Patho/pharm II exam 3

Nephron structure

Renal corpuscle (glomerulus and Bowman’s capsule), proximal tubule, loop of henle, distal tubule

Urine output

Oliguria: <500mL in 24 hours

Anuria: <100mL in 24 hours

Polyuria: >2000mL in 24 hours

Assessment of renal function

Urine output

Labs: dipstick, urinalysis, C&S (culture and sensivity), 24hr

Serum: BUN (10-20mg/dl, increases if dehydrated), ceratinine (0.5-1.5mg/dl, more accurate about kidney function)

Serum BUN and creatinine

BUN: end product of protein metabolism, liver problems, dehydrated

Ceratinine: end product of muscle metabolism, excreted only by kidney, focus more on this, renal function

Ratio of BUN to Cr normal: 20:1

Any elevationis important

Tests for renal function

Glomerular filtration rate: 95 and above, how well kidneys are working

Cytoscopy: looking into urinary tract

Ultrasonography: structures specifically, mass?, enlargement?, necrosis?, cold but painless

Radiologic and other image studies: size and shape, KUB: kidney ureter bladder

Disorders of the kidney

Subject to many of the same types of disorders that affect other body structures

Developmental defects, infections, altered immune responses, neoplasms

Organ development

Dysgenesis: failure of an organ to develop normally

Agenesis: the complete failure of an organ to develop, nothing you can do

Hypoplasia: failure of an organ to reach normal size, doesn’t grow with you, fall with you

Cystic disease of the kidney

Fluid filled sacs or segments of a dilated nephron

Causes: tubular obstructions that increase intratubular pressure

Changes in the basement membrane of the renal tubules that predispose to cystic dilatation

Causes of urinary tract obstruction

Developmental defects, calculi (stones), pregnancy, benign prostatic hyperplasia, scar tissue resulting from infection and inflammation, tumors, neurologic disorders such as spinal cord injury

Damaging effects of urinary obstruction

Stasis of urine: predisposes to infection and stone formation

Development of back pressure: interferes with renal blood flow and destroys kidney tissue

Manifestations of urinary obstruction

Depends on: the site of obstruction, the cause, rapidity with which the condition developed

Common symptoms: pain, signs and symptoms of UTI, manifestations of renal dysfunction

Kidney stones

Definition: crystalline structures that form from components of the urine

Requirements for formation: a nidus to form (allows crystals to accumulate), a urinary environment that supports continues crystallization of stone components

Factors influencing the formation of kidney stones

The concentration of stone components in the urine, the ability of stone components to complex and form stones, the presence of substances that inhibit stone formation

Types of kidney stones

Calcium stones: 75% of stones, oxalate or phosphate

Magnesium ammonium phosphate stones: strubite, infection, too big to pass

Uric acid stones: gout

Cystine stones: least common, autosomal recessive defect

Kidney stone treatment

Preventative: dietary restriction, calcium salt supplementation, thiazide diuretics, cellulose phosphate

Treatment for pain, antibiotic for infection, removing stones

Diagnosis: urinalysis, radiography, IV pyelography, ultrasonography

Types of UTIs

Asymptomatic bacteriuria, symptomatic infections, lower UTIs (cystitis), upper UTIs (pyelonephritis)

Causes of UTIs

Most uncomplicated UTIs caused by E. Coli

Other uropathic pathogens include: Staphylococcus saprophyticus in uncomplicated UTIs, Both E. Coli gram negative rods (Proteus mirabilis, Klebsiella pneumoniae, Enterobacter, Pseudomonas, and Serratia)

Most caused by bacteria that enter through the urethra

Causes of UTIs associated with stasis urine flow

Anatomic obstructions (stones, prostatic hyperplasia, pregnancy, malformation of uretervesical junction)

Increased pressure resulting in reflux

Functional obstructions: neurogenic bladder, infrequent voiding, detrusor (bladder) muscle instability, constipation

