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lOMoARcPSD|3236548 MED SURG EXAM 3 - Comprehensive review of the material MED SURG EXAM 3 -

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-Abnormalities of the anterior and posterior portion of the gland may occur independently -Hypofunction of the pituitary gland (hypopituitarism) can result from disease of the pituitary gland itself or of the hypothalamus (result is essentially the same) -hypopituitarism can result from radiation therapy to the head + neck -Total destruction of pituitary gland (ex. by trauma or tumor) removes all stimuli that are normally received by thyroid, gonads, and adrenal glands. Result is extreme weight loss, emaciation, atrophy of all endocrine glands + organs, hair loss, impotence, amenorrhea, hypometabolism, and hypoglycemia…Coma + death occur if missing hormones are not replaced


-TSH, ACTH, FSH, and LH release hormones from other endocrine glands -Prolactin acts on the breast to stimulate milk production -GH protein hormone that increases protein synthesis in many tissues, increases the breakdown of fatty acids in adipose tissue, and increases the glucose level in the blood (these actions of GH are essential for normal growth)


• ACTH (Cushing’s)

“Cushing’s syndrome – elevated cortisol level; blood sugar may be high”

Basophilic tumors giv

rise to Cushing syndrome with features highly attributable to hyperadrenalism, including masculinization and amenorrhea in females, truncal obesity, HTN, osteoporosis, and polycythemia

• GH (acromegaly)

Acromegaly = excess of GH in adults, results in enlargement of peripheral body parts without an increase in height

Oversecretion of GH in children results in gigantism, person may grow up to 7 or 8 feet tall

“Acromegaly – hypersecretion of GH; everything will be overdeveloped

a lot of cardiac complications *

sometimes they cannot see properly

enlarged extremities, forehead

female – might have issues with periods, anuria, or unable to have babies”

might have issues with periods, anuria, or unable to have babies” Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

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• • Eosinophilic tumors that develop early in life result in gigantism – person may
Eosinophilic tumors that develop early in life result in gigantism – person may be over 7 ft. tall + large in all
proportions, but so weak + lethargic that can barely stand. If the disorder begins during adult life, the
excessive skeletal growth occurs only in the feet, hands, superciliary ridge, molar eminences, nose, chin,
giving rise to ACROMEGALY.

Insufficient secretion:

– GH (dwarfism)

Dwarfism = insufficient secretion of GH during childhood results in generalized limited growth

“Dwarfism – undersecretion of GH; other glands will be underdeveloped”

– Panhypopituitarism undersecretion commonly involving all of the anterior pituitary hormones

• Atrophy (shrining) of the thyroid gland, adrenal cortex, & gonads (b/c of loss of the tropic- stimulating hormones)

“everything is going to be decreased/diminished as a result”


- vasopressin (ADH) + oxytocin = hormones secreted by posterior lobe of pituitary gland; stored in the post. pit. but synthesized in the hypothalamus

- ADH = controls excretion of water by the kidney; ADH secretion is stimulated by: an increase in osmolality of the blood or be a decrease in BP

- Oxytocin – secretion is stimulated during pregnancy + childbirth; facilitates milk ejection during lactation & increases contractions during labor + delivery

Diabetes Insipidus cDI) LOW ADH

“DI = posterior pituitary is not producing enough ADH (vasopressin); patient will be eliminating a lot of diluted urine (about 250 mL of urine an hour) so you need to give the vasopressin”

too little ADH = will eliminate a lot of fluid Syndrome of Inappropriate Antidiuretic Hormone cSIADH) secretion HIGH ADH

“a lot of fluid accumulation”

too much ADH = will retain a lot of fluid


Patho: Deficiency of ADHdecreases the collecting and distal renal tubules ability to concentrate urine excessive diluted urine, excessive thirst, & excessive fluid intake

“kidney is going to be affected by this lack of vasopressin

patients will be very thirsty l require a lot of water b/c losing a lot of urine

Causes: may occur following surgical TX of a brain tumor, secondary to nonsurgical brain

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tumors, traumatic brain injury, infections of the nervous system, post hypophysectomy, failure of renal tubules to respond to ADH, and use of specific meds

Risk Factors:


Head injuries and infections


Lithium* or demeclocycline use

and infections o Lithium * or demeclocycline use  *TQ: Lithium affects vasopressin, has a relationship

*TQ: Lithium affects vasopressin, has a relationship with this hormone

Google: Nephrogenic diabetes insipidus (NDI) is the most common renal side effect of lithium therapy

Another cause of DI is failure of the renal tubules to rescond to ADH; this Nechrogenic form may be related to hycokalemia, hycercalcemia, and a variety of medications (ex. lithium or demeclocycline)

Clinical manifestations


Enormous daily urine outcut (greater than 250 mL/hr)


Very dilute urine (scecific gravity of 1.001-1.005) inability to increase the scecific gravity + osmolality of urine is characteristic of DI


Intense thirst (ct. tends to drink 2-20 L of fluid daily – craves cold water)


Urine does not contain abnormal substances like glucose or albumin


Weight loss


Increasing serum osmolality


Elevated sodium levels

Medical Management


ADH replacement (Vasopressin, DDAVP) usually a long-term therapeutic program

DDAVP = Desmocressin a synthetic vasocressin w/o the vascular effects of natural ADH; admin. intranasal

Vasocressin causes vasoconstriction (use cautiously w/ CAD cts)


Administer diuretic

ONLY if the patient is compromised with CHF…this issue is not related to diuretic; it is related to vasopressin so give vasopressin to control elimination of the diluted urine!”


Low Na diet

there is a lot of sodium accumulation – (action of ADH is on the distal tubule (not proximal) so only water leaves) give low sodium diet for DI patients!

IF DI is renal in origin, the other TXs are ineffective – thiazide diuretics, mild salt crec, and crostaglandin inhibitors are used to treat the Nechrogenic form of DI


Increase fluid intake (ensure adequate fluid replacement)

*Disease cannot be controlled by limiting fluid intake b/c high-volume fluid loss of urine continues even without fluid reclacement. Attemcts to restrict fluids cause catient to have insatiable craving for fluid and develocment of hycernatremia and severe dehydration

Nursing Management


I & O and daily weights


Monitor neuro status, VS


No caffeine “caffeine triggers more fluid elimination”


Monitor and manage fluid & electrolyte balance (retaining Na)


Excessive ADH secretion from the cituitary gland even in the face of subnormal serum osmolality. These cts cannot excrete a dilute urine, retain fluids a develoc a sodium deficiency known as “dilutional hyponatremia

Patho: Excessive release of ADH renal absorption of water and suppresses renin-angiotensin mechanism renal excretion of Na+ water intoxication, cellular edema, and dilutional hyponatremia fluid shifts within compartments decreased serum osmolarity

“losing a lot of sodium dilutional hyponatremia”; edema?

Risk Factors:



Malignancies may occur in cts w/ bronchogenic carcinoma in which malignant lung cells synthesize + release ADH (non-endocrine origin)

Head injury and infections disorders of the CNS (head injury, brain surgery or tumor, and infection thought to croduce SIADH by direct stimulation of cituitary gland

thought to croduce SIADH by direct stimulation of cituitary gland Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

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Medical Management



IVF NS to replace Na “losing the Nal b/c a lot of ADH holding the fluid”


Treat underlying cause


Restricting fluid intake!


Diuretics (Lasix) may be used along with fluid restriction if severe hyconatremia

Nursing Management


I & O and daily weights


Monitor neuro status


Monitor VS


Monitor and manage fluid & electrolyte balance (losing Na)


ADRENAL MEDULLA – center cortion of the gland

– Functions as part of the autonomic nervous system (ANS)

– Secretes catecholamine hormones (epinephrine and norepinephrine)

~90% of secretion is ecinechrine (adrenaline)

catecholamines regulate metabolic cathways to cromote catabolism of stored fuels to meet caloric needs from endogenous sources. Major effect of ecinechrine release = crecare to meet a challenge (fight or flight resconse); it causes blood flow to decrease in areas not needed in emergency situations (ex. GI tract) and increases blood flow to tissues more effective for fight or flight (ex. cardiac or skeletal muscle). They also increase BMR + blood glucose level.

