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69 Cards in this Set

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What are the S/S of pheochromocytoma?
paroxysmal hyper or hypo tension from circulating excessive catecholemines--epi and norepi--usually due to a tumor of the adrenal medulla. what else? diaphoresis, palpatations, tachycardia, weight loss, hyperglycemia, HA,tremor, --sounds like hyperthyroidism except postural hypotension or hypertension--labile BP!!!.
whats the treatment for pheo?
surgical removal of the tumor with adrenergic meds presurgery and watch post op for HYPOTENSION AND HEMMORHAGE .
whats the 1st test you would order for pheo?
--TSH--then the fastest serum test--the plasma metanephrines.
Also the assay of urine catecholemine, vma and creatinine and metanephrine--its a 24H urine collection. to confirm the diagnosis you would order a CT.
What is DKA?
a state of intracellular dehydration becaue of elevated glucose. it may be the first presentation of a type 1. look like a diabetic in shock.
S/S of DKA?
polyuria, polydipsia, Kussmauls (fast breathing to blow off CO2--the fruity breath), orthostatis, hypotension. glucose > 250 or 300 but not 1200--thats HHNK pt. KETONEMIA AND KETONURIA
hyperkalemia too because pt is acidic!!! acidosis = hyperkalemia alkalosis=hypokalemia
what is the mgmt of DKA?
protect airway, 3 volume resusitation that goes on.
1. NS or maybe ringers until more hemo stable--isotonic
2. hypotonic solution--1/2 NS to bathe cells
3. as glucose drops to 250-300 at D5 to keep from rebounding. Then an insulin gtt.
How do you start an insulin gtt?
0.1 units/kg of regular followed by 0.1u/kg/hr.--dont need to treat bicarb
HHNK--what is it?
type 2--no ketosis!!! greatly elevated glucose, hyperosmolality, hyperglycemia, severe dehydration but NO KETONES. SS--like DKA except glucose is really high, over 1000 alot, serum osmo high, bun high, creat high, elevated A1c ,normal anion gap!!!
Management for HHNK?
same as DKA--3 step fluid but give them alot more fluid. start with isotonic, add hypotonic solution then add D5 when BG drops to around 250-300. Insulin gtt? controversial. can give 15u of reg IV followed by 15u reg SQ. depends on severity of the pt. They get off gtt faster than the type 1 pt.
Hyperthyroidism S/S?
bulging eyes--graves disease is the leading presentation. most common presentation of hypothyroidism is hashimotos. SS OVERDRIVE. nervousness, anxiety, tremors, diaphoresis, sweating, tachycardia (AF), lid lag, stare, increased DTRs, goiter, (hyperreflexia, increased appetite but a weight loss, smooth warm moist skin, fine thin hair,) bug eyes. exopthalmos. tachycardia and heat intolerance.
Cause of hyperthyroidism?
causes: tsh secreting tumor of the pituitary, and high dose amiodorone!
What is the TSH in hyperthyroism?
TSH is low in hyperthyroidism, and T3, T4,and resin uptake as well as free indeX is high. ANA also elevated. TSH low and t3 up
How do we treat hyperthyroidism?
Inderal (propanalol), Thioureas: Tapazole, PTU, Radioactive Iodine can be used, Surgery (but have to be euthyroid before surgery)
What is thyroid storm? what are the S/S?
hyperthyroid crisis! fever, confusion, CV collapse, respiratory distress if goiter is large
What does the thyroid do?