Protective mechanisms for UTIs

Washout phenomenon, mucin layer (prevent bacteria from entering area, film like), local immune responses (prevent bacteria from colonizing), normal flora of the periurethral area in women, prostate secretions in men

Characteristics of acute episode cystitis

Frequency of urination (as often as every 20 minutes), lower abdominal or back discomfort, burning and pain on urination, cloudy and foul-smelling urine on occasion

Special considerations of UTI patients

Sexually active women, pregnant women, age related effects (infants, toddlers, adolescents, adults, elderly)

Diagnosis and treatment of UTIs

Diagnosis based on symptoms and on examination of the urine for the presence of microorganisms, X-ray films, ultrasonography, and CT and renal scans are used to identify contributing factors

Urine dipstick, treatment of UTI is based on the pathogen causing the infection

Drug therapy of UTIs

Sulfonamides, Trimethoprim, Penicillins, Aminoglycosides, Cephalosporins, Fluoroquinolones, Carbapenems, Methanamine, Nitrofurantoin

Characteristics of glomerulonephritis

Immune mechanisms (glomerular antibodies, curculating antigen-antibody complexes)

Characteristics: hematuria with red cell casts, a diminished GFR, azotemia (presence of nitrogenous wastes in the blood), oliguria, HTN

Causes of glomerulonephritis

Diseased that provoke a proliferative inflammatory response of the endothelial, mesangial, or epithelial cells of the glomeruli

The inflammatory process: damages capillary wall, permits red blood cells to escape into the urine, produces hemodynamic changes that decrease the GFR

Cellular changes in glomerular disease

Proliferative (endothelial, mesangial, leukocyte, cresent formation), basement membrane thickening, sclerosis, fibrosis, diffuse glomerular changes, focal glomerular changes, segmental glomerular changes, mesangial changes

Urinary changes in glomerulonephriitis

Proteinuria, hematuria, pyuria, oliguria, edema, hypertension, azotemia

Types of glomerular diseases

Actice proliferative glomerulonephritis, rapidly progressing glomerulonephritis, nephrotic syndrome, membranous glomerulonephritis, minimal disease change (lipoid nephrosis), focal segmental glomerulosclerosis, IgA nephropathy, chronic glomerulonephritis

Tubulointersitial disorders

Damage to the proximal loop or distal portion of the nephron

Acute tubular necrosis, renal tubular acidosis, pyelonephritis, the effects of drugs and toxins

Proximal and distal tubular acidosis

Renal tubular acidosis: proximal tubular disorders that affect bicarbonate reabsorption, distal tubular defects that affect the secretion of fixed metabolic acids

Renal failure

A condition in which the kidneys fail to remove metabolic end products from the blood and regulate the fluid, electrolyte, and pH balance of the extracellular fluids

Underlying causes: renal disease, systemic disease, urologic defects of nonrenal origin

Prevention and early diagnosis of acute renal failure

Assessment measurements to identify persons at risk for development of acute renal failure

Those with preexisting renal insufficiency and diabetes (damage to basement membrane of glomeruli)

Elderly persons (due to the effects of aging on renal reserve)

Also medications toxic to kidneys

Types of renal failure

Acute: abrupt in onset, often reversible if recognized early and treated appropriately

Chronic: the end result of irreparable damage to kidneys, it develops slowly, usually over the course of a number of years

Prerenal causes of acute renal failure

Hypovolemia (decreased blood volume, affect kidneys ability to perfuse properly)

Decreased vascular filling

Heart failure and cardiogenic shock

Decreased renal perfusion due to vasoactive mediators, drugs, diagnostic agents

Postrenal causes of acute renal failure

Bilateral ureteral obstruction, bladder outlet obstruction

Intrinsic or intrarenal causes of acute renal failure

Acute tubular necrosis: prolonges renal ischemia, exposure to nephrotoxic drugs metals and organic solvents, intratubular obstruction resulting from hemoglobinuria, myoglobinuria, myeloma light chains, or uric acid casts