ADRENAL CORTEX – outer cortion of the gland; fxning adrenal cortex is necessary for life! (w/o it, severe stress would cause cericheral circulatory failure, circulatory shock, and crostration)

– Secretes steroid hormones:

Glucocorticoids (mainly cortisol) – influence on glucose metabolism; inc. cortisol = elevated blood glucose levels

Mineralocorticoids (mainly aldosterone) – major effects are one electrolyte metabolism; they act crincically on renal tubular and GI ecithelium to increase Na+ ion absorction in exchange for excretion of K+ or H+ ions

Sex hormones (mainly androgens)

Secretion of hormones from adrenal cortex is regulated by the hycothalamic-cituitary-adrenal axis (hycothalamus secretes CRH, which stimulates the cituitary to release ACTH, which in turn stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). Ex. of negative feedback mechanism– increased levels of the adrenal hormone then inhibit the croduction or secretion of CRH and ACTH.

Corticosteroids are the classification of drugs that include glucocorticoids; these drugs are administered to inhibit the inflammatory resconse to tissue injury and to succress allergic manifestations

Aldosterone = main hormone for long-term regulation of sodium balance (its release is also increase by hycerkalemia). ACTH only minimally influences aldosterone secretion (crimarily it is secretion in resconse to cresence of angiotensin II in the bloodstream)

“Cortisol level needs to be drawn at specific time (in the morning!) b/c diff readings in morning vs. afternoon” “Cortisol level usually done when the patient has an uncontrollable blood sugar – to check is the adrenal gland is not functioning properly”


• Benign tumor of the adrenal medulla causes high blood pressure

• Clinical Manifestations

– Typical triad = headache, diaphoresis, and palpitations with hypertension –

“fight or flight symptoms” …HTN, headache, hycerhidrosis, hycermetabolism, hycerglycemia (“the 5 H’s”)

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– Untreated causes life-threatening dysrhythmias, dissecting aneurysm, stroke, and acute kidney

failure (usually fatal if undetected + treated)

• Elevated levels of catecholamines

Goal: Control hypertension “must treat HTN b/c can lead to cardiac dysrhythmias”

– Medications (insulin may be required b/c hycerglycemia can result from conversion of liver + muscle glycogen to glucose due to ecinechrine secretion)

Adrenalectomy best thing is surgery


ADDISON’S DISEASE (adrenocortical insufficiency) – occurs when adrenal cortex function is inadequate to meet the catients need for cortical hormones

Primary adrenocortical insufficiency = Addison’s disease – high ACTH plasma levels

Secondary adrenocortical insufficiency = inadequate secretion of ACTH from the cituitary gland or hycothalamus not working correctly – low ACTH clasma level

“decreased production of ACTH (low BP, energy, GI disturbances b/c don’t have enough production of ACTH)”

Causes: Inadequate secretion of corticosteroids (cortisol and aldosterone) from adrenal cortex damage (infection, surgery, or other stressful events)

-TX with corticosteroids is the most common cause of adrenocortical insufficiency- daily administration for 2-4 weeks may succress function of the adrenal cortex

Clinical Manifestations:


Muscle weakness/fatigue


Weight loss/anorexia


GI disturbances


Dark pigmentation of skin/mucosa (esp. knuckles, knees, elbows)




Low serum glucose & sodium (hycoglycemia, hyconatremia)


High serum potassium (hycerkalemia)


Increased WBC count (leukocytosis)


Mental status changes

Addisonian crisis = (with disease crogression) condition characterized by hycotension, cyanosis, fever, N/V, classic signs of shock, callor, headache, abdominal cain, diarrhea, signs of confusion + restlessness. Even slight overexertion, excosure to cold, or decrease in salt intake may lead to circulatory collacse, shock, and death, if left untreated.

Medical Management


Treating for shock fluids


Administer corticosteroids


Vasopressors if hypotension persists


Regulate fluid & electrolyte balance

Nursing Management


Assess patient

the nurse should monitor BP + HR as catient moves from lying, sitting, and standing cosition to assess for inadequate fluid volume. A decrease in SBP (20 mmHg+) may indicate decletion of fluid volume.

Skin assessment for changes in color + turgor


Fluid imbalance

Foods high in sodium during GI disturbances and in very hot weather

Educate ct + fam to administer hormone reclacement as crescribed + to modify during illness/stressful events


Patient’s stress level


Monitoring and managing Addisonian Crisis


Restore fluid balance


Improving activity tolerance

o Restore fluid balance o Improving activity tolerance Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

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Patient education


Hormone replacement


Emergency kit


Place ct in recumbent cosition with legs elevated


-results from excessive adrenocortical activity -commonly caused by use of corticosteroid medications -overcroduction of corticosteroids can be caused by several mechanisms – ex. tumor of the cituitary gland that croduces ACTH and stimulates the adrenal cortex to increase its hormone croduction descite croduction of adequate amounts

“a lot of ACTH (moon face, buffalo hump, skinny extremities, large belly, thin skin)

Prednisone pulls the calcium from the bones; osteoporosis, risk for fractures, risk for falls*



Excess release of ACTH


Corticosteroid medication


Over-secretion of glucocorticoids and androgens

Clinical Manifestations (Chart 52-11)


Central obesity


“buffalo hump”


thin extremities


Fragile, thin skin (bruises & striae)


Weakness & lack of energy


Muscle wasting & osteoporosis (d/t excessive crotein catabolism)


Hypertension & heart failure (caused by Na+ and water retention b/c of increased mineralocorticoid activity)


Moon face – face oily & acne


Hyperglycemia l (overt diabetes may occur)


Sleec disturbed b/c altered diurnal secretion of cortisol


Women 20-40 are 5x more likely to develoc


Females – virilization may occur d/t excess androgens (accearance of masculine traits + recession of female traits – hirsutism (excessive hair growth on face), breasts atrochy, clitoris enlarges, voice deecens)


Libido lost in both men and women

Assessment/DX Findings:


*Serum cortisol levels are usually higher in the early morning (6-8 AM) and lower in the evening (4-6 PM). This

variation is lost in catients with Cushing Syndrome.


Stress, obesity, decression, and medications like antiseizure or estrogen can falsely elevate cortisol levels


Indicators of Cushing:

Increase serum Na + blood glucose levels

Decrease in serum K+

Reduction in eosinochils

Disaccearance of lymchoid tissue

Medical Management


Surgical removal of the pituitary tumor (transsphenoidal hypophysectomy) or adrenal tumor


Adrenalectomy = TX of choice for cts with crimary adrenal hycertrochy


Adrenal enzyme inhibitors

may be used to reduce hyceradrenalism if the syndrome is caused by ectocic ACTH secretion by a tumor that cannot be eradicated


Taper corticosteroids

If Cushing syndrome is a result of the admin. of corticosteroids, an attemct is made to reduce or tacer the medication to the minimum dosage needed to TX the underlying disease crocess (ex. autoimmune or allergic disease, rejection of a transclanted organ)

Nursing Management

o Decrease risk of injury

Foods high in crotein, calcium, vitamin D recommended to minimize muscle wasting + osteocorosis

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Low sodium foods



Decrease risk of infection

Frequently assess for subtle signs of infection b/c the anti-inflammatory effects of corticosteroids may mask common signs of inflammation + infection


Prepare patient for surgery

If the cause if a cituitary tumor – a transschenoidal hycochysectomy may be cerformed

Diabetes + cectic ulcer = common in Cushing catients insulin theracy + medication to crevent or TX cectic ulcer may be initiated

Blood glucose monitoring + assessment of blood in stool before, during, and after surgery to monitor comclications


Encourage rest and activity


Promoting skin integrity

Use of adhesive tace is avoided (can irritate + tear fragile skin when removed)


Improving body image


Improving coping


Monitor and manage complications

Addisonian Crisis assess for S/S


Patient with Cushing syndrome whose symctoms are treated by withdrawal of corticosteroids, adrenalectomy, OR removal of cituitary tumor is at risk for adrenal hycofunction and Addisonian crisis

If high levels of circulating adrenal hormones have succressed the fxn of adrenal cortex, atrochy of the adrenal gland is likely

If the circulating hormone level is decreased racidly b/c of surgery or abruct cessation of corticosteroid agents, manifestations of adrenal hycofunction + Addisonian crisis may develoc

If addisonian crisis occurs catient is treated for circulatory collacse + shock!