EVERYTHING! affects CHO metabolism by enhancing the actions of epi to stimulate glycogenolysis and gluconeogenisis. Increases AV node depolarization (tachy), incr resp drive, mental alertness, GI motility, involved in protein synthesis and protein catabolism, involved in the temp regulation
What 3 things does the thyroid produce?
T3, T4, calcitonin. 90% of its production is T4, 10% is T3. Regulated through a negative feedback loop
Describe the patho of thyroid-hypothal-pituitary.
Hypo releases TRH in response to Reduced circulating levels of T3 and T4 OR when cerebral cortex responds to a drop in body temp or exposure to cold.
What does TRH stimulate? what secretes the TRH?
TRH stimulates the anterior pituitary to release TSH. TRH comes from the hypoth.
What is the difference in T3 and T4?
thyroid secretes mostly T4. The T3 is the unbound active hormone and 90% of T3 is derived from the deiodination of T4. Only the free (unbound) form of T3 enters the cell to regulate metabolic activities. IODINE IS NEEDED TO SYNTHESIZE T3 and T4
What are the labs for the thyroid?
TSH--measures the amount of TSH released from the ant. pit. Normal is 2-5.4; TSH is elevated in hypothyroidism and low in primary hyperthyroidism. When diagnosing do TSH, T3, and T4. follow up just do TSH. If it is secondary (problem in the pituitary) in hypo the tsh is low and so is the T4
what are the s/s of hypothyroidism?
weakness, fatigue, cold intolerance, constipation, arthralgias, delayed DTRs, hyponatremia, loss of 1/3 eyebrows, hoarseness, amenorrhea,cardiac enlargement (myxedema heart)
what would you test for if you suspected hypothyroidism?
TSH (which would be high if there if person is hypo)
T4 would be below normal
what are some complications of hypothyroidism?
megacolon! myxedema, assess for cardiac s/s
if you palpate nodules on the thyroid, what diagnostic testing would you do?
fine needle aspiration, US
whats the difference in primary hypothyroidism and secondary hypothyroidism?
in primary, the dysfunction is in the thyroid gland. in secondary, the problem is in the pituitary gland--you'll see low or normal TSH.
what are the complications of hypothyroidism?
advanced atherosclerosis secondary to increase in lipid levels; increased suseptability to infections, megacolon (decr gastric motility), myxedema (crisis--has signif mortality)
what is the treatment for hypothyroidism?
synthroid! > 70y.o. start low and slow for heart--25-50mcg for a week, gradually increase dose every 4 wks to a total dose of 75-100 mcg. in the younger adult, can start at 50-100 and increase every 1-3 wks by 25 mcg until TSH normalizes. see them in a month--assess for CP!!! once TSH is at desired level and pt feels better monitor once a yr. Too rapid replacement or too high a dose--rapid HR, dyspnea, orthopnea, angina, palpitations, nervousness, insomnia
T3 influences seratonin--low levels of T3 can cause depression.
hyperthyroidism complication is agranulocytosis--call NP with fever or infection.
SEVERE hypothyroidism--altered mental status, altered thermal regulation, precipitating event or illness. get big fluid and electrolyte imbalances, increased capillary permiability.--see non-pitting edema of hands and feet.
what are the presenting s/s of myxedema?
stupor or coma