Acute renal disease

Phases of ATN

Onset phase: lasts hours or days, the time from the onset of the precipitating event until tubular injury occurs (hemorrhage)

Maintenance phase: characterized by a marked decrease in the GFR (person is oliguric, increased nitrogenous wastes, increased fluid retention, HTN, can be fatal, hyperkalemia)

Recovery phase: period during which repair of renal tissues takes place (edema resolves, returns to normal)

Common causes of chronic renal disease

Hypertension, diabetes mellitus, polycystic kidney disease, obstructions of the urinary tract, glomerulonephritis, cancers, autoimmune disorders, diseases of the heart or lungs, chronic use of pain medications

Signs of the progression of chronic renal failure

Diminished renal reserve, renal insufficiency, renal failure, end stage renal disease

Mild reduction of GFR to 60 to 89mL/min

Moderate reduction of GFR to 30 to 59mL/min

Severe reduction in GFR to 15 to 29mL/min

Kidney failure with a GFR <15mL/min with a need for renal replacement therapy

Clinical manifestations of chronic renal failure

Accumulation of nitrogenous wastes, alterations in water electrolyte and acid-base balance, mineral and skeletal disorders, anemia and coagulation disorders, hypertension and alterations in cardiovascular function

GI disorders, neurologic complications, disorders of skin integrity, immunologic disorders

Treatment during the renal insufficiency stage of renal failure

Using measures to retard deterioration of renal function and assist the body in managing the effects of impaired function

Treating urinary tract infections promptly, avoiding medications with renal damaging potential, controlling blood pressure, controlling blood sugar in persons with diabetes, stopping smoking

Disorders of water, electrolyte, and acid-base balance

Sodium and water balance: the kidneys function in the regulating of extracellular fluid volume

Potassium balance: approximately 90% of potassium excretion is through the kidneys

Acid-balance balance: the kidneys normally regulate blood pH by eliminating hydrogen ions produces in metabolic processes and regenerating bicarbonate

Hematologic disorders accompanying renal failure

Anemia: decreased hemoglobin, can be chronic, decreased RBCs

Coagulopathies: bleeding disorders, GI bleeding, easy bruising, clotting issues

Cardiovascular disorders accompanying renal failure

Hypertension, heart disease (left ventricular hypotrophy, impaired filling, overload anemia), pericarditis (uremia, hemodialysis, cardiac tamponade, chest pain, friction rub)

Altered drug metabolism in kidney disease

CKD and its treatment can interfere with the absorption, distribution, and elimination of drugs

Altered drug absorption (antacid treatment), altered metabolism (results of less protein bound drugs, increased intermediates of drug metabolism), alterations in dosage may be required

Treatment of renal failure

Medical management: dialysis (hemodialysis and peritoneal dialysis), transplantation (based on patient preference and donor ability)

Dietary management: protein (decreased, reduces symptoms because it gets turned into wastes), carbohydrates (with fat and calories), potassium (should decrease, easily become hyperkalemic), sodium and fluid intake

Depends on type or severity of kidney disease, special diets

CKD in children

Causes: congenital malformations, inherited disorders, acquired diseases, metabolic syndromes (polycystic kidney disease)

Manifestations: severe growth impairment, developmental delay, delay in sexual maturation, bone abnormalities, development of psychosocial problems

CKD in elderly

Normal decrease in GFR with age, increased detrimental effects of nephrotoxic drugs

Greater incidence of cerebrovascular, cardiovascular, and skeletal system effects

Diuretics

Increased urinary output

Therapeutic uses: hypertension, removal of edematous fluids, prevention of renal failure (by increasing circulation of fluids)

Renal physiology

Functions: cleansing of ECF, maintaining ECF volume and composition, maintaining acid-base balance, excreting metabolic wastes and foreign substances (drugs, toxins), secreting regulatory substances (renin, erythropoietin, vitamin D)

