T3 - Internal Medicine - Endocrine

Front 1

If you suspect primary hypo-adrenals, what's a good test?

what about if you suspect secondary?

Back 1

cosytropin test - it functions like ACTH.

give cosytropin, look at cortisol level. If it goes up, then you don't have a primary problem.

for secondary (brain problem): look at 8am ACTH/cortisol. If the brain is screwed up, ACTH/cortisol will be normal or low (note that ACTH will be REALLY HIGH IN PRIMARY DISEASE, as there's no good feedback).

Front 2

what do you do to treat someone with suspected addison's?

Back 2

don't wait, treat.

give DEXAMETHASONE and, if primary, fludrocortisone too. Note that dexamethasone won't screw up your tests.

Front 3

Cushing's : what are the potential causes, how do you test for it?

Back 3

Cushing's disease = pituitary adenoma making ACTH. Also could have ectopic site making ACTH.

Alternative is an adenoma in the adrenals cranking out cortisol.

Test: look at 24 hour free cortisol. If >3x normal = one of the 3 diseases.

Also, dexamethasone suppression: if cushing's DISEASE (pituitary), HIGH DOSE dex WILL SUPPRESS (pituitary still can be regulated). If ectopic/adrenal, high does will NOT suppress.

differentiate ectopic vs. adrenal by basal ACTH level: adrenal cortisol will negatively feed back to turn off, ectopic will NOT.
Pituitary and ectopic are 'acth dependent' - meaning that the cortisol increase depends on ACTH. So, do a test for ACTH.

Front 4

Conn syndrome: dx?

Back 4

High aldosterone = high salt, low K.

also, down-regulates RENIN. an ald:renin ratio >23 = con's.

Front 5

what random conditions/drugs cause osteoperosis?

Back 5

hyperthyroidism, smoking, alcohol, neuroleptics/antiseizures.

Front 6

what's the osteoperosis scan you do? scores mean what?

when do we screen people?

when do we treat?

Back 6

dexa.

T-score < -2.5 = positive. Between -1 and -2.5 = osteopenia

women > 65 years.

treat if T score >-2.
Bisophosphanates, ralixofen, TERIPARATIDE is expensive but is the only one that increases formation.

injectable calcitonin possible.

Front 7

what random things can raise a prolactin level?

Back 7

pregnancy, hypothyroidism (high TRH stimulates both thyroid AND prolactin release)

Front 8

what big common drug must you NOT be on if you're going to get contrast?

Back 8

metformin - it accumulates if your kidneys fail. contrast is potentially renal toxin.

this includes arteriography/ct studies.

Front 9

what counts as impaired glucose tolerance?

Back 9

fasting 100-125, OGTT 140-200

remember that diabetes is diagnosed as fasting >126 or >200 plus symptoms.

Front 10

if you have DM and are being treated, what are the values for blood glucose/lipids you want?

Back 10

fasting 90-130
post-food, 2 hr = <180
Bp: 130/80
TG: <150
HDL >40
LDL <100

Front 11

type 1 diabetics - how much insulin do they need, and how should it be broken up?

Back 11

typically need 0.5 units/kg. if 60 kg = 30 units.

typically that's broken up half and half long-acting and bolus with meals.

Front 12

when do you correct sodium and how?

Back 12

hyperglycemia - for each 100 of glucose high, need to add 1.6 to the sodium. remember this especially in HHS syndrome.

Front 13

what are the equivelant conditions?

Back 13

those that are equivalent to having had CAD.

DM, AAA, PAD, carotid disease, framingham risk >20, symptomatic CAD. SO having diabetes is as as bad a risk factor for future heart disease as current CAD.

Front 14

thyroiditis - what are the physical signs and lab tests? what's a common cause of this?

Back 14

non-tender, decreased RAI uptake, low TSH and normal/high T4/T3.

this is commonly found after pregnancy: patients will get hyperthyroid after birth for awhile due to lymphocitic infiltration of the thyroid.

RAI will be negative, TSH low, and FT4 high.

Treat with beta blockers.

This is followed by hypothyroidism (you had inflamed thyroid leaking out all stores) - most people end up normal within a year.

Front 15

what do you see with a myxedema coma?

Back 15

hypothyroidism in old lady. hypotension, hypothermia, bradycardia, hyponatremia. comes from not having enough thyroid - likely an old thyroidectomy and not taking her medication.

Front 16

what is 'silent' thyroiditis? treatment?

Back 16

low TSH, high T4/T3, non-painful, but ELEVATED anti-thyroid peroxidase antibodies, like you see in grave's.

difference is that grave's has increased RAI uptake - silent thyroiditis has NORMAL/LOW RAI.

only treatment is beta blockers for the hyperthyroid stage (followed by hypo, then euthyroid eventually...like post partum).

