3220 Final

Seizure Disorders
2 Major Pathways Result in Brain Damage
Hypoxia brain uses 20% of oxygen in body
Uses a lot more oxygen than other organs
Ischemia less oxygen & glucose, more wastes
Focal stroke, collateral circulation
Each section in brain has a specific job so depending where it is, effect function
Brain has good collateral circulation to deal with focal damage
Block off 1 arteryblood travel through different path to get to tissue
Global reversible to irreversible
Entire brain effected at same time
When cut off entire oxygen supply
Some areas of brain are damaged faster

Causes of brain damage:
Ischemia from heart attack, cardiac arrest
Head trauma concussions, hematomas
Infections in brain: encephalitis
Brain tumor
Stroke, Brain Attack, or Cerebrovascular Accident (CVA)
Hypoxia from drug use, respiratory arrest
Seizures
Low glucose levels in brain cause brain damage

Global Brain Injury
Treatments: oxygen & perfusion, cooling to decrease metabolic needs, blood sugar control
During recovery, damage from:
excitatory amino acids & calcium cascade,
&
brain swelling vasogenic, & cytotoxic (toxins built up)
nowhere for swelling to go, but babies have this ability

Manifestations of Diffuse / Global Brain Injury:
Stepwise, rostral to caudal descent into coma
First - Level of consciousness (LOC)
Can be subtle.. talking and then sleepy
Pupillary changes
Tell if difference between pupils.. control of dialation is effected by reflex that occurs with brain injury
Oculomotor response
Motor response
Patterns of breathing, circulation

Your most important assessment: Level of Consciousness
Alert
Confusion & Disorientation
Delirium-inability to pay attention
Obtundation extremely sleepy but can wake up
Stupor-barely waking up
Coma (Glasgow)

Pupillary changes
Indicates the presence and level of brain stem dysfunction

Oculomotor Response
Eye movement
Nystagmus uncontrolled rapid movements from side to side and the room feels like its spinnin
Dolls Eyes- eyes fixed in one direction and when turn head, eyes go in same direction
Alert, awake eyes will track straight ahead even if turn head

Motor Response
Level of brain dysfunction
Determine most severely damaged side

Patterns of Breathing
Rate, rhythm, pattern
Sighing & yawning
Cheyne-Stokes- rapid deep breathing follow by slower shallow breathing
Gasping breath
Hyperventilation
Very irregular

Increased Intracranial Pressure (ICP) causes
-when brain swells and no where to go, compression of tissue so blood cant low easily and the heart has to force blood
inat higher pressure to get circulation into brain
Increased blood volume
Increased cerebral spinal fluid
Increased brain tissue

High Intracranial pressure Effects
Obstructs cerebral blood flow
Destroys brain cells
Herniation part of brain normally position in certain areas due to membrane s and base of skull.. moves into
compartments normally wouldnt be

Cushings Triad
High blood pressure - WHY???
Brain tells heart to produce higher pressure
Slow pulse
Good perfusion but doesnt create more pressure
Wide pulse pressure
LATE signs of increased ICP

Whats a brain attack?
Do you know someone who has had a stroke?
A. yes
B. no
What manifestations did they have? Dysfunction on 1 side of body, facial droop, aphasia

Cerebrovascular Accident (CVA)
BRAIN ATTACK!!!!
TYPES:
Ischemic stroke- blockage so lack of blood supply to certain part of brain
Hemorrhagic stroke-blood vessel bursts and leaks out

Ischemic Stroke Types:
Transient ischemic attack (TIA)
Last 1 hrspasm of blood vessel or short term blockage
Thrombotic stroke (large vessel)
Clot forms at specific location (atherosclerosis)
Lacunar infarct (small vessel stroke)
Embolic stroke (moving clot)
Clot moving around body

Temporary Ischemic Attack (TIA)
-may need treatment to prevent major stroke
Focal ischemic cerebral neurological deficits
Usually last less than 1-2 hours
Temporary disturbance in cerebral blood flow reverses before infarction occurs

Where would embolus be most likely to occur from?
A. Left side of heart
B. Lower extremities
C. Right side of heart
D. Lungs

Most frequent sites of arterial and cardiac abnormalities causing ischemic stroke
Clinical Manifestations
Sudden in onset, not LOC
Usually one-sided
Most common weakness of face and arm
Other unilateral numbness, vision loss, aphasia, dysarthria, and sudden, unexplained imbalance or ataxia

Treat based on damage: embolic and thrombi

Location of brain damage
RIGHT Brain Damage
Paralysed LEFT side
Behavior: quick, impulsive
Spacial & perceptual deficits

LEFT Brain Damage
Paralysed RIGHT side
Behavior: slow, cautious
Speech & language deficits
Depression

3 hours attack! Treatment of the Brain
Must be immediate use of early identification, special medical teams
Differentiate type of stroke WHY?
Treatment with new medications and procedures
Better recovery if area surrounding ischemic area (penumbra) has circulation restored fast

What medication is used to treat ischemic stroke first?
A. Anticoagulants heparin, warfarin
Too late already coagulating
B. Anti platelet aggregation aspirin, Plavix
C. Thrombolytics tPA, tissue plasminogen activator
D. Vitamin K, coagulation factors

Which should not use tPA?
A. Ischemic stroke
B. Myocardial infarction
C. Pulmonary embolism
D. Hemorrhagic stroke

Seizure disorders
-not a disease but symptom of several types of disorders
Seizure = Sudden, disorderly discharge of a group of cerebral neurons (focus)
Convulsion motor seizure: moving of arm and legs.. cause convulsion(rhythmic changes in muscle length)
Not a disease but symptom
Common in children, elders
Epilepsy seizure disorder without identifiable cause
Idiopathic- dont know cause

Seizure Treshold affected by:
Congenital defects
Tumors
Vascular lesions
Metabolic abnormalities
Head injury
Fever
Drug and alcohol use/withdrawal
Infections
Medications

Manifestations of seizures depends on how far of neuron movement spreads
+/- Bizarre muscle movements-smacking of eyes, licking of lips
+/- Unusual sensations, perceptions
(Tactile, odors, sounds, visual)
+/- Loss of consciousness: when middle centers of brain are effected
EXACT MANIFESTATIONS DEPEND ON LOCATION OF FOCUS AND SPREAD IN THE BRAIN

Seizure Terms
Aura-change in sensation person notices shortly before going to have seizure
Earliest part of the seizure, can protect self so dont get hurt
Prodroma
Hours-days leading up
Postictal state-wake up from deep sleep can become combativeness
Post seizure, global change

Have you been with someone having a seizure?
A. Yes
B. No
What do you do?
Protect their head, lower them to the floor, turn them on their side

Local (Partial) or Widespread (generalized)
Partial start in one lobe, so no loss of consciousness if simple, or, if complex, spreads to both lobes, leading to
impaired consciousness
Simple stays in location, complex spread to both lobe lead to impaired consciousness
Generalized spread widely and fast to both lobes, so loss of consciousness

Absence Seizures
Often confused with simple partial
NOT just a blank stare
Motion (automatisms, eyelid movement)
Lasts a few seconds
Cease in adulthood or evolve into motor seizures
PHENOBARBITOL, PHENYTOIN WORSEN!!!

