Medsurg Exam 4

Front 1

Accute suppurative thyroiditis

Back 1

Caused by bacteria
S/s: unilaterla neck pain, fever, sweating
Tx: antibiotics

Front 2

Subacute granulomatous thyroiditis

Back 2

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

Front 3

Chronic thyroiditis (hashimotos)

Back 3

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.

Front 4

Thyroid nodules

Back 4

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

Front 5

Hyperparathyroidism
S/S?
Diagnosis?
Tx?

Back 5

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

Front 6

Hypoparathyroidism:
Causes?

Back 6

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

Front 7

s/s

Back 7

s/s of hypoparathyroidism: muscle spasms, irritabiltiy, tingling, laryngospasm, arrhythmias, lethargy, thin hair, cataracts, psychosis

Front 8

Dx of hypoparathyroidism

Back 8

Dx: + Chvostek's sign (face), trousseau's sign, labs show low serum Ca and high serum Phos, low Urine Ca, cataracts

Front 9

Tx of hypoparathyroidism

Back 9

Tx: 10% IV Ca gluconate, oral Ca and Vit D, high Ca diet, no surgery because that is what causes the disorder

Front 10

Adrenal medulla secretes:

Back 10

Catecholamines: epinepherine, adrenalin, norEpi, dopamine.

Front 11

Which hormones does the adrenal cortex produse?

Back 11

Cortisol, androgens, aldosterone

Front 12

What does hyperaldosteronism (Conn's disease)look like?
Labs?

Back 12

Hypertension, hypernatremic, hypokalemic, muscle weakness, fatigue, metabolic alkalosis-> tetany, cardiac arrhythmias.

Front 13

How is hyperadlosteroneism managed?

Back 13

Surgically: adrenalectomy
K-sparring diuretic, antiHTNs
Aldosterone receptor antagonists
Low Na diet
Correct hypoK with K supplements
Prevent kidney damage

Front 14

What is cushing's syndrome?

Back 14

High levels of ACTH becaues of hypertrophy of adrenal cortex/tumor/hypersecretion. Too much corticosteriods.

Front 15

What happens as a result if Cushing's?

Back 15

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

Front 16

How is Cushings treated?

Back 16

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

Front 17

What are the 2 types of adrenal insufficiency?

Back 17

Primary - Addison's disease
Secondary - Lack of pituitary ACTH secretion

Front 18

Explain Addison's disease. (s/s)

Back 18

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

Front 19

Explain secondary adrenal insufficiency. (s/s and causes)

Back 19

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.

Front 20

What is an Addinsonian crisis?

Back 20

Complication of adrenal insuffiency: cardiovas collapse, profound hypovolemia, hypotension, shock, sudden weakness, severe abd px, back and leg px, renal shutdown, death.

Front 21

How is Addison's treated?

Back 21

Treat the cause, replace lost corticoids, salt additives for excess heat, IV hydrocortisone, manage shock, monitor cardiac fxn, watch EKG for hyperK, I/O

Front 22

What should you tell your patient on steroids?

Back 22

Adherence to schedule is very important. Updose if pt will be stressed, never stop therapy abruptly --> addisonian crisis. Increase salt intake

Front 23

What disorder affect the adrenal medulla and what does it look like (s/s)?

Back 23

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

Front 24

What is osteoporosis? What causes it?

Back 24

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)

Front 25

What labs/diagnostics can help in diagnosing osteoporosis?

Back 25

calcium, Vit D, phosphorus, ALP, urin calcium, parathyroid hormone levels.
Xray can show bone density loss, CT, DEXA scan

Front 26

What tests can be done if you suspect osteomyelitis?

Back 26

Increased WBCs, erythrocyte sedimentatino rate, blood dultures, bone scan, MRI, bone biopsy

Front 27

How is osteomyelitis managed?

Back 27

Antibiotics, sequestrectomy (excision of necrosed bone) bone grafts, amputation, muscle flaps

Front 28

What is a good sign of infection in the elderly?

Back 28

Confusion, not fever always

Front 29

What hormones are secreted by the posterior pituitary?

Back 29

ADH, Oxytocin

Front 30

Thyroid stimulating hormone (TSH)is regulated by ___ from the ___ which sends the signal to the _____ to secrete TSH.

Back 30

TRH, hypothalamus, anterior pituitary.

Front 31

A _____ feedback mechanism is controlled by ciruclating concentrations of __ and __ which have profound effects on ____ _________ ________.

