygen. Carbon monoxide is the most common toxic inhalants; this bond is 200 times greater than the one with oxygen. Airway obstruction High altitude: atmospheric O2 concentration is lower Fever: increase metabolic rate and tissue O2 demand

Decreased chest wall motion: prevents lowering of the diaphragm

Oxygen Therapy - Alteration in respiratory function Hyperventilation: excess ventilation more than required to eliminate the normal venous carbon dioxide commonly seen in anxiety, infections, drugs, or acid base imbalances. Fever: increases the metabolic rate and the production of CO2 Salicylate poisoning causes excessive stimulation of the respiratory center Amphetamines increase ventilation Acid base imbalance: the body tries to compensate for metabolic acidosis by producing a respiratory alkalosis COPD: inappropriate administration of excessive oxygen results in hypoventilation because this type of client has adjusted to high levels of carbon dioxide and their stimulus to breath is a low oxygen level. If excessive O2 is given the O2 requirement is satisfied and the stimulus to breath is negated. Hypoventilation: ventilation is inadequate to meet the bodys demand or to eliminate sufficient carbon dioxide commonly seen in atelectasis (collapse of the alveoli). Sign and symptoms of hypoventilation: mental status change dysrrhythmias cardiac arrest convulsion unconsciousness death

Hypoxia: low O2 concentration at the cellular level. Causes: low hemoglobin level, high altitudes, cyanine poisoning, pneumonia, shock and impaired circulation as in multiple ribs fractures. Can occur from either severe pulmonary disease or from extrapulmonary disease affecting gas exchange at the cellular level. The need for oxygen is assessed by ABGs analysis and pulse oximetry as well as by clinical evaluation. Sign and symptoms: Apprehension Restlessness inability to concentrate decrease level of consciousness dizziness behavioral changes The patient appears fatigue and agitated Tachycardia with tachypnea is also present.

Cyanosis: a late sign of hypoxia although is a not reliable measure of oxygen status. Peripheral cyanosis is often a result of vasoconstriction. Is a bluish coloring of the skin, is a very late indicator of hypoxia. The presence or absence of cyanosis is determined by the amount of unoxygenated hemoglobin in the blood. A patient with anemia rarely manifest cyanosis, and a patient with polycythemia may appear cyanotic may appear cyanotic.

Oxygen Therapy - Implementation: The airway is patent when the trachea, bronchi, and large airways are free from obstructions. Airway maintenance requires adequate hydration to prevent thick, tenacious secretions. Proper coughing removes secretions and keep the airway open. Implementation - Humidifier: adds H2O to the gas. It helps loosen and mobilize pulmonary secretions. Needed when O2 therapy >4 liters. Nebulizer: adds moisture or medication to the inspired air. It improves clearance of pulmonary secretions. Implementation - CPT (chest physiotherapy): is a group of therapies use in combination to mobilize pulmonary secretions. It includes postural drainage, chest percussion, and vibration. Percussion and vibration is needed for those clients who produce more than 30 ml of sputum per day. Oxygen Therapy - Oxygen supply Three types of O2: compressed, liquid, and concentrators. O2 concentration in the air with breath is about 21%. OXYGEN SUPPLY Device Nasal canula Face mask Venti mask Non-rebreather Flow rate 1 L-6L 5L-8L 2-14 L --------O2 concentration 24%-44% 40-60% 28-55% 100%

When the atmosphere is 21% and you give 1 liter you increase concentration. Respiratory system o o o o Medulla oblongata and the pons control inspiration and expiration O2 is required for oxidation of CHO, fats, and proteins Oxidation produces CO2 Respiratory system is responsible O2 and CO2 transport (gas exchange)

Respiratory system signs and symptoms o Dyspnea: difficult or labored breathing, breathlessness, shortness of breath. Is a symptom common to many pulmonary and cardiac disorders particularly when there is decreased lung compliance or increased airway ressitance. Sudden dyspnea in a healthy person may indicate pneumothorax, acute respiratory obstruction. In immobilized patients sudden dyspnea may denote pulmonary embolism. Orthopnea (inability to breathe easily except in an upright position) may be found in patients with heart disease and occasionally in patients with COPD. Placing the patient at rest with the head elevated and administering oxygen sometimes achieve relief of the symptom. o Cough: although cough is a reflex that protects the lungs form the accumulation of secretions or the inhalation of foreign bodies, it can also be a symptom of a number of disorders of the pulmonary system or it can be suppressed in other disorders. It results from the irritation of the mucous membranes anywhere in the respiratory tract. The stimulus that produces a cough may arise form an infectious process or from an air bone irritant such as smoke, smog, dust, or a gas. A dry, irritative cough is characteristic of an upper respiratory tract infection or viral origin. Coughing

at nighttime may herald the onset of left-sided heart failure or bronchial asthma. A cough in the morning with sputum production may indicate bronchitis. A persistent cough may affect a patients quality of life and may produce embarrassment, exhaustion, inability to sleep, and pain. Cough suppressants must be used with caution, because they may relieve the cough but do no address the cause of the cough. o Sputum production: a patient who coughs long enough almost invariably produces sputum. Violent coughing causes bronchial spasm, obstruction, and further irritation of the bronchi and may result in syncope (fainting). Bacterial infection: a profuse amount of purulent sputum thick and yellow, green, or rustcolored. Viral bronchitis: thin, mucoid sputum Chronic bronchitis: gradual increase of sputum over time Cancer: pink-tinged mucoid sputum Pulmonary edema: profuse, frothy, pink material, often welling up into the throat Infection: foul-smelling sputum and bad breath point to the presence of a lung abscess, bronchiectasis and infection caused by fusospirochetal or other anaerobic organisms. Relief measures: if the sputum is too thick for the patient to expectorate, is necessary to increase water content through adequate hydration and inhalation of aerosolized solutions. Smoking is contraindicated because it interferes with ciliary action, increases bronchial secretions causes inflammation. The nurse encourages adequate oral hygiene and wise selection of food. Also, encourage the patient and family to remove sputum cups, emesis basins and soiled tissues properly o Chest pain: chest pain associated with pulmonary conditions may be sharp, stabbing, and intermittent. Chest pain may occur with pneumonia, pulmonary embolism and pleurisy. The nurse assesses the quality, intensity, and radiation of pain and identifies and explores precipitating factors and their relationship to the patients position. Analgesic medications may be effective in relieving chest pain. o Wheezing: is often major finding in a patient with bronchocostriction or airway narrowing. Oral or inhalant bronchodilator medications reverse wheezing in most instances o Clubbing of the fingers: is a sing of lung disease that is found in patients with chronic hypoxic conditions, chronic lung infections, or malignancies of the lung. o Hemoptysis: expectoration of blood form the respiratory tract is a symptom of both pulmonary and cardiac disorders. Diagnostic evaluation to determine the cause includes several studies: chest xray, chest angiography, and bronchoscopy. o Cyanosis: a bluish coloring of the skin is a very late indication of hypoxia. The presence or absence of cyanosis is determined by the amount of unoxygenated hemoglobin in the blood. In the presence of a pulmonary condition, observing the color of the tongue and lips assesses central cyanosis. Peripheral cyanosis results from decreased blood flow to a certain area of body, as in vasoconstriction of the nail beds or earlobes from exposure to cold.

PNEUMONIA

Inflammation of the lung parenchyma caused by an infection Pneumonitis: inflammatory process in the lung tissue that may predispose or place pt at risk for microbial invasion. 7th leading cause of death in the United States, and in those over 65 years of age the 5th leading cause. Caused by various microorganisms including bacteria, mycobacteria, chamydiae, mycoplasma, fungi, parasites, and viruses.

Pneumonia classification: Community acquired pneumonia: (CAP) onset prior to hospitalization or within the first 48 hours of hospitalization. The causative agents for CAP are S. pneumoniae, H. influenzae, Lengionella, Pseudomonas aeruginosa. o Pneumonia caused by s. pneumoniae is the most common CAP in people younger than 60 years of age. Most prevalent in winter and spring. Lives in the upper respiratory tract. It may occur as a lobar or bronchopneumonic form in patients of any age and may follow a recent o mycoplasma pneumonia occurs most in children and young adults and is spread by person to person. o H. influenzae: affects elderly people and those with COPD, alcoholism, diabetes mellitus. Chest xray may reveal multibolar, patchy bronchopneumoniae or areas of consolidation (tissue that solidifies as a result of collapsed alveoli or pneumonia). Hospital acquired pneumonia: (HAP): onset 48 hours after admission. Also know as nosocomial pneumonia. Occurs when at least one of the three conditions exits: host defenses are impaired, and inoculum of organisms reaches the lower respiratory tract and overwhelms the hosts defenses. The common organism responsible for HAP include the pathogens E. coli, h. influenzae, serratia marcescens, p. aeruginosa, MRSA, s. pneumoniae. o Pseudomonal pneumonia: occurs in patients who are debilitated, those with altered mental status, and prolonged intubation o MRSA: highly virulent. Patients with MRSA are isolated in a private room, and contact precautions are used. o Pneumonias from E. coli, proteus, serratia are characterized by destruction of lung structure and alveolar walls, consolidation and bacteremia. Pneumonia in the immunocompromised host: occurs with use of corticosteroids or othter immunosuppressive agents, chemotherapy, nutritional depletion, use of broad spectrum antimicrobial agents, AIDS, genetic immune disorders. Patients with compromised immune system commonly develop pneumonia from organisms of low virulence. Can be caused by host seen in CAP, HAP (s. pneumoniae, s. aureus, h. influenza, p. aeruginosa, m. tuberculosis.) has a subtle onset, with progressive dyspnea, fever, and nonproductive cough. The organism that causes CPC is pneumocystitis carinii. Aspiration pneumonia: refers to pulmonary consequences resulting form entry of endogenous or exogenous substances into the lower airway. Common pathogens are S. pneumoniae, h. influenzae, s. aureus. Other substances can be aspirated such as gastric contents, exogenous chemical contents. This type of aspiration or ingestion may impair lungs defenses, cuase inflammatory changes and lead to bacterial growth and resulting of pneumonia.

Broncho pneumonia: pneumonia that is distributed in a patchy fashion, having originated in one or more localized areas whitin the bronchi and extending to the adjacent surrounding lung parenchyma. Lobar pneumonia: substantial portion of one or more lobes. An entire lobe is consolidated. Pneumonia Risk factors: o o o Heart failure: risk for pneumoccocal disease because of chronic illness Diabetes: risk for pneumoccocal disease because of chronic illness Alcoholism: alcohol suppresses the bodys reflexes, may be associated with aspiration, and decreases white cell mobilization and ciliary motion. o COPD: condition that produces mucus or bronchial obstruction and interfere with normal lung drainage. o AIDS: compromised defenses against infections

Pneumonia Sign and symptoms o o o o o o o o o Sudden onset of shaking chills Rapidly raising fever (101-105 degree) Pleuritic chest pain (aggravated by deep breathing and cough) Tachypnea (25-45 b/min) SOB (shotness of breath) Tachycardia and bounding pulse Pt may exhibit orthopnea (shortness of breath when reclining) Appetite is poor Sputum is purulent

Walking pneumonia signs and symptoms o o o o o o o o Headache Low grade fever Pleuritic pain Myalgia Pharyngitis Mucopurulent sputum Consolidation CXR COPD (purulent sputum may be the only sign)

Pneumonia Diagnostic tools o The diagnosis of pneumonia is made by history, physical exam, chest x-ray, blood culture CBC (increased WBC), sputum examination o The sputum example is obtained by having pt rinsing the mouth with water, breath deeply, cough deeply, and expectorate the raised sputum. Also, it may be obtained from a bronchoscopy.

Pneumonia Management o o o Antibiotics for bacterial infectiosn Supportive treatment for viral infections Respiration support measures O2 administration

 o

Endotracheal intubation Mechanical ventilation

Prompt administration (within 4 to 8 hours) of antibiotics in patients in whom CAP is strongly suspected or confirmed is the key treatment meauser.

o o

For patients with MRSA vaconmysisn is used. The recommended duration of treatment for pneumoccocal pneumonia is 72 hours after the patient become afebrile. Patient with most other forms of pneumonia caused by bacterial pathogens are treated for 1 to 2 weeks after they become afebrile. Those with atypical pneumonia are usually treated for 10 to 21 days.