Attonic or akinetic seizures
Drop attacks - sudden loss muscle
tone for a few minutes
Familial
Rule out syncope

Generalized motor seizures (Tonic-clonic grand mal)
Tonic phase
- simple partial seizure is prodrome
- loss of consciousness
- sharp tonic muscle contractions
- incontinence
Clonic phase
- brain fights back, alternating contraction and relaxation, slowing
- postictal: altered LOC, sleepy

Drugs wont help up to 40%
Other treatments:
Brain surgery
Ketogenic diet
Vagal nerve stimulator

Anti Epileptic Drugs (AEDs)
Lack of adherence (compliance) is the major reason for poor control!!
Balance of seizure control and adverse effects of the AEDs
Important to diagnose type of seizure, as it affects choice of AEDs
May need to adjust doses and add meds
Adjust dosages using plasma drug levels

Why use plasma drug levels?
A. Seizures may be infrequent, making it hard to monitor effectiveness
B. Non-compliance may be an issue
C. With multiple drugs, hard to know which is causing effects
D. All of the above

4 mechanisms of AEDs:
Block sodium channels, neurons repolarize more slowly, stops rapid firing
Block calcium channels, same
Block glutamate (excitatory neurotransmitter) receptors
Block excitiatory response
Increase GABA (inhibatory neurotransmitter)

Common problems with AEDs
Rapid withdrawal can lead to severe seizuresmust do so gradually
Most AEDs cause CNS depression, ESPECIALLY with other CNS depressants like alcohol
Many AEDs are metabolized by the liver, induce liver enzymes, and change metabolism of other meds, including other
AEDs
Enzyme induction leads to inactivation of normal dose oral contraceptives, and warfarin
-unanticipated pregnancytoxic to the fetus
Most AEDs can have negative effects on the fetus, but seizures have worse effects on the fetus

Two major types of AEDs
Traditional, including:
phenytoin (Dilantin)
carbamazepine more tolerated by people
valproic acid
phenobarbitol cheap , many adverse effects
ethosuximide
Well known, cheaper, more adverse effects
Newer, including:
gabapentin, lamotrigine, topiramate dont need to know
Not as tested, more expensive, but fewer adverse effects

Phenytoin (Dilantin)
Normalizes sodium flux in neurondoesnt fire as often
Raises seizure threshold
For partial and tonic clonic seizures, but NOT absence seizures

Phenytoin adverse effects
CNS: dizziness, sluggishness, confusion
(Avoid alcohol, other CNS depressants)
GI: nausea, constipation
Rashes stop! Dangerous to immune system
Gingival hyperplasialoss of teeth
(use folate rinse)

Drug Nutrient interactions of phenytoin
INDUCES hepatic metabolism of vitamin
B12, folate, vitamin D, vitamin K
DISPLACES folate from plasma proteins
Phenytoin metabolism USES UP folate

Adverse effects of phenytoin
Teratogenic (palate, lip, heart)
Folate supplementation REDUCES RISK

Monitor Phenytoin serum levels!
Highly bound to plasma proteins
Note FREE, UNBOUND phenytoin levels
NARROW THERAPEUTIC INDEX! Of what is therapeutic and what is actually toxic
Liver has limited ability to metabolize keep 10-20 mcg/mL therapeutic range

Phenytoin Toxicity
Sedation
Nystagmus
Ataxia lose balance
Diplopia double vision
Cognitive impairment

Phenytoin has many drug interactions
Many drug incompatibilities
(Do NOT mix C/ other parenteral Rxs)
INDUCES hepatic p-450 enzymes
DISPLACES other drugs, nutrients from plasma proteins
BINDS to proteins in enteral feedings

Carbamazepine
Similar to phenytoin, but fewer side effects
Can cause leukopenia, anemia, thrombocytopenia, even fatal aplastic anemia (bone marrow shut down) - rarely

Phenobarbital
Can be used for simple partial
Also used (infrequently) for complex-partial, tonic-clonic and febrile seizures
Similar adverse effects as phenytoin but NO EFFECT ON FOLATE, NO GINGIVAL HYPERPLASIA
Long time to stabilize blood levels

Valpoic acid (Depakote)
Gamma aminobutyric acid (GABA), an inhibitory neurotransmitterincreasing GABA
For ALL generalized seizures
75% of partial seizures controlled also
Also used for bipolar disorder

Valproic Acid Adverse Effects
Teratogenic (neural tube defects) - avoid in pregnancy
Hepatotoxicity, pancreatitis (avoid infants, elderly)
CNS depression (avoid alcohol, etc.)
Inhibits platelet aggregation
NO BEHAVIORAL EFFECTS

Every time have seizure compromise oxygen and can injure fetus

Benzodiazepinesstop seizures rapidly
Diazepine receptors potentiate GABA
Used for rapid cessation of seizures
MONITOR for respiratory depression

Clonazepam (klonopin)
A benzodiazepine for maintenance therapy of absence, akinetic seizures

2
nd
generation AEDS
oxcarbazepine (Trileptal)
lamotrigine (Lamictal)
gabapentin (Neurontin)
pregabalin (Lyrica)
topiramate (Topamax)

Magnesium Sulfate
For seizures caused by hypomagnesemia (eclampsia, hypothyroidism, alcohol withdrawal)
Side effects from hypocalcemia (CNS depression, hypotension, hypothermia, circulatory collapse)
Monitor serum magnesium levels
Treat toxicity with IV calcium gluconate (antidote)

Emergency: Status Epilepticus
Continuous tonic-clonic seizures for over 20 min., unconscious
Cause permanent brain damage
The longer the seizure activity, the more resistant to stopping the seizure, start treatment within 5 min.
Seizures using up oxygen and glucose, cause acidosis, brain damage, even death
Goals: maintain ventilation, treat hypoglycemia, stop seizures
Start IV, draw labs, give benzodiazepine
Lorazepam (Ativan), long acting (72 hr), preferred
Diazepam (Valium), short acting, need repeat