Renal processes: urine formation

Filtration: glomerulus, filtrate is left with Na+, Cl-, HCO3-, K+

Reabsorption: diuretics work here, proximal convoluted tubule, loop of henle, distal convoluted tubule

Active tubular secretion: proximal convoluted tubule, maintains acid/base balance

Maintenance of ECF volume and composition

Roles of aldosterone and ADH

Aldosterone: acts on distal tubule to stimulate reabsorption of Na+ and excretion K+

ADH: acts on collecting duct to reabsorb water

Mechanism of action of diuretics

Blocks sodium/ chloride reabsorption so osmotic pressure retained to keep water in filtrate and increase urine output

Site of action depends on type of diuretic; the higher up in the tubule the action, the greater the diuresis

Adverse effects: hypovolemia, acid-base balance, electrolyte balance, hypotension

Classification of diuretics

Loop (high-ceiling): furosemide (Lasix)

Thiazide: hydrochlorothiazide

Potassium sparing: Spironolactone (Aldactone)

Ostomic: mannitol

Carbonic anhydrase inhibitors: carbonic acid → H2O + carbon dioxide, not used often

Loop diuretics

Ascending loop of henle, nonpotassium sparing

Rapid onset; given orally (onset 60 minutes, lasts 6-8 hours but if given parenterally then faster)

Uses: pulmonary edema of congestive heart failure, edematous states (hepatic, renal, cardiac), hypertension

Others: Ethacrynic acid (Edecrin), Bumetanide (Bumex), Torsemide (Demadex)

Adverse effects: hypotension, hypokalemia, hyponatremia, ototoxicity, NEVER use with aminoglycosides

Drug interactions with loop diuretics

Negative: Digoxin- risk of decreased potassium accentuates problem of digoxin toxicity

Positive: potassium sparing diuretics help retain potassium so they may counteract loss of potassium

Thiazide diuretics

Hydrochlorothiazide, most widely used

Action on distal convoluted tubule, peaks 4-6 hours, lasts 12

Used in: hypertension, edematous states

Increases uric acid and glucose levels, less diuresis (used for those with fairly decent kidney function, not ototoxic)

Drug interactions with thiazides: augment effects of antihypertensive agents, NSAIDS may decrease effectiveness of thiazides

Potassium sparing diuretics

Spironolactone (aldactone)- blocks aldosterone in the distal nephron (aldosterone antagonist), rentention of potassium and loss of sodium

Uses: Hypertension (most commonly in association with thiazide or loop diuretic), edematous states, severe heart failure (decreases mortality), primary hyperaldosteronism

Adverse effects: hyperkalemia, teach patients to be cautious of eating too much K+

Drug interactions with K+ sparing diuretics

DO NOT use with potassium supplements

DO NOT use with angiotensin converting enzyme inhibitors because they suppress aldosterone secretion and thereforre, can increase potassium

Osmotic diuretic

Mannitol (Osmitrol)

Osmotic pressure in lumen of nephron increased so sodium and water retained rather than being reabsorbed

Uses: shock, hypotension (situations where blood flow to the kidney is decreased), increased intracranial pressure, increased intraocular pressure

Erythropoietin (Epogen)

Used for renal disease, peptide growth factor secreted by kidneys, IV, SC, usually 3x/week

Stimulates erythrocyte development in bone marrow leading to more RBCs, available in recombinant form that can be given parenterally, Anemia of CKD responds to this, for chronic CKD not acute

Adverse effects: HTN, increased clotting, CV events, malignancy progression, arthalgia

Discontinue therapy when HGB levels are above: 10-11gm/dl

Sodium polystyrene sulfonate (Kayexalate)

Used to treat hyperkalemia, exchanges sodium ions for K+ ions in the gut; after binding K+, it is expelled in feces

Given orally or rectally (followed by saline irrigation), 15-30gms four times a day

Adverse effects: colonic necrosis, anorexia, constipation, hypernatremia, hypokalemia, hypocalcemia, hypomagnesemia