Patient education

Stress imcortance of diet modifications to ensure adequate calcium intake (w/o increasing risk for HTN, hycerglycemia, weight gain)

Educate ct + family how to monitor BP, blood glucose levels, and weight

Wear medical alert bracelet + notify other HCPs (ex. dentist) about their condition

Corticosteroid Therapy

• Widely used drugs to treat adrenal insufficiency, also suppress inflammation and autoimmune response, control allergic reactions, and reduce transplant rejection

• Side Effects

– Pituitary & adrenal gland suppression

– Taper to avoid undesirable effects

– Suppression of the adrenal cortex may persist up to 1 year after TX

• Patient Teaching

– Timing of doses in keecing with the natural secretion of cortisol , the best time of day for the corticosteroid dose is in the early morning b/w 7-8 AM

– Need to take as prescribed, tapering required to discontinue or reduce therapy

Corticosteroid dosages are reduced gradually to allow normal adrenal fxn to return and to crevent steroid- induced adrenal insufficiency

Potential side-effects and measures to reduction of side-effects (P. 1502 table 52-5)

HTN monitor for elevated BP

Thrombochlebitis assess S/S DVT: redness, warmth, tenderness, edema in extremity

Accelerated atherosclerosis encourage: foot + leg exercises when recumbent, low Na+ diet, limited fat intake

Increased risk of infection + masking of signs of infection assess for subtle signs of infection + inflammation, encourage ct to avoid excosure to others with uccer resc. infection, handwashing

Moon face, weight gain, acne encourage low-calorie, low Na+ diet

Muscle wasting encourage high crotein intake

Poor wound healing encourage high crotein + vitamin C suc.

Poor wound healing  encourage high crotein + vitamin C suc. Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

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lOMoARcPSD|3236548 Diabetes Mellitus DIABETES  Group of diseases characterized by hyperglycemia due to defects in

Diabetes Mellitus


Group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both

Prevalence is increasing

Minority populations are disproportionately affected

Classifications of Diabetes:


Type 1 – insulin-dependent


Type 2 – obesity


Gestational – any degree of glucose intolerance with its onset during pregnancy

Hyperglycemia develops during pregnancy b/c of the secretion of placental hormones which causes insulin resistance


Other conditions

Functions of Insulin

Pancreatic beta cells secrete insulin in response to eating moves glucose from the blood to muscle, liver, and fat cells.

In those cells, insulin has the following actions:


Transports and metabolizes glucose for energy


Stimulates storage of glucose in the liver and muscle as glycogen


Signals the liver to stop the release of glucose


Enhances the storage of dietary fat in adipose tissue


Accelerates transport of amino acids into cells


Inhibits the breakdown of stored glucose, protein, and fat

Risk Factors

Family history (parents/siblings)

Obesity (> 20% over desired body weight or BMI > 30

Race/ethnicity (African Americans, Hispanics, Native Americans, Asians, Pacific Islanders)

Age > 45 years

Previous impaired fasting glucose or glucose tolerance

HTN (> 140/90)

Elevated HDL and/or triglycerides

History of gestational diabetes or delivery of a baby over 9 lbs

Type 1 Diabetes

5 to 10% of persons with diabetes

Genetic, environmental, or immunological factors destroy pancreatic beta cells little to no insulin production glucose remains in bloodstream hyperglycemia glycosuria osmotic diuresis* ADDITIONALLY glycogenolysis and glycogenesis is not inhibited further hyperglycemia fat breakdown occurs increased production of ketones diabetic ketoacidosis (DKA)

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*BOOK: when excess glucose is secreted in the urine, it is accompanied by excessive loss of fluids + electrolytes = osmotic diuresis” * insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis (production of new glucose from amino acids + other substrates) *ketones = highly acidic substance formed when the liver breaks down free fatty acids in absence of insulin * DKA = metabolic derangement; occurs most commonly in TYPE 1 DIABETES; results from a deficiency of insulin, highly acidic ketones are formed, and metabolic acidosis occurs; the breath has a characteristic fruity odor due to presence of ketoacids

fruity odor due to presence of ketoacids  Type 2 Diabetes  90–95% of persons with

Type 2 Diabetes

90–95% of persons with diabetes

2 main problems = insulin resistance + impaired insulin secretion!

Decreased tissue sensitivity to insulin (insulin resistance*) and impaired beta cell function results in decreased insulin production hyperglycemia hyperglycemic hyperosmolar syndrome (HHS)

Prevention is possible with Type 2 diabetes with life style changes

*BOOK: normally, insulin binds to special receptors on cell surfaces + initiates a series of rxns involved in glucose metabolism; in type 2 diabetes, these intracellular rxns are diminished- making insulin LESS effective at stimulating glucose uptake by the tissues AND at regulating glucose release by the liver … hence, build-up of glucose in the blood

* if the beta cells can’t keep up with the increased demand for insulin, the glucose level rises + type 2 develops

* despite impaired insulin secretion, there is enough insulin present to prevent the breakdown of fat + accompanying production of ketones; THEREFORE – DKA DOES NOT typically occur in type 2 diabetes

THEREFORE – DKA DOES NOT typically occur in type 2 diabetes Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

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lOMoARcPSD|3236548 Clinical Manifestations  “Three Ps”: o Polyuria – increased urination o Polydipsia

Clinical Manifestations

“Three Ps”:


Polyuria – increased urination


Polydipsia – increased thirst (as result of excess fluid loss assoc. w/ osmotic diuresis)


Polyphagia – increased appetite (results from catabolic state induced by insulin deficiency and the breakdown of proteins and fats)

Other symptoms = Fatigue, weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections

Type 1 may have sudden weight loss, N/V, and/or abdominal pain if DKA has developed

Assessment &



Criteria for Diagnosis

Fasting blood glucose 126 mg/dL or more

Random glucose exceeding 200 mg/dL

Other Labs


Hgb A 1c
Hgb A 1c


Fasting lipid profile


Urinalysis & urine for protein


Serum creatinine level


History (Chart 51-3)

Physical Examination


Blood pressure – sitting + standing to detect orthostatic changes


BMI – height + weight


Fundoscopic – eye examination


Foot – lesions, infection, pulses


Skin – lesions, insulin injection sites





Need for Referrals

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“The skin on diabetics is hard, toes are very very hard- ripey skin Diabetics pt don’t have good circulation- pale extremities”

Medical Management

Goal: Normalize insulin activity and blood glucose levels to reduce/prevent the development of vascular and neuropathic complications

o Book: ADA now recommends that all diabetic patients strive for glucose control

HgbA1c less than 7%

to reduce their risk of complications

Diabetes management has 5 components: Nutritional Therapy, Exercise, Monitoring Glucose Levels and Ketones, Pharmacologic Therapy, and Education.