Heart Failure
Preload
Systole- pumping action (S1) felt in carotid pulse
Diastole- filling (S2)
Volume and pressure generated in the ventricle at the end of diastole
Determined by 2 factors:
Amount of venous return entering the ventricle during diastole
blood left in the ventricle after systole

Afterload- resistance left heart has to over come to eject blood
-increased afterload caused by hypertension
Resistance to ejection of blood from the left ventricle
Pressure in the left ventricle must exceed aortic pressure before blood can be pumped out during systole

Contractility-for any muscle
Change in tension at a given resting fiber length
Ability of the heart muscle to shorten

Stroke Volume
Volume of blood ejected per beat during systole (normal is about 70 ml for each ventricle_
Depends on force of contraction, which depends on myocardial contractility

Frank-Starling Mechanism
THE MORE THE MYOCARDIAL FIBERS ARE STRETCHED, THE GREATER THE FORCE OF CONTRACTION
-healthy heart should do whats asked of it, if more volume can stretch and contraction will be stronger
-in heart failure, contractility is decreased so less cardiac output

Congestive Heart Failure: Scope of the Problem
Nearly 900,000 annual hospital admissions (increased 90% in past 10 years)
6.5 million hospital days per year


Most common discharge diagnosis for patients older than 65 years
12-15 million office visits per year
Single largest expense for Medicare


Annual hospital/nursing home costs: $15.4 billion

Heart Failure-SYNDROME
-Effects diastole and systole
Complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the
ability of the ventricle to fill with or eject blood.
May be caused by any interference with normal mechanisms regulating cardiac output
Preload- volume; too much or too little
Afterload; hypertension or CAD inc afterload ventricle will have a lot of ressitance and will have to work
harder
Myocardial Contractility force of contraction
Heart Rate CO= sv x hr
Invasive: lines into neck floating into pulmonary artery
Other ways: are you making urine (indicated good blood flow to kidneys)

Heart Failure: Primary Cause
**biggest one is MI
Coronary artery disease
Hypertension
Rheumatic heart disease- comes from rheumatic fever
Developed from streptococcus infectionif not treated with antibiotics or on time
Fever cause damage to heart valves
Congenital heart defects
Pulmonary hypertension- right side
Cardiomyopathy-
Hyperthyroidism- overactive; increased oxygen demand
Valvular heart disease

Heart Failure: Precipitating Causes (at risk for HF, may not have it, stable HF without symptoms that cause acute
exacerbation of HF)

Anemia
Infection- fever, tachycardia
Thyrotoxicosis
Hypothyroidism
Bacterial endocarditis IV drug users, poor mouth care, bacteria stick to valve effect blood flow
Pulmonary disease- COPD
Hypervolemia too much preload

Left Heart Failure
Categorized as systolic or diastolic
Do not always exist independent of one another: Patients with systolic dysfunction may also have diastolic dysfunction.

Left hear failure: systolic failure more common
CO will be low because not difusing vital organs
Systolic failure
Inability of heart to pump blood effectively and perfuse vital organs
Most common causes are coronary heart disease, dilated cardiomyopathy, htn, and valvular disease
End result: left ventricle dilated & hypertrophied
Huge/floppy and not contracting well
Hallmark decreased ejection fraction

Ejection Fraction- calculate using echocardiogram
Systolic failure: may be 5-10%, not pumping enough blood, cause left over blood sit in left ventricle back up to left
atrium and into lungs causing shortness of breath
Amount of blood ejected per beat
Estimated by doing an echocardiogram
Normal is 60-75%
Decrease is hallmark of ventricular failure

Left heart failure: Systolic Failure
Systolic heart failure
Increased workload enlarges left ventricle leading to decreased function
Prevents forward flow of blood
Blood backs up into the left atrium & pulmonary veins
Can lead to pulmonary edema
Can lead to stress on right ventricle
Symptoms
Pulmonary vascular congestion
Dyspnea
Orthopnea
Cough/frothy sputum
Fatigue
Decreased urine output
Edema

Exam Systolic Failure
Cyanosis- seen in finger tips
Rales similar to crackles
Pleural effusions
Hypotension/hypertension- low cardiac output
S3 gallop- heart in heart failure ; sounds like when you say Kentucky
Extra blood slashing around ventricle
Evidence of underyling CAD or hypertension

Compensatory Mechanisms
-in low cardiac output state; want to inc cardiac output and overtime leading to worsening heart failure
Sympathetic Nervous System Activity
Triggered by low CO state
Increased catecholamine release
Increased heart rate
Increased myocardial contractility
Peripheral vasoconstriction
Neurohormonal Response
Decreased CO causes decreased blood flow to kidneys
Kidneys release renin, which converts to angiotensinogen to angiotensin I
Angiotensin I, converted by angiotensin converting enzyme in lungs, to angiotensin II
Adrenal cortex releases aldosterone
Retain Na and H20
Peripheral vasoconstriction
Neurohormonal response continued
Decrease in cerebral perfusion pressure
Posterior pituitary secretes antidiuretic hormone (ADH)
Water reabsorption in renal tubules
Proinflammatory cytokines also released
Endothelin released
Dilation
Enlargement of the chambers of the heart
Muscle fibers of the heart stretch
Increased contraction initially leads to increased CO
Eventually mechanism fails
Hypertrophy
Increase in muscle mass & cardiac wall thickness
Will lead to an increase CO but poor contractility and increased 02 consumption

Myocardial Hypertrophy
Myocyte growth
Up to 6x increase left ventricle
Ventricular stiffness

Left heart failure: diastolic failure
Heart failure with preserved systolic function or ejection fraction
Can occur alone or with systolic heart failure
More common in women
Results from decreased compliance of left ventricle

Symptoms:
Dyspnea on exertion
Fatigue
Crackles

Diagnosis
Based on 3 factors:
Signs/symptoms of heart failure
Normal ejection fraction
Evidence of diastolic dysfunction

Pulmonary Edema or Acute Decompensated Heart Failure
Symptoms:
-dyspnea
-increased work of breathing
-pink, frothy sputum

Exam:
-VQ mismatch
-crackles up to neck, feel like they are drowning (given ativan and lasix) may need to be put on ventilator

Right Heart Failure (can be caused by pulmonary hypertension)
-Inability of the right ventricle to provide adequate blood flow into the pulmonary circulation
can result from left heart failure, copd, cystic fibrosis
pressure rises in the systemic circulation, causing edema and hepatosplenomegaly (large liver and spleen)
-blood back up to right ventricle, to atrium and to the rest of body.. will see edema, fluid build up in systemic
circulation

