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90 Cards in this Set

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Accute suppurative thyroiditis
Caused by bacteria
S/s: unilaterla neck pain, fever, sweating
Tx: antibiotics
Subacute granulomatous thyroiditis
Self limiting an dinflammatory
Sometimes follows viral illness, genetic predisposition
S/s: painless goiter
Labs show hyperthyroidism with elevated T3 and T4
Tx: salicylates, NSAIDS, predisone, B-blockers
Chronic thyroiditis (hashimotos)
most commont, autoimmune, genetic, hypothyroidism with goiter
s/s Painless goiter--> dysphagia and resp distress, most pts are euthyroid, 30% hypo.
Tx: thyroid replacement if necessary, may resolve or come back.
Thyroid nodules
Hard, palpable deformities that are hard and painless, (cold)malignant or (hot) benign, t-scans done, pt given I131 to see what areas uptake it. Needle biopsy is gold standard, increased levels of serum calcitonin are associated with thyroid cancer.
Tx for malignancy: partial/total thyroidectomy, radiation
Hyperparathyroidism
S/S?
Diagnosis?
Tx?
Overactivity of parathyroid gland. PTH is secreted to increase bone resorption (into the blood) and in hyperPT there is too much hormone in the blood leading to bone damage, hyperCa (in blood)(stones, bones, abdominal moans, psychic groans, cardiac - short QT interval), and kidney damage.
Diagnosed with increased serum/urine Ca levels, decreased phosphate in serum, increase in urine.
Tx: REDUCE Ca LEVELS! IV NS, lasix (to escrete Ca), glucocorticoids to reduce Ca, surgery to reduce gland that is oversecreting
Hypoparathyroidism:
Causes?
Hyposecretion of PT glands causing hypoCa and high PHOS lvls, tetany may occur.
Result of accidental removal of glands or ischemia of area during surgery.
s/s: muscle spasms, irritabiltiy, tingling, laryngospasm, arrhythmias, lethargy, thin hair, cataracts, psychosis
s/s
s/s of hypoparathyroidism: muscle spasms, irritabiltiy, tingling, laryngospasm, arrhythmias, lethargy, thin hair, cataracts, psychosis
Dx of hypoparathyroidism
Dx: + Chvostek's sign (face), trousseau's sign, labs show low serum Ca and high serum Phos, low Urine Ca, cataracts
Tx of hypoparathyroidism
Tx: 10% IV Ca gluconate, oral Ca and Vit D, high Ca diet, no surgery because that is what causes the disorder
Adrenal medulla secretes:
Catecholamines: epinepherine, adrenalin, norEpi, dopamine.
Which hormones does the adrenal cortex produse?
Cortisol, androgens, aldosterone
What does hyperaldosteronism (Conn's disease)look like?
Labs?
Hypertension, hypernatremic, hypokalemic, muscle weakness, fatigue, metabolic alkalosis-> tetany, cardiac arrhythmias.
How is hyperadlosteroneism managed?
Surgically: adrenalectomy
K-sparring diuretic, antiHTNs
Aldosterone receptor antagonists
Low Na diet
Correct hypoK with K supplements
Prevent kidney damage
What is cushing's syndrome?
High levels of ACTH becaues of hypertrophy of adrenal cortex/tumor/hypersecretion. Too much corticosteriods.
What happens as a result if Cushing's?
Aldosterone is hypersecreted so Na and H2O retention-> HTN, edema and increased K excretion (hypoK).
Increased sex hormones (secondary sex characteristics seen). Increased glucocorticoids so muscle wasting, hypertension, decreased immune function.
Bruising, high risk of fractures, increased fat storage so moon faced, buffalo hump, increased GNG so hyperglycemia
How is Cushings treated?
Goal is to minimalize hormone secretion so discontinue/alter corticosteriod adminstration.
Surgical management with transsphenoidal hypophysectomy if pituitary problem, adrenalectomy if adrenal tumor, treat tumor/cancer. These pts will have to be on corticosteroids for life because they will no longer produce them
What are the 2 types of adrenal insufficiency?