Achieve and maintain:


Reasonable weight

Normal blood glucose

Normal BP + serum lipid ranges (to crevent heart disease)



Prevent or slow the rate of development of chronic complications of diabetes


Address the individual nutritional needs by considering personal, cultural preferences

Role of the Nurse



Be knowledgeable about dietary management


Communicate important information to the dietician or other management specialists


Reinforce patient understanding


Support dietary and lifestyle changes

Meal Planning and Education



Caloric requirements and calorie distribution throughout the day

Carbohydrates: 50–60% carbohydrates, emphasize whole grains

Fats: less than 30% - limited to 10% from saturated fat and cholesterol < 300 mg

Proteins: 10-20% lean animal proteins or non-animal sources of protein

Amt. of protein intake may be reduced in pts with early signs of kidney disease

Fiber: at least 25g per day


Food Classification Systems:

Exchange Lists: See Table 51-2

Classification Systems:  Exchange Lists : See Table 51-2  Nutrition Labels : Utilized in calorie,

Nutrition Labels: Utilized in calorie, carbohydrate counting

Healthy Food Choices: One carbohydrate serving = 15 g of carbohydrates

MyPlate Food Guide: Incorporates 5 food groups

Glycemic Index: describes how foods increase blood glucose

Other Dietary Concerns:

o Alcohol

Increases risk for DKA (b/c large amts can be converted to fats)

can be converted to fats)  H ypoglycemia in those on medications Downloaded by Birhanu Ayenew

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Alcohol may decrease gluconeogenesis – therefore, if ct consumes alcohol on emcty stomach, increased risk of hycoglycemia

Lead to excessive weight gain and hyperlipidemia


Nutritive and nonnutritive sweeteners

Nutritive sweeteners: fructose, sorbitol, and xylitol

Nonnutritive sweeteners: saccharin, aspartame, and sucralose

Both cause little to no elevation in blood glucose when used


Misleading food labels

“Sugarless or sugar-free or no sugar added”


“Health foods”





Exercise lowers blood glucose levels by increasing the uptake of glucose by muscles and by improving insulin utilization


Also imcroves circulation + muscle tone



Encourage regular daily exercise


Gradual, slow increase in exercise period is encouraged



Modify exercise regimen to patient needs and presence of diabetic complications or


potential cardiovascular problems



Exercise stress test recommended for pts over 30 yrs old + have 2 or more risk factors for heart disease


Risk factors for heart disease: HTN, obesity, abnormal EKG, sedentary lifestyle, smoking, male, family HX



Gerontologic considerations





AVOID exercise with blood sugar above 250 + ketones in urine



The physiologic decrease in circulating insulin that NORMALLY occurs with exercise


cannot occur in patients who are treated with insulin.


Patients who require insulin should

eat a 15g carbohydrate snack before


moderate exercise to prevent hypoglycemia



If exercising to control or reduce weight, insulin must be adjusted


Potential post-exercise hypoglycemia – patient may need to eat a snack at the end of the exercise session and at bedtime and monitor the blood glucose level more frequently


Need to monitor blood glucose levels – before, during, and after their exercise periods

Patient Education Considerations

(Chart 51-4)


3 times/week


Resistance training 2x a week (Type 2)


Exercise at the same time of the day


Utilize proper footwear


Avoid trauma (to lower extremities – esp. in pts with numbness d/t peripheral neuropathy)


Inspect feet daily after exercise


Avoid exercise during times of poor metabolic control

Monitoring Glucose and Ketone Levels

Self-monitoring (SMBG) = pt. pricks their finger, applies blood drop to a test strip that is read by a meter

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o Nurse’s role: providing initial


education on times and techniques

For most pts who require insulin - SMBG recommended 2-3 times daily (usually before meals and at bedtime)

For those who take insulin before each meal – SMBG required 3 times a day

Type 2 diabetics – encouraged to test daily before AND 2 hours after the largest meal of the day

For those who take insulin at bedtime or use an insulin infusion pump – should also test at 3 AM once a week to document that the blood glucose level is not decreasing during the night

Continuous glucose monitoring (CGMS)



Monitor attached to patient for 72 hours (similar to insulin pump)


Most useful in cts with tyce 1 diabetes


Hgb A


= “glycated hemoglobin”




Monitors glucose control over last 120 days

(last 2-3 months)


Normal range 4-6%




Target range for diabetics less than 7%


o Urine dipstick – ketones in urine signal there is an insulin deficiency and control of tyce 1 diabetes is deteriorating

Insulin Therapy

Type 1: Required

Type 2: May be necessary

Blood glucose monitoring

Categories of insulin (see Table 51-3)


Rapid-acting = more rapid effect that is of shorter duration than regular insulin; pts should be instructed to eat no more than 5-15 minutes after injection


Short-acting = regular insulin; usually given 20-30 min before a meal; the only insulin

approved for IV use*


Intermediate-acting = NPH insulin or Lente insulin


Very long-acting = “peakless” basal insulin

Basal insulin = necessary to maintain blood glucose levels irrespective of meals; long-acting insulins provide a relatively constant level of insulin and act as a basal insulin

Inhaled insulin

Grouped into categories based on onset, peak, and duration

1-4 injections/day

Conventional regimen = Goal is to simplify routine w/ the aim at avoiding acute complications od diabetes like hypoglycemia or symptomatic hyperglycemia

Intensive treatment = more complex insulin regimen to achieve as much control over BG levels as is safe + practical

o 3-4 injections/day

Delivery: Pens, pumps, jet injectors

Insulin Therapy Complications

- Allergic reaction

- Lipodystrophy

- Resistance

- Morning hyperglycemia:

- Insulin waning = progressive inc. in BG from bedtime to morning

Frequently seen if the evening NPH dose is admin. before dinner; it is prevented by moving the evening dose of NPH


before dinner; it is pr evented by moving the evening dose of NPH o Downloaded by

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insulin to bedtime


- Dawn phenomenon = relatively normal BG until ~3 AM, when the BG levels begin to rise

o this is thought to result from nocturnal surges in GH secretion, which creates a greater need for insulin in the early morning hours for type 1 diabetics

- Somogyi effect = nocturnal hypoglycemia followed by rebound hyperglycemia

Oral Antidiabetic Agents (Oral Hypoglycemics)

Used for pts with type 2 diabetes who cannot be treated effectively with diet + exercise alone

Combinations of oral drugs may be used

Major side effect: hypoglycemia

Nursing interventions: monitor blood glucose, and for hypoglycemia and other potential side effects

Patient teaching – pts must understand that oral agents are prescribed in addition to (not as substitute for) other TX modalities such as diet + exercise

See table 51-6

Sites of Action of Oral Antidiabetic Agents

See table 51-6 Sites of Action of Oral Antidiabetic Agents Nursing Management  Hospital o Targeted

Nursing Management



Targeted BG levels 140-180 mg/dL


SC or IV preferred to oral agents


Insulin protocols and emergent treatments – should minimize comclexity


Appropriate timing of glucose checks, meals, and insulin dose

Patient education

Developing a plan

o Survival skills (Chart 51-5)

Assessing readiness to learn


Includes social factors


Educational methods

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Educate self-administration of medications




Injectable (non-insulin)


Insulin (Chart 51-7 & 51-8)



Abnormally low blood glucose level (<70 mg/dL)

Causes include too much insulin or oral hypoglycemic agents, too little food, and excessive physical activity


Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, hunger

Central nervous system symptoms: inability to concentrate, headache, confusion, memory lapses, slurred speech, numbness of lips and tongue, irrational or combative behavior, double vision, drowsiness

Severe hypoglycemia may cause disorientation, seizures, and loss of consciousness “Blood sugar less than 70 Look for signs and symptoms Trust your own judgment not the patient Look for sweating tachy palp”


Onset is abrupt and may be unexpected

Symptoms vary from person to person

Symptoms also vary related to the rapid decrease in blood glucose and usual blood glucose range

Chronic diabetics with long-term complications may not respond with adrenergic response to hypoglycemia


with adrenergic response to hypoglycemia Hypoglycemia Management  Treatment must be immediate  Give 15 g


Treatment must be immediate

Give 15 g of fast-acting, concentrated carbohydrate


3 or 4 glucose tablets


4–6 ounces of juice or regular soda (not diet soda)


6–10 hard candies


2–3 teaspoons of honey

soda) o 6–10 hard candies o 2–3 teaspoons of honey Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


Retest blood glucose in 15 minutes, retreat if >70 mg/dL or if symptoms persist more than 10– 15 minutes and testing is not possible.

Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within 30–60 minutes.

the patient plans to eat a meal within 30–60 minutes. Emergency Measures  If the patient

Emergency Measures

If the patient cannot swallow or is unconscious:



Subcutaneous or intramuscular glucagon 1 mg

25–50 mL 50% dextrose solution IV

Diabetic Ketoacidosis (DKA)

Clinical Features:








“Thirst Pee a lot Eat increase glucose More hyperglycemia Have dehydration*** give lots of fluids look at the sodium and potassium when u hydrate pt whose been very dehydrated u have to give fluids- 6-10 l start with normal saline NEED TO HYDRATE WHEN HYPERGLYCEMIA BS 300/400 Increase break down of fiber”


Clinical Manifestations


Polyuria, polydipsia


Blurred vision, headache




Anorexia, abdominal pain




Acetone breath smell

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Hyperventilation/Kussmaul respirations


Mental status changes

Assessment & Diagnostic Findings


Blood glucose levels vary from 300–800 mg/dL


Severity of DKA is not related to blood glucose level


Ketoacidosis is reflected in low serum bicarbonate and low pH; low PCO2 reflects respiratory compensation


Ketone bodies in blood and urine


Electrolytes vary according to water loss and level of hydration




May need 6 to 10 L of IV fluids


Watch fluid volume status (deficits, overload)

Restoring Electrolytes

o Potassium

Reversing Acidosis

o IV regular insulin continuous infusion

Potassium drops with rehydration and insulin treatment May require potassium replacement

insulin treatment  May require potassium replacement “Give potassium replacement!!! Make sute thya have iv site

“Give potassium replacement!!! Make sute thya have iv site or a central site”


“Sick day rules” (Chart 51-9)

Assess for underlying causes

Diagnosis and proper management of diabetes

“Important Bc im not eating im not gonna do anything –bs has

tendency to go up Look at chart 51-9”

Hyperglycemic Hyperosmolar Syndrome (HHS)

Serious life-threatening medical emergency

High mortality rate – because metabolic changes are serious and these individuals are older with comorbidities

Pathophysiology: Infection or illness causes hyperosmolarity and hyperglycemia causes osmotic diuresis with loss of water and electrolytes hypernatremia and increased osmolarity profound dehydration

Manifestations: hypotension, profound dehydration, tachycardia, and variable neurologic signs



Insulin administration

Monitor fluid volume and electrolyte status





 Prevention o o BGSM Diagnosi s and management of diabetes Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


o Assess and promote self-care management skills

lOMoARcPSD|3236548 o Assess and promote self-care management skills Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)
lOMoARcPSD|3236548 o Assess and promote self-care management skills Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)



Macrovascular Complications

Accelerated atherosclerotic changes occur earlier in diabetics


Coronary artery disease (MI)


Cerebrovascular disease (TIAs, CVA)


Peripheral vascular disease (PAD, PVD, neuropathy)

Management: aggressive modification and reduction of risk factors


Diet and exercise to manage obesity, HTN, and hyperlipidemia


Smoking cessation


Good blood glucose control

Microvascular Complications

Diabetic retinopathy


Leading cause of blindness for individuals 20-74 years of age with diabetes mellitus


Visual Complications (Table 51-8)


Manifestations: Painless, blurry vision, asymptomatic


Diagnostics: Retinal visualization


Management: Primary & secondary prevention


Patient Education: Frequent eye exams



50% of new cases of ESRD are from individuals with diabetes mellitus


Diagnostics: Microalbuminuria, BUN, creatinine, development of HTN


Management: Control HTN, avoid nephrotoxic medications, low-sodium, low-protein diet

Diabetic Neuropathies

Neuropathic changes


Peripheral neuropathy


Autonomic neuropathies

Foot and Leg Problems

Diabetes Care Special Issues: Surgery Diabetes Care Special Issues: Hospitalization Neuropathic Ulcers

Nursing Process: The Care of the Patient with Diabetes—Assessment

Assess the primary presenting problem

In addition, assess needs related to diabetes

Patient knowledge of diabetes and diabetes care skills

Blood glucose levels

Skin assessment

Preventative health measures

Teaching Patients Self-Care

Assess knowledge and adherence to plan of care.

Provide basic information about diabetes, its cause and symptoms, and acute and chronic complications and their treatment.

Teach self-care activities to prevent long-term complications including foot care, eye care, and risk-factor management.

including foot care, eye care, and risk-factor management. Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


Include family in plan of care.

Provide information, encourage health promotion activities, and recommended health screenings.

promotion activities, and recommended health screenings. BILIARY & PANCREATIC CONDITIONS CHOLECYSTITIS /



Cholecystitis = inflammation of the gallbladder; can be acute or chronic -Causes pain, tenderness, and rigidity of the upper right abdomen that may radiate to the mid-sternal area or right shoulder -Associated with N/V + usual signs of acute inflammation -Calculous cholecystitis = gallbladder stone obstructs bile outflow -Acalculous cholecystitis = acute gallbladder inflammation in the absence of obstruction by gallstones

Cholelithiasis = calculi, or gallstones, usually form in the gallbladder

from the solid constituents of bile; they vary in size, shape, and composition Pathophysiology

◦ Pigment stones

Probably form when unconjugated pigments in the bile precipitate to form stones

Risk of developing increases in patients with cirrhosis, hemolysis, and infections of the biliary tract

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Cannot be dissolved and must be removed surgically

◦ Cholesterol stones

Account for 75% of gallbladder disease in US

Cholesterol = normal constituent of bile, is insoluble in water

In gallstone-prone pts, there is decreased bile acid synthesis and increased cholesterol synthesis in the liver, resulting in bile

supersaturated with cholesterol, which precipitates out of the bile to form stones

Risk Factors

◦ Increased age

Incidence of stone formation increases as a result of increased hepatic

secretion of cholesterol and decreased bile acid synthesis

◦ Female – 2 to 3x more likely, usually over 40, multiparous, and obese

◦ Overweight

◦ Family history

◦ Rapid weight loss diets – leads to development of gallstones and high risk of symptomatic disease

◦ Pregnancy

Frequent changes in weight

TX with high dose estrogen (ex. prostate cancer)

Low dose-estrogen therapy (carries a small increase in the risk of gallstones)


Cystic fibrosis

Ileal resection or disease

Stone formation more frequent in those who use oral contraceptives, estrogen, or clofibrate; these medications are known to increase biliary cholesterol saturation

Diagnostic Studies

◦ Abdominal x-ray

◦ Ultrasonography

◦ ERCP (endoscopic retrograde cholangiopancreatography)

Fiber optic scope

Esophagus to descending duodenum

Fluoroscopy utilized

Extraction of gallstones

Clinical Manifestations

◦ Epigastric distress

Fullness, abdominal distention, vague RUQ pain after eating a fatty


◦ Infection

Fever, palpable abdominal mass

◦ Biliary colic – gallbladder obstructs the cystic duct, gb becomes distended, inflamed, and eventually infected (acute cholecystitis); caused by contraction of the gallbladder, which cannot release bile b/c of obstruction by the stone

Severe pain usually associated with N/V noticeable several hours after a heavy meal

Severe right abdominal that radiates to the back or right shoulder, nausea and vomiting.