Right Failure
Fatigue
Dependent edema
Distention jugular veins
Liver engorgement
Ascites result of liver disease
Anorexia, GI distress
Cyanosis
Inc. peripheral venous pressure

Diagnostic Tests
CBC: elevated WBC cause infection increase work load on heart
Low HandH is anemia
Chemistries
LFTs
TFTs-hypo/hyperthyroidism
BNP level elevated sign of heart failure
ABG looking at pO2 may show hypoxia
Echo- measure ejection fracture, look at valves itself
EKG-changes may be indicative of left ventricular hypertrophy
CXR- xray fluid in lungs, heart enlarged
Angiogram- look at coronary arteries, invasive, risks involved, determine if any calcification

BNP levels
Brain Natriuretic Peptide
Secreted from the left ventricle in response to stretch
-comes from left ventricle in response to stretch
-normal in pneumonia but elevated in heart level
-false high in kidney failure because secreted in kidney
Can be elevated in patients with:
Renal dysfunction
Large pulmonary embolism (due to atrial stretch)
Severe sepsis

Heart Failure
Severity of heart failure graded on the New York Heart Associations functional classification scale
Scale indicates how little or much activity it takes to make patient symptomatic
Class I: No symptoms with activity
Class II: Symptoms with ordinary exertion-walking to mailbox
Class III: Symptoms with minimal exertion-getting up to bathroom
Class IV: Symptoms at rest may be on transplant list

Stages of Heart Failure
A. at risk for HF but without structural heart disease or symptoms
B. Structural heart disease but without signs or symptoms of HF
C. Structural heart disease with prior or current symptoms of HF
D. refractory HF requiring specialized interventions-not responding to intervention

Disorders of the myocardium: cardiomyopathies
Diverse group of diseases that primarily affects myocardium
Most result of remodeling caused by MI/neurohormonal response to ischemic heart disease and hypertension
Can be secondary to toxic exposure, connective tissue disorders, infiltrative & proliferative disorders, nutritional
deficiencies
Many cases are idiopathic
Many different forms of cardiomyopathy: dilated, hypertrophic, or restrictive

Disorders of the myocardium: cardiomyopathies
1. Dilated
Most common form
Left ventricle becomes enlarged & dilated. cant pump as efficientlydecreases CO
Contractility decreased in left ventricle
Sinus tachycardia, atrial & ventricular dysrhythmiasv tach- lethal
Systemic or pulmonary thromboembolism
Eventually leads to left heart failure
Associated conditions: ischemic heart disease, alcoholism, pregnancy, infection, nutritional deficiencies,
exposure to toxins

2.Hypertrophic cardiomyopathy
Chamber volume decreased (left ventricle)
Compliance decreased, particularly left ventricle
Heart wall thickens, less space for blood
Less blood fills from chamber & is pumped out
Can develop atrial & ventricular dysrhythmias
Associated conditions: hypertension, aortic stenosis, inherited defect of muscle growth
Young athletes drop dead without symptosm
Inherited
Need inc preload to give blood a push out .. need more volume

3. Restrictive cardiomyopathy
Portions of heart wall become rigid & lose flexibility- decrease contractility
Compliance decreased
Eventually leads to right heart failure
Conditions associated with: amyloidosis, sarcoidosis, hemochromatosis protein build up in heart

Takotsubo cardiomyopathy
-broken heart syndrome
-stress inducedintense sudden stress release of catecholamine; inc workload on heart might feel like have heart attack
-sudden weakening of heart
-octopus pot in japaneese
-can cause lethal heart rhythms

Parkinsons Disease
What is happening to the brain?
-Extra pyramidal system controls movement
Deliver dopamine through striatum to the globus pallidus which converts nerve impulses and coordinates our
movements
-not enough dopamine because neurons that produce dopamine are being killed and dying off so balance of GABA is
thrown off (too much ACH) causing disturbed movement
-takes a lot of damage and long period of time in order to see symptoms


A disorder of balance
1. Not enough dopamine (dopamine producers are dying) and
2. Relatively too much acetylcholine, in the striatum
3. Not enough GABA inhibition of the control center for movement coordination, the Globus Pallidus
4. Uncontrolled neuron firing leading to DYSKINESIA, other symptoms of PD

Why do people develop Parkinsons or its symptoms?
Parkinsons Disease caused by:
Genetic problems with the destruction of alpha synuclein, a toxin that kills dopaminergic neurons.
Alpha synuclein forms fibrils called Lewy bodies seen on autopsy, diagnostic for PD
Environmental toxins, like cocaine, pesticides
Brain damage due to vascular diseases (diabetes, etc.), tumors, viruses, encephalitis
Parkinsonism (symptoms of Parkinsons) caused by anti-psychotic medications (reversible) meds
block dopamine receptors in the extrapyramidal system
Not disease itself, not cause by killing off neurons

Progressive death of dopaminergic neurons
Early symptoms:
Tremors at rest, especial a hand, on one side
Pill rolling
Head bobbing
Late symptoms:
Rigidity, cogwheel movement
Inability to initiate movement, bradykinesia, akinesia
Gait problems, hunched, forward leaning
Balance problems, cant stop

Bradykinesia
Slowness in initiating movements
Cannot stop easily
Shuffling gait
Micrographia (very small handwriting)
Cannot move slowly (fall risk)
Fenestration- big to tiny movements and cant stop
Top part of body continute to propel forward and feet get caught up
POSTURAL INSTABILITY IS VERY CONCERNINGmore and more steps to compensate

Problems beside movement, gait
Facial expression stiff, appears unemotional, less blinking so looks like staring
Eating difficult swallowing, drooling, prone to choking, difficult to feed self
Speech soft voice, poor articulation
Cant distinguish words
Emotions labile, depression
Increase tear formation
Weight loss loose clothing
Dementia 20-40%

Off balance, too much ACH
Diaphoresis sweating
Salivation - drooling
Lacrimation crying
Sebaceous secretion oily skin
Constipation
Urinary incontinence
Prolonged urination

How does this person look socially?
What is the initial reaction to this person?
Need for support, vs. appearance
Difficulties with ADLs, quality of life HUGE role for nursing care!
http://www.youtube.com/watch?v=IYbFFevRW_Q&feature=share&list=PL54C9B18894D14360

How can this condition be treated?
Symptom control, vs. cure
Medications more dopamine, less acetylcholine
Nutrition proteins inhibit absorption, Vitamin B 6 needed to convert meds to dopamine
Activity may respond to focused activities
Continuous motion stop shaking
Surgery medication delivery, stem cell/transplants, brain stimulation, destruction of pallidus
Pump deliver medication directly into blood streaminstead of GI tract where protein can iinterfere
with absorption
Electrode into brain and stimulateadjust stimulation until symptoms go away
Destrcructive surgery to globus pallidus and this reduces over stimulation

Strategies with medication
Goal: more stimulation of dopamine receptors in the striatum
1. Make more dopamine
2. Recycle dopamine (reuptake inhibitor)
3. Stimulate dopamine receptors without dopamine
4. Stop dopamine breakdown by stopping COMT and MAO-B
Goal: less acetylcholine stimulation (anti-cholinergics)

Most effective: treatment of levodopa
Levodopa CAN cross blood brain barrier
Levodopa gets converted to dopamine in a reaction using dopa decarboxylase enzyme and Vitamin B6
PERFECT, right?