Back 31

Negative, T3, T4, basal metabolic rate

Front 32

Therefore, under normal conditions high levels of cirulating T3 and T4 will lead to a ______ in TSH levels.

Back 32

Decrease

Front 33

The target cells for adrenocorticotropin (ACTH) are in the ________ and produces and releases _________ and _________.

Back 33

Adrenal cortex, glucocorticoids and mineral corticoids

Front 34

Who is at risk for developing SIADH?

Back 34

Head injury, brain surgery, CVA/aneurysm, Guillina-Barre, Cancer, infections, hypoxia, chemo agents.

Front 35

What are the s/s of SIADH?

Back 35

Wg gain w/o edema, orthostatic hypotension, looks dehydrated, CNS: Headache, lethargy, confusion, N/V/D,

Front 36

What will the labs of a pt with SIADH look like?
Plasma osmolality?
Na?
H/H?
I/O?
BUN/Cr?
ADH levels?

Back 36

decreased plasma osmolality, decreased serum Na levels (dilutional), decreased H/H, Urinary: low UO, decreased BUN and Creatnine.
High plasma ADH levels

Front 37

What is your treatment of the pt with SIADH?

Back 37

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.

Front 38

What are the 3D's of diabetes insipidus?

Back 38

Diabetes insipidus
decreased ADH
diuresis

Front 39

What causes diabetes insipidus?

Back 39

Lesions of hypothalmus or post pituitary that prevent ADH synthesis or realease
decreased renal response to ADH

Front 40

What are the clincial s/s of DI?

Back 40

Polyuria, polydypsia, 5-20 L urine output with spec gravit < 1.003, fatigue, hypovolemic, wt loss, tachycardia, hypotension, shock, irritability, coma, alterered mental staus

Front 41

What will labs reveal for PTs with DI?

Back 41

Serum osmolality> 295
Hypernatremia
Urine SG 1.001-1.005
Low serum ADH

Front 42

What hormones does the thyroid produce? What regulates this?

Back 42

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)

Front 43

The pt with ___________ is at an especially high risk for an MI or cardiac incident.

Back 43

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

Front 44

Two manifestations of hyperthyroidism are _______ and ____________.

Back 44

Graves Disease and thyroid storm

Front 45

What is Graves disease? Presentation?

Back 45

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

Front 46

Is the hyperthyroid pt hyperglycemic or hypoglycemic?

Back 46

Hyperglycemic, they have a low glucose tolerance.

Front 47

How does Thyroid storm present? Lab abnormalities?

Back 47

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

Front 48

Thyroid storm is treated with _____(3)______.

Back 48

Saturated solution of K Iodide, beta blockers, and steriods

Front 49

What should the nurse watch for in a patient post thyroid surgery?

Back 49

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

Front 50

What are the clinical manifestations of hypothyroidism?

Back 50

Impaired memory, slow speech, fatigue, cold intolderance, alopecia, wt gain, menorrhagia, decreased pulse, hyperlipidemia, myxedema (waxy deposits on face), anemia.

Front 51

What will labs show of the hypothyroid pt?

Back 51

Decreased T4 and T3, increased TSH

Front 52

What is the treatment of a hypothyroid patient?

Back 52

Synthetic thyroxine, advise pt to report chest px, meds must be taken daily.

Front 53

What may trigger myxedema coma?

Back 53

Infection, trauma, exposure to cold, tranquilizers, physical stress, hashimoto's thyroiditis, hypophysectomy, insufficient replacement therapy.

Front 54

What will physical assessment reveal on pt with myxedema coma?

Back 54

Hypothermia, nonpitting edema, enlarged tongue, loss of eyebrows/scalp hair, goiter, delaed deep tendon reflexes, bradycardia, shallow respirations

Front 55

What will labs reveal on this pt?

Back 55

HypoNa, respiratory acidosis, hypoglycemia, prolonged QT interval, low T3, T4, elevated TSH, hyperlipidemia

Front 56

What are the (6) main functions of the liver?

Back 56

CHO metabolism
Fat Metab.
Protein met. (albumin, globulin, urea)
Bile production
Circulatory/drug megabolism
Vitamin storage

Front 57

What causes Lannec's cirrhosis?

Back 57

Alcohol leads to fatty infiltration of hepatocytes, lumps, and scarring. Reversible if ETOH stopped.

