Endo-UWORLD Flashcards
81-Q 10. What does primary hypoparathyroidism do on
- renal handling of Ca2+ and phosphate
- gut handling of Ca2+ and phsopate
- renal handling
: reduced Ca2+ reabsorption -> reduced Ca2+
: reduced phosphate excretion -> increased phosphate - gut handling
: reduced activation of vitamin D
-> reduced absorption of Ca2+ and phosphate - active vitamin D is responsible for absorption of BOTH
Ca2+ and phosphate.
81- Q 12. Amenorrhea in a girl with low BMI. What is underlying pathophysiology?
low fat -> low leptin -> decreased GnRH (hypothalamus)
-> decreased FSH/LH (pituitary) -> amenorrhea
- This is called functional hypothalamic amenorrhea
It is HYPOTHALAMIC DYSREGULATION
81- Q 21. Effect of OCP on
- free T3/T4
- Total T3/T4
Explain physiology
- normal free T3/T4, but increased total T3/T4
OCP increases level of TBG, causing initial transient decrease in free T3/T4 (as free T3/T4 goes to bind TBG)
With normal physiology however, body can sense hypothyroid state, increasing synthesis of free T3/T4 until it becomes saturated to TBG, and get to normal T3/T4 range (EUTHYROID state)
81- Q 25. Hypothyroidism vs. Hyperthyroidism: How myopathy look different?
Hypothyroidism: elevated CK
Hyperthyroidism: normal CK
- both present with myopathy
81- Q 26. Lab tests for Diabetes: Hb1Ac, fasting glucose level, oral glucose tolerance test. Which two methods are preferred over another?
Hb1AC and fasting glucose level
oral glucose tolerance test is too much work. Let patient take sugar water and wait 2 hours. more expensive, more time consuming
81- Q 32. Sheehan syndrome vs. Pituitary apoplexy: compare etiologies
Sheehan: ISCHEMIC INFARCT due to postpartum hemorrhage
Pituitary apoplexy: HEMORRHAGE of PITUITARY gland, usually in the setting of pre-existing pituitary adenoma
(pituitary adenoma, gets bigger, rupturing vessel)
81- Q 38. Thyroidecomy
- what nerve is damaged during ligation of inferior thyroid artery?
- what nerve is damaged during ligation of superior thyroid artery? what muscle is innervated by this nerve?
- recurrent laryngeal -> hoarseness
- superior laryngeal -> innervates cricothyroid
82- Q 9. Increased level of which metabolite is diagnostic for 21-hydroxylase deficiency
17-hydroxyprogenelone
82- Q 11. sympathetic vs. parasympathetic: compare how these two autonomic systems innervate pancreatic cells for regulation of insulin release
- sympathetic
Alpha 2 -> Gi -> inhibition of insulin release
Beta 2 -> Gs -> insulin release - alpha 2 action predominates, thus overall sympathetic tones inhibit insulin release
- parasympathetic
M3 -> Gq -> insulin release - BOTTOM LINE: sympathetic decreases insulin release, while parasympathetic increases insulin release
82- Q 21. Phenotype of congenital adrenal hyperplasia in terms of external genitalia and secondary sexual development in
- 17 alpha hydroxylase deficiency
- 21 hydroxylase deficiency
- 11 beta hydroxylase deficiency
17
- normal external genitalia: no need for androgen for external genitalia development. estrogen can be used from other sources
- lack of secondary sexual development: androgen is required for secondary sexual development
21 & 11
- ambiguous external genitalia; excess androgens mess up with normal external genitalia development
- virilization during secondary sexual development
82- Q 33. Fever, low BP, high pulse, signs of acidosis. what is happening? why there is acidosis?
septic shock -> hypoperfusion -> lack of oxidative phosphorylation -> lactic acidosis
82- Q 34. Which beta blockers are preferred to patient with diabetes? why?
selective Beta 1 blockers (A to M) are preferred over non-selective (N to Z).
blocking beta 2 exacerbates hypoglycemia by inhibiting gluconeogenesis and lipolysis (beta 2 is associated with gluconeogenesis and lipolysis)
83- Q 4. Special two phenotypes that are only seen in Graves, but not other hyperthyroidisms.
- exophthalmos
- peritibial myxedema
- these two are mediated by TSI, specific for Graves
83- Q14. Diabetic drugs “-gliflozin”
- MOA
- contraindicated in what circumstance
- SGLT-2 inhibitors
- moderate to severe renal impairment
- > lack of efficacy and increased chance for UTI
- renal function test (creatinin and BUN) needs to be done prior to prescription
83-Q 26. Chronic glucorcorticoid treatment, levels of
- CRH
- ACTH
- cortisol
ALL GO DOWN
- it is true that chronic glucorcorticoid causes adrenal hypoplasia, but later CRH and ACTH also give up.
ALL hipothalmus-pituitary- adrenal axis is messed up
83- Q 36. Cortisol cross-talks to catecholamine synthesis pathway by stimulating what enzyme? what reaction does this enzyme stimulate?
PNMT (Phenylethanolamine-N-MethylTransferase)
last step: norephi -> ephi
84- Q 4. level of plasma sodium in primary aldosteronism? why?
normal
Aldosterone escape: ANP/BNP works to pee out retained sodium (by aldosterone) and equilibrate sodium/volume status
=> why hypernatremia and peripheral edema is rarely seen in PHA
84- Q 16. What is primary polydypsia? What is underlying pathophysiology? What lab tests can differentiate it with Diabetes insipidus?
Primary polydypsia is polydypsia due to excess intake of water, usually has underlying psychological disorder
water deprivation test: with prolonged water deprivation, urine osmolarity will increase. Addition of ADH after few hours of deprivation will not change urine osmolarity that much. (patient has intact ADH synthesis/ kidney’s response to ADH
84- Q19. Migratory necrolytic dermatitis. what endocrine tumor is this?
glucagonoma
85- Q2. Hypothyroidism
- TSH
- T4
- T3
- high TSH
- low T4
- NORMAL T3
- T3 is not accurate. even with hypothyroidism, T3 can be normal as it can be made from T4. It is T4 that is primarily released from thyroid
85- Q 18. Thyroid hormone (T3/T4) vs. TSH: compare signaling pathway
Thyroid hormone (T3/T4): intracellular receptor -> txn *like steroids, vitamin D
TSH: Gs-> cAMP
XX karyotype. Clitoromegaly and fused labia majora. what condition should I think abut?
congenital adrenal hyperplasia
: either 21 or 11 hydroxylase deficiency
=> excess androgens result in ambiguous female external genitalia and virilization during secondary sexual development.
vs. 17 hydroxylase deficiency, where female external genitalia is normal, while secondary sexual development is lacking
* androgen is not required for female external genitalia , but it is required for appropriate secondary sexual development
XX karyotype. Clitoromegaly and fused labia majora. Differential diagnosis comes down to either 21 or 11 hydroxylase deificiency. Now what? how to differentiate these two?
check sodium and potassium level
with 11 hydroxylase deficiency, 11-deoxycorticosterone is accumulated, and this one has MR activity. Thus hypernatremia ( so does increased BP) and hypokalemia will be observed