Problems with levodopa treatment
Destruction of neurons continues, so dose has to increase, and meds stop working in a few years
Absorption problems: gradual and On-Off phenomenon
Levodopa is broken down peripherally (outside of brain) too, so only 2% actually reaches the brain
Need for Vitamin B6 to change levodopa to dopamine, but higher B6 levels cause more peripheral breakdown
Side effects of excess dopamine itself are severe dyskinesias, and psychosis
Amino acid compete, poor absorption, blood levels drops (good control bad control) and patients will
drop
Need b6 to be converted, b6 that changes rest of body cant pass the brain (accumulate b6 peripherally
causing breakdown)

On-Off phenomenon
Dyskinesia suddenly turns to bradykinesia
Large neutral amino acids in proteins in foods
compete with levodopa for absorption
Remedies:
Nutritional - redistribute protein in evening meal
More protein in evening meal and not morning when they are taking medication
Use implanted pump to deliver constant dose of levodopa

Levodopa side effects
All directly related to dosage
Nausea and vomiting effect on chemoreceptor trigger zone in brain
Dyskinesias like head bobbing, grimacing, ballismus, choreoathetosis
Postural hypotension
Dysrhythmias
Psychosis with hallucinations, night terrors, paranoia (use clozapine)
Cant treat with antipsychosis
BEST THING TO DO IS TO REDUCE TOTAL DOSE OF LEVADOPA
Darkening of urine, sweat
What do you do for each?
Drug holidays in hospital, dangerous
Take off levadopa, then put back on and patient will do better
When stop levadopa can go into freezing mode where cant intiate movement at all

Adding carbidopa to levadopa decreases these problems
Reduces total peripheral levodopa, and all side effects
Less need for Vitamin B6
Delivers 10% of levodopa dose to brain, not 2%

Drug of FIRST choice: dopamine agonist
-more likely to cause psychosis as reaction than dysknesia
5 drugs, main one is pramipexole (Mirapex)
Stimulate dopamine receptor even though not dopamine, cross of BBB, and causes same effect as
dopamine itself
Less dyskinesia, but more chance of psychosis
Side effects: sleep attacks, hallucinations, and postural hypotension
First drug used in younger patients
Not good for older patients or those with advanced disease

Other PD meds
COMT inhibitors Entacapone stop breakdown of levodopa
Increase levodopa avail to make into dopamine
Seligiline MAO-B inhibitor, stops breakdown of dopamine, may stop destruction of dopamine neurons,
stopping PD progression!!!
Stop neuron from dying and prevent progression of Parkinson disease
Amantadine many actions, inhibit dopamine uptake and increase release
Central Anticholinergics block cholinergic (acetylcholine) receptors, side effects like dry mouth, blurred vision,
tachycardia, constipation

Non medication treatments
Transplanted cells:
Stem cells
Fetal brain cells
Pallidotomy - unilateral
Deep brain stimulation - reversible
Nutritional
Activity

Heart Failure Treatment
Medical Nutritional Therapy in Heart Failure
Should promote a diet to control sodium and fluid retention, maintaining a healthy body weight, and providing a
diet adequate in vitamins, minerals, and proteins
May have other comorbidities such as diabetes, hypertension, obesity, or kidney failure
Heart failure may need low sodium but id diabetic teach about carbohydrate too
Kidney failure need low protein

Nutrition
Sodium should be restricted
If preserved or depressed EF, restrict to 2-3 gm/day
Moderate to severe, <2 gm/day
Should be taught major sources of dietary sodium, not adding salt, where to find sodium content on labels, and
to choose foods low in sodium
Canned vegetables, process foods, deli meet,
DASH (dietary approaches to stop hypertension)
Salt substitutes , spices, and low sodium marinades and sauces may be good substitution but watch for
potassium in patients with kidney failure
Potatoes, tomatoes, oranges and banana
Weight Monitoring
Weigh yourself at the same time everyday, wearing the same thing
Keep a record
If gain 2 pounds in one day or 5 pounds in a week, call provider

Cardiac Cachexia
Weight loss of more than 6% of the previous normal weight over 6 months associated with heart failure
Need more calories because greater work of breathing
Occurs in 10-15% of clients with heart failure
Seen in advanced disease
Undernutrition due to one or a combination of:
Increased nutrient losses
Unmet increased nutritional requirements
Decreased nutritional intake
malabsorption

Medical treatment
Diuretics
Inhibitors of RAAS system
Beta blockers
Digoxin
Effect preload, afterload, contractility, RAAS system

Diuretics
First line drugs for patients with signs of volume overload
Lose too much volume- dehydration case dry mucus membrane, low BP, high heart rate
Reduce blood volume and therefore decrease preload and afterload, edema, and cardiac dilation.
Must watch blood pressure

Diuretics: Thiazides
Ex. Hydrochlorothiazide (Hydrodiuril): oral agent
Produce moderate diuresis
Used for long term therapy
Ineffective when GFR is low
If CO is low, not good filtration of blood to kidneys so GFR is low
Should be above 60
Adverse effect: hypokalemia, hyponatremia

Diuretics: Loop Diuretics
Ex. Furosemide (Lasix)
Produce profound dieresis
Patient may take water pill for CHF but if come in with acute exacerbation (pilm edema) will treat with
IV lasix
Also called high ceiling agents
Promotes fluid loss even with low GFR
Will still have effect of dieresis
Used for severe heart failure
Oral or IV
Adverse Effects: hypokalemia, dehydration, ototoxicity
Hypokalemia can cause digoxin otoxicity

Loop Diuretics: drug interactions
Digoxin
Ototoxic drugs : aminoglycoside antibiotics
Potassium sparing diuretics
Lasix with potassium sparing diuretics to keep potassium normal

