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UWorld > Endo > Flashcards

Endo Flashcards

1
Q

What does POMC give rise to?

A

ACTH
MSH
b-Endorphins

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2
Q

Explain pathogenesis of high PTH and Calcium deficiency in Celiac.

A

Can’t absorb the Calcium

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3
Q

XX virilization
Salt Wasting
Increased serum 17-hydroxyprogesterone

Diagnosis?

A

CAH, 21-hydroxylase deficiency

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4
Q

Spindle cells on amorphous background with extracellular amyloid
Proliferation of parafollicular, calcitonin secreting C cells

Diagnosis?

A

Medullary thyroid cancer

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5
Q

What syndrome and oncogene is medullary thyroid cancer associated with?

A

MEN 2, RET pro-oncogene (TK)

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6
Q

What is the MOA of Thiazolidinediones (ex. Pioglitazone)?

A

Decrease insulin resistance by binding PPAR-g, a TF of genes in glucose and lipid metabolism

(DM)

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7
Q

What is an adverse effect of the Thiazolidinediones in treating DM?

A

Increase adiponectin >
increase fluid retention >
exacerbate CHF

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8
Q

What is osteitis fibrosa cystica?

A

Skeletal manifestation of primary hyperparathyroidism

  • Cortical bone involvement
  • Subperiosteal erosions, osteolytic cysts in long bones
  • Salt and pepper skull
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9
Q

Lesion to what part of the brain will affect production of ADH and cause permanent central DI?

A

Hypothalamus

- ADH is made int he hypothalamic nuclei

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10
Q

Lesion to what part of the brain will affect release of ADH and cause transient central DI?

A

Posterior Pituitary

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11
Q

What is the effect of glucocorticoids in the periphery?

A

Catabolism

  • Antagonist of insulin in skeletal and adipose tissue
  • Decreased enzymes
  • Provide substrate to the liver instead

(Peripheral wasting with steroid use)

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12
Q

What is the effect of glucocorticoids on the liver?

A

Anabolism

Gluconeogenesis:
- Increase enzymes: PEPCK, G6Phosphatase

Glycogenesis
- Increase enzymes: Glycogen synthase

(Central obesity with steroid use)

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13
Q

What is the Na+ level in primary hyperladosteronism?

A

Normal!

Low K+ and H+

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14
Q

What is the pathogenesis of a normal Na+ level in primary hyperaldosteronism?

A

“Aldosterone Escape”

Aldo retains a lot of water and Na+ >
ANP tries to diurese >
Overall negative charge in lumen pulls out K+ and H+ >
Normal Na, hypoK, alkalosis

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15
Q

What hormones promote gluconeogenesis?

A

Cortisol (through steroid Rs)
GH (through JAK/STAT)
Epi, NE, Glucagon (through GPCRs)

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16
Q

Where are thyroid hormone receptors located?

A

In the nucleus

NOT in the cytoplasm and later translocated to the nucleus

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17
Q

What are the volume and sodium levels in SIADH?

A

Euvolemic Hyponatremia

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18
Q

What is the pathogenesis of euvolemic hyponatremia in SIADH?

A

Increased ADH causes transient fluid overload >
Increased ANP and Decreased aldo in rxn >
Natriuresis (pee out sodium) >
Euvolemia with profound hyponatremia

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19
Q

What is the location and function of chromaffin cells?

A 
Adrenal medulla (stimulated by Ach)
Release catecholamines (NE and Epi)