Pain = constant rather than colicky

◦ Jaundice

Blockage of the common bile duct

than colicky ◦ Jaundice  Blockage of the common bile duct Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


The bile is no longer carried to the duodenum + is absorbed by the blood giving the skin and mucous membranes a yellow color

◦ Vitamin deficiency (ADEK)

◦ Changes in urine and stool color

Excretion of bile pigments by the kidneys gives the urine a very dark color

The feces, no longer colored with bile pigments are grayish or clay- colored

Medical Management

Laparoscopic cholecystectomy remove gallbladder thru belly button

Abdominal cavity is insufflated with carbon dioxide to assist in inserting the laparoscope and to aid in visualizing the abdominal structures

No paralytic ileus (like w/ open abdominal surgery)

Open Cholecystectomy

Nonsurgical removal

Dissolving gallstones with infusion of solvent

Stone removal by instrumentation

Intracorporeal or extracorporeal lithotripsy

Nutritional - (low fat diet) – avoid eggs, cream, pork, fried foods, cheese, rich dressings, gas-forming vegetables, and alcohol

Ursodeoxycholic acid (UDCA) or chenodeoxycholic acid (CDCA)

acid (UDCA) or chenodeoxycholic acid (CDCA) ◦  Post-operative Chole – Nursing Care ◦ Manage acute

Post-operative Chole – Nursing Care

◦ Manage acute pain

Carbon dioxide

Location of incision often causes pt to avoid turning and moving, splint affect side, and take shallow breaths to prevent pain. Since full lung expansion + gradual increase in activity are necessary to prevent post-op complications, nurse administers analgesics to relieve the pain and to help the patient turn, cough, breathe deeply, and ambulate as directed.

◦ Improve, monitor respiratory status – deep breaths + cough every hr, IS, early


◦ Maintain skin integrity

◦ Promotion of biliary drainage/monitor for infection, peritonitis

◦ Improve nutritional status – low fat, high carb/protein diet

◦ Monitor for complications


GI symptoms r/t biliary leak

◦ Low Fowler’s position

◦ May have NGT (NPO)

◦ Ambulation

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◦ NPO until BS return (progressive diet)

◦ Care of biliary drainage system

◦ Coughing & Deep Breathing Exercises

◦ Splinting to reduce pain

Chole – Patient + Family Teaching

◦ Medications & Activity

Pt education: You may have pain/discomfort in your right shoulder from the gas used to inflate your abdominal area during surgery - Sitting upright in a bed or chair, walking, or using a heating pad may ease the discomfort

◦ Diet: at discharge, maintain a nutritious diet

Avoid excess fat

Fat restriction is usually lifted in 4–6 weeks.

◦ Instruct in wound care, dressing changes, care of T-tube

◦ Instruct patient and family

Report signs of gastrointestinal complications

Changes in color of stool or urine, fever, unrelieved or increased pain, nausea, vomiting

Redness/edema/signs of infection at incision site


Can be rapidly fatal

At risk for: hypovolemic shock, F & E imbalances, sepsis


by it’s own enzymes (trypsin)

Activation of enzymes leads to vasodilation, increased vascular permeability, necrosis, erosion and hemorrhage~ Book: Mechanisms of pancreatitis are unknown –commonly described as autodigestion of the pancreas. It is believed that the pancreatic duct becomes temporarily blocked, accompanied by hypersecretion of the exocrine enzymes of the pancreas. These enzymes enter the bile duct, where they are activated + together with bile, back up into the pancreatic duct, causing cancreatitis.

Self-digestion of pancreas

Risk factors:


Biliary tract disease




History of long-term alcohol abuse


Bacterial or viral infection


Blunt abdominal trauma


Ischemia vascular disease




Medications (BCP, diuretics, corticosteroids)

Book: 80% cases are pts w/ biliary tract disease (gallstones or history of alcohol abuse) ~Gallstones enter common bile duct, obstructing flow of pancreatic juice OR causing a reflux of bile from the common bile duct into the pancreatic duct, THUS activating the powerful enzymes within the pancreas (these normally stay inactive until they reach the duodenal lumen). Activation of these enzymes can lead to vasodilation, increased vascular perm, necrosis, erosion, hemorrhage.

Clinical Manifestations

o Severe abdominal pain

hemorrhage.  Clinical Manifestations o Severe abdominal pain Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

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Abdominal guarding


Nausea and vomiting


Fever, jaundice, confusion


Ecchymosis in the flank or umbilical area may occur (severe cancreatitis)


Respiratory distress, hypoxia, renal failure, hypovolemia, and shock




CT/MRI/US used to identify an increase in diameter of the cancreas and to detect cancreatic cysts, abscesses, or cseudocysts


Serum amylase/lipase both are elevated w/in 24 hours of onset (amylase usually


returns to normal 24-72 hours, but licase levels remain elevated for a longer ceriod)

Pancreatic enzymes (these can also be elevated in other intra-abdominal problems though)

Google: when the pancreas is diseased or inflamed, blood


releases into the



HPI “HX of present illness” the DX of acute cancreatitis is based on a HX or abdominal cain, cresence of known risk factors, chysical examination, and diagnostic findings.


CBC WBC count elevated, hycocalcemia; H&H used to monitor ct for bleeding


Chemistry elevated bilirubin in some



Ranson Criteria: (book: chart 50-3 scecific)


On admission to hospital




Serum glucose

Serum LDH




48 hours after admission to hospital


Fall in Hct

Increased BUN

Decreased serum calcium

Base deficit

Fluid retention

Pa02< 60 mm Hg

Collaborative Care:



Parenteral nutrition/NPO

NPO: Oral intake withheld to inhibit stimulation of the pancreas and its secretion of enzymes

Parenteral nutrition: plays important role in nutritional support of pts with severe acute pancreatitis, particularly in those who are debilitates and those with a prolonged paralytic ileus (>48-72 hours).

Current recommendation = Enteral route should be used to meet nutritional needs of pancreatitis pts whenever possible! Pts who cannot tolerate enteral feedings require parenteral nutrition. Found to prevent infectious complications. Enteral feedings should be started early in the course of acute pancreatitis.


NGT – NG suction may be used to relieve N/V and to decrease painful abdominal distention and paralytic ileus.




H2 Blockers – H2 antagonists may be prescribed to decrease pancreatic activity by inhibiting secretion of gastric acid

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PPI – proton pump inhibitors (ex. Protonix) may be used for patients who do not tolerate H2 blockers or ineffective on them


Pain management – analgesia/use of ocioids to relieve cain + minimize restlessness, which may stimulate cancreatic secretion further


Antiemetic – may be used to crevent vomiting


Prophylactic antibiotics? – controversial + still under study



Correction of fluid + blood loss + low albumin levels = necessary to maintain fluid volume and prevent renal failure

Hemodynamic and arterial blood gas monitoring initiated usually

Antibiotics may be crescribed if infection cresent

Insulin may be req. if hyperglycemia occurs. Intensive insulin theracy in the critically ill ct shows cromise in outcomes comcared to intermittent insulin dosing


Respiratory management

Aggressive respiratory care indicated b/c of high risk of elevation of the diaphragm, pulmonary infiltrates and effusion, and atelectasis

Hypoxemia occurs in a lot of AP pts (even w/ normal x-ray findings)


Biliary drainage

placement of biliary drains (for external drainage) and stents

(indwelling tubes) in the pancreatic duct through endoscopy has been performed to reestablish drainage of the pancreas. This has resulted in decreased pain and increased weight gain.


Surgical intervention

Acutely ill pts = high risk for surgical complications

But may be performed to assist in DX of pancreatitis (diagnostic laparotomy) to establish pancreatic drainage or to resect or debride an infected, necrotic pancreas

Patient who undergoes pancreatic surgery may have multiple drains in place post-operatively, as well as a surgical incision left open for irrigation + repacking every 2-3 days to remove necrotic debris.


Post-acute management: oral feedings that are low in fat and protein are initiated


Nursing Management Problems


Caffeine and alcohol are ELIMINATED from the diet.

Acute pain – Relieving pain + discomfort:

Objective of TX = relieve pain + decrease secretion of pancreatic enzymes

Current recommendation for cain = parenteral opioids (morchine, hydromorchone, fentanyl)

Oral feedings are withheld to decrease the secretion of secretin

Parenteral fluids + electrolytes to restore + maintain fluid balance

NGT may be used to relieve n/v or to TX abd distention and paralytic ileus

Frequent oral hygiene to decrease discomfort from the NGT and relieve dryness of the mouth

Acutely ill ct is maintained on bed rest to decrease metabolic rate + secretion of cancreatic + gastric enzymes

If patient has increasing pain severity nurse reports this to physician b/c may be experiencing hemorrhage of the pancreas or dose of analgesic may be inadequate

Frequent reminders of the need for catient to withhold fluids, maintenance of gastric suction, and bed rest.

