Endocrine

Question 1

causes of Cushing’s syndrome

Answer 1

1. exogenous steroids: low ACTH, adrenal atrophy
2. primary adrenal adenoma: low ACTH, big adrenal w/ c/l atrophy
3. ACTH pit adenoma: high ACTH, suppression with dexamethasone
4. Ectopic ACTH, (SC lung carcinoma): high ACTH, no suppression

*think carcinoma/ectopic source is a cancer who listens to no one.

Question 2

what are the ways Cushing’s syndrome produces immunosuppression

Answer 2

dec in phospholipase A2> no arachodonic acid
dec in IL-2> no growth of T cells
dec in histamine> no vasodilation, no increased permeability

Question 3

Cushing’s presents with moon facies, buffalo hump, truncal obesity (via ____ ____). with HTN and dec K with met alk (via ____).

Answer 3

fat deposits> due to high insulin (via the excess cortisol which has stimulated high glucose)
HTN with met alk> incr a1 receptors on arterioles, making it more sensitive to catecholamines.

Question 4

pituitary adenoma mass effect

Answer 4

bitemporal hemianopsia= at optic chiasm

Question 5

types of functional pituitary adenoma

Answer 5

1. prolactinoma: produces prolactin (no GnRH, no LH, no FSH)> galactorrhea, 2 amenorrhea in females; dec libido in males. tx: bromocriptine (D2 agonist)
2. GH adenoma: produces GH> in kids= gigantism, growth of long bones before epiphyseal plate closes
   > in adults, acromegaly. **diagnosed via insulin GF1- produces the symptoms. tx: octreotide (somato anolog)
3. ACTH adenoma> Cushing’s syndrome. suppressed with dex.

Question 6

Sheehan syndrome

Answer 6

postpatrum hemm that leads to pit infarct. presents with amennorrhea, difficulty breastfeeding (no prolactin), no pubic hair (no androgens), fatigue
gland grows, but not blood flow.

Question 7

central diabetes insipidus labs

Answer 7

absent ADH
inc Na, high serum osmolality
dec urine osmolality (highly diluted urine)
*low specific gravity= hyperhydrated urine
water depravation fails to correct osmolality
tx: desmopressin corrects (ADH analog)

Question 8

nephrogenic diabetes insipidus labs

Answer 8

no response, present ADH (V2R mutation, lithium)
inc Na, high serum osmolality
dec urine osmolality (highly diluted urine)
*low specific gravity= hyperhydrated urine
water depravation fails
desmopressin fails

Question 9

SIADH labs

Answer 9

excessive ADH= holding onto alot free H2O= diluted serum= “hypotonic hyponatremia”
low Na, low serum osmolality> mental status alter
inc urine osmolality, inc Na urine
tx: free water restriction, demeclocycline (ADH block)

risk: carbamazepine, ecstasy, chloproamide all inc kidney sensitivity to ADH.

Question 10

Graves Disease labs

Answer 10

inc T4, dec TSH
HYPOcholesteroemia
HYPERglycemia
IgG autoantiboides at TSH receptor (HS II)

Question 11

thyroid storm

Answer 11

stress/infection> stimulates epi> excesssss T4/T3.
commonly presents as n/v, hypovolemic shock, hyperthermia, arrhythmias.
tx: PTU, B-, steroids. PTU is key to prevent the peripheral conversion of T4 to T3.

Question 12

thioamide blocks ____

Answer 12

blocks peroxidase (TPO). so prevents organification (thyroglobulin + I2), oxidation of iodine, and coupling to make T3/T4 synthesis.
** so does PTU.

Question 13

subacute granulomatous de Quervain thyroiditis

Answer 13

presents as tender thyroid
s/p viral infection, makes granuloma inflammtory response

Question 14

riedel fibrosing thyroiditis

Answer 14

presents as nontender thyroid ~40F
extensive fibrosis & inflame of the thyroid, but not malignant> fibrosis can restrict the airway/local structures

Question 15

how do you biopsy thyroid

Answer 15

fine needle aspiration.
thyroid is bloody and will not see anything otherwise

Question 16

how do you differentiate follicular adenoma vs. follicular carcinoma

Answer 16

carcinoma= invasion thru the capsule.
key is that you can’t tell via the fine needle aspiration, need a gross specimen most often.

Question 17

pathonomic feature of papillary carcinoma

Answer 17

orphan-annie nuclei> papillae are lined by nuclei with white clearing at center.
nuclei grooves> little lines w/in nuclei
psomma bodies> can help, but can be found elsewhere.
*this is most common thyroid cancer

Question 18

pathonomnic feature of medullary carcinoma

Answer 18

malignant proliferation of parafollicular C cells.
> local amyloidosis stroma
> calcitonin+, they are also neuroendocrine, so perhaps chromogranin+

Question 19

pathonomnic feature of anaplastic carcinoma

Answer 19

> undifferentitated cells of thyroid of an elderly lady with dysphagia/respiratory compromise.
*often via p53 loss to anaplastic.