Pneumonia Nursing interventions: o Improve airway patency: remove secretions is important. The nurse encourage hydration. Humidification may be used to loosen secretions and improve ventilation. The nurse encourages the patient to perform an effective, directed cough. Chest physiotherapy is important. Change position and after that encourage patient to breathe deeply and cough. o o Promote fluid intake: encourage fluid intake of at least 2 liter per day, unless contraindicated Maintain adequate nutritional intake: fluids such as Gatorade may help provide fluid, calories, and electrolytes. In addition, IV fluids and nutrients may be administered if necessary o Promote rest

Pneumonia Nursing diagnosis o o o o o Ineffective airway clearance related sputum production Activity intolerance Risk for deficient fluid volume related fever and dyspnea Imbalance nutrition: less than body requires Knowledge deficit related treatment regimen

EMPHYSEMA
Impaired gas oxygen and carbon dioxide exchange results from destruction of the walls of overdistended alveoli. An abnormal distention of the air spaces beyond the terminal bronchioles with destruction of the walls of the alveoli. It is the end stage of a process that has progressed slowly for many years. The alveolar surface area in direct cotact with the pulmonary capillaries continually decreases causing impaired oxygen diffusion, which leads to hypoxemia. In the later stages of the disease CO2 elimination is impaired resulting in an increased CO2 in arterial blood ( hypercapnia) and causing respiratory acidosis. Right sided heart failure ( cor pulmonale) is one of the complications of emphysema. Hypercapnea: o o o CO2 elimination is impaired Increased CO2 tension in the arterial blood Respiratory acidosis

o o o o

Increased pulmonary blood flow Right ventricle is forced to maintain a higher BP in the pulmonary arteries Right sided failure (cor pulmonale) most common complication Types of emphysema Palobular and centrilobular signs and symptoms Hyperinflated chest (barrel chest) Weight loss Polycythemia Central cyanosis

Emphysema - Risk factors o o o o 80% exposure to tobacco smoke Occupational exposure Air pollution Genetic abnormalities Cigarette smoking It depress the activity of the scavenger cells Affects the ciliarys cleansing mechanism Free passage of inhaled irritants, bacteria, and other foreign matter Obstruction of air flow, and air becomes trapped behind the obstruction Irritates the globet cells and mucous glands Increase accumulation of mucous Formation of carboxyhemoglobin equal less O2 carry capacity

Emphysema - Sign and symptoms o o o o o o o o o Cough Sputum Dyspnea on exertion Weight loss due to dyspnea and the use of energy and accessory muscles for respiration Barrel chest Ribs fixation in the inspiratory position Shoulders to heave upward Anxiety Fatigue

Emphysema - Diagnostic findings o Pulmonary function studies o o o Perfusion Diffusion Ventilation

ABGs Spirometry CXR

Electrolyte studies

Emphysema - Complications o o o o o o Respiratory insufficiency Respiratory failure Pneumonias Atelectasis Pneumothorax Cor pulmonale

Emphysema - Management o o Smoking cessation is the most important and effective treatment Medications (improve breathing) Bronchodilators (albuterol): relieve bronchospams and reduce airway obstruction by allowing increased oxygen distribution throughout the lungs and improving alveolar ventilation. o o o o o o Diuretics: decrease the fluids retained on the lungs Corticosteroids: decrease inflammation of the alveolis

Influenza (flu) vaccines every year Pneumovax (pneumonia vaccine) every 5 years Lung reduction surgery Bullectomy Lung transplant Oxygen therapy Hypoxemia: stimulates breathing, high flow of O2 will suppress the respiration drive High O2 administration equal increased CO2 retention

Emphysema - Nursing implementations o Promoting smoking cessation: the nurse must discuss smoking cessation strategies with the patient. The nurse should educate the patient regarding the hazards of smoking and cessation strategies and provide resources regarding smoking cessation, counseling and formalized programs available in the community o Improve gas exchange and airway clearance: monitor patient for dyspnea and hypoxemia. The nurse instructs the patient in directed or controlled coughing. Chest physiotherapy with postural drainage, intermittent positive pressure breathing, increased fluid intake. o Improve activity tolerance: education is focused on rehabs therapies to promote independence in executing activities of daily living. o Promote self -care: emphasize the importance of setting goals, avoiding temperature extremes, and modifying lifestyle. o Monitor complications: the nurse must assess for various complications of COPD such as atelectasis, infections. Cognitive changes, increased dyspnea, tachypnea, tachycardia, hypoxemia. The nurse monitors pulse oximetry values to assess the patients need for oxygen and administer supplemental oxygen.

COPD
Chronic obstructive pulmonary disease: airflow limitation, and irreversible condition. o o Includes chronic bronchitis, emphysema, and asthma (reversible inflammation) Currently COPD is the fourth leading cause of mortality and the 12th leading cause of diability in the USA. o o 5th leading cause of death among men and 4th for women, 3rd cause of home care services Incidence increases with age

Chronic bronchitis o Disease of the airway, is defined as the presence of cough and sputum production for at least 3 months in each of two consecutive years. o How chronic bronchitis occurs: o o o Higher incidence in the winter months Inspired irritants Increased mucous production Impaired ciliary function Thick and tenacious mucous perfect medium for bacteria to growth Increase susceptibility to infections Inflammation and thickness of bronchial wall Airway obstruction, air trapping, dyspnea Hypventilation (increased CO2) and hypoxemia

Chronic Bronchitis Risk factors: Active and passing smoking Genetics Occupational exposure Air pollution

Chronic Bronchitis Sign and symptoms Productive cough (smoker cough) Activity intolerance SOB, wheezing Hypoxemia Polycythemia Cyanosis Pulmonary hypertension

Chronic Bronchitis Management: Bronchodilators Expectorants Chest physiotherapy Antibiotics Steroids (late) Low-flow oxygen

Chronic Bronchitis Nursing implementation (teaching) Nutrition: counseling about meal planning and supplementation is part of the rehabiliation process. Continual monitoring of weight and interventions as necessary are important part of the care of patients with COPD. Respiratory hygiene Recognition of early signs of infection Techniques to relieve dyspnea (pursued lips breathing): pursued lip breathing helps slow expiration, prevent collapse of small airways, and control the rate and depth of respiration. It also promotes relaxation, which allows patients to gain control of dyspnea and reduce feeling of panic

ASTHMA
Asthma is chronic inflammation disease of the airways that causes airway hyperresponsivenss, mucosal edema, and mucus production. This inflammation ultimately leads to recurrent episodes of asthma symptoms: cough, chest tightness, wheezing, and dyspnea. Asthma differs from other obstructive lung diseases in that it is largely reversible, either spontaneously or with treatment. Asthma (how it happens) o o o o o Airway hyper response Mucosal edema: recurrent episodes (cough, chest tigness, wheezing) Reduction of airway diameter and bronchospasm Mucous production Bronchi obstruction

ASTHMA Classification based on severity o o o o Step 1: mild intermittent (symptoms no more than two weeks) Step 2: mild persistent (symptoms more than two weeks, but less than once/day) Step 3: moderate persistent ( daily symptoms) Step 4: severe persistent (continual symptoms)

ASTHMA Triggers o o o o o o Airway irritants (air pollutants, cold, heat, weather changes, strong odors or perfume, smoke) Exercise Medications Post nasal drip Viral respiratory tract infections Gastroesophageal reflux

ASTHMA Sign and symptoms o o o o Attacks: night or early morning ( circadian variations that influence airway receptor thresholds) Cough, dyspnea, wheezing ( the most common symptoms of asthma) Chest tightness Prolonged expiration ( expiration requires effort and becomes prolonged)

o o o

Diaphoresis, tachycardia, widened pulse Hypoxemia Central cyanosis

ASTHMA Diagnostic tools o o o o Family, environmental, and occupational history Increased serum levels of immunoglobulin E (allergy) Increased eosinophils Spirometry o ABGs Hypoxemia Early respiratory alkalosis or late respiratory acidosis Decreased expiratory flow rate Decreased forced expiratory volume Increase total lung capacity

ASTHMA Complications o o o o Status asthmaticus Respiratory failure Pneumonia Atelectasis

ASTHMA Management medications o Short acting meds o Beta adrenergic agonist

Long acting medications Corticosteroids ( most potent and effective anti inflammatory medications ) Beta adrenergic agonist (control asthma symptoms at night) Leukotriene modifiers ( are potent bronchoconstrictors that also dilate blood vessels and alter permeability

ASTHMA Nursing interventions o o o o o o o Monitor severity of symptoms Breath sounds Pulse oxymetry Vital signs Administer fluids Teach the pt to rinse mouth after inhaled corticosteroids use Advise smoking cessation and to avoid allergens

ASTHMA Nursing diagnosis o o o Ineffective airway clerance Knowledge deficit related to disease process noncompliance

Muscoloskeletal chapters (66-69) Class notes A fracture is a break in the continuity of the bone. It happens when there is trauma to the bone. Risk factors: bone cancer, osteoporosis Osteoporosis: brittle bones Osteomalacia: soften of the bones (lack of calcium, vitamin D) Osteomyelitis: infections of the bone Diagnostic tools: x-ray, CT scan, bone scan, MRI Bone scan: athletes use it the most Complete fracture: complete cut in the bone. Require surgery most of the time. Aligning of the bones. Incomplete: greenstick (irregular) it doesnt go directly to the bone. The bones still attach. Communited fracture: a lot of bone pieces Avascular necrosis: dying of the bone. You need bone transplant Open fracture: the piece of bone comes out through the skin. Open fracture wounds: o o o Grade 1: clean wound and less than 1 cm Grade 2: clean wound but larger. Not too much trauma to the skin Grade 3: highly contaminated, dirty, big, really bad

Stress fracture: you can hardly see it on an x-ray. Common in athletes (runners, aerobic instructors). It is a fine fracture. Most common in lower extremities Sign and symptoms o o o #1 pain Loss of function Deformity

Pain at fractures is constant. Immobilize first the extremeties and then administer analgesics Loss of function: bone affected because of the pain Deformity; malformation secondary to fracture Shortening: common in hip fracture Hip fracture: classic sign is shortening of the extremity that is fracture Crepitus: feeling of bone rubbing. Echymosis, hematoma in the affected area Prevention: o Vitamin D, calcium

o o o o

Delay and decreased severity of osteoporosis Activity Smoking Alcohol intake

Goal: reduction, immobilize extremities, to regain normal strength and function through rehab Priority: o o o Immobilize the affected area Moving: hold above the fracture and below the fracture Open fracture: cover the bone with sterile dressing to prevent further contamination with normal saline to keep moist. Then proceed with immobilization. o Do not reduce fraction. It is done by the doctor

Reduction: realignment of the fracture bone. Surgery as soon as possible to prevent further damage Pt having orthopedic surgery loose a lot of blood Place the pt in traction. The weight should be hanging so it can pull the skin. Close reduction: manipulate from the outside Open reduction: surgery Most fractures heal in 4-6 weeks (simple fractures) The swelling and strength takes another 4-6 weeks. Simple fractures heal in 8-12 weeks Complications o o o o o Compartment syndrome Fat embolism Gas gangrene (1-14 days after fracture) Thromboembolus Delayed complications (most common in elderly)

Compartment syndrome: takes 6 hr in order to cause severe damage (permanent damage) to lower extremities. Cast is very tight and there is swelling. That pressure compress the veins and arteries. There is some nerve damage, no blood supply. this can lead to permanent damage and avascular necrosis happens.

It is very important to assess the cast The result from compartment syndrome is irreversible muscle ischemia within 6 hours. Compartment syndrome assessment o Assess pain (pain is not relief with anything) localized everywhere.

o o o

Assess for numbness and tingling Assess for ability to flex and move fingers Assess skin temp, color, and pulsations

The difference between fracture pain and compartment syndrome pain is that compartment syndrome pain is unrelieved. The first thing you do is elevate the extremities to relief pressure and pain in compartment syndrome Do not document that the patient has dorsalis pedis pulse when there is a cast covering the foot. Application of cold packs and removal of dressing you need to call physicians To test for tightness of the cast put your finger in and you should be able to put some The nurse needs to assess the cast edges for erythema and irritation Instruct pt not to put anything inside the cast Handle cast by grabbing it from the bottom. Do not grab it from the top. You may cause indentation on the cast Skin traction: weight should be hanging to pull the skin. Phantom pain: pt tells you they have pain in an amputated limb. You need to believe the pt pain and administer pain medications Osteomyelitis: infection of the bone. Treatment with IV antibiotics ORIF: open reduction internal fixator 45-70% with orthopedic surgeries develop DVT. You need to administer anticoagulant postoperative to the pt 20% orthopedic postoperative to the pt develop pulmonary embolism and 3% result in death Prevention of joint dislocation prosthesis (until 4 months) o o o o o do not cross the legs shouldnt sit in more than 60 degrees use high seat and high toilet seats prevent bending 90 degree place pillow between legs

Dislocation: pt tells, I felt something pop up. You need to take pt to bed, call the physician. Provide pain medication, keep pt as flat as possible

AMPUTATION

Is the removal of a body part, usually an extremity. Amputation of a lower extremity is often necessary because progressive peripheral vascular disease. Amputation is used to relieve symptoms, to improve function, and most importantly to save or improve the patients quality of life.