Primary - Addison's disease
Secondary - Lack of pituitary ACTH secretion
Explain Addison's disease. (s/s)
Adrenal insuffiency or cortex failure, autoimmune in nature. All 3 corticosterioids fail: glucocorticoids (decreased GNG, glucose, weakness), mineral corts (Na lost, K is retained), and androgens (decreased hair and sex drive).
s/s:Increased H2O loss -> decreased BP, hyper K, dehydration, shock, metabolic acidosis.
With decreased corticosterioids, AntPit keeps making ACTH --> melanocyte stimulating hormone --> increased pigmentation, bronze rash
Explain secondary adrenal insufficiency. (s/s and causes)
There is a lack of ACTH secretion.
S/s hypotension, hypovolemia, shock, hypoNa, confusion, syncope, hyperkalemia (wide QRS,peaked Twave) fatigue, n/v, wt loss, hypoglycemia.
Causes: Pituitary disease, pit tumors, metastatic disease, postpartum necrosis, granulomas, withdrawl from chronic steroid use.
What is an Addinsonian crisis?
Complication of adrenal insuffiency: cardiovas collapse, profound hypovolemia, hypotension, shock, sudden weakness, severe abd px, back and leg px, renal shutdown, death.
How is Addison's treated?
Treat the cause, replace lost corticoids, salt additives for excess heat, IV hydrocortisone, manage shock, monitor cardiac fxn, watch EKG for hyperK, I/O
What should you tell your patient on steroids?
Adherence to schedule is very important. Updose if pt will be stressed, never stop therapy abruptly --> addisonian crisis. Increase salt intake
What disorder affect the adrenal medulla and what does it look like (s/s)?
Pheochromocytoma: neoplasm produces excess cathecolamines
s/s: severe episodic htn, headache, tachycardia, sweating lasting minutes to hours. May lead to DM or cardiomyopathy if not treated
What is osteoporosis? What causes it?
It is an age related metabolic disease in whihc bone demineralization -> decreased density and fractures.
Decreased osteoblast activity and increase osteoclast activity.
Can happen on its own or secondary to hyperthyroidism, hyperparathyroidsm, LT drug therapy (steroids)
What labs/diagnostics can help in diagnosing osteoporosis?
calcium, Vit D, phosphorus, ALP, urin calcium, parathyroid hormone levels.
Xray can show bone density loss, CT, DEXA scan
What tests can be done if you suspect osteomyelitis?
Increased WBCs, erythrocyte sedimentatino rate, blood dultures, bone scan, MRI, bone biopsy
How is osteomyelitis managed?
Antibiotics, sequestrectomy (excision of necrosed bone) bone grafts, amputation, muscle flaps
What is a good sign of infection in the elderly?
Confusion, not fever always
What hormones are secreted by the posterior pituitary?
ADH, Oxytocin
Thyroid stimulating hormone (TSH)is regulated by ___ from the ___ which sends the signal to the _____ to secrete TSH.
TRH, hypothalamus, anterior pituitary.
A _____ feedback mechanism is controlled by ciruclating concentrations of __ and __ which have profound effects on ____ _________ ________.
Negative, T3, T4, basal metabolic rate
Therefore, under normal conditions high levels of cirulating T3 and T4 will lead to a ______ in TSH levels.
Decrease
The target cells for adrenocorticotropin (ACTH) are in the ________ and produces and releases _________ and _________.
Adrenal cortex, glucocorticoids and mineral corticoids
Who is at risk for developing SIADH?
Head injury, brain surgery, CVA/aneurysm, Guillina-Barre, Cancer, infections, hypoxia, chemo agents.
What are the s/s of SIADH?
Wg gain w/o edema, orthostatic hypotension, looks dehydrated, CNS: Headache, lethargy, confusion, N/V/D,
What will the labs of a pt with SIADH look like?
Plasma osmolality?
Na?
H/H?
I/O?
BUN/Cr?
ADH levels?
decreased plasma osmolality, decreased serum Na levels (dilutional), decreased H/H, Urinary: low UO, decreased BUN and Creatnine.
High plasma ADH levels
What is your treatment of the pt with SIADH?
Fluid restrictins (800-100mL/d).
IV NS with mild hypoNa, Hypertonic NS with severe HypoNa
Siezure precautions
Loop diuretic to decrease effectiveness of ADH.
Demeclycycline blocks action of ADH.
What are the 3D's of diabetes insipidus?
Diabetes insipidus
decreased ADH
diuresis
What causes diabetes insipidus?