Do not give with sorbitol, can increase the risk of colonic recrosis, which can be FATAL

Disturbances of endocrine function

Caused by inappropriate amounts of hormones delivered to target cell, inappropriate response by target cell

Hyperfunction: excessive hormone production

Hypofunction: underproduction of hormone

Diseases of posterior pituitary

Hyperfunction: too much antidiuretic hormone effects

Ex. syndrome of inappropriate antidiuretic hormone secretion

Hypofunction: too little antidiuretic hormone effects

Ex. diabetes insipidus, neurogenic, nephrogenic, dipsogenic

Syndrome of inappropriate antidiuretic hormone secretion

ADH levels abnormally high

Hyponatremia sodium: <135mEq/L

Hypoosmolarity: <280mOsm/kg

Hypervolemia

Decreased urine output, water retention, weight gain, increased urine osmolarity, decreased serum osmolarity

Treatment for SIADH

Correction of severe hyponatremia: very dangerous, 3% saline IV treatment (slow electrolyte replacement)

Diuretics: furosemide and electrolyte replacement

Vaptans: Tolvaptan (samsca, Jynarque), Conivaptan (Vaprisol)

Fluid restriction between 800 and 1000mL/day

Resistant or chronic SIADH: demeclocycline

Diabetes insipidus

Insufficient ADH, polyuria, nocturia, urine output: 8-12L/day

Polydipsia: continual thirst, hypovolemia, hypernatremia, increase in plasma osmolarity, inability to concentrate urine

Emergencies: Vasopressin, but not for long term use because it elevates BP

Types and treatment of diabetes insipidus

Neurogenic: insufficient amounts of ADH, administer DDAVP (Desmopressin), not enough being made

Nephrogenic: insensitivity of the renal collecting tubules to ADH, administer thiazide diuretics, kidneys are not responding to ADH

Dipsogenic: excessive fluid intake, lowers plasma osmolarity, suppression of ADH secretion, management of water ingestion- drink too much water, not respond to “not thirsty anymore”, TBI, manage fluids

Major functions of thyroid hormone

T3 and T4

Increases metabolism and protein synthesis, influence growth and development in children, mental development and attainment

Thyroid hormones

T3 (triiodothyronine) and T4 (thyroxine), will later turn into T3

Secretion regulated by hypothalamic pituitary thyroid feedback system

Iodine necessary to make T3 and T4

Protein bound

Measures used to diagnose thyroid disorders

Measures of T3, T4, and TSH

Resin uptake test (how much hormone is present), assessment of thyroid antibodies, radioiodine uptake test, thyroid scans, ultrasonography, Ct and MRI scans, fine needle aspiration biopsy of a thyroid nodule

Alterations of thyroid function

Hypothyroidism: primary causes- autoimmune, irradiation, trauma, gland removal; secondary causes- pituitary hyposecretion of TSH

Hashimoto thyroiditis (most common) autoimmune disorder- decreased metabolic rate, accumulation of hydrophilic mucopolysaccharide substance inn the connective tissues, elevated serum cholesterol

Congenital, malfunction, trauma

Manifestations of hypothyroidism

Mental and physical sluggishness, myxedema (orange peeling skin), somnolence/lethargy, decreased CO, byadycardia, hypotension, constipation, decreased appetite, hypoventilation, cold intolerance, decreased reflexes, weight gain

Congenital hypothyroidism

Thyroid hormone is essential for normal growth and brain development, almost half of which occurs during the first 6 months of life

If untreated, congenital hypothyroidism causes mental retardation and impairs physical growth

The manifestations of untreated congenital hypothyroidism are referred to as cretinism

Thyroid hormone replacement

Levothyroxine (Synthroid)

Synthetic preparation of T3, conversion to T4, highly bound to protein, half life of 7 days so long time to see plateau, drug of choice for hypothyroidism

Adverse effects: symptoms fo hypothyroidism (arterial fibrillation)
Drug interactions: occur with several common drugs, check before giving with other drugs, give on empty stomach