Perform at the most distal point that will heal successfully. The site of amputation is determined by two factors: circulation in the part and functional uselfuness. AEA (above elbow amputation) BEA (below elbow amputation AKA (above knee amputation) BKA (below knee amputation)

Contributing factors Fulminating gas gangrene Trauma Congenital deformities Chronic osteomyelitis Malignant tumors

Advantages Relieve symptoms Improve function Save pts life (sepsis)

Complications Hemorrhage: because major blood vessels have been severed, massive bleeding may occur. Infection: is a risk with all surgical procedures. It increases with contaminated wounds after traumatic amputation. Skin breakdown: skin irritation caused by the prosthesis. Phantom limb pain: is caused by severing of peripheral nerves Joint contracture: caused by positioning and a protective flexion withdrawal pattern associated with pain and muscle imbalance

Influencing factors: Muscle and skin perfusion are evaluated with Doppler flow meter, segmental BP readings, and PaO2 levels. The circulatory status of the extremity is evaluated through physical examination and diagnostic studies.



Preservation of knee and elbow joint for post-op prosthesis use Staged amputation: (1st guillotine amputation is done to remove the infected tissue and systemic ABTs (antibiotics) therapy is started) few days after 2nd stage an amputation with skin closure is done.

Management: The objective of treatment is to achieve healing of the amputation wound, the result of being a non-tender residual limb with healthy skin for prosthesis use. Gentle handling of the residual limb, control of residual limb edema through rigid enhances healing or soft compression dressings, and use of aseptic technique in wound care to avoid infection. Systemic antibiotics (ABTs)

Nursing implementation Assessment (post-op): evaluate the neurovascular and functional status of the extremity through history and physical assessment. Assess circulatory status and function of the unaffected extremity. Evaluate the patient nutritional status. Assess the psychological status. Assess circulatory status of residual limb and unaffected one. Assess function of residual limb and unaffected one. Signs and symptoms of infection (enlarge lymph nodes, fever, drainage, increased WBC, erythema, wound dehiscence). Assess for concurrent health conditions such as dehydration, anemia, cardiac insufficiency, chronic respiratory problems and diabetes mellitus. Assess grief response. Pain management: evaluation of the patients pain and responses to interventions is an important part of the nurses role in pain management. Surgical pain can be controlled with analgesics. Minimize altered sensory perception: when a patient describes phantom pains or sensations the nurse acknowledges these feelings and helps the patient modify these perceptions. Distraction techniques and activity are helpful. In addition, beta-blockers may relieve dull, burning discomfort; antiseizure medications control stabbing and cramping pain; and tricyclic antidepressants are used to improve mood and coping ability. Phantom pain described as usual sensation before the amputation. Numbness, tingling, cramps, pain, presence of the amputated extremity, legitimate feelings. The cause is unknown. Promotion of wound healing: whenever dressing is changed, aseptic techniques is required to prevent wound infection and possible

osteomyelitis. The nurse instructs the patient and family in wrapping the residual limb with elastic dressings. Monitor signs and symptoms of infection. Proper handling of limb Increase level of activity: postoperative ROM exercises are started early because contracture deformities develop rapidly. Strength and endurance are assessed and activities are increased gradually to prevent fatigue. Promotion of self-care: the patient is encouraged to be an active participant in self -care. The nurse encourages the patient to do selfcare activities. The nurse and the therapist work with the patient to achieve maximum independence. Encourage pt to actively participate in self-care. Independence in toileting, dressing, bathing. o Prevention of contractures FRACTURES o A fracture is a break in the continuity of bone and is defined according to its type and extent. o o Fractures occur when the bone is subjected to stress greater that it can absorb. Direct blows, crushing forces, sudden twisting motions, and extreme muscle contractions cause fractures. o Risk factors: o o Tumor Osteoporosis Osteomyelitis Osteomalacia Can cause the bone to break regardless of trauma Encourage patient to turn from side-to-side and to assume prone position: prevents flexion contractures of the hips ROM of knee: important for prosthesis fitting Use of over-head trapeze to strengthen the biceps

Diagnostic tools X-ray of the affected area CT scan to evaluate the degree of displacement, and for compression fractures Bone scan, useful to identify occult stress fractures MRI to detect lesions that affect the bone

Types of fractures



Complete fracture: involves a break across the entire cross-section of the bone and is frequently displaced (removal from its normal position) Incomplete fracture (eg. Greenstick fracture): involves a break through only part of the cross-section of the bone. Comminuted fracture: is one that produces several bone fragments Closed fracture (simple fracture): is one that does not cause a break in the skin. Open fracture (compound, or complex, fracture): is one in which the skin or mucous membrane wound extends to the fracture bone.

Open fractures are graded according to the following criteria: Grade I is a clean wound less than 1 cm long Grade II is a larger wound without extensive soft tissue damage Grade III is highly contaminated, has extensive soft tissue damage, and is the most severe.

Stress fracture Fine fracture line that results from indirect trauma to the bone. Not easily seen in x-rays Most commonly seen in athletes: runners who participate in repetitive activities (jumping). Most common sites: calcaneous, patella, metatarsal, etc.

Fracture signs and symptoms Pain: the pain is continuous and increases in severity until the bone fragments are immobilized. Loss of function: after the fracture the extremity cannot function properly because normal function of the muscles depends on the integrity of the bones to which they are attached. Pain contributes to the loss of function. Deformity: displacement, angulation, or rotation of the fragments in a fracture of the arm or the leg causes a deformity that is detectable when the limb is compared with he uninjured extremity. Shortening: in fractures of long bones, there is actual shortening of the extremity because of the contraction of the muscle that are attached distal and proximal to the site of the fracture. Crepitus: when the extremity is examined with the hands, a grating sensation is felt. Caused by the rubbing of the bone fragments against each other.

Local swelling and discoloration: localized edema and discoloration of the skin (ecchymosis) occurs after fracture.

Prevention and screening Weight bearing and physical activity makes the bone stronger and reduces calcium loss Adequate dietary intake of calcium Avoid smoking Avoid excessive alcohol intake

Management: Goal: reduction, immobilization, and regaining normal strength and function through rehab Emergency care: Immediately after injury, whenever a fracture is suspected, it is important to immobilize the body part (priority #1) before the patient is moved. If an injured patient must be removed from a vehicle before splints can be applied, the extremity is supported distal and proximal to the fracture site to prevent rotation as well as angular motion. With an open fracture, the wound is covered with a sterile dressing to prevent contamination of deeper tissue. No attempt is made to reduce the fracture, even if one of the bone fragments is protruding through the wound. Reduction: Reduction of a fracture refers to restoration of the fracture fragments to anatomic alignment and rotation. The physician reduces a fracture as soon as possible to prevent loss of elasticity from the tissues through infiltration by edema or hemorrhage. In most cases reduction becomes more difficult as the injury begins healing. Before fracture reduction and immobilization, the patient is prepared for the procedure, permission is obtained, and an analgesic is administered. o Close reduction: is accomplished by bringing the bone fragments into apposition through manipulation and manual traction. The immobilizing device maintains the reduction and stabilizes the extremity for bone healing. X-rays are obtained to verify that the bones are correctly aligned.

Open reduction: through surgical approach, the fracture fragments are reduced. Internal fixation devices such as pins, wires, screws, plates, nails or rods may be used to hold the bone fragments in position.

Fractures complications: Factors that can impair fracture healing include: 1) inadequate fracture immobilization, 2) inadequate blood supply to the fracture site or adjacent tissue, 3) extensive space between bone fragments, 4) interposition of soft tissue bone ends, 5) infection, 6) metabolic problems. Compartment syndrome: occurs when there is increased tissue pressure within a limited space (eg, cast, muscle compartment) that compromises the circulation and the function of the tissue within the confined area. (an anatomic compartment is an area of the body encased by bone or fascia that contains muscles, nerves, and blood vessels.) Is a complication that develops when pressure within a compartment is greater than normal. The patient complains of deep, throbbing, unrelenting pain, which continues to increase despite the administration of opioids and seems out of proportion to the injury. A hallmark sign is pain that occurs or intensifies with passive ROM. The pain can be caused by reduction in size of the muscle compartment because the enclosing muscle fascia or an increase in compartment contents because of edema or hemorrhage. The pressure within a muscle compartment may increase to such an extent as to decrease microcirculation, causing nerve and muscle anoxia and necrosis. Permanent function can be lost if the anoxic situation continues for longer than 6 hours. Paralysis, sensory loss, and permanent disability occur within the next 24-48 hours. Compartment syndrome assessment o Frequent assessment of neurovascular function after a fracture is essential and focuses on the 5 P: pain, paralysis, paresthesia, pallor, and pulselessness. Sensory deficits include: deep, throbbing, escalating pain that increases with passive stretching. Paresthesia (burning and tingling sensation) and

numbness are early signs of nerve involvement. Ask the patient to move the fingers or toes. Peripheral circulation is evaluated by assessing color, temperature, capillary refill, swelling, and pulses. o Medical management: prompt management of acute compartment syndrome is essential. The physician needs to be notified immediately if neurovascular compromise is suspected. Is managed by elevation of the extremity to the heart level, release of restrictive devices. Application of cold packs. Remove restrictive dressing (elastic bandage). Assess dressing for drainage and tightness o Nursing documentation: patient with right lower extremity cast, from below the knee to the toes. Toes with good color, warm to touch, capillary refill within 2 seconds. Pt is able to wiggle his toes with minimal discomfort, as voiced. Right popliteal pulse present, strong and equal to left one. Fat embolism: at the time of fracture, fat globules may diffuse into the vascular compartment because the marrow pressure is greater than the capillary pressure. The fat globules may occlude the small blood vessels that supply the lungs, brain, kidneys, and other organs. The onset of symptoms is rapid, usually within 24 to 72 hours of injury. Presenting features include hypoxia, tachypnea, tachycardia, and pyrexia. Cerebral disturbances are manifested by mental status changes varying from headache and mild agitation to delirium to coma. Immediate immobilization of fractures, minimal fracture manipulation, adequate support for fractured bones during turning and positioning, and maintenance of fluid and electrolyte balance are measures that may reduce the incidence of fat emboli. Gas gangrene (1-14 days post fracture) Thromboembolus: includes DVT and PE (pulmonary embolism). Immobility, bed rest put patients at risk for thromboembolus. Delayed complications (delayed union or no-union): nonunion results from failure of the ends of a fractured bone to unite, whereas malunion result from failure of the ends of fracture bone to unite in normal alignment. Factors contributing to nonunion and malunion include

infection at the fracture site, interposition of tissue between the bone ends, inadequate immobilization or manipulation that disrupts callus formation, excessive space between bone fragments, limited bone contact, and impaired blood supply resulting in AVN (avascular necrosis) o Cast care: A cast is a rigid external immobilizing device that is molded to the contours of the body. A cast is used specifically to immobilize a reduced fracture, to correct deformity, to apply uniform pressure to underlying soft tissue, or to support and stabilize weakened joints. Nursing implementation: Observe skin at cast edges for erythema and irritation Assess for signs and symptoms of infection (odor and drainage coming from under the cast) Elevate casted extremity Assess for neuro-vascular changes of the affected extremity. Pruritus: o Instruct pt to gently rub the area below and above the cast to retard the desire to scratch o o Not to stick sharp objects underneath the cast Use of diversional activities

Weight bearing (as per MD orders) Handling the new cast o Support the wet cast with palm of the hands to avoid indentations that cause pressure on underlying skin o Placed the casted extremity on pillows

A patients unrelieved pain must be immediately reported to the physician to avoid possible paralysis and necrosis. The nurse must never ignore complaints of pain from the patient in a cast because of the possibility of problems, such as impaired tissue perfusion or pressure ulcer formation.