respiratory depression
50-80% mortality (primary cause is hypoventilation and hypercapnea)
what are the clinical findings of mixedema?
severe hypothermia******
hyponatremia (kidneys not working well)
hypoglycemia (down regulation)
lactic acidosis
what are the goals of therapy in myxedema?
stabilize hemodynamics
assist respiratiry function
adjunctive thyroid therapy
treatment for myxedema?
fluid replacement and possible vasopressors. intubatio and vent support. IV syndhroid (2mcg/kg IV); daily synthroid dose of 100 mcg IV or PO; gradual rewarming to avoid generalized vasodilation and CV collapse.
patho of thyroid storm?
extreme hyperthyroidism--brought on by stressful illness or trauma or thyroid surgery. high mortality rate./
S/S of thyroid storm?
high fever
severe agitation
cardiovascular collapse
resp distress if goiter large
how do you treat thyroid storm?
sodium iodine
what is the end result of the renin angiotensin thingy?
aldosterone!!! aldosterone regulates Na and K
aldosterone is a mineralocorticoid
cortisol is a glucocorticoid
what is addisons?
chonic adrenocortical insufficiency--an autoimmune disease. a chronic insufficiency.
presenting symptoms with addisons?
weakness, fatigue, weight loss, N/V and abd. pain, amenorrhea, increased skin pigmentation (look tan), hypotensive, hyponatremic, hyperkalemic, neutropenic. also hyperuremia.
What do you see clinically in a patient with addisons?
low plasma cortisol (<5mg/dL) at 8a.m.; decreased ACTH levels
what is the diagnostic test for addisons?
Cosynthropin Stim Test
give corticotropin and test to see if plasma cortisol levels rise. in addisons disease they dont rise or are too low. there isnt a change.
what is replacement therapy in addisons disease?
glucocorticoids/mineralocorticoids--get 2/3 in a.m., 1/3 in afternoon or 3 equal doses.
Prednisone (assess for avascular necrosis!)
Fludrocortisone Acetatye (Florinef Acetate)--Rx if pt not retaining sufficient salt--actiion: renal tubules to increase reabsorption of Na and excretion of K
monitor bp, K and wt
how do you treat hyperthyroidism?
specialist referral as needed, esp w/ pts who have co-morbidities
interal for symptomatic relief, begin dosing w/ 10mg PO, may go to 80mg 4x dauy
Thiourea drugs for pts w/ mild cases, small goiters or fear of isotopes, ex: Methimazole (Tapazole) 30-60mg daily in 4 divided doses
also--radioactive iodine--destroys goiters
thyroid surgery (must be euthyroid)
Lugols solution 2-3 gtts PO qday x 10 days to reduce vascularity of the gland.
Pts w/ subacute thyroiditis are best treated symptomatically w/ propranolol
how do you treat thyroid crisis?
Propylthiouracil 150-250mg q 6 H OR
Methimazole (tapazole( 15-25mg q 6H with the following in one hour:
Lugols solution 10gts t.i.d. OR
Sodium iodide 1gm slow IV along with
Propranolol 0.5 - 2gm IV q4H with hydrocortisone 50mg q6H w/ rapid reduction as situation improves
what med do ppl w/ hyperthroidism avoid?
aspirin--they will have to be tylenol ppl
what are some of the causes of hyperthyroidism?
toxic adenoma, subacute thyroiditis, TSH secreting tumor of the pituitary, HIGH DOSE AMIODARONE
what are the side effects of amiodarone?
lung damage--fever, shortness of breath, wheezing, other breathing problems, cough, or coughing or spitting up blood.

