Endo-UWORLD Flashcards

1
Q

81-Q 10. What does primary hypoparathyroidism do on

  • renal handling of Ca2+ and phosphate
  • gut handling of Ca2+ and phsopate
A
  • 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.
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2
Q

81- Q 12. Amenorrhea in a girl with low BMI. What is underlying pathophysiology?

A

low fat -> low leptin -> decreased GnRH (hypothalamus)
-> decreased FSH/LH (pituitary) -> amenorrhea

  • This is called functional hypothalamic amenorrhea

It is HYPOTHALAMIC DYSREGULATION

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3
Q

81- Q 21. Effect of OCP on
- free T3/T4
- Total T3/T4
Explain physiology

A
  • 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)

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4
Q

81- Q 25. Hypothyroidism vs. Hyperthyroidism: How myopathy look different?

A

Hypothyroidism: elevated CK
Hyperthyroidism: normal CK

  • both present with myopathy
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5
Q

81- Q 26. Lab tests for Diabetes: Hb1Ac, fasting glucose level, oral glucose tolerance test. Which two methods are preferred over another?

A

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

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6
Q

81- Q 32. Sheehan syndrome vs. Pituitary apoplexy: compare etiologies

A

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)

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7
Q

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?
A
  • recurrent laryngeal -> hoarseness

- superior laryngeal -> innervates cricothyroid

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8
Q

82- Q 9. Increased level of which metabolite is diagnostic for 21-hydroxylase deficiency

A

17-hydroxyprogenelone

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9
Q

82- Q 11. sympathetic vs. parasympathetic: compare how these two autonomic systems innervate pancreatic cells for regulation of insulin release

A
  • 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
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10
Q

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
A

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
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11
Q

82- Q 33. Fever, low BP, high pulse, signs of acidosis. what is happening? why there is acidosis?

A

septic shock -> hypoperfusion -> lack of oxidative phosphorylation -> lactic acidosis

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12
Q

82- Q 34. Which beta blockers are preferred to patient with diabetes? why?

A

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)

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13
Q

83- Q 4. Special two phenotypes that are only seen in Graves, but not other hyperthyroidisms.

A
  • exophthalmos
  • peritibial myxedema
  • these two are mediated by TSI, specific for Graves
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14
Q

83- Q14. Diabetic drugs “-gliflozin”

  • MOA
  • contraindicated in what circumstance
A
  • 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
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15
Q

83-Q 26. Chronic glucorcorticoid treatment, levels of

  • CRH
  • ACTH
  • cortisol
A

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
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16
Q

83- Q 36. Cortisol cross-talks to catecholamine synthesis pathway by stimulating what enzyme? what reaction does this enzyme stimulate?

A

PNMT (Phenylethanolamine-N-MethylTransferase)

last step: norephi -> ephi

17
Q

84- Q 4. level of plasma sodium in primary aldosteronism? why?

A

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

18
Q

84- Q 16. What is primary polydypsia? What is underlying pathophysiology? What lab tests can differentiate it with Diabetes insipidus?

A

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

19
Q

84- Q19. Migratory necrolytic dermatitis. what endocrine tumor is this?

A

glucagonoma

20
Q

85- Q2. Hypothyroidism

  • TSH
  • T4
  • T3
A
  • 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
21
Q

85- Q 18. Thyroid hormone (T3/T4) vs. TSH: compare signaling pathway

A
Thyroid hormone (T3/T4): intracellular receptor -> txn
*like steroids, vitamin D

TSH: Gs-> cAMP

22
Q

XX karyotype. Clitoromegaly and fused labia majora. what condition should I think abut?

A

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

23
Q

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?

A

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