Skin traction Skin traction is used to control muscle spams and to immobilize an area before surgery. Skin traction is accomplished by using a weight to pull on traction tape or on a foam boot attached to the skin. The use of weight to exert pulling force on the affected extremity Provides support and comfort (treatment of muscle spasm)



Temporally measure until more definitive treatment is initiated Potential complication: skin breakdown, nerve pressure, and circulatory impairment. Nursing diagnosis related to fracture Risk for trauma related to loss of skeletal integrity, movement of skeletal fragments, use of traction Acute pain related to muscle spasm, movement of bone fragments, tissue trauma/edema, or traction/immobility device Risk for peripheral neurovascular dysfunction Impaired physical mobility related to pain, discomfort, and restrictive devices.

OSTEOMYELITIS Osteomyelitis is an infection of the bone. The bone becomes infected in one of three ways: Extension of soft tissue infection Direct bone contamination from bone surgery, open fracture, or traumatic injury Hematogenous spread from other sites of infection.

Osteomyelitis is an infection of the bone that can be caused by microbial agents. Osteomyelitis affects about two out of every 10,000 people. Osteomyelitis etiology: An open injury to the bone: o Open fracture

An infection from elsewhere in the body: o Spread to the bone through the blood

A minor trauma: o Can lead to a blood clot around the bone creating a medium for bacteria growth

Bacteria in the bloodstream: o Localized infection of the bone, resulting in destruction of the bone tissue, however new bone often forms around the site

A chronic open wound or soft tissue infection: o Extending to the bone surface

Osteomyelitis risk factors: Diabetes Patients receiving hemodialysis



Immuno-compromised patients Sickle cell disease Intravenous drug abusers The elderly

Osteomyelitis signs and symptoms Pain/and or tenderness in the infected area Swelling and warmth in the infected area Fever Nausea, secondarily from being ill with infection Drainage of pus through the skin Excessive sweating Chills Lower back pain Swelling of the ankles, feet, and legs Changes in gait (walking pattern that is painful, yielding a limp)

Diagnostic tools: Blood tests: (elevated WBC and ESR (erythrocyte sedimentation rate) Blood culture: a blood culture is a test used to detect the causative micro-organism Needle aspiration: to obtain a specimen for culture and sensitivity. Biopsy: tissue sample Bone scan: a small amount of technetium 99 pyrophosphate is injected. If the bone tissue ishealthy, the material will spread in an uniform fashion. However, a tumor or infection in the bone will absorb the material and show an increased concentration of the radioactive material. Detect abnormality before x-rays.

Management: Goal: to control and halt the infective process. Eliminate the infection and prevent the development of chronic infection Antibiotic therapy depends on the result of blood and wound cultures The area affected with osteomyelitis is immobilized to decrease discomfort and to prevent pathologic fracture of the weakened bone.

As soon as the culture specimens are obtained, IV antibiotic therapy begins, based on the assumption that infection results from a staphylococcal organism that is sensitive to a semisynthetic penicillin.

Surgery: destroyed bone is scrapped out. In the case of spinal abscesses, surgery is not performed unless there is compression of the spinal cord or nerve roots

Some cases of chronic osteomyelitis can be so resistant to treatment that amputation may be required. Chronic infectious draining sites can evolve into a squamous cell type of skin cancer (rare)

ORTHOPEDIC SURGERY Many patients with musculoskeletal dysfunction undergo surgery to correct the condition. Conditions that may be corrected by surgery include unstabilized fracture, deformity, joint disease, necrotic or infected tissue, and tumors. Frequent surgical procedures include ORIF (open reduction internal fixator) and closed reduction with internal fixation. Orthopedic surgery goal: improving function by restoring motion and stability and relieving pain and disability. Surgical procedures: ORIF: open reduction with internal fixation Closed reduction with internal fixation (bone fragments are not surgically exposed) Arthroplasty: the repair of joint problems through the operating arthroscope or through open joint surgery Meniscectomy: the excision of damaged joint fibrocartilage Joint replacement: the replacement of the joint surfaces with metal or synthetic materials Amputations: the removal of a body part Bone graft: the placement of bone tissue to promote healing to stabilize, or to replace disease bone Tendon transfer: the movement of tendon insertion to improve function Athrodesis: immobilizing fusion of a joint

Fasciotomy: the incision and diversion of the muscle fascia to relieve muscle constriction, as in compartment syndrome, or to reduce fascia contracture.

Joint replacement: o Patient with severe joint and disability may undergo joint replacement. Conditions contributing to joint degeneration include osteoarthritis (degenerative joint disease), rheumatoid arthritis, trauma, and congenital deformity. Some fractures may cause disruption of the blood supply and subsequent avascular necrosis. Joints frequently replaced include the hip, knee, and finger joints. Less frequently more complex joints shoulder, elbow, wrist, ankle are replaced. o Procedures: most joint replacement consist of metal and high density polyethylene components. The joint implants may be cemented in the prepared boen with polymethyl methacrylate. Press fit, ingrowth prostheses tha allow the patients bone to grow into and securely fix the prosthesis in the bone are alternative to cement prosthese. With joint replacement, excellent pain relief is obtained in most patients. Return of motion and function depends on preoperative soft tissue condition, soft tissue reactions, and general muscle strength.

Total hip replacement: is the replacement of a severely damaged hip with an artificial joint. Indications for this surgery include arthritis, femoral neck fractures, and conditions resulting from congenital hip disease. The surgeon selects the prosthesis that is best suited to the individual patient, considering various factors, including skeletal structure and activity level. Most consist of a metal femoral component topped by a spherical ball fitted into a plastic acetabular socket.

Complications: Dislocation of the hip prosthesis, excessive wound drainage, thromboembolism, infection, and heel pressure ulcer. Other complications are related to immobility, heterotopic ossification (formation of bone in the periprosthetic space), avascular necrosis, and loosening of the prosthesis

Nursing interventions:

Obtain baseline assessment of the affected extremity: Prevent infection: prophylactic antibiotics are prescribed. If indwelling urinary catheters or portable wound sucntion devices are used, they are removed as soon as possible to avoid infection. Acute infection may occur within 3 months after surgery. Adhere to strict aseptic techniques in the OR. Monitor for sign and symptoms of infection. Avoid osteomyelitis. Hand washing

Monitor wound drainage: expect wound drainage of 200-500 ml day one post. Mark borders of drainage in the dressin. Reinforce initial surgical dressing as needed. Accurate intake and output. Monitor for active bleeding under patient dressing

Promote increase level of activity: assist patient with early ambulation as ordered. OOB to bed chair, standing for short periods to walking for progressing greater distance. Watch for orthostatic hypotension. Weight bearing as ordered. Use of appropriate assistive devices such as walker and or cane.

Prevention of DVT: the incidence of DVT is 45 to 70%. The peak occurrence is 5 to 7 days after surgery. About 20% patient with DVT develop pulmonary embolism of which 3% of cases are fatal. Signs of DVT include calf pain, swelling, and tenderness. The nurse encourages the patient to consume adequate amounts of fluids, to perform ankle and foot exercises hourly while awake, to use elastic stockings and sequential compression devices as prescribed. Low molecular weight heparin.

Preventing dislocation of hip prosthesis: the nurse teaches the patient about positioning the leg in abductio, which helps prevent dislocation of the prosthesis. Use pillow between the legs to prevent dislocation. The patient hip is never flexed more than 90 degrees. To prevent hip flexion, the nurse does not elevate the head of the bed more than 60 degrees. For use of the fracture bedpan, the nurse instruct the patient to flex the good leg and use the trapeze to lift the pelvis onto the pan. High seat chairs, semireclining wheelchairs and raised toilet seats may be used to minimize hip joint flexion. At not time the patient cross his or her legs. The patient should not bend at waist to put

on shoes and socks. Occupational therapist can provide the patient with devices to assist. Patient education: never cross legs, avoid bending forward (no flexion >90 degree), use high seated chair and raised toilet seat, use assistive devices provided by OT to put on clothing (socks, shoes, pants), keep knees apart at all times, put pillows between legs when sleeping. Signs and symptoms of hip dislocation: Increased pain at the surgical site, swelling, and immobilization Acute groin pain in the affected hip or increased discomfort Shortening of the leg Abnormal external or internal rotation Restricted ability or inability to move the leg Reported popping sensation in the hip

If a prosthesis becomes dislocated the nurse immediately notifies the surgeon because the hip must be reduced and stabilize promptly so that the leg does not sustain circulatory and nerve damage. Stresses to the new hip joint should be avoided for the first 3 to 6 months. After close reduction, the hip may be stabilizing with Bucks traction or a brace to prevent recurrent dislocation.

Total knee replacement Total knee replacement surgery is considered for patients who have severe pain and functional disabilities related to destruction of joint surfaces by arthritis or bleeding into the joint. Post op: Affected knee with compression dressing Ice to reduce edema and poss. Bleeding Encourage active flexion of the foot q1hr Monitor CPM (continuous passive motion device): the patients leg is placed in this device, which increases circulation and range of motion of the knee joint. Inspect immobilizing devices (splints, cast, or brace) Follow weight bearing orders Assist pt with ambulation, as ordered.

Nursing diagnostic Acute pain related to orthopedic problem Acute pain related to inflammation

Risk for peripheral neurovascular dysfunction related to inflammation and or constricting devices Impaired physical activity related to pain inflammation, and or presence of immobilization device

Hip fracture Elderly people who have brittle bones from osteoporosis and who tend to fall frequently have high incidence of hip fracture. The patient who has sustained a hip fracture frequently has a comorbid condition (cardiovascular, pulmonary, renal and endocrine). There are two major types of hip fracture. Intracapsular fractures are fractures of the neck of the femur. Extracapsular fractures are fractures of the trochanteric region. Avascular necrosis is common in femoral neck fractures. Sign and symptoms: the leg is shortened, adducted, and externally rotated. The pt complains of pain in the hip and groin or in the medial side of the knee. The diagnostic of fractured hip is confirmed with an x-ray. Management: Bucks extension traction, a type of temporary skin traction, may be applied to reduce muscle spasm, to immobilize the extremity and to relieve pain. The goal of surgical treatment of hip fractures is to obtain a satisfactory fixation so that the patient can be mobilized quickly and avoid secondary medical complications. Displacement femoral neck fractures may be treated as emergencies with reduction and internal fixation performed withing 12 to 24 hours after fracture. Adequate reduction is important for fracture healing: the better the reduction, the better the healing. Nursing intervention: Attention is given to pain management, prevention of secondary medical problems, and early mobilization of the patient. The nurse encourages deep breathing, coughing, and foot flexion exercises every 1 to 2 hours. Elastic compression stockings and pneumatic compression devices are used and anticoagulants. A pillow is placed between the legs. The patient is encourage to exercise as much as possible by means of overbed trapeze. Encourage the pt to drink fluids and ankle foot exercises to

prevent DVT. The nurse assess every 4 hours for DVT. Change positions every 2 hours. Complications: DVT, atelectasis, and pneumonia are most common complications. Delayed complications of hip fracture include infections, nonunion, AVN of the femoral head.

Med-surge notes (WOMENS HEALTH)

6/11

OSTEOARTHRITIS (Non-inflammatory arthritis) o o o o o o o o Known as degenerative joint disease It affects women and men but women have more symptoms than men Women are mainly affected at: hand and knee Men are mainly affected at: hip There are changes in the joints. It happens over time. The joint become rough and softer The joint becomes thinner and the bones would rub together Joint mice: bones become spur a small moveable stone formed in or near a joint, usually a knee. Risk factors: o Modifiable: obesity, repetitive joint stressor, post menopausal bone loss Non-modifiable: age, gender, family history, trauma, fractures, infections

By 40 years old most people have osteoarthritis pain. They are asymptomatic, asymmetrical, redness, swelling, and tenderness at the heberdens nodes,

Heberdens nodes: an abnormal cartilaginous or bony enlargement of a distal interphalaneal joint of a finger, usually occurring in degenerative diseases of the joint.

Patient is so stiff that takes time (usually 30 minutes or so) and a lot of activity to start the day. They should take warm shower

Crepitus and limited ROM in weight bearing joints. Crepitus is associated with gas gangrene, rubbing of bone fragments, air in superficial tissues, or crackles of a consolidated area of the lung in pneumonia.