Aldosterone
Promotes ventricular remodeling
Promotes myocardial fibrosis
Activation of SNS (causes tachycardia)and suppression of norepinephrine uptake in the heart
Promotion of vascular fibrosis
Acts to promote sodium uptake in exchange for potassium excretion

Diuretics: Potassium Sparing Diuretics
Ex. spironolactone (Aldoactone) - nonselective
eplerenone (Inspra)- selective
Promote small amount of diuresis
Used to counteract K loss caused by thiazide and loop diuretics
Adverse Effect: Hyperkalemia, gynecomastia
Be cautious if combined with an ACE I or ARB
Pregnancy category C
Can give with loop thiazide diuretics
Give with foods high in potassium

Spironolactone
Prolongs survival in patients with HF primarily by blocking receptors for aldosterone
Guidelines recommend adding to standard therapy in patients with moderately severe or severe therapy

Drugs that inhibit RAAS
RAAS plays important role in hemodynamic changes that occur when cardiac output is low
4 groups:
ACE inhibitors
ARBs
Direct renin inhibitors
Aldosterone agonists

Ace Inhibitors
Ex. Captopril, enalapril
Block production of angiotensin II, decrease release of aldosterone, and suppress breakdown of bradykinins
Results in dilation of arterioles and veins
Can prolong life
Usually combined with beta blocker and diuretic
Preload and afterload will decrease if dialation in vessels because dont have to pump hard against increases
resistance
Start on LOW DOSE due to dialation can become hypotensive

Benefits
Improved blood flow to kidneys
Reduces preload and afterload
Excretion of sodium and water
stops progression of cardiac remodeling


Adverse Effects
Hypotension
Hyperkalemia
Intractable cough
Angioedemalips and tongue swell up (most severe reaction)
Renal failure in patients with bilateral renal artery stenosisno blood flow to kidneys
Pregnancy category X

ARBs
Effects are similar to ACE
Reserved for those who cannot tolerate an Ace
Improve ejection fraction, reduce heart failure symptoms, increase exercise tolerance, decrease hospitalization,
enhance quality of life, and reduce mortality

Direct Renin Inhibitor
Only 1 available aliskiren(Tekturna)
Effects similar to ACE I and ARBs
Acts on renin to inhibit conversion of angiotensin into angiotensin I
Causes less angioedema and cough than ACE I

Beta Blockers
Ex. carvedilol (Coreg), bisoprolol (Zebeta), sustained release metoprolol (Toprol XL)
Can improve LV ejection fraction , increase exercise tolerance, slow progression of heart failure, reduce the need
for hospitalization, and prolong survival
Protects the heart from excessive stimulation and dysrhythmias
Doses initiated at low dose and gradually increased
May take 1 -3 months to see benefits
**AFFECT HR MORE THAN BP

Adverse Effects
Fluid retention and worsening heart failure
Fatigue
Hypotension
Bradycardia or heart block
SLOW HEART RHYTHYMS CAN BE DANGEROUS

Inotropic AgentsCONTRACTILITY: FORCE OF CONTRACTION
Chronotropy: rate of contraction
Digoxin
Sympathomimetics
Increase cardiac output by increasing contractility and reducing neurohormonal activation
Used for systolic heart failure (bc systolic is the PUMPING diastolic is the FILLING)

DigoxinTreat symptoms at the time; not used for acute episode of heart failure
Cardiac glycoside
Can be given po or IV
Positive inotropic agent
Increases cardiac output
Can alter the electrical activity of the heart
Second line agent
Cannot prolong life

Digoxin and Potassium (inverse: when dig is low, potassium is high)
K ions compete with digoxin on the Na/K ion pump
When K is low, binding of digoxin is increased, causing toxicity
When K is high, digoxin is reduced

Digoxin: Adverse Effects
Narrow therapeutic window- -want to keep levels normal
On high level of window, will see side effects of toxicity
Normal level 0.5-1.5
Must be monitored closely
Decreased dose if renal impairment
Nausea, vomiting (usually happens first)
fatigue
visual disturbances yellow tinge
Dysrhythmias
IV dose = digloading

Drug Interactions
Diuretics
ACE inhibitors and ARBs
Sympathomimetics
Quinide- increase dig level by decrease renal excretion of dig
verapamil calcium channel blocker

Pharmokinetics
Absorption is variable
decreased by foods high in bran
Eliminated by renal excretion
Can take 6 days to reach plateau

Treatment of Digitals Intoxication
Stop drug
Gastric lavage
Activated charcoal
Hemodialysis
Digibind
antidysrhythmics

Sympathomimetics: Dopamine
Must be given IV in hospital
Weight based
Catecholamine, activates:
beta adrenergic receptors in the heartincrease HR
Dopamine receptors in the kidneyinc blood flow to kidney so inc urine output
Alpha adrenergic receptors in blood vessels (at high doses)down side bc when activate alpha
andrenergic will inc vascular resistance leading to constriction
Short term rescue measure for severe acute heart failure

Dobutamine
Given IV in the hospital
Preferred over dopamine
Synthetic catecholamine, causes:
Selective activation of beta adrenergic receptors
Does not activate alpha receptors
Phosphodiesterase Inhibitors
Ex. Milrinone
Continuous IV infusion
increased contractility and promotes vasodilation
dec preload/afterload
results from an increase in cAMP secondary to inhibition of PDE3
cAMP should allow heart to pump more effic and inc contractility.. and phos tries to ibhibit this from
happening soooo inhibitor prevents phos from inhibiting
Used for patients in acute heart failure, not responding to traditional treatment

Vasodialator
Isosorbide and hydralizine are usually combined
Can be used as an alternative to ACE or ARB
Isosorbide casues dilation of veins, can improving congestive symptoms
Can cause hypotension, tachycardia
Hydralizone causes dilation of arterioles, improving cardiac output and renal blood flow
Can cause hypotension, tachycardia

Intravenous Vasodialators
Nitroglycerin
Venodilator, decreases venous pressure-dec preload/afterload used for chest pain
Used for acute pulmonary edema
Sodium nitroprusside (Nitropress)
Dilates arterioles and veins, reduces afterload and increases cardiac output
Used for short term therapy
Nesiritide (Natrecor)
Synthetic human BNP

Meds to avoid in heart failure
NSAIDS
Calcium channel blockers
TZDs
theophylline

Surgical treatment heart failure
Cardiac transplantation is ultimate treatment for end stage heart failure
Coronary revascularization
Mitral valve repair
LV reconstruction

Device Therapy abnormal/fast heart rhytyms
Implanted cardioverter defibrillator-zap into normal heart rhythms
Cardiac resynchronization
Ventricular assist device (VAD) usually on left side
Mechanical devices that can assist and support the circulation
Used for:
Bridge to transplant
Bridge to decision
Destination therapy