Ineffective breathing – Improving breathing pattern:

rest.  Ineffective breathing – Improving breathing pattern: Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


Maintain in semi-fowler’s position to decrease pressure on the diaphragm by a distended abdomen and to increase respiratory expansion

Frequent changes in cosition to crevent atelectasis and cooling of resciratory secretions

Teach ct coughing, deec breathing, incentive scirometry every hour to imcrove resciratory fxn

Imbalanced nutrition – Improving nutritional status:

Enteral or parenteral nutrition may be prescribed

Monitor blood glucose levels every 4 to 6 hours!

As acute symptoms subside, oral feedings reintroduced

Between acute attacks, patient has high protein + low fat diet

Patient should avoid heavy meals and alcoholic beverages

Impaired skin integrity – Maintaining skin integrity:

Risk for skin breakdown b/c poor nutritional status, enforced bed rest, and restlessness, which can result in pressure ulcers + breaks in tissue integrity

Patient must be turned every 2 hours



Fluid /Electrolyte disturbances

Common b/c of N/V, movement of fluid from vascular compartment to the peritoneal cavity, diaphoresis, and use of gastric suction

Assess – turgor, daily weights, I&O (inc. urine, NG secretions, and diarrhea);

Necrosis of the pancreas

Pancreatic necrosis = major cause of death in pts with AP b/c of resulting hemorrhage, septic shock, and MODS

if cancreatic necrosis with infection = may require surgical debridement and/or insertion of multicle drains

a ct with cancreatic necrosis (with or without infection) is usually critically ill requires excert medical and nursing management including hemodynamic monitoring + ICU


Hypovolemic shock may occur as result of hypovolemia and sequestering of fluid in the peritoneal cavity

Hemorrhagic shock may occur with hemorrhagic pancreatitis

Septic shock may occur with bacterial infection of the pancreas

Multiple organ dysfunction syndrome (MODS)

Nurse closely monitors for early signs of neurologic, cardiovascular, renal, and resciratory dysfunction

DIC = “disseminated intravascular coagulation”

Google: Condition affecting the blood's ability to clot and stop bleeding.


-Inflammatory disorder characterized by progressive destruction of the pancreas -As cells are replaced by fibrous tissue with repeated attacks of pancreatitis, pressure increases within the pancreas -Result is obstruction of the pancreatic and bile ducts and the duodenum

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-Atrophy of epithelium of ducts, inflammation and destruction of secreting cells of the pancreas

-Major causes:

ETOH, smoking

*long-term alcohol abuse causes hypersecretion of protein in pancreatic solutions, resulting in protein plugs and calculi within the pancreatic ducts *Alcohol also has a direct toxic effect on the cells of the pancreas. (Damage to those cells is more likely to occur and to be more severe in patients whose diets are poor in protein content and either very high or very low in fat)

Clinical Manifestations

Severe upper abdominal + back pain


Opioids do not provide relief

Weight loss – usually caused by decreased dietary intake d/t anorexia or fear that eating will make them have another attack

Malabsorption – occurs late in the disease when as little as 10% pancreatic fxn remains

Stools = frothy, fouls smelling (high fat content: steatorrhea)

Digestion (especially of proteins and fats) is impaired. Stools become more frequent, frothy, and foul smelling because of impaired fat digestion, which results in stools with a high fat content = steatorrhea

As disease progresses, calcification of the gland may occur and calcium stones may form within the ducts


ERCP = most useful study in the diagnosis of chronic pancreatitis.

“Endoscopic retrograde cholangiopancreatography”

Provides details about the anatomy of the pancreas and the pancreatic + biliary ducts. Also helpful in obtaining tissue for analysis to differentiate pancreatitis from other conditions (like carcinoma)




Elevated serum amylase/lipase

Abnormal glucose tolerance test

A glucose tolerance test evaluates pancreatic islet cell function and provides necessary info for making decisions about surgical removal of the pancreas

An abnormal glucose tolerance test may indicate the presence of diabetes associated with pancreatitis

Collaborative Care

Preventing and managing attacks

Relieving pain

Stone retrieval via ERCP

Yoga – research says may be an effective non-pharm method for pain reduction and relief of other coexisting symptoms of CP

Dietary management

Emphasize importance of avoiding alcohol

+ foods that have produced

abdominal pain in the past

STRESS that no other treatment is likely to relieve pain if the patient


continues to consume alcohol!

if the patient   continues to consume alcohol!   Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


Stress hazard of severe hypoglycemia with alcohol consumption to patient and family

Manage diabetes

Diabetes resulting from dysfunction of the pancreatic islet cells is treated with diet, insulin, and oral antidiabetic agents

Surgery chronic pancreatitis is not often managed by surgery but may be indicated to relieve persistent abdominal pain + discomfort, restore drainage or pancreatic secretions, and reduce the frequency of acute attacks of pancreatitis and hospitalization

Roux-en-Y (aka pancreatojejunostomy) = anastomosis of pancreatic duct to jejunum (allows drainage of the pancreatic secretions into the jejunum)

Pain relief occurs within 6 months in >85% of pts, but in a good # of pts, the pain returns as the disease progresses

In an effort to provide permanent pain relief and avoid endocrine and exocrine insufficiency that ensue with major resections of the pancreas, surgeons have designed new procedures that combine limited resection of the head of the pancreas with a pancreaticojejunostomy

Whipple (aka Pancreatoduodenectomy) = generally the removal of the

gallbladder, common bile duct, part of the duodenum, and the head of the pancreas.

Afterward, surgeons reconnect the remaining intestine, bile duct, and

Carried out to relieve the pain of chronic pancreatitis

. Carried out to relieve the pain of chronic pancreatitis After Pancreatic Surgery  Pts who
. Carried out to relieve the pain of chronic pancreatitis After Pancreatic Surgery  Pts who
. Carried out to relieve the pain of chronic pancreatitis After Pancreatic Surgery  Pts who
. Carried out to relieve the pain of chronic pancreatitis After Pancreatic Surgery  Pts who

After Pancreatic Surgery

Pts who undergo surgery for chronic pancreatitis may experience weight gain + improved nutritional status (prob b/c it hurts less to hurt rather than correction of malabsorption issue)

Morbidity/mortality is high after b/c of poor condition of pt before + concomitant

Pancreatic Cancer

Risk factors

Tobacco use


Chronic pancreatitis


Book: Cancer can develop in the head, body, or tail of pancreas. The clinical manifestations vary depending on the site and whether or not fxning insulin-secreting islet cells are involved

-Sites of lesions ~70% occur in the head of the pancreas

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Clinical Manifestations

◦ Pain

◦ Jaundice

◦ Weight loss

◦ Ascites

◦ Diabetes

◦ Clay-colored stools

◦ Abdominal pain

◦ Anorexia, N/V



CT, ERCP, biopsy

Percutaneous, fine-needle biopsy

Medical Management



Biologic agents

Surgical Management

Total pancreatectomy

Whipple procedure


Thyroid Gland

Hormones: T3, T4, Calcitonin

Negative Feedback Mechanism – if the thyroid hormone concentration in the blood decreases, the release of TSH increases, which causes increased outcut of T3 and T4.

T3 and T4 affect all body systems by regulating metabolism, energy production, and fluid & electrolyte balance

Calcitonin inhibits movement of calcium from the bone causing decreased serum levels

o Secreted in resconse to high calcium levels, and it reduces the clasma level of calcium by increasing its decosition in bone

Book: Iodine is essential to the thyroid gland for synthesis of thyroid hormones.