Administration of thyroid replacements

Usually given PO, IV for myxedema coma, assess baseliem weight/height and vitals, monitor cardiac status, thyroid function

Assess s/s of hyperthyroidism, administer on empty stomach

Contraindicated with adrenal insufficiency, untreated thyroiditis or thyrotoxicosis

Myxedema coma

Causes: untreated hypothyroidism, sudden withdrawl of thyroid meds, acute illness and surgery

Results: decreased cardiac output, lack of perfusion to vital organs including the brain

Manifestations: decreased BP, tachycardia then badycardia, decreased or change in LOC

Treatment: IV normal saline and glucose, thyroid hormone replacement, respiratory support

Alterations in thyroid function

Hyperthyroidism: primary causes- tumor related, inflammatory, autoimmune; secondary- hypersecretion of TSH by pituitary

Graves disease- most common, increased metabolic rate and oxygen consumption, increased use of metabolic fuels, increased sympathetic nervous system responsiveness

Manifestations of hyperthyroidism

Exothalamos, restlessness, irritability, anxiety, hyperactive reflexes, increased cardiac output, tachycardia and palpations, diarrhea, increases appetite, dyspnea, heat intolerance, increased sweating, thin hair, scalp hair loss, weight loss

Graves disease

State of hyperthyroidism, goiter, and ophthalmopathy

An autoimmune disorder characterized by abnormal stimulation of the thyroid gland by thyroid stimulating antibodies that act through the normal TSH receptors

Labs: low TSH, high T3 and T4

Tx: antithyroid drugs, beta blockers, radioactive iodine, surgery

Manifestations of thyrotoxic crisis (thyroid storm)

Very high fever, extreme cardiovascular effects (tachycardia, congestive HR, and angina), severe CNS effects (agitation, restlessness, and delirium), high mortality rate (cannot maintain homeostasis)

Antithyroid agents

Interfere with formation, release, or action of thyroid hormones

Methimazole (Tapazole) and Propylthiouracil PTU (propyl-thyracil inhibit hormone synthesis)

Radioactive Iodine (RAI): collects in thyroid, destroys cells, slows production of thyroid hormones

Methimazole

Treatment for hyperthyroidism: (Tapazole), first line drug for hyperthyroidism, prototype of the thionamides

Does not cause the liver damage associated with propylthiouracil, does not destroy existing stores of thyroid hormone, may take 3-12 weeks

More dangerous than PTU during lactation and during the first trimester of pregnancy, agranulocytosis

Propylthiouracil

Treatment for hyperthyroidism: (PTU), inhibits thyroid hormone synthesis, second line drug for Graves disease, short half life (90 minutes), full benefits may take 6 to 12 months

Therapeutic uses: Grave’s disease, adjunct to radiation therapy, preparation for thyroid gland surgery, thyrotoxic crisis

Radioactive iodine

Treatment for hyperthyroidism-(131I), radioactive isotope of stable iodine, emits gamma and beta rays, half life of 8 days, 2-3 months for full effect

Used in Graves disease: effect on the thyroid, advantages and disadvantages of therapy

Candidates over over age 30, not children, action: destruction of thyroid gland, disadvantage: hypothyroidism

Nonradioactive iodine

Strong iodine solution (Lugol’s solution)

Used to suppress thyroid function in preparation for thyroidectomy

Adverse effects: brassy taste, burning sensation in the mouth and throat, soreness of the teeth and gums, frontal headache, salivation, various skin eruptions, coryza (cold symptoms)

Actions of parathyroid hormone

Increases intestinal absorption of calcium, increases intestinal absorption of phosphate, decreases renal excretion of calcium, increases renal excretion of phosphate, increased bone resorption, decreases bone formation, promptly increases serum calcium levels, prevents increase in serum phosphate levels

Hypoparathyroidism

Low secretion of parathyroid hormone by the parathyroid gland- Idiopathic, autoimmune, low magnesium or surgery