Manifestations: Bad Weather affects joints - Rising humidity and falling barometric pressure often aggravates the symptoms Advanced groin pain Hip most common in man Hip: point at groin, buttocks, medial side of the thigh or knee. Pain is poorly differentiated. Lowering the body becomes different. Knee; pain with motion with decreased flexion, vagus deformity, crepitus. Spine: a lot of pain. Patient tells you lower back pain. Weakness of lower extremeties, decreases reflexives and leg pain

o o o

Diagnostic: medical history, arthroscopy, x-ray, physical assessment Goal: control pain, disability, pt be able to perform ADL as much as possible with less assistance Treatment: Non-drug: physical therapy (increase joint movement), occupational therapy (assistive devices), dietitian Aquatic exercise: increase joint flexibility, muscle strengths and increase self -confidence. Isometric exercises: increase muscle tension



Warm bath or shower Dietary supplements: restore and maintain cartilage, analgesics Drug therapy: acetaminophen: first line of treatment NSAID: avoid as possible. Inflammation is not a main sign of osteoarthritis. COX-2 inhibitor (less GI problem seem with NSAID)

Surgery: Arthrodesis: immobilization Arthroplasty: diseased joint components are replaced with artificial joint products Osteotomy the sawing or cutting of a bone. In this case Displacement Osteotomy in which a bone is redesigned surgically to alter the alignment or weight-bearing stress areas.

Alternative treatments: Acupuncture, Massage therapy Osteoarthritis Progressive, not systemic (only on specific joints Primary affects weight bearing joints Pain, swelling and tenderness Affects all connective tissue in the body Warm, tender, erythematosis, and painful joints Crepitus, heberdens nodes Severe joint deformities Rheumatoid arthritis Systemic, autoimmune condition

Nursing intervention: o o o Anticipate immoblization when acute problems (splint) Encourage to participate in ADLS, allow rest periods Maintaining a regular exercise program

OSTEOPOROSIS (a disorder characterized by abnormal loss of bone density and deterioration of bone tissue, with an increased risk or fracture) o o o o o o o Most common bone condition Female 80% Occurs at about 55 years of age 1 out of every 2 women will be affected 1 out of every 8 men over 50 years will develop delayed fracture metabolic bone disease types: Primary: age related type 1: estrogen deficiency induced (menopause) type2: elderly with declined vitamin D production and decreased GI calcium absorption (as you get older, less absorption of vitamin D and Calcium in the GI tract) Secondary: related to any other medical condition Risk factors: nonmodifiable: age, gender, euro-american ethnicity, thin, small frame, family Hx, Caucasians modifiable: chronic Ca deficiency, vitamin D deficiency, sedentary lifestyle, smoking, ETOH, diet high in proteins and fats o A diet high in acid forming foods is counteracted by the body by releasing calcium from the bone into the bloodstream o people who consumed a diet rich in alkaline forming fruits and vegetables have higher bone mass o secondary osteoporosis risk factors: o o o o diabetes, chronic exercise related to suppression of menses (reduced hormones) medications: corticosteroids, anti-seizures, aluminum, diuretics

sign and symptoms: called the silent thief (no warning signs). No S and S until fractures occurs acute back pain: vertebral fracture hip fracture spontaneous or with little trauma. Wrist fracture: overstretching or past falls

Complications: pain, loss of function, deformity, muscle weakness, social isolation X-ray is not a good tool to Dx fractures Bone density test (DEXA Dual Energy Absorptiometry): an imaging technique that uses two low-dose X-Ray beams with different levels of energy to produce a detailed image of body components. It is used primarily to measure bone mineral density

o o

Labs: serum levels of calcium, phosphorus. Screening guidelines: all post menopausal women under 65 all post menopausal women with fractures

 o

women considering treatment of osteoporosis women in hormone replacement treatment.

Treatment: Calcium and vitamin D Calcium minimum: 1200-1500 mg/day for all persons. Sources: low fat dairy products, canned salmon, vegetables, almonds, cereals, pasta, grains Vitamin D 400-800 daily Source: milk, cereal, egg yolks, salt water fish, liver

o o o o

Calcium interferes with the absorption of iron Exercises: walking Smoking cessation Drugs: Hormone replacement therapy, fosamax, calcitonin, raloxifen

Goal: decrease pain and promote activity to minimize functional decline Administer analgesia, provide periods of rest, assess ABD for constipation, provide safe environment, teach pt about proper body mechanics

6/14 STDs Trichomoniasis (trichomonas) a vaginal infection caused by the protozoan trichomonas vaginalis Incubation can be years. It is symptomatic. Takes years to be diagnosed Sign and symptoms: o Off-white, yellow, greenish purulent discharge, foul smelling drainage, itching, irritates vagina

Some women are asymptomatic The cervix looks like a strawberry. It is called strawberry cervix. Cervix has petechiae which are tiny purple or red spots appearing on the skin as a result of tiny hemorrhages within the dermal or submucosal layers.

Treatment: o o Single dose of metronidazole per 7 days If it doesnt go away. They need to call CDS because there is resistance and they would tell what to do. They would take report. o o You need to report STDs to the CDC Treat it with flagil if metronidazole doesnt work

CHLAMYDIA (a genus of microorganisms that live as intracellular parasites, have a number of properties in common with gram negative bacterias) Most common bacterial STD in the US Whenever you treat a patient with Chlamydia you need to treat for Gonorrhea Chlamydia and Gonorrhea go together Sign and symptoms o o o o A lot of women are asymptomatic Pelvic inflammatory desease (PID), it is the main sign and symptom of Chlamydia Men: testicular pain Men diagnostic test: you need to collect the first voided urine in the morning

Treatment: o o o Zithromax (1 g) PO single dose Vibramycin 100 mg PO bid for seven days Erythromycin (pregnant women)

GONORRHEA Gonorrhea is the most common venereal disease in the USA Incubation period 3-4 days Homosexual male has 10x greater incidence Transmission: Direct contact with exudates via sex or neonatal passage through birth canal. Signs and Symptoms o o o Woman has no discharge Men has discharge. Purulent urethral discharge (white, yellow, green color) Complications: Infertility Ectopic pregnancy



Blindness for babies Prostatitis Sterility

Gonorrhea is the only STD that would cause low grade fever Diagnostic test for males: you need to collect the first voided urine in the morning When patient had low grade fever and discharge there is possibility that he/she has gonorrhea Treatment: o o Rocephin (125 mg IM single dose) Oral and pharyngeal respond best to rocephin

All patient treated for gonorrhea need to be treated for Chlamydia

SYPHILIS (an STD caused by the spirochete Treponema pallidum, characterized by distinct stages of effects over a period of years.) Is being around for many years Has 3 stages Invades through intact skin or mucous membranes. Goes to the lymph nodes Affects many organs including the integumentary system South has the highest rate in the nation Secondary stage is the most contagious stage (you can get it by kissing). Incubation: about 3 weeks (range 10-90 days post exposure) The First Stage (Primary syphilis): o o o Chancre: painless ulcer (filled with spirochetes) Extra genital lesions may be painless Heals spontaneously in 1-5 weeks

The Second Stage (Secondary syphilis): o o o o Spirochetes have increased in number and spread throughout the body Rash Lymph nodes and nerves Condyloma lata: flat lesions that may appear in moist areas

Tertiary stage: o o Absence of clinical symptoms Appearance of soft rubber tumors, called gummas, that ulcerate and heal by scarring. Gummas form anywhere on the surface of the body and in the eyes, liver, lungs, stomach, or reproductive system. o Systemic involvement with cardiovascular and CNS

Diagnosis o RPR (rapid plasma reagin test): an agglutination examination, the test detects two groups of antibodies. The first is a nontreponemal reagin directed against a lipoidal agent resulting from the Treponema pallidum infection. The second is an antibody directed against the Treponemal pallidum organism itself.

Nursing intervention

Administer parenteral penicillin

HERPES GENITALIS (a chronic infection caused by type 2 herpes simplex virus (HSV2), usually transmitted by sexual contact which causes painful vesicular eruptions on the skin and mucous membranes of the genitalia of males and females.) Type 1 and type 2 Person get herpes when person comes in contact with the vesicles Herpes has no cure. You will always have herpes. Assessment: tingling and itching before the vesicle appears Complications: cervical cancer, pregnant women should have C section HSV2 may be transmitted to the newborn by direct contact with infected tissue during natural child birth. Treatment: Sitz bath, analgesia, Acyclovir (an antiviral agent) taken PO results in partial control of the S&S

GENITAL WARTS (a small soft, moist pink or red swelling of the genitals that becomes pedunculated and may be painless. The growth may be solitary, or a cauliflower-like group may be present in the same area of the genitalia.) Etiology: Condyloma acuminate a wart-like growth Caused by the human papilloma virus (HPV) Treatment: burn wart by wart

BREAST CANCER (a malignant neoplastic disease of breast tissue) Non hormone dependant Estrogen and progesterone receptors, are present in some breast cancers. Estrogen and progesterone affect the rate of cells division and thus affect the risk of breast cancer by causing proliferation of breast epithelial cells. Thus drugs that block these receptors may be useful in treating tumors with the receptors. Tamoxifen for example. A womens lifetime risk for developing breast cancer is 1 in 8 Risk factors o o o o o Genetic Alcohol Obesity Hormone replacement therapy Early menarche and late menopause (high risk). Should be late menarche and early menopause ( reduces the risk) Screening by: o Breast cancer genetic screening test which is a blood test used to detect the presence of breast cancer genes. o Breast cancer self examination: Go around the breast with your finger pads in a clock wise motion until you reach the lymph nodes in the arm pit. Can be performed standing or in supine position. Should be performed on the 7th day from the first day of your period. Look for drainage, size, lumps, retraction Diagnosis by: o Mammography - Breast imaging of non-palpable lesions, Baseline mammogram between the age of 35 40 years-old o o o Ultrasound -Sound waves to produce an image MRI Biopsy

Treatment: o Drug therapy - Tamoxifen if the tumor is influenced by estrogen receptor proteins, an anti-estrogen drug is given o Surgical o Lumpectomy Removal of axillary node resection followed by low-dose radiation Simple mastectomy - Removal of the entire breast and facia Modified radical mastectomy - Removal of breast and nodes only Radical mastectomy - Removal of breast, lymph nodes, pectoralis major and minor

Post operative: Radiotherapy and/or chemotherapy

Post Operative Treatment: o o Implantation of a prosthesis Reconstructive surgery is also an option Transverse Rectus Abdominis Myocutaneous Flap (TRAM flap): go into the abdomen, remove muscle from the ABD and reconstruct the breast. One complication is hernia.

Gastritis / Peptic Ulcer Disease

Gastritis Gastritis is a mild irritation, inflammation, or infection of the stomach lining. Gastritis may be a sudden attack or chronic. Gastritis may be acute, lasting several hours to a few days, or chronic resulting from repeated exposure to irritating agents or recurring episodes of acute gastritis. Gastritis may be the first sign of an acute systemic infection The gastric mucous membrane becomes edematous and hyperemic (congested with fluid and blood) and undergoes superficial erosion. Secretes gastric juice, containing very little acid but much mucus. Gastritis Causes: Acute gastritis may be caused by: o Dietary indiscretion o Over use of aspirin or other NSAID o Ingestion of strong acid or alkali. o Pyloric stenosis or obstruction. o Tramatic injuries, burns, severe infections, hepatic renal or respiratory failure or major surgery. Chronic gastritis (may be cause by either benign or malignant ulcers of the stomach or by H. pylori) o Bacterial or viral infection (infection by a virus is contagious) o Excess stomach acid caused by: heavy smoking alcohol use Caffeine o improper diet such as spicy, greasy foods o Non-steroidal anti-inflammatory meds o Cortisone o Stress

Gastritis Sign and symptoms Abdominal discomfort Headache Lassitude Nausea Anorexia Vomiting Hiccupping Sour taste in the mouth Intolerance to spicy or fatty foods Malabsorption of vitamin B12 Gastritis Diagnostic tools GI x-ray series or endoscopy and histologic examination of a tissue specimen obtained by biopsy Gastritis Medical management The gastric mucosa is capable of repairing itself after a bout of gastritis. The patient recovers in about 1 day and appetite returns 2-3 days Refrain from alcohol and food IV Fluids is administered if symptoms persist Modifying patients diet, reducing stress, recommending avoidance of alcohol and NSAIDs Gastritis Assessment: A diet history plus a 72 hours dietary recall. The nurse also identifies the duration of the current symptoms, any methods used by the patient to treat these symptoms and whether the methods were effective. Signs to note during the physical examination include abdominal tenderness, dehydration, and evidence of any systemic disorder.