Exercise training
In past, bed rest was recommended
Now we know that inactivity is detrimental
Exercise can improve clinical status, increase exercise capacity, and improve quality of life
No blood pressure
Judge CO by pink, warm, making urine, not lethargic
INR kept at 2.5/3high so dont have clotting but this may cause a hemmorhagic stroke
If CO is lowinc RPM to improve it

Monitoring
Watch for reduction in symptoms
JVD, edema, rales
Increased capacity for physical activity
Lower BNP
Improved quality of life

Thyroid Problems and Treatment
A negative Feedback System

Endocrine System
Glands
Hormones-attach to cells that are receptive and hormones turn activity of cell of or on?
Feedback Mechanisms

Altered Endocrine Function: 2 types
Hyposecretion of hormone
Hypersecretion of hormone
Pituitary hormones, target tissues, and feedback mechanisms
`
Anterior pituitary gland produce specific hormones and determine if turn on or off
-when it becomes aware the metabolism is too low, produces TSH
-stimulates thyroid gland and will produce 2 hormones (t3 and t4) and provides feedback to pituitary gland to
shut off tsh if messed up producing too much or too little hormone

Thyroid Hormone production
Thyroid takes up iodide (50 x other tissue), joins to glycoproteins using enzyme
Released as T3 and T4, over 99% protein bound in blood
Only free amount (1%) act on tissues
In peripheral tissues all converted to bioactive form, T3
T4 is precursor, T3 is active and change production in nucleus to change degree of energy use in cell
speeds it up to create heat and change way cell is acting will cause heart to beat harder and faster
T3 goes into cell nucleus, changes DNA to increase energy use

What happens if not enough iodine intake?
To T3 and T4 levels? Decrease
To TSH levels? Increase
To the thyroid gland itself? Inc in size, press on trachea so person cough, hoarse voice, difficult to swallow, hard
to flex the neck

3 effects of increased cellular energy use due to T3
1. Increased metabolic rate
2. Increased heart rate and strength
3. Growth and development, esp. brain, nervous system, and skeletal muscle

Hypothyroidismlow and slow
Congenital or acquired
Decreased production of thyroid hormones (T3, T4)
Causes symptoms & Myxedematype of edema develops for mucoid fluid (diff texture)
Primary type from the thyroid glanddue to damage, surgically removed, exposed to radiation
Secondary type from the anterior pituitaryisnt working in negative feedback so not creating TSH the way it
should more trouble than hypothyroidism

Primary Hypothyroidism
Thyroid gland cannot produce thyroid hormones (T3, T4), so these are low
Because low T3 and T4, anterior pituitary produces more TSH to stimulate the thyroid, and serum TSH is high
tSH much more sensitive indicator.. t3/t4 will go down but TSH will be increased
t3/t4 not as sensitive because protein bound.. tsh will detect much earlier
Secondary Hypothyroidism
Anterior pituitary doesnt produce TSH to stimulate thyroid, so
Thyroid doesnt make T3 and T4
Serum levels of BOTH TSH and T3 & T4 are low

When T3 is low
First, subtle changes like cold intolerance, low temp, slow reflexes, slower mentation
Then dry skin, facial edema, hair loss/brittle hair, eyebrows thin, constipation, lethargy, decreased facial
expression, mental slowness
Finally, MIXEDEMA mucoid edema, and coma

Hypothyroidism treatments
Replace missing T3as early as possible in newborn
Needed in newborn, for brain development
Treat underlying cause, if secondary
Monitor treatment with TSH & decreasing symptoms
Exemplar: Levothyroxine - synthetic, identical, brands NOT interchangable
Some brands more active than others
Overdose = hyperthyroid symptoms

Hyperthyroidism manifestationstoo much t3
-Excess thyroid hormone secretion
-Causes sympathetic NS symptoms: inc HR, temp, BP, resp rate, go through calories quickly, eat a lot and lose weight,
tremor, nervous
-Thyrotoxicosisthyroid is toxic
-Thyroid storm crisis, hyperthermia, tachycardia, delerium, due to stressor

Clinical Manifestations
Increase in metabolism
Increase in oxygen consumption
Increase in sensitivity to stimulation of SNS

Hyperthyroidism labs:
High serum T3, T4
High metabolic rate, O2 consumption
LOW TSH (feedback to anterior pituitary!), can be normal or sl. high
Radioactive iodine uptakehow fast concentrate into thyroid gland determine if uptake is too fast and if it is
hyperactive

Graves Diseasemost common cause of hyperthyroidism
Autoimmune disordercreates antibodies that take place of TSH on thyroid gland and stimulate thyroid gland
causing overgrowth of thyroid gland from overstimulation
Thyroid Stimulating Antibodies
Goiter
Exophthalmos eyeballs bulging out
Hyperthyroid to hypo

Hyperthyroidism treatments
Deal with dangerous symptoms!
Medications to decrease thyroid function
Radioactive iodine to kill thyroid cells, then replace thyroid hormones if needed (131 I)
Surgical removal of gland tissue
Treat autoimmune disease

2 main anti-thyrotoxic medications
Propylthiouriacil (PTU) good in pregnancy, less crosses placenta, less peripheral conversion to T3
Methimazole (Tapazole) longer half life, so only once a day
Same main mechanism: inhibits enzyme (peroxidase) needed to make T3 & T4
Same problem effects: rare agranulocytosis, rashes

Giving non-radioactive iodine
Immediately suppresses T3, T4
Cant use long term
Lugols

Managing severe symptoms
Beta blockers- slow HR so dont go into heart failure
Coolinguse a cooling blanket
Sedation
Exopthalamos: eye drops, surgery, steroids





Polypharmacy
Administration of many drugs together
Administration of more medication than are clinically indicated
Precise number is variable, but generally 5 to 10
Includes prescribed medications, over the counter medications, herbal supplements

Balance is required between over and underprescribing
Multiple medications usually needed to manage clinically complex older adults
Ex. 76 y/0 female patient with COPD, T2DM, osteoporosis, htn, and osteoarthritis would probably
require 12 medications

Factor Contributing to Polypharmacy
Multiple providers- doctor shop to get medications they want
Non adherence-
Underreporting symptoms-not getting right medications
Taking others medications-daughter has metformin so take her medications for own diabetes
Diastolic and lopressorboth beta blockers; low heart rate
Expense
Confusion between brand name and generic name

Example
Doctor changes from one med to another within the same therapeutic class; but the patient doesnt stop
taking the first med. (two drugs doing the same thing, maybe not educated to stop the first drug)
For example: You are taking Protonix 40mg and Dr. gives you a prescription for Prevacid 30mg. Both of these drugs are
in the same therapeutic class Proton Pump Inhibitors and work the same way. No one should be on both these meds.