Question 20

21yr M has 1 testis in scrotum. inc FSH, normal LH. what is decr in patient?

Answer 20

inhibin B.
GnRH>FSH/LH release> FSH releases inhibin B
*LH @ leydig> testosterone (neg feedback for GnRH)

the sertoli cells are temp sensitive (incr temp in abdomen)> atrophy from heat damage> low inhibin B> no feedback on FSH> inc FSH.
BUT leydig cells are not as affected by temp> normal LH fxn> normal androgens.

Question 21

Pt has testicular torsion>u/l orchiectomy. Pt is concerned about sexual dysfxn and infertility. how do they change s/p procedure?

Answer 21

u/l orchiectomy has initial drop in T> + LH secretion> compensatory T production and Leydig hyperplasia in remaining testis> libido, erection, and sexual characteristics normal/unchanged.

loss of inhibin B> inc FSH> + spermatogenesis, but the loss of seminiferous tubules in the u/l testis most pt have decreased net spermatogenesis> reduced fertility.

Question 22

f/u pt has DM2, on max metformin dose. Pt started on sodium-glucose-cotransporter2 inhibitor. what is the likely additional effect of new med?

Answer 22

decreased BP (lowers intravascular volume, preload reduction, afterload reduction, natriuresis slows glomerular hyperfiltration).
*good for BP, heart failure, diabetic nephropathy

MOA: inhibit PCT absorption of Na and glucose (not one for the other)> giving osmotic diuresis> causing glucosuria> common to get UTIs w/ med

Question 23

what anti-diabetic med causes fluid retention?

Answer 23

thiazolidinediones= pioglitazone

Question 24

pit apoplexy> causes loss of ACTH> no cortisol. what kind of shock does this make?

Answer 24

severe hypotension, distributive shock.
tx: glucocorticoids + neurosurgery consult

Question 25

cabergoline

Answer 25

dopamine agonist (D2+); also bromocriptine

Question 26

high levels of 17-hydroxyprogesterone indicates

Answer 26

adrenal cortical hyperplasia, specifically 21OH def
17hydroprogesterone–> 11deoxycortisol usually

Question 27

what is the treatment for 21OH def?

Answer 27

low dose exogenous corticosteroids> will also suppress ACTH> stop the overproduction of androgens
*suppression of LH/Testosterone will help the peripheral conversion of the androgens>feedback on GnRH> but that doesn’t stop the ACTH from leading to more DHEA

Question 28

insulin> inhibits glucagon. glucagon> stimulates insulin

Question 29

effects of insulin

Answer 29

inc glucose uptake into cells: muscle, fat, liver
inc glycogen synthesis (store it, prevent glycogenlysis breakdown)
inc protein synthesis in muscle

dec glucagon
dec lipolysis/ketogenesis

Question 30

congenital adrenal hyperplasia forms:
17a hydroxlyase
21OH hydroxlyase
11OH hydroxlyase

common presentations of them?

Answer 30

starts with the 1: HTN
ends with a 1: female virilization/clitomegaly

17a: impaired sex steroids, cortisol. all aldosterone pathway. HTN & hypokalemia with boys having ambigous genitalia.
21: impaired aldosterone, cortisol. all sex steroids, clitomegaly at birth, hypoBP, hyperkalemia, boys with odor ~3yrs
11: more upstream impairment of cortisol, aldosterone. all sex, but aldo precursor has minimal fxn so will give HTN with virilization

Question 31

36yr DM1 has recurrent hypoglycemic episodes, difficulty controlling sugars. now at <50mg/dL. Pt has CKD 2/2 with GRF @ 20mL/min. Pt awaiting dialysis. What is the most likely reason for current glycemic disturbances?

Answer 31

dec renal insulin clearance.
declining GFR is unable to filter> unable to degrade insulin>insulin around for longer to push more glucose into cells> hypoglycemic episodes
*originally thought that dec GFR would inc glucose excrete> but in order to get inc excrete would need inc GRF (more filtered, more out), or reach max reabsorb capabilities (DM2). afferent>filter>excrete.

Question 32

Pt undergoing a total thyroidectomy for papillary carcinoma. During surgery a nearby nerve is injured while ligating the artery running superior and entering the superior portion of the thyroid. What muscle is denervated as a result?

Answer 32

cricothyroid muscle, damage to the superior laryngeal n> leads to dysphonia with changes in pitch/tone
superior thyroid artery> branch of external carotid artery runs with superior laryngral n.
*the recurrent laryngeal n innervates (post, lateral, transverse, oblique cricoarytenoid, thyroartytenoid)> all coming from the 6th phar arch