Gastritis Nursing diagnosis Anxiety related to treatment Imbalanced nutrition, less than body requirements, related to inadequate intake of Nutrients Risk for imbalanced fluid volume related to insufficient fluid intake and excessive fluid loss subsequent to vomiting Deficient knowledge about dietary management and disease process Acute pain related to irritated stomach mucosa Gastritis Nursing Implementations Use calm approach to assess the patient and to answer all questions as completely as possible Monitor intake and output Introduce solid food as soon as possible to provide adequate oral nutrition Discourage the intake of caffeinated beverages, alcohol, cigarette smoking Assess electrolytes values every 24 hours to detect any imbalance Instruct the patient to avoid any food or beverages that may irritate the gastric mucosa Instruct the patient about the correct use of medications to relieve chronic gastritis

Peptic Ulcer Disease

~500,00 new cases per year Duodenal ulcers 95% Gastric ulcers less common Higher incidence among young adults (30-55 years of age) Male > Female Ratio 1.3:1 Most common in Jewish descent Peptic ulcers are open sores that develop on the inside lining of your stomach, upper small intestine or esophagus A person who has peptic ulcer has peptic ulcer disease. A peptic ulcer is an excavation that forms in the mucosal wall of the stomach, in the pylorus, in the duodenum and esophagus Erosion of a circumscribed area of mucous membrane is the cause. Peptic ulcers are more likely on the duodenum than in the stomach. Peptic ulcer result from the infection of H. pylori. Excessive secretions of HCL in the stomach and stress may contribute to peptic ulcers People with type O are more susceptible to peptic ulcers than are those with blood type A, B, or AB.

Peptic Ulcer Causes Bacterial infection (H. pylori) Long-term use of nonsteroidal anti-inflammatory agents (NSAIDs) Cancerous tumors (stomach or pancreas) Peptic ulcer disease Risk factors: Chronic NSAID use (increase risk of gastric ulcers) Corticosteroids use Smoking Stress (contributes) Peptic ulcer disease - Helicobacter pylori H. Pylori is a bacterium that has adapted to living on the surface lining of the stomach. Impairs the ability of the stomach and duodenum to protect themselves from acid and pepsin (predisposes these areas for ulcer formation) Risk factor for gastric cancer. ~20% of people <40 years of age

~ 50% of people >60 years of age Transmission: Overcrowded areas, from person to person Test: H. Pylori serum antibody. (+) test may persist for up to 18 Months after successful treatment. Meds should be held for 7 days prior serum test.

Peptic Ulcer Disease Prevention: Use of newer NSAID (COX2 inhibitors spare gastric mucosal prostaglandin synthesis) Proton pump inhibitors BID in conjunction with NSAID prophylaxis Smoking cessation Stress management Peptic Ulcer Disease Diagnostic Tools: LABS Endoscopy biopsy for H. Pylori CBC (anemia-blood loss) (leukocytosis-ulcer formation) Pancreatic enzyme (Amylase excludes pancreatic involvement) Fasting serum gastrin level TESTS Upper endoscopy Barium upper GI series Urea breath test (H. Pylori generates urease) Endoscopy is the preferred diagnostic procedure because it allows direct visualization of inflammatory changes, ulcers, and lesions. Peptic Ulcer Disease: Sign & Symptoms Classic Sign - Dyspepsia Possible signs of an ulcer Feel better when you eat or drink and then worse 1 or 2 hours later (gastric ulcer) Feel worse when you eat or drink (duodenal ulcer) Stomach pain that wakes you up at night Feel full fast Heavy feeling, bloating, burning or dull pain in your stomach Vomiting Unexpected weight loss Pyrosis: heartburn Constipation and diarrhea Peptic Ulcer Disease Emergency Symptoms Sharp, sudden, persistent stomach pain Bloody or black stools Bloody vomit or vomit that looks like coffee grounds Signs of a serious problem o Perforation o Bleeding (when acid or the ulcer breaks a blood vessel) o Obstruction (when the ulcer blocks the path of food trying to leave the stomach) Peptic Ulcer Disease Management: The goal of management is eradicate H. pylori and to manage gastric acidity Stop NSAID Well balanced diet Surgeries: Rare Meds: o Proton pump inhibitors (prevacid, prilosec) o H2 (histamine ) receptor antagonists and proton pump are used to treat NSAID induced ulcers and others associated with H.pylori. o Bismuth compounds o Antacids

Proton Pump Inhibitors (PPI) Suppresses gastric acid secretion. Give 1 hr ac (at meal time) Drugs: o Omeprazole (Prilosec) o Lansaprazole (Prevacid) o (Protonix) H2 Receptor Antagonists Suppress basal and nocturnal gastric secretion Less effective inhibitor of meals stimulated acid secretion. Drugs: o Ranitidine (Zantac) o Famotidine (Pepcid) o Nizatidine (Axid) Bismuth Compounds Promotes ulcer healing o Stimulates mucosal bicarbonate o Stimulates prostaglandin production o Antibacterial action against H. Pylori Dark stools with use Antacids Provide symptom relief. Peptic Ulcer Disease H. Pylori Treatment: Omeprazole 20 mg bid Metronidazole 500mg bid or Bismuth subsalicylate (10 to 14days) Peptic Ulcer Disease Complications Internal bleeding Perforation (a hole through the wall of your stomach or small intestine) Peritonitis Scar tissue that can obstruct passage of food through the digestive tract. (This causes nausea, vomiting and weight loss.) Peptic Ulcer Disease Assessment The nurse asks the patient to describe the pain and the methods used to relieve it. Nurse determines how often emesis has occurred and notes important characteristics of the vomitus. The nurse asks the patient to list his or her usual food intake for a 72 hour period. Describe food habits, assess pt vital signs and reports tachycardia, hypotension. Stool tested for occult blood, and physical examination including palpation of the abdomen for localized tenderness Goals: relief of pain, reduced anxiety, maintenance of nutritional requirement, knowledge about the management and prevention of ulcer recurrence, and absence of complications Peptic Ulcer Disease Nursing Implementations Monitor for potential complications: Melena (tarry stools) Hematemesis S&S anemia (dizziness, fatigue, tachycardia) Abd distention Constipation

Peptic Ulcer Disease Nursing Diagnosis Acute pain R/T effect of gastric secretion on damaged tissue Anxiety related to an acute illness Imbalanced nutrition related to changes in diet Deficient knowledge about prevention of symptoms and management of the condition. The nurse reviews with the patient and family the signs and symptoms of complications to be reported. These complications include hemorrhage (cool skin, confusion, increased heart rate, labored breathing, and blood in the stool), penetration and perforation (severe abdominal pain, rigid, and tender abdomen, vomiting, elevated temperature, and increased heart rate), and pyloric obstruction (nausea, vomiting, distended abdomen, and abdominal pain)

Intestinal Obstruction
Caused by any condition that prevents the normal flow of chyme through the intestinal lumen Intestinal obstruction Classifications Simple: Mechanical blockage of the lumen by lesions, (most common fibrous adhesions). Is an intraluminal obstruction or a mural obstruction from pressure on the intestinal wall occurs. o Adhesions, hernias, tumors, inflammatory disorders, stenosis, strictures, abscess. Functional: o Failure of motility (paralytic ileus). The intestinal musculature cannot propel the contents along the bowel. The blockage can be temporary and the result from surgery. o Examples: amyloidosis, muscular dystrophy, endocrine disorders such as diabetes and neurological disorders such as parkinsons disease. Most bowel obstructions occur in small intestine. Adhesions are the most common cause of small bowel obstruction, followed by hernias and neoplasms. Other causes can be twisting of the bowel ( intussusception, volvulus). Most obstruction in the large bowel occur in the sigmoid colon. The most common cause are carcinoma, diverticulitis, inflammatory bowel disorders and benign tumor. Intestinal obstruction Sequestration of gas and fluid proximal to the obstruction Distention Colicky ABD pain Nausea & vomiting Decrease nutrient absorption Decrease CHO reserve Ketosis Loss of H2O and Electrolytes Dehydration Hypokalemia & Hypochloremia Intestinal bowel wall edema Release of toxins Bacterial translocation Fever, hypovolemia, peritonitis Shock

Intestinal obstruction Pathophysiology Obstruction causes intestinal distention and loss of fluids and electrolytes Fluid accumulation proximal to the obstruction site Gas accumulation (swallowed air and bacterial fermentation) Pathophysiology of Small Bowel Obstruction: intestinal contents, fluids, and gas accumulates above the intestinal obstruction. The abdominal distention and retention of fluid reduce the absorption of fluids and stimulates gastric secretions. The pressure increases and the pressure of venous and arteriolar capillary decreases. This causes edema, congestion, necrosis, and eventual rupture of the intestinal wall with peritonitis. Reflux vomiting may be caused by abdominal distention. Vomiting results in the lost of electrolytes leading to metabolic alkalosis. Dehydration and acidosis occurs from the loss of water and sodium. With acute fluid losses, hypovolemic shock may occur.

Pathophysiology of Large Bowel Obstruction: In the large intestine dehydration occurs more slowly than in the small intestine because the colon can absorbs its fluids contents. Adenocarcinoid tumor account for the majority of large bowel obstructions. Most tumors occur beyond the splenic flexure.

Intestinal obstruction Pathophysiology Hypochloremia: obstruction at the pylorus or higher in the small intestines leads to metabolic alkalosis due to hydrogen ion lost from inhibition of gastric juice reabsorbtion. Metabolic acidosis: Develops from obstruction lower in the intestines because bicarbonate from the pancreatic secretions and bile cannot be reabsorbed. Also due to ketosis caused by starvation Severe distention causes impaired arterial circulation thus causing ischemia, necrosis, and peritonitis Fever and leukocytosis Sepsis Intestinal obstruction Sign & Symptoms Colicky pain that progresses to constant and severe as ischemia progresses to necrosis or perforation Nausea and vomiting ABD distention Partial obstruction causes diarrhea or constipation Lower causes vomiting or emesis containing fecal material Complete, increases the number of bowel sounds S&S of hypovolemia Fever Intestinal obstruction Diagnostic tools Physical exam Ultrasound Radiography (CT scan and abdominal x-ray findings include abnormal quantities of gas, fluids, or both in the intestines. Also, distended colon and pinpoint the site of obstruction Labs (electrolytes studies and a complete blood cell count) reveal picture of dehydration, loss of plasma volume, and possible infection. Barium studies are contraindicated in large bowel obstruction Intestinal obstruction Management Fluid abd electrolytes replacement Gastric or intestinal suction to decompressed the lumen Immediate surgical intervention for strangulation & complete obstruction When the bowel is completely obstructed, the possibility of strangulation warrants surgery Before surgery IV fluids is necessary to replace lost Cl, Na, K A colonoscopy is performed to untwist and decompress the bowel. A cecostomy may performed in patients who are poor surgical risk and urgently need relief form the obstruction (opening in the cecum) A rectal tube may be used to decompress an area that is lower in the bowel. The usual treatment is surgical resection to remove the obstructing lesion. Intestinal obstruction Nursing diagnosis Acute pain R/T distention/edema or ischemia of intestinal tissue as evidenced of guarding behavior or changes in vital signs. Diarrhea R/T presence of obstruction as evidenced by changes in consistency and frequency of bowel movements. Constipation R/T changes in peristalsis as evidenced by decreased bowel sounds and/or absence of stools. Risk for deficient fluid volume R/T V&D and decrease intake.

Intestinal obstruction Vocabulary Adhesions: loops of intestines become adherent to areas that heal slowly or scar after abdominal surgery Intussusception: one part of the intestine slips into another part located below it Volvulus: bowel twists and turns on itself Hernia: protrusion of intestine through a weakened area in the abdominal muscle wall Tumor: a tumor that exits within the wall of the intestine extends into the intestinal lumen, or a tumor outside the intestine causes pressure on the wall of the intestine.