Front 58

What is postnecrotic cirrhosis?

Back 58

Occurs after massive livercell necrosis, bands of scar tissue destroy entire lobes of liver.
Caused by viral hepatitis or industrial chemicals.

Front 59

What is biliary cirrhosis?

Back 59

results from obstruction/tumor of hepatic or common bile duct -> bile stasis in liver.

Front 60

What is Cardiac cirrhosis?

Back 60

Associated with severe rt sided HF. Liver is congested by blood and becomes edematous.

Front 61

What are some complications of cirrhosis (7)?

Back 61

Jaundice
Portal hypertension
Esophageal varicies
Coagulation defects
Ascites
Portal-systemic encepalopathy
hepatorenal syndrome

Front 62

Folks with portal hypertension often develop __________ and _______ because the blood is trying to find other ways to get back to the heart.

Back 62

Esophageal varicies and hemmoroids.

Front 63

Why do pts with cirrhosis develop coagulation defects?

Back 63

Vitamin K clotting factors synthesized in the liver are not produced.

Front 64

What causes the encephalopathy in pts with cirrhosis?

Back 64

High levels of circulating NH3

Front 65

_________ is the promary cause of death in pts with cirrhosis. and is evidenced by ________ UO, _________ BUN and CR, and ________osmolarity.

Back 65

Hepatorenal syndrome
decreased, elevated, fixed.

Front 66

What are your treatment options in cirrhosis pts with ascites?

Back 66

Low Na diet
diuretics
daily weight and I/O
paracentesis
peritoneovenous shunt

Front 67

Along with Vit K, what med would you give a pt with a ruptured esophageal varicie?

Back 67

Vasopressin to constrict arteries and decrease portal presure

Front 68

What lab tests can one do to assess for liver disease?

Back 68

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.

Front 69

High amonial levels in the blood can cause ___________ and _______.

Back 69

Hepatic encephalopathy and coma

Front 70

If your patient presents with fector hepaticus and asterixis, this could be a complication of what?

Back 70

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

Front 71

S/S of encephalopathy include:

Back 71

confusion, mood changes, asterixis, no relfexes, sweat breath (fetor hepaticus)

Front 72

How is hepatic encephalopathy/coma managed?

Back 72

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

Front 73

What is fulminant hepatitis?

Back 73

Rapid onset necrosis of liver cells resulting from Hep B or C or caused by CCL4.

Front 74

What are the s/s of fulminant hepatitis?

Back 74

depression, confusion, anorexia, jaundice->coagulation defects, renal failure, *cerebral edema, increased ICP* , need transplant

Front 75

How is Hep A transmitted?

Back 75

oral/fecal, sex with infected person

Front 76

What labs assist in Hep A diagnosis?

Back 76

Alt and AST will be 4-1000 times normal

Front 77

There are vaccines available for hep_____ and hep______.

Back 77

A and B

Front 78

Hep B is transmitted by:

Back 78

blood and body fluids

Front 79

What labs assist in diagnosing a pt with Hep B?

Back 79

ALT, AST, HBsAg,

Front 80

_________ is the #1 reason for liver transplant in the US.

Back 80

Hepatits C

Front 81

How is Hepatitis C detected?

Back 81

Enzyme immunoassay detects antibodies to it. Test confirmed with anti-HCV assay and viral load test.

Front 82

What causes pancreatitis?

Back 82

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

Front 83

What are s/s of pancreatitis?

Back 83

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

Front 84

What diagostic tests will help in diagnosing pancreatitis?

Back 84

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.

Front 85

How is pancreatitis treated?

Back 85

NPO to prevent more secretion of pancreatic juices
TPN, IVF
NG suctioning
Pain control with demerol *not morphine*

Front 86

What is the most common surgical procedure in the US?

Back 86

Cholecystectomy

Front 87

What are the s/s of cholesystitis?

Back 87

Px and fullness, cna be vomitting and jaundice if CBD is obstructed.
Fever and increased WBCs

Front 88

How is cholecystitis diagnosed?

Back 88

Ultrasound is gold standard
Radionuclide image
Elevated WBC and LFTs

Front 89

How is cholecystitis treated?

Back 89

antibiotics
IVF
Px control
Low fat diet
chenodial (cholesterol solvent)
Removeal of gallbladder

Front 90

What is Conn's disease?

Back 90

excessive secretion of aldosterone from one or both adrenal glands, which is most commonly caused by an adenoma.