liver damage--nausea, vomiting, dark colored urine, excessive tiredness, yellowing of the skin or eyes, itching, or pain in the upper right part of the stomach

Amiodarone may make your skin sensitive to sunlight. Exposed skin may turn blue-gray and may not return to normal even after you stop taking this medication.

you should know that amiodarone may cause vision problems including permanent blindness.
what is the interaction of amiodarone and digoxin cause?
Amiodarone increases the blood levels of digoxin (Lanoxin) when the two drugs are given together. It is recommended that the dose of digoxin be cut by 50% when amiodarone therapy is started.

Amiodarone can interact with some cholesterol-lowering medicines of the "statin" class, such as simvastatin (Zocor), atorvastatin (Lipitor), and lovastatin (Mevacor), increasing the risk of severe muscle breakdown and kidney failure or liver disease. This interaction is dose-related, meaning that lower doses of statins are safer than higher doses when used with amiodarone. An alternative statin, pravastatin (Pravachol), does not share this interaction and is safer in patients taking amiodarone.
what does the interaction of dilantin and amiodarone cause?
Amiodarone can result in phenytoin (Dilantin) toxicity because it causes a two- or three-fold increase in blood concentrations of phenytoin. Symptoms of phenytoin toxicity including unsteady eye movement (temporary and reversible), tiredness and unsteady gait.
what happens when you mix amiodarone w/ beta blockers or CCB?
Amiodarone may interact with beta-blockers such as atenolol (Tenormin), propranolol (Inderal), metoprolol (Lopressor), or certain calcium channel blockers, such as verapamil (Calan, Isoptin, Verelan, Covera-HS) or diltiazem (Cardizem, Dilacor, Tiazac), resulting in an excessively slow heart rate or a block in the conduction of the electrical impulse through the heart.
what does amiodarone do when mixed with coumadin?
Amiodarone interacts with warfarin (Coumadin) and increases the risk of bleeding
in hyperthyroidism, is t3 or t4 effected? tsh?
T3 is high, TSH is low
in hypothyroidism, is T3 or T4 affected? TSH?
T4 is low, TSH is high
what 2 lab findings do you find in hypothyroidism?
what test is done to establish the etiology of hyperthyroidism?
thyroid radioactive iodine uptake scan
what is the cause of Cushings disease?
ACTH hypersecretion by the pituitary OR adrenal tumors, OR chronic administration of steroids
what causes addisons disease?
dificient cortisol, androgens, and aldosterone; autoimmune destruction of the adrenal glands; metastatic CA; bilateral adrenal hemorrhage (e.g., w/ anticoag therapy); pituitary failure resulting in decreased ACTH
what are the significant labs you see with cushings?
what are the significant labs you see with addisons?
how do you treat cushings?
depends on the cause, maybe d/c meds inducint symptoms, transphenoidal resection of a pituitary adenoma, surgical removal of the adrenal tumors, resection ACTH secreting tumors, manage electrolyte balance
how do you treat addisons?
specialist referral
glucocorticoid and mineralocorticoid replacement (hydrocortisone and fludrocortisone acetate (Florinef)

Inpatient Mgmt:
replace volume w/ D5NS
vasopressors ineffective
what causes SIADH? and what does it do?
release of ADH occurs independent of blood osmolality or volume dependent stimulation so you get inappropriate WATER RETENTION. Can be from a tumor producing ADH, skull fracture, CNS disorder or even chronic lung disease. think hyponatremia--serum Na (and osmo) low and urine Na (and osmo) high! cant hold onto the sodium so its all in the pee.
what kinds of S/S do you see w/ SIADH?
neuro changes from the hyponatremia--mild HA, seizures, coma, decreased DTRs, hypothermia, wt gain/edema, N/V, cold intolerance
what labs will you see with SIADH?
low serum Na, decreased serum osmo; increased urine Na and osmolality BUT renal, cardiac, thyroid function is normal.
what is the cause of diabetes insipidus?
2 kinds of DI: central and nephrogenic.

central is related to pituitary or hypothalamus damage resulting in ADH deficiency. there are idiopathic causes, damage to hypothal. or pituitary, surgical dmg, accidental trauma, infections, metastatic carcinoma.

Nephrogenic: due to a defec in the renal tubules resulting in renal insensitivity to ADH. it is a familial X-linked trait; acquired due to pyelonephritis, K+ depletion, sickle cell anemia, chronic hypercalcemia, meds like lithium, methicillin.

if its psychogen: refer
what labs do you see with DI?
elevated BUN/creat
Urine Spec gravity low
if central DI is suspected, a vasopressin desmopressin challenge test is done. if no apparent cvause an MRI should be ordered to look for a mass/lesion
How do you treat SIADH?
treat the underlying cause
If serum Na+ > 120, restrict total fluids to 1000cc/24H and monitor

If serum Na+ 110-120 without neuro symptoms, restrict fluids to 500cc/24H and monitor

If serum Na+< 110 or neuro s/s present, replace w/ isotonic or hypertonic saline (3%) and chase w/ lasix. monitor Na+K+ losses hourly and replace slowly.
how do you treat in diabetes insipidus?
if Na+ > 150, give D5W IV to replace 1/2 volume deficit in 12-24H; Note: more rapid lowering of Na+ can cause cerebral edema

When Na+ < 150, substitute 1/2 or .9 NS

DDAVP 1-4 ug IV or SQ every 12-24H for acute situations
Maintenance dose of DDAVP is 10ug q 12-24H intranasally

ddavp is just synthetic adh.