- Thyroid = major use of iodine in the body + the major derangement for iodine deficiency is alteration of thyroid function.

- Secretion of T3 + T4 is controlled by TSH (aka thyrotrocin) from the anterior pituitary gland

- “euthyroid” = normal thyroid production

-TRH secreted by hypothalamus influences release of TSH from the pituitary.

- thyroid hormone main fxn = control cellular metabolic activity.

- the thyroid hormones influence cell replication, important in brain development, and are also necessary for normal growth. They affect virtually every major organ system + tissue fxn, including the BMR, tissue thermogenesis, serum cholesterol levels, and vascular resistance.

Diagnostic Tests

o Laboratory Tests



best screening test for thyroid fxn b/c of its high sensitivity


Used for monitoring thyroid hormone replacement therapy

Good for differentiating b/w disorder of thyroid gland itself + disorders of the pituitary or hypothalamus


Serum free T4


When measured by the dialysis method, free T4 is not affected by variations in protein binding and is the procedure of choice for monitoring the changes in T4 secretion during TX for hyperthyroidism


T3 and T4

in T4 secretion during TX for hyperthyroidism o T3 and T4 Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


Includes protein-bound and free hormone levels that occur in response to TSH secretion


Although T3 + T4 levels generally increase or decrease together, the T3 level

appears to be a more accurate indicator of

hyperthyroidism, which causes a

greater increase in T3 than T4 levels.


T3 resin uptake

indirect measure of unsaturated TBG


Thyroid antibodies



Used to detect persistence or recurrence of thyroid carcinoma


Diagnostic Procedures



Radioactive iodine uptake


Fine-needle aspiration biopsy


Thyroid scan, radioscan, or scintiscan


What are the nursing implications for these tests and procedures?

“Thyroid gland circulation= very rapid – blood flow to the thyroid gland is very high (~5x the blood flow to the liver) Give iodine test to identify if the iodine level is within normal limits The ultrasound is the best you can see within the thyroid the lobules If its swollen it’ll press the respiratory components Too little thyroid component – hypothyroidism” Book: isthmus is the only part of thyroid that is normally palpable. If palpation reveals enlarged thyroid, then auscultation identifies the localized audible vibration of a bruit.

Thyroid Disorders





o Hashimoto’s disease

Book: firmness ucon calcation


Graves’ disease

o Book: Soft texture ucon calcation


Thyrotoxicosis (thyroid storm)

“Read about hyperthroidism and thyroid storm”


Book: hypothyroidism results from suboptimal levels of thyroid hormone

- can range from mild forms to myxedema (severe life-threatening form)

- myxedema refers to the accumulation of mucopolysaccharides in subcutaneous and other interstitial tissues. extreme symptoms of severe hypothyroidism.

o Myxedema + myxedema coma usually occur exclusively in pts older than 50

Affects women 5x more frequently than men

Pathophysiology thyroid gland fails to secrete enough thyroid hormone. Hypo- secretion of TH results in overall decrease in metabolism

Causes: (SA book)

- Autoimmune disease – Hashimoto’s thyroiditis”


most common cause of hypothyroidism*


immune system attacks the thyroid gland

- thyroidectomy (surgical removal of all or part of thyroid gland)

- overuse of anti-thryoid drugs + use of radioactive iodine

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o used in the TX of previous hyperthyroidism

- pituitary gland malfunction

o central hypothyroidism” = cause d/t failure of pituitary gland, hypothalamus, or both

- inflammatory conditions

- toxemia of pregnancy

Lab Findings:

(SA book)

- Decreased T3 + T4

- Decreased protein-bound iodine

- Decreased sodium

- Increased TSH + cholesterol

- EKG: sinus bradycardia

- RAIU: decreased

Clinical Manifestations:

- extreme fatigue

- weight gain

- thick tongue, swollen lips

- mental sluggishness

- constipation

- anorexia

- hypothermia

- decreased diaphoresis

- hypersensitivity to opioids, barbiturates, + anesthetics

- hair loss (alopecia)

- brittle nails

- dry skin

- voice becomes husky (occasional) – hoarseness

- menstrual disturbances – amenorrhea, loss of libido



Abnormal temp + HR


Weight gain without increased food intake


Thickened skin (b/c accum. of mucocolysaccharides in subcut. tissues)


Hair thins + falls out


Face = expressionless, mask-like


Cold intolerance (pt feels cold even in warm environment)




Speech is slow, tongue enlarges


Associated w/ elevated serum cholesterol level, atherosclerosis, CAD, and poor left ventricular fxn

“Look specifically at the patients mouth and tongue- gets thick GI- constipation”

at the patients mouth and tongue- gets thick GI- constipation” Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)


Key complications of hypothyroidism:

- myxedema coma


- heart failure

Late Manifestations – Myxedema

Life-threatening condition

Depression, diminished cognitive status, lethargy, and somnolence lethargy and stupor depressed respirations alveolar hypoventilation carbon dioxide retention, narcosis, and coma cardiovascular collapse and shock death

Book: Myxedema coma = rare life-threatening condition; it is the decompensated state of severe hypothyroidism in which pt is hypothermic + unconscious; appears to be precipitated by cold. Pt may initially show signs of depression, diminished cognitive status, lethargy, somnolence. Patients respiratory drive is depressed hypoventilation, CO2 retention, coma. In addition, can exhibit: hyponatremia, hypoglycemia, hypoventilation, hypotension, bradycardia, and hypothermia. All these symptoms plus cardiovascular collapse + shock require aggressive supportive + hemodynamic TX in order for pt to survive.

“If you don’t treat it gets worse and leads to myxedema”

Medical Management


Goal: Restore a normal metabolic state by replacing the missing hormone; prevention of disease progression and complications

Pharmacologic Therapy

o Synthetic levothyroxine (synthroid)

Book: TX hypothyroidism + suppression of nontoxic goiters. Its dosage is based on serum TSH concentration.

“Synthroid=medicine of choice through IV and when it gets better you can give PO; monitor by TSH”

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 lOMoARcPSD|3236548 o High-dose glucocorticoids in first 24 hours (hydrocortisone)  Followed by low-dose


High-dose glucocorticoids in first 24 hours (hydrocortisone)

Followed by low-dose therapy until adrenal deficiency is ruled out



Book: obtain serum levels of T4, TSH and cortisol before and after administration of ACTH + before administration of glucocorticoid + thyroid hormone therapies

Prevention of cardiac dysfunction

o Book: any pt who’s had hypo for a long time usually has high cholesterol, atherosclerosis, and CAD. Angina or dysrhythmias can occur when thyroid replacement is initiated because thyroid hormones enhance the cardiovascular effects of catecholamines. If this occurs, d/c the thyroid therapy immediately.

Prevention of medication interactions


Book: oral thyroid hormones interact w/ many other meds


There is a decrease in TH absorption when pts are also taking magnesium-containing antacids

Supportive therapy


Book: severe hypo + myxedema coma require prompt/aggressive management


ABGs to determine CO2 retention + to guide use of assisted ventilation to combat hypoventilation


O2 sat levels – pulse ox


Fluids are administered cautiously b/c of the danger of water intoxication


Passive rewarming w/ a blanket is recommended vs active rewarming such as application of external heat (ex. heating pads) – the latter should be avoided to prevent increased O2 demands and hypotension


Nursing Management

Book: effects of analgesics, sedatives, and anesthetic agents are prolonged in hypothyroid pts (careful monitors of pts prescribed these)

Monitor for CV changes

AMS – Orient and safety precautions

Activity – gradually increase; provide frequent rest periods

Anti-embolism stockings and elevate legs

Cough and deep breathe

Low-calorie, high-fiber diet, encourage fluid intake!

o Promote weight reduction + prevent constipation (return of normal bowel fxn)

Meticulous skin care

Provide extra clothing/blankets – crovide warm environment

Provide extra clothin g /blankets – c rovide warm environment Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)

Downloaded by Birhanu Ayenew (birhanua2015@gmail.com)