Diverticular Disease
Diverticular Disease In the Western societies 30% of the population is affected at age 60, and 50% over age 80 (with Diverticulosis) Developing countries life expectancy is much lower, no comparison is poss. Most cases are asymptomatic, discovered incidentally with endoscopies and barium enemas. The exact cause of diverticulosis has not been identified. A low intake of dietary fiber is considered a predisposing factor Almost all patients have colonic involvement (it affects the lower part of the large intestine such as sigmoid colon because thats where more pressure is exerted on the walls of the colon) due to higher intraluminar pressure. Over time the contracted colonic musculature, working against greater pressure to move small, hard stools develop hypertrophy, thickening, rigidity, and fibrosis. Diverticulosis looks like swiss cheese which is why you shouldnt eat seeds and peanuts. Bowel contents can accumulate in the diverticulum ( a saclike herniation of the lining of the bowel that extends through a defect in the muscle layer.) causing inflammation and infection Diverticular Disease Risk Factors Believe to arise after many years of diet deficient in fiber Hereditary (unknown) Abnormal connective tissue disorders (sclerodema, Marfan syndrome, etc) Diverticular Disease Complications o Lower GI bleeding o Diverticulitis (infestation of the holes in the walls of colon, swelling and possible complications such as peritonitis) o Fistulas (tunnelling of hole to other tissue or organs o Constipation Uncomplicated Diverticulosis o More than 2/3 of patients Sign&Symptoms sign and symptoms of diverticulosis are relatively mild and include bowel irregularities with intervals of diarrhea, nausea, anorexia, and bloating or abdominal distention with repeated local inflammation of the diverticula the large bowel may narrow with fibrotic strictures, leading to cramps, narrow stools, and increased constipation. Weakness, fatigue, and anorexia are common symptoms If the condition is untreated can lead to septicemia Chronic constipation ABD pain (left lower quadrant, tenderness and abdominal pain/ sigmoid involvement so either diverticulosis or itis) Fluctuating bowel habits Mild left lower quadrant tenderness upon assessment Mild cramps Bloating Uncomplicated Diverticulosis Management High fiber diets Fiber supplements Fiber Containing Foods Fruits o Apple, raw, with skin1 medium =3.3 g o Peach, raw1 medium = 1.5 grams o Pear, raw1 medium = 5.1 grams o Tangerine, raw1 medium = 1.9 grams

Fiber Containing Foods Vegetables o Asparagus, fresh, cooked 4 spears = 1.2 grams o Broccoli, fresh, cooked1/2 cup = 2.6 grams o Brussels sprouts, fresh, cooked1/2 cup = 2 grams o Cabbage, fresh, cooked1/2 cup = 1.5 grams o Carrot, fresh, cooked1/2 cup = 2.3 grams o Cauliflower, fresh, cooked1/2 cup = 1.7 grams o Romaine lettuce1 cup = 1.2 grams o Spinach, fresh, cooked1/2 cup = 2.2 grams o Summer squash, cooked1 cup = 2.5 grams o Tomato, raw1 = 1 gram o Winter squash, cooked1 cup = 5.7 grams Fiber Containing Foods Starchy Vegetables o Baked beans, canned, plain1/2 cup = 6.3 g o Kidney beans, fresh, cooked1/2 cup = 5.7 g o Lima beans, fresh, cooked1/2 cup = 6.6 g o Potato, fresh, cooked1 = 2.3 g Fiber Containing Foods Grains Bread, whole-wheat1 slice = 1.9 grams Brown rice, cooked1 cup = 3.5 grams Cereal, bran flake3/4 cup = 5.3 grams Oatmeal, plain, cooked3/4 cup = 3 grams White rice, cooked1 cup = 0.6 grams

Diverticulitis
Perforation of the colonic diverticulum causing infection that vary in size. Localized inflammation (most common) to macro-perforation with abscess and peritonitis The symptoms manifested generally result from complications: abscess, fistula formation, perforation, obstruction, peritonitis, and hemorrhage

Diverticulitis Complications A fistula is an abnormal connection of tissue between two organs or between an organ and the skin E.g., diverticulitis to the bladder - feces passing thru the urine The organs usually involved are the bladder (most common), small intestine, and skin. Peritonitis ( abdominal pain, rigid-board like abdomen, loss of bowel sounds and signs and symptoms of shock occur during peritonitis) abscess formation ( tenderness, palpable mass, fever, and leukocytosis) Bleeding ( noinflamed or slightly inflamed diverticula may erode areas adjacent to arterial branches, causing massive rectal bleeding) Diverticulitis Signs & Symptoms Mild to moderate aching ABD pain (left lower quadrant) Constipation or loose stools N&V (nausea & vomiting) Low grade fever and chills Left lower quadrant tenderness with palpation (guarding is 10 on pain scale of 0 to 10) (+) stool occult blood (area is irritated and could have a perforation, wbc count in the 20 & 30, fever) Perforation: Systemic presentation (which could lead to peritonitis and systemic infection such as sepsis) Leukocytosis Test questions you do not do a colonoscopy on someone with suspected diverticulitis because the area is so inflamed and damaged and the scope can perferate the wall. Diverticulitis Diagnostic tools KUB X-Ray: Free ABD air represents perforation (there is serous fluid and no air or gas in the peritoneum)

Colonoscopy and barium enema (avoid during the initial stage because of the risk of perforation) ABD CT Scan (Abscess formation, wall thickening, inflammation obstruction, etc) CT scan is the diagnostic test of choice if the suspected diagnosis is diverticulitis; it can also reveal abscesses. Laboratory tests that assist in diagnosis include a complete blood cell count, revealing and elevated WBC (5000-10,000 normal values)

Diverticulitis Management Mild symptoms: outpatient with clear liquids diet and broad spectrum ABTs. (No laxatives, no fleets enemas and pt needs to go on liquid diet.) Antibiotics are prescribed for 7-10 days The liquid diet is recommended because increase stool volume, decrease colonic transit time, and reduce intraluminal pressure. Pts with fever, increased pain and unable to tolerate PO diet needs hospitalization. Severe cases, immuno-suppressed, elderly, and those with co-morbid disease require acute hospitalization Diverticulitis Hospital patients NPO No eating IVF ( intravenous fluid) NGT placement (ileus) IV ABTs (to cover anaerobic and gram negative bacteria) for 7-10 days An opiod is prescribed (DEMEROL) for pain relief. Morphine is contraindicated because increase intraluminar pressure in the colon. Diverticulitis Surgical Management 20-30% of the 1/3 of cases need surgical intervention Required for large abscesses and peritonitis 1sr stage diseased segment of the colon is removed. Proximal colon brought out to form a temporary colostomy. This is done through traditional surgical or laparoscopically. 2nd stage: After inflammation and infection subsides the colon can be reconnected electively. The double barrel temporary colostomy is then reanastomosed in a later procedure Diverticulitis Prognosis Reoccurs in 1/3 of patients which warrant elective surgical resection. Assessment: ask the patient about the onset and duration of pain. Past and present elimination patterns, review dietary habits, history of constipation with periods of diarrhea, tenesmus, abdominal bloating, and distention. Auscultate bowel sounds, palpate four quadrants, and inspect stools for mucus, blood, pus. Temperature, BP is monitored. Diverticulitis Nursing Diagnosis Altered nutrition: Less than body requirement R/T dietary restrictions, N&D, and ABD pain (someone who is NPO) Pain R/T intestinal inflammatory process, pt unable to move bowels for days, etc. Constipation R/T inadequate dietary intake of fiber Impaired skin integrity (perianal) R/T diarrhea (extremely acidic damages the skin) Infection, risk for (even if the infection is self evident) Goal: attainment and maintenance of normal elimination patterns, pain relief, and absence of complications Diverticulitis Nursing Implementation 1. Nutrition: Recommend daily intake of fluid at least 2 l per day (if pt doesnt have renal or cardiac problems) Dietary consult Daily weight Monitor lab results (albumin) normal values are adult/elderly: 3.5-5 g/dl or 35-50 g/L Offer frequent small meals (6 per day, snacks and shakes like glucerna & jevity) Monitor Parenteral alimentation Diverticulitis (NSG)

2. Pain: Provide optimal pain relief with prescribed analgesics (opiods like Demerol) Assess effectiveness of analgesics 30min after administration Teach non-invasive pain relief methods; relaxation techniques Assess location, intensity, aggravating & alleviating factors, radiation, onset Diverticulitis (NSG) 3. Constipation: Teach diet high in fiber: fresh fruits with skin, whole grain breads and cereals, vegetables, Encourage increase fluid intake (8-10 glasses of H2O/day) Establish a regular time for evacuation Explain the hazard of enema and laxative use Increase ambulation and level of activity Diverticulitis (NSG) 4. Skin integrity: Use of skin protecting cream Keep skin clean and dry Consult with dietitian: increase protein and CHO intake Monitor serum albumin level (3.5-5) Monitor skin integrity, turn & reposition q2h Protect bony prominence areas Refer to wound team Diverticulitis (NSG) 5. Infection: Assess for S&S of infections, especially temp. Assess ABD for distention & bowel sounds Administer ABTs as ordered Administer IVF as ordered Obtain specimen to lab ad culture for C&S

CAD
Coronary Artery Disease Male patients with higher incidence Overall ratio is 4:1 (men vs. women) but before age 40 the ratio is 8:1 Male peak incidence is 50-60 Female peak incidence is 60-70 CAD - Atherosclerosis formation steps Abnormal lipid metabolism and/or excessive intake of cholesterol and saturated fats. Fatty streaks (sub-endothelial accumulation of lipids and monocytes (macrophages). LDL (low-density lipoproteins) undergo in situ oxidation. Microphages migrate into the site to take up lipids Smooth muscle cell also migrate into the lesion Fibrous cap formation over the stable lesion which becomes calcified Lumen slowly become narrowed. CAD: Risk Factors Family history Age Gender Elevated blood homocysteine levels Elevated C-reactive protein, Sedimentation rate Elevated serum fibrinogen Blood lipid abnormalities Metabolic syndrome HTN Diabetes mellitus Physical inactivity Cigarette smoking Hormone replacement therapy CAD: Risk Factors Abnormal lipid metabolism High levels of LDL cholesterol and low levels of HDL Ratios LDL: HDL (below 3 lower risk) LDL: HDL (above 5 high risk) CAD: Management Smoking cessation Lowering of blood pressure Decrease levels of homocysteine Folic acid 1mg/daily (+) Vit B6 and B12 Treatment of dyslipidemia Statins to decrease LDL levels Niacin to increase HDL levels Vit E as antioxidant therapy-- questionable Anti-platelet therapy ASA 81-325mg/daily Omega-3 fatty acid 1g/daily Hormone replacing therapy Combined estrogen-progesterone therapy in not protecting ACE inhibitors Reduces the risk for recurrent cardiac events by 20-25%

Myocardial Infarction
Myocardial oxygen supply is severe compromised by impaired coronary blood flow. Myocardial cells are permanently destroyed. Myocardial Infarction Causes: Coronary thrombosis 2nd to ruptured atherosclerotic plaque. Coronary spasm Polycythemia vera Decreased O2 supply ( BP, Anemia, acute blood loss) Increased O2 demand (Cocaine, amphetamines) MI Development O2 supply or O2 demand Ischemia cellular injury Necrosis (death of heart muscle) Myocardial Infarction Incidence: 1 million people every year suffer of AMI. 25% mortality rate. 50% men and 63% of women with sudden cardiac death, had no previous symptoms. Myocardial Infarction Risk Factors: CAD 1st degree relative with MI prior to age 55 Smoking Diabetes Mellitus HTN Hyperlipedemia Menopause sedentary life style Aging Personality type A Myocardial Infarction Diagnostic tools: EKG Cardiac Enzymes LDH Troponin Thallium scan CXR Myocardial Infarction S&S Oppressive retrosternal chest pain Pain radiation Pain at rest or with minimal activity N/V Diaphoresis SOB Apprehensive Ashen color Hypotension Tachycardia New murmurs

MI - Medical Management M Morphine Sulphate O Oxygen Therapy N Nitroglycerin A Aspirin

MI - Medical Management Ischemic area reperfusion (Thrombolytics &/or PTCA) Meds O2 demand O2 Bed Rest O2 supply MI - Treatment: Meds: Thrombolytics Analgesics ACE inhibitors Beta-Blockers MI - NSG: Relieve pain Promote adequate tissue perfusion Reduce anxiety Monitor for potential complications