Doctors also may have a patient on a brand name drug and write the next prescription for a generic drug.
For Example: A patient is taking Coumadin 5mg daily; the Doctor gives patient a prescription for Warfarin 5mg, another
trade name for Coumadin. The patient continues to take both not realizing they are the same medication. This could
have devastating consequences.

Prescription drugs switching to over-the-counter (OTC) status
For Example: A patient may take Prilosec (OTC) and get a script for Protonix, Prevacid,, etc. This is why it is so important
that you take all the meds you take on a regular basis with you when you go to the doctor.

Risks
Side effects-how do you know which medication is causing a side effect
Allergic reactions
Interactions-how they are metabolized
Metabolism
Compliance secondary to complexity
Cost

Elderly at risk
12% of US population but 31% of nations prescribed drugs
Increased severity of illness, multiple pathologies, excessive prescribing
More sensitive to drugs
Wider individual variation
Experience more drug reactions and drug-drug interactions

Why elderly at risk
Altered pharmacokinetics
Multiple and severe illnesses
Multidrug therapy
Poor adherence
May be taking a drug that they found in medicine cabinet

To ensure safe medication practicemainly REDUCE SYMPTOMS
Individualization of treatment
Monitored closely for desired and adverse responses
Regimen adjusted carefully

Pharmokinetic changes in elderly
Gradual progressive decline on organ function, altering the absorption, distribution, metabolism and excretion
of drugs
Effect drug sensitivity
Extent of change varies among patients

Absorption
Rate of absorption may be delayed because of delayed gastric emptying and reduced blood flow to the gut
Drug responses may be delayed

Distribution
4 major factors can effect:
1. increased percent body fat
2. decreased percent lean body mass
3. decreased total body water
4. reduced concentration of serum albumin

Metabolism
Rates of hepatic drug metabolism decline with age because of reduced hepatic blood flow, reduced liver mass,
and decreased activity of some hepatic enzymes
Half lives of certain drugs may be increased, prolonging response
Stick around longer than it is supposed to

Excretion
Renal drug excretion undergoes progressive decline beginning in early adulthood
** drug accumulation secondary to reduced renal excretion is the most important cause of adverse drug
reactions in the elderly
Decline in renal function is result of reductions in renal blood flow, GFR, and number of nephrons
Should monitor creatinine clearance
**Less lean muscle mass (creatinine is measure of kindey function but also reflects muscle mass) you must look
at GFR or creatinine clearance, will give adequate estimeate of kidney functionjust bc low muscle mass, creatinine will
be low but doesnt mean kindey is functioning properly

Pharmodynamic changes
Alteration in receptor properties
Ex. Beta blockers less effective in elderly
A reduction in beta receptors
Reduction in affinity of beta receptors for beta receptor blocking agents
Warfarin produce effects that are more intense in the elderly possibly due to an increase in receptor
affinity

Adverse drug reactions (ADR) and drug interactions
ADRs are 7 times more common in the elderly
Usually dose related
Symptoms nonspecific
Multiple factors predispose older adults:
Drug accumulation secondary to reduced renal function
Polypharmacy
Greater severity of illness
greater use of drugs with a low therapeutic index
Poor adherence

Measures to reduce ADR
Taking a thorough drug history , including OTC
Accounting for pharmacokinetic and pharmacodynamic changes that occur with aging
Initiating therapy with low doses
Monitoring responses and drug levels in order to adjust doses
Employing simplest regimen possible
Monitoring for reactions
Periodically reviewing the need for medications, and discontinuing if appropriate
Encouraging the patient to dispose of old medications
Avoiding drugs on the Beers list

Nonadherance
Between 26% and 59% of elderly dont take their meds as prescribed
Never fill or refill prescriptions
Account for 10% of all hospital admissions because of therapeutic failure

Factors for nonadherance
Unintentional:
Forgetfulness
Failure to understand instructions
Inability to pay
Use of complex medications

Factors for nonadherance
Intentional: (about 75%)
Patient thinks that drug not needed
Unpleasant side effects
expense

promoting adherence
Simplify regimen
Explain the treatment regimen in a clear, concise way
Choose appropriate dosage form
Labeling drug containers clearly
Suggest recording drug administration
Asking patient if they have access to pharmacy and can afford the medication
Enlisting friend or relative to help

Prescribing cascade
Develops when an adverse drug event is mistaken as a new medical condition and additional medication is
added
Patient is at risk for developing additional adverse drug events

Beers criteria
Most widely used criteria to assess inappropriate drug prescribing
List of 53 meds considered inappropriate for prescribing to older adults because of adverse reactions or
ineffectiveness
3 categories: meds that should be avoided, meds considered inappropriate, and those that should be used with
caution

High risk medications
First generation antihistamines
Analgesics
Antidepressants
Antihypertensive
Sedative hypnotics
Drugs for urge incontinence
Muscle relaxants

Anticholinergic activity
Associated with multiple adverse drug effects:
Memory impairment, confusion, hallucinations, dry mouth, blurred vision, constipation, nausea, urinary
retention, impaired sweating, tachycardia
glaucoma
closed angle glaucoma can go blind this is an emergency

Atypical antipsychotics
Increased risk for falls
Limited evidence to support use of these meds in elderly

Herbal supplements
Common in elderly
Dont always tell provider
Dont consider them medications

Most commonly usedserotonin syndrome = tachycardia
Three Gs:
Ginko Biloba, ginseng, garlic
Have antiplatelet effect, problematic with prescription antiplatelet medication
Ex. Warfarin and ginko biloba

Most commonly used
St johns wort
Potential for serotonin syndrome when taken with SSRI
Valerian root
Not to be used with benzos , alcohol, sedatives

Med reconciliation
Average hospitalized patient is subject to one medication error per day
Formal process for creating the most accurate and complete list possible of the patients medications and
comparing those to the patients records
Attempt to avoid duplications, omissions, errors, or potential for interactions
Should be done at every transition of care
Should include all medications, herbals, vitamins, otc drugs

Brown bag medication review
Patients are asked to bring all their medications including OTC, herbal supplements, and vitamins
Answer questions about medications, verify what is being taken and how much, identify possible errors

Nursing Responsibilities
Preparing, administering, and evaluating client responses to medications
Developing an up to date knowledge base of medications, including uses, mechanism of action, safe dosage, side
effects, and contraindications