Front 17

compare the secondary sexual characteristics of high cortisol in women vs. men

Back 17

women get hairy, fat, acne.

men loose hair, libido, get erectile dysfunction.

Front 18

how does hyperthyroidism/hypothyroidism affect blood pressure, and why?

Back 18

both can cause hypertension.

hyperthyroidism = 'hyperdynamic state' - high thyroid probably increases andrenargic receptors on heart, making more contractile. see high SYSTOLIC, normal diastolics (wide pulse pressure).

hypothyroidism typically causes HIGH DIASTOLIC (narrow pulse pressure).

Front 19

pericardial effusion causes what EKG change?

Back 19

electrical alternans - the QRS complex height varies from beat to beat.

something to do with the heart swinging back and forth inside of a fluid-filled bag.

note that this usually comes from pericarditis (infected heart = leaky heart).

Front 20

old people with isolated systolic hypertension probalby have what?

Back 20

stiff artery walls. note that during systole, elastic arteries 'absorb' some of the pressure, then squeeze back in and are responsible for some of the diastole pressure.

if they're stiff, get high systolic and lowered diastolic.

this is a new hot topic and new risk factor - treat with HCTZ.

Front 21

someone is having a cocaine-induced MI. what's going on, and what drug do you NOT use?

Back 21

vasospasm - this can cause STEMi's which are treated just like normal STEMI's.

with the exception of BETA BLOCKERS - note that vasculature has some beta on it, and if you block it, alpha will be left unopposed and you'll vasoconstrict MORE.

Ca++ blockers and alpha blockers (phentolamine) are good ideas.

Front 22

Acromegaly - what's the gold standard diagnostic test? signs?

Back 22

GH level after giving glucose.

remember that GH is like anti-insulin: when insulin goes up, GH should bottom out.

If you give glucose and GH stays high, it means it can't be suppressed and you have acromegaly.

pts have coarse facial features, swollen fingers, skin tags, oily skin.

Front 23

if you strongly suspect a thoracic aortic dissection (pregnancy especially), how do you manage?

Back 23

often associated with high BP - this has to be treated aggressively first. use IV BETA BLOCKER - this lowers HR and vasodilates. Simple vasodilators will up HR and will INCREASE WALL STRESS.

then get TEE (gold standard) or, failing that, a CT scan.

Front 24

what does low cortisol levels do to blood counts?

Back 24

eosinophelia and lymphocytosis common.

Front 25

thyroid nodule - what's the basic workup framework?

Back 25

1. get TSH, regardless of symptoms.

if TSH is high (low thyroid), look for hashimoto's antibodies. if nodule >1.5cm, do FNA for cancer.

If TSH is LOW (high thyroid), do radio-uptake to figure out toxic nodule vs. thyroiditis. probably not cancer, no need for FNA.

Front 26

a kid has a syncopal episode. also, past history is hard of hearing. what happened?

Back 26

jervell - lang - nielsen syndrome. congenital long QT with deafness. Recessive, prone to TORSADES, treatment is BETA BLOCKER and implantable defibrilator.

Front 27

men syndomes: go over them

Back 27

men 1 = 3p's = pancreatic islet cell, pituitary adenoma, parathyroid.

men 2a = medullary carcinoma, pheochromocytoma, and parathyroid hyperplasia

men 2b = medullary, pheo, and mucosal neuromas

Front 28

what are some of the symptoms in heat stroke?

Back 28

temp >105 = definition.

enzymes stop working = ARDS and DIC (so low platelets, long PT/PTT)

skin is hot.

Front 29

what are the symptoms of hypercalcemia?

Back 29

groans = abdominal pain, constipation.

polyuria and polydypsia.

don't forget that excessive vitamin D intake will raise Ca++ and cause the same thing.

Front 30

how do you correct calcium for albumen difficulties?

Back 30

[Ca] + 0.8 (4-alb)

Front 31

pt on high dose NSAIDS and hyponatremia: what happened?

Back 31

SIADH - nsaids potentiate ADH and make you retain tons of water, and give you concentrated urine.

Front 32

what's the triad for tamponade? why?

Back 32

hypotension, muffled heart sounds, and JVD.

fluid around the heart, when pressure is high enough, gets beyond diastolic pressure and prevents blood from returning to the LV, so pressure drops.

pulsus paradoxus happens on INSPIRATION, because more blood returns to the RV, which pushes the septum into the LV, preventing blood from making it in.

note that you don't need blood to back up into the lungs to get JVD...the RV has trouble filling all on its own.

Front 33

why does hyperventilating make your muscles twitch?

Back 33

blowing off H+.

remember that a lot of Ca++ is bound to albuin. Also, H+ binds as a buffer.

When you loose H+ from blood, it detaches from albumen and Ca++ takes its place...

so you have transient hypocalcemia.