Lesions of hypothalmus or post pituitary that prevent ADH synthesis or realease
decreased renal response to ADH
What are the clincial s/s of DI?
Polyuria, polydypsia, 5-20 L urine output with spec gravit < 1.003, fatigue, hypovolemic, wt loss, tachycardia, hypotension, shock, irritability, coma, alterered mental staus
What will labs reveal for PTs with DI?
Serum osmolality> 295
Hypernatremia
Urine SG 1.001-1.005
Low serum ADH
What hormones does the thyroid produce? What regulates this?
T3, T4, Calcitonin (lowers plasma calcium and phosphate levels)
The secretion of these is regulated by Thyroid Stimulating hormone.
Hypothalamus (TRH)->Ant pit (TSH)->Thyroid (T3, T4)
The pt with ___________ is at an especially high risk for an MI or cardiac incident.
Hyperthyroidism, thyroid hormones affect the heart, The increased heart rate and stroke volume in hyperthyroidism cause an increased in cardiac output and peripheral blood flow
Two manifestations of hyperthyroidism are _______ and ____________.
Graves Disease and thyroid storm
What is Graves disease? Presentation?
Autoimmune disease in which antibodies attack thyroid gland causing it to over produce. Goiter development, buldging eyes. Tachycardia, SOB, increased apetite with wt loss, muscular weakness, edema, muscle wasting, nervousness, tremors, amenorrhea, decreased libido
Is the hyperthyroid pt hyperglycemic or hypoglycemic?
Hyperglycemic, they have a low glucose tolerance.
How does Thyroid storm present? Lab abnormalities?
Like GD to another level: Severe tachycardia, heart failure, shock, hyperthermia, restlessness, abd px/n/v coma. Confsion, weakness, heat intolerance.
Labs will show increaed T4 and T3 with decreased TSH
Thyroid storm is treated with _____(3)______.
Saturated solution of K Iodide, beta blockers, and steriods
What should the nurse watch for in a patient post thyroid surgery?
It may be difficult to talk, watch for hemorrhage, trachea compression, place pt in semifowlers, watch for tetany (if parathyroids were removed too--> give calcium gluconate). Watch for hypothyroidism
What are the clinical manifestations of hypothyroidism?
Impaired memory, slow speech, fatigue, cold intolderance, alopecia, wt gain, menorrhagia, decreased pulse, hyperlipidemia, myxedema (waxy deposits on face), anemia.
What will labs show of the hypothyroid pt?
Decreased T4 and T3, increased TSH
What is the treatment of a hypothyroid patient?
Synthetic thyroxine, advise pt to report chest px, meds must be taken daily.
What may trigger myxedema coma?
Infection, trauma, exposure to cold, tranquilizers, physical stress, hashimoto's thyroiditis, hypophysectomy, insufficient replacement therapy.
What will physical assessment reveal on pt with myxedema coma?
Hypothermia, nonpitting edema, enlarged tongue, loss of eyebrows/scalp hair, goiter, delaed deep tendon reflexes, bradycardia, shallow respirations
What will labs reveal on this pt?
HypoNa, respiratory acidosis, hypoglycemia, prolonged QT interval, low T3, T4, elevated TSH, hyperlipidemia
What are the (6) main functions of the liver?
CHO metabolism
Fat Metab.
Protein met. (albumin, globulin, urea)
Bile production
Circulatory/drug megabolism
Vitamin storage
What causes Lannec's cirrhosis?
Alcohol leads to fatty infiltration of hepatocytes, lumps, and scarring. Reversible if ETOH stopped.
What is postnecrotic cirrhosis?
Occurs after massive livercell necrosis, bands of scar tissue destroy entire lobes of liver.
Caused by viral hepatitis or industrial chemicals.
What is biliary cirrhosis?
results from obstruction/tumor of hepatic or common bile duct -> bile stasis in liver.
What is Cardiac cirrhosis?
Associated with severe rt sided HF. Liver is congested by blood and becomes edematous.
What are some complications of cirrhosis (7)?
Jaundice
Portal hypertension
Esophageal varicies
Coagulation defects
Ascites
Portal-systemic encepalopathy
hepatorenal syndrome
Folks with portal hypertension often develop __________ and _______ because the blood is trying to find other ways to get back to the heart.