Hypertension (HTN)
Hypertension Blood pressure (p. 662) Is the product of cardiac output multiplied by peripheral resistance. (BP= CO x PVR) Pressure exerted on the wall of the arteries during diastole and systole. Influencing factors: cardiac output, distension of the arteries, blood volume, blood velocity, and blood viscosity. Hypertension Called the silent killer because it is sometimes asymptomatic. Major contributor factor of death from cardiac, renal, and PVD. Usually accompanies Diabetes and atherosclerotic heart disease p. 855 Hypertension Definition: SBP>140 mm Hg & DBP>90 mm Hg 2 or more reading during 2 or more doctors visit. Hypertension Incidence: 21-36% of the adult population has HTN. 90-95% with primary HTN 5-10% with secondary HTN Hypertension Primary hypertension: (Unknown etiology). Secondary hypertension: o Known etiology: Chronic kidney disease Coartation of the aorta Thyroid/parathyroid disease Chronic steroid therapy and Cushing syndrome. others

Regulating Systems: Sympathetic Nervous System Renin-angiotensin-aldosterone System Peripheral resistance Insulin resistance Hypertension Classifications: Pre-hypertension: o SBP 120-139 & DBP 80-89 mm Hg Stage 1 HTN: o SBP 140-159 & DBP 90-99 mm Hg Stage 2 HTN: SBP >160 & DBP> 100 Hypertension Risk factors: Cigarette smoking (increases the risk of dying from a cardiac event) Obesity Physical inactivity ETOH African American Family history Hypertension Target organ damage: Left ventricular hypertrophy Angina Heart failure CVA Kidney failure Peripheral arterial disease Retinopathy Hypertension: S&S Retinal changes Papilledema (optic nerve edema) R/T target organ damage (CVA, Kidneys,) Morning headaches & cervical pain Hypertension p. 858, table 32-3

Hypertension: Life style modification

Weight reduction (BMI 18.5-24.9 kg/m2) Change eating habits: Diet rich in fruits, vegetables, low fat dairy products and reduce saturated fats. Reduction of dietary sodium intake to 2.4g/day Limit ETOH intake, 2drinks/male/day & 1/female Regular aerobic exercises, 30 minutes Monday to Friday.

Hypertension: MEDS Diuretics - blockers ACE inhibitors Angiotensin 2 antagonists Calcium channel blockers vasodilators Hypertension: NSG Obtain V/S BP in both arms, apical and peripheral pulses. Assist in identifying modifiable risk factors

Assist in developing a health maintenance plan (set realistic goals) (smoking, exercise, diet, and stress)

Hypertension: HTN animation Hypertension case study Hypertensive Urgency (p.865) Situation in which blood pressure must be lowered within few hours. (Brunner & Suddarth) Close Hemodynamic monitoring is required, most patients are admitted to intensive care units. Life threatening side effect of medications is a sudden drop in blood pressure which requires immediate action to restore blood pressure to allow appropriate tissue perfusion. o SBP>90 mm Hg

Congestive Heart Failure (CHF)

Inability of the heart to pump sufficient blood to meet the needs of the tissues of oxygen and nutrients. Fluid overload and inadequate tissue perfusion. Heart abnormality that leads to decreased systole and/or diastole (contraction and/or filling)

CHF Etiology: Primary cause: Atherosclerosis. Causes: CAD, HTN, Valvular disorders. Incidence increases with age. Most common cause of hops. of people older than age 65

(p. 789)

Congestive Heart Failure (CHF) Positioning: (p.803) Increase head of the bed 8-10 inches with the use of pillows of blocks under the bed with arms supported by pillows. OOB sitting in armchair. High fowlers with feet dangling. Advantage: Venous return to the heart (preload) is reduced. Pulmonary congestion is alleviated. Impingement of the liver in the diaphragm is minimized. CHF: Diagnostic tools Echocardiogram (EF) Cardiac cath CXR ECG Labs: Electrolytes BUN and Creat. BNP TSH CBC U/A CHF: Diagnostic tools BNP B-type natriuretic peptide Marker of ventricular systolic and diastolic dysfunction. Elevated with ventricular volume expansion and fluid overload. CHF: Medical Management Goal:

o Meds: o o o o o

Reduce the workload on the heart by reducing afterload and preload. ACE inhibitors ARB (angiotensin 2 receptor blocker) Digitalis -blockers Diuretics

CHF: NSG V/S Daily weights Educate about Na restriction Educate to avoid excessive fluid intake (fluid restriction), smoking cessation, and ETOH. O2 based on pts condition. Accurate I&O Auscultate lungs Monitor for dehydration & hypotension due to meds Assess skin turgor and mucous membranes Assist with ADLs

Angina Pectoris
Angina Pectoris Clinical syndrome characterized by pain or pressure in the anterior chest. Result of insufficient blood flow R/T significant obstruction of a major coronary artery. Coronary oxygen needs exceeds the supply. Most often caused by arteriosclerosis & atherosclerosis. Angina Pectoris Arteriosclerosis o Thickening, hardening, loss of elasticity, and calcification of the arterial wall. Atherosclerosis o Yellowish plaque of lipids and cellular debris in the inner layer of the arterial wall. Angina Pectoris Influencing Factors: Physical exertion: myocardial oxygen demand Exposure to cold: Oxygen demand due to vasoconstriction, which BP. Eating a heavy meal: blood flow to the mesenteric area which blood supply to the coronaries. Stress/emotions: BP, HR, myocardial workload. Angina Pectoris S&S Chest pain subsides with rest and/or nitroglycerin. Angina Pectoris Management: Surgery: o PTCA o CABG o Intra-coronary stents. Angina Pectoris Medications: Nitroglycerin: Dilates veins and arteries (systemic vasodilator) myocardial oxygen consumption coronary blood flow preload Beta adrenergic blocking agents: myocardial Oxygen consumption by blocking -adrenergic sympathetic stimulation BP, myocardial stimulation Use cautiously with Asthma and Diabetes (mask hypoglycemia symptoms) Calcium Channel Blockers o SA node automaticity and/or AV node conduction o Relax blood vessels. Prevent/treat vasospasm o Dilates smooth muscle wall of coronary arteries o Workload of the heart Anti-platelets & anticoagulant ASA Plavix Ticlid Heparin Angina Pectoris Oxygen administration: Increase oxygen delivered to the myocardium to decrease pain

EKG
EKG - Properties of Cardiac Cells Automaticity: o Ability to spontaneously generate and discharge an electrical impulse Excitability: o Ability to respond to an electrical impulse Conductivity: o Ability to transmit an electrical impulse from one cell to another Contractility o Ability to shorten and lengthen its muscle fibers Extensibility: o The ability of the cell to stretch. EKG - Electrical Impulses Depolarization o Contraction of the cardiac cell (electrical activation) o systole Repolarization Relaxation of the myocardial cell (recovery) Diastole Depolarization of one electrical cell stimulates adjacent cells causing a propagation of the electrical stimulus producing an electrical current.

EKG Records the electrical current of the cardiac cells as waves in a paper/strip. EKG - Electrical Conduction System SA node (sinoatrail) o Called the pacemaker cells because they poses the highest level of automaticity. o Discharge impulses at a rate of 60-100 beats/min AV node (atrioventricular) o Escape pacemaker. Discharge impulses at a rate of 40-60 beats/min Bundle of His (R + L branches) Purkinje fibers o Escape pacemaker. Discharge impulses at a rate of 30-40 beats/min P wave: (atrial contraction) o Atrial depolarization. Spread of the impulse from the SA node through the atria. QRS wave: (ventricular contraction) o Ventricular depolarization. Spread of the impulse through the ventricles. T wave: o Later phase of ventricular Repolarization One heart beat = P-QRS-T sequence

Peripheral Vascular Disease

Types Arterial Occlusion Type 1: o 10-15% of patients. o Plaque formation limited to the aorta and the common iliac arteries. o Higher incidence among young adults (ages 40-55)- heavy smokers + hyperlipidemia. Type2: o 25% of patients o Involves the aorta, the common iliac artery, and external iliac artery. Type 3: o Most common, affects 60-70% of patients. o Affects the aorta, iliac, femoral, popliteal, and the tibial arteries. Peripheral Vascular Disease S&S Impotence (iliac arteries occlusion) Claudication Rest pain Gangrene Atrophy of skin, subcutaneous tissue and muscles of the calves Hair loss Coolness of the skin Dependent Rubor Claudication Pain and numbness or weakness in the calves, thighs, or buttocks produced by exercise and relieve after a few minutes of rest. Reproducible pain Ischemic Rest Pain Pain at rest, nocturnal located across the dorsum of the foot at the metatarsal heads. Relieve by placing the affected extremity in a dependent position. Impending gangrene. PVD - Medical Management: Meds Pentoxifylline 400 mg TID o Deforms RBC. Phosphodiesterase inhibitor cilostazol 100mg BID o Impairs platelet aggregation and increases Ca-mediated vasodilatation. o Improves walking distance Propionyl-L-carnitine 1g BID o Increases walk distance Ginko biloba extract 120mg daily o Increases walk distance o Risk of bleeding ASA 325 mg daily PVD - Medical management: Sx Stent angioplasty Thomboendarterectomy Arterial bypass Lumbar sympathectomy (reserve for symptomatic patients) Hyperbaric oxygen PVD - Surgery Complications Percutaneous procedures: Distal emboli

Contrast nephropathy Puncture site complications: Hematoma Pseudo aneurysm Arteriovenous fistulas Retroperitoneal hemorrhage Occlusion

PVD - Prognosis 25% will develop Claudication and rest pain 10% will face amputations Pts with CAD: 50% survival/5years PVD - Acute Limb Ischemia Etiology: Emboli Thrombus Trauma PVD - Acute Limb Ischemia Characteristics of acute ischemia (6 Ps) Pain (common early symptom) Pallor Pulselessness Paresthesias (common early symptom) Poikilothermia Paralysis PVD - Arterial Embolism 80%-90% arise from the heart 60%-70% of patients suffer from A.Fib Non-cardiac: R/T atherosclerosis PVD - Arterial Embolism: Treatment Heparin sodium to prevent distal thrombosis Emergent embolectomy Percutaneous thrombolysis &/or thrombolytic therapy Endarterectomy PVD - Arterial Embolism: Complications Compartment syndrome post embolectomy Foot drop 2nd to peroneal nerve ischemia Renal failure Amputations PVD - Arterial Embolism: Prognosis 25%-30% in hospital mortality (heart disease) Depends on the location of the occlusion. PVD - Acute Arterial Thrombosis Usually results from atherosclerosis Other Risk Factors: Trauma Low flow rate: hypovolemia & Cardiogenic shock Polycythemia Dehydration Hypercoagulopathy

PVD - Venous Disease: DVT 80% of thrombosis begins in the deep vein of the calf. 25% of cases progression in to the popliteal and femoral veins. 30% of post/op patients develop asymptomatic thrombosis. 3% of post/op patients develop S&S of thrombosis. PVD - DVT: Risk Factors Total hip replacement Cardiac failure Stroke Ventilatory support Pelvic bone or limb fracture Paralysis Extended air travel Lengthy surgery Hypercoagulopathy R/T malignancy, etc PVD - DVT: Risk Factors It is estimated that about 20% of patients with new DVT have an underlying malignancy. Others:

Advance age A blood group Obesity Multiple pregnancies Oral contraceptives IBS

PVD - DVT: S&S 50% of patients do not present with S&S Dull ache Tightness Calf pain (pronounced with walking) Edema of the affected extremity Low grade fever Tachycardia (+) Homans sign (50% of patients) PVD - DVT: Diagnostic Tools Duplex ultrasound PVD - DVT: Complications Pulmonary Embolism Varicose veins Chronic venous insufficiency PVD - DVT: Treatment Anticoagulation with Heparin to reach a goal of PTT (partial thromboplastin time) of 1.5-2 times normal). Warfarin after heparinization. Exonaprin (does not require monitor labs) Comparison Arterial vs. Venous Arterial Occlusion Claudication and rest pain Hair loss, coolness of the skin. Unequal peripheral pulses.

R/T atherosclerosis mainly Dx with Duplex Ultrasound

DVT (venous) Pain and edema of the calf and /or thigh 50% of patients are asymptomatic Hx of CHF, recent Sx, trauma, neoplasia, oral contraceptives, and/or prolonged inactivity. Dx with Duplex ultrasound