Front 34

how do primary and metastatic-to-bone cancers differ in their increase in serum Ca++

Back 34

those that travel into bones release cytokines that cause lytic bone lesions. these will suppress PTH.

primary tumors that cause high Ca++ come from making PTHrP.

Front 35

lady testosterone - where does it come from. if someone's virilzed, what test is good?

Back 35

testosterone comes from the ovaries (or more precisely, from ovarian estrogen getting coverted in peripheral fat into testosterone).

also comes from adrenals = DHEAS.

so, if someone virilzed, do DHEAS/testosterone test.

Front 36

what is pulsus paradoxus and what are the potential causes?

Back 36

drop in SBP >10 on INSPIRATION.

seen in tamponade
seen in tension pneumo
seen in asthma.

Front 37

differentiate papillary carcinoma from follicular cell

Back 37

papillary is most common, has orphan annie nuclei/ground glass, has a good prognosis (even if metistatic),

follicular is hard to diagnose, but more deadly. looks like follicular adenoma - need evidence of invasion/hematogenous spread to diagnose, harder to treat.

remember that colloid overgrowth is the most common cause of thyroid nodules.

Front 38

pt on amiodarone - what should you look out for?

Back 38

thyroid abnormalities! as well as pulmonary fibrosis.

Front 39

HHS + focal neuro deficits is what?

Back 39

HHS. This is a normal finding in HHS, don't let this make you get a head CT.

Front 40

what's the treatment for diabetic gastric paresis?

Back 40

better glycemic control (hint is that people's sugars are really low post-meals, as they aren't absorbing fast enough).

METOCLOPRAMIDE is pro motility. Any dopamine antagonist (domperidome).

Erythromycin is pro-kinetic

Bethanochol (ACh mimic)

Front 41

how can you tell the difference between cushing disease and an ectopic tumor making ACTH?

Back 41

you'll have signs of high cortisol/aldosterone in both.

low dose dexamethasone will fail to repress both pituitary adenomas (diseas) and ectopic ACTH tumors.

high dose WILL repress pituitary adenomas. Ectopic ACTH tumors are resistant to dexamethasone-suppression.

just remember that the brain is only partially resistant to dexamethasone treatment.

Front 42

what's the treatment for a prolactinoma?

Back 42

this is usually in the pituitary - if it's under 1cm = microadenoma.

either way, treat with DOPAMINE AGNOISTS - bromocriptine or new one, CABEROLINE.

Front 43

what happens to the Ca++ levels of people who can't move, and what can you do?

Back 43

goes way up - bones get broken down when you don't move.

prevent with bisphosphonates - they kill off the osteoclasts.

Front 44

define metabolic syndrome:

Back 44

3/5 needed:

glucose 100-110
HTN: >130
waist >40 men, >25 women
dyslipidemia: HDL < 40 men, <50 women
triglycerides >150

Front 45

primary hyperparathyroidism is pretty common. how can you tell between this and someone with renal failure?

Back 45

primary hyperparathyroidism will cause HIGH CALCIUM.

that caused by renal failure will have low/normal calcium. remember that renal failure patients will have VitD deficiency and low Ca++, which is partly driving the high PTH.

the PTH in renal failure will never get high enough to give someone hypercalcemia.

Front 46

what's a good screen for the Men2 syndromes?

Back 46

calcitonin - remember that medullary carcinomas will be made of C cells and make calcitonin.

don't assume that the serum calcium will be affected, however.

Front 47

what's a really bad outcome of hashimoto's you have to look out for?

Back 47

lymphoma - these patients are 60x more likely to get it.

Front 48

how do you differentiate DI (2 kinds) and psychogenic polydypsia?

Back 48

water deprivation and test urine concentration. if deprive and urine gets more concentrated = crazy.

if not, it's DI.

next, is it central vs. peripheral resistance: give ddAVP (vasopressin = ADH) and see if there's a response. If so, it's central. if not, it means the receptors for it on the kidney don't work.

Front 49

what's the treatment for siADH?

Back 49

demelocycline - it induces nephrogenic DI (makes kidney resistant to ADH).

demelo = DI.

Front 50

what do you see in tropical sprue?

Back 50

someone who's traveled. biopsy looks like celiac's, and they'll have malabsorption symptoms (megaloblastic anemia).

Front 51

if you aren't going to look for gastrin levels in the blood, what's a good test for a gastrinoma?

Back 51

secretin test - gastrin stays up if you give secretin.

think of men1 syndrome.

Front 52

quick review of how you can tell transudate from exudate:

Back 52

expect transudate most of the time.

1. PROTEIN: a pleural fluid to serum ratio BELOW 0.5

2. LDH: a pleural fluid to serum ratio BELOW 0.6

remember that you're expecting less stuff in transudate than in serum (and certainly less than exudate).