Esophageal varicies and hemmoroids.
Why do pts with cirrhosis develop coagulation defects?
Vitamin K clotting factors synthesized in the liver are not produced.
What causes the encephalopathy in pts with cirrhosis?
High levels of circulating NH3
_________ is the promary cause of death in pts with cirrhosis. and is evidenced by ________ UO, _________ BUN and CR, and ________osmolarity.
Hepatorenal syndrome
decreased, elevated, fixed.
What are your treatment options in cirrhosis pts with ascites?
Low Na diet
diuretics
daily weight and I/O
paracentesis
peritoneovenous shunt
Along with Vit K, what med would you give a pt with a ruptured esophageal varicie?
Vasopressin to constrict arteries and decrease portal presure
What lab tests can one do to assess for liver disease?
ALT, AST (not specific to liver dysfunction) GGT, direct and total bilirubin levels, serum proteins, albumin:globulin, PT, Cholesterol, serum amonia levels.
All will be increased except h/h, serum protein and albumin.
High amonial levels in the blood can cause ___________ and _______.
Hepatic encephalopathy and coma
If your patient presents with fector hepaticus and asterixis, this could be a complication of what?
Portal-Systemic Encephalopathy- Buildup of ammonia and urea in the body to toxic levels- patient will appear confused, lethargic, have an altered level of consciousness, impaired thinking processes
S/S of encephalopathy include:
confusion, mood changes, asterixis, no relfexes, sweat breath (fetor hepaticus)
How is hepatic encephalopathy/coma managed?
Lactulose to reduce serum ammonia levels
Give glucose to prevent protein breakdown (which causes increased NH3 levels)
restrict protein intake
Monitory lytes and NH3
Neomycin sulfate - allows free conversion of NH3->NH4->out in urine
What is fulminant hepatitis?
Rapid onset necrosis of liver cells resulting from Hep B or C or caused by CCL4.
What are the s/s of fulminant hepatitis?
depression, confusion, anorexia, jaundice->coagulation defects, renal failure, *cerebral edema, increased ICP* , need transplant
How is Hep A transmitted?
oral/fecal, sex with infected person
What labs assist in Hep A diagnosis?
Alt and AST will be 4-1000 times normal
There are vaccines available for hep_____ and hep______.
A and B
Hep B is transmitted by:
blood and body fluids
What labs assist in diagnosing a pt with Hep B?
ALT, AST, HBsAg,
_________ is the #1 reason for liver transplant in the US.
Hepatits C
How is Hepatitis C detected?
Enzyme immunoassay detects antibodies to it. Test confirmed with anti-HCV assay and viral load test.
What causes pancreatitis?
Autodigestion by trotolytic enzymes.
Obstruction of common bile duct (gall stones)
ETOH abuse (causes regurgitation of duodenal contents into pancreatic duct)
Trauma
Viral infection, duodenal ulcers, drugs
What are s/s of pancreatitis?
Intense Abd px radiating to back
Dyspnea
N/V
hypotension secondary to losing fluid to third spacing
Tachycardia secondary to fluid loss and shock
low grade fever
increased WBC
jaundice
Cullen's sign due to seepage of blood from pancreas
What diagostic tests will help in diagnosing pancreatitis?
Increased amulase and lipase
Increased glucose (secondary to beta cell damage, decreased insulin)
Decreased calcium (body feeds off of fatty acids that Ca is bound to)
ERCP fiber optic scope to duodenum to view common bile duct and pancreatic duct.
How is pancreatitis treated?
NPO to prevent more secretion of pancreatic juices
TPN, IVF
NG suctioning
Pain control with demerol *not morphine*
What is the most common surgical procedure in the US?
Cholecystectomy
What are the s/s of cholesystitis?
Px and fullness, cna be vomitting and jaundice if CBD is obstructed.
Fever and increased WBCs
How is cholecystitis diagnosed?
Ultrasound is gold standard
Radionuclide image
Elevated WBC and LFTs
How is cholecystitis treated?
antibiotics
IVF
Px control
Low fat diet
chenodial (cholesterol solvent)
Removeal of gallbladder
What is Conn's disease?
excessive secretion of aldosterone from one or both adrenal glands, which is most commonly caused by an adenoma.