Results in hypocalcemia and increased serum phosphorus level

S/S: increased neuromuscular excitability- remember PTH (paresthesia, tetany, hypocalcemia and hyperphosphatemia

Emergency: IV calcium gluconate and/or calcitriol, long term- oral Ca++ supplement and vitamin D

Drugs to treat hypocalcemia

10% calcium gluconate IV: IV push (undiluted, given SLOWLY, max of 50-100mg/min)

Monitor BP, pulse, ECG while giving

Calcitriol (Rocaltrol): daily oral dose or IV 3 times a week

Hyperparathyroidism

High secretion of parathyroid hormone by the parathyroid gland. Primary: something is wrong with the parathyroid glans itself (hyperplasia, adenoma, cancerous tumor); secondary: disease is causing the prarthyroid gland to not work properly (hypocalcemia, vitamin D deficiency, often main cause is chronic renal failure)

Manifestions due to hypercalcemia

Treatment: surgical excision of abnormal parathyroid gland, calcimimetics

Adrenal glands

Disorders of the adrenal cortex: hyperfunction or hypofunction

Disorders of the adrenal medulla: no known hypofunction, hyperfunction

Steroid hormones produced by the adrenal cortex

Mineralcorticoids: aldosterone, function in sodium, potassium, and water balance

Glucocorticoids: cortisol, aid in regulating the metabolic functions of the body and in controlling the inflammatory process, essential for survival in stress situations

Adrenal sex hormones: androgens, serve mainly as source for androgens for women

Adrenal cortical insufficiency

Primary adrenal cortical insufficiency: Addison’s disease, ACTH levels are elevated because of a lack of feedback inhibition

Secondary adrenal cortical insufficiency: Occurs as a result of hypopituitarism or because pituitary gland has been surgically removed

Acute adrenal crisis: life threatening situation occurs

Addison’s disease

Primary adreno-cortical deficiency (adrenal cortex does not produce enough cortisol and aldosterone)

Causes: autoimmune, idiopathic, TB, adrenal trauma, neoplasia

Up to 90% of tissue nonfunctional before recognized in some patients

Clinical findings of Addison’s disease

Anorexia and weight loss, fatigue and weakness, myalgia, arthralgia, abdominal pain, orthostatic hypotension, hyponatremia, hyperkalemia, hypoglycemia, hyperpigmentation of the skin, GI symptoms, nausea, diarrhea

Addisonian crisis

Medical emergency

Triad to recognize: fluid imbalance (hypotension/shock), electrolyte imbalances (hyperkalemia, hyponatremia), glucose issues (hypoglycemia)

Glucocorticoids

Hydrocortisone (Solu-Cortef), Prednisone (Deltasone), Dexamethsone (Decadron)

Used for adrenocortical insufficiency, allergic reactions, anaphylaxis, collagen disorders, neoplastic disease, respiratory disorders, rheumatic disorders, shock

Pharmacologic actions: antiinflammatory, maintenance of normal BP, fat metabolism, immunosuppressant actions, stress effects, mood and behavior

Complications of glucocorticoids

Suppression of adrenal function, hyperglycemia, euphoria, increased appetite, restlessness, insomnia, lowered resistance to infections, bone loss, osteoporosis, myopathy, fat redistribution, peptic ulcer disease

Nursing considerations for glucocorticoids

Monitor Vs, weight, I/O, BP, glucose, labs, assess for edema, lung sounds, check skin, change in hair growth, acne, skin will become fragile with long term use, oral doses with meals, weight reduction diet

Hydrocortisone

A glucocorticoid, IV bolus is preferred route, IM and oral are available

If in acute adrenal insufficiency, may need additional hydrocortisone 100mg by continuous infusion over 8 hours and 50mg IM Q12 hours along with hydration

Higher doses adverse effects: adrenal suppression and cushings syndrome (rapid weight gain, round face, fluid retention)

Dexamethasone is an alternative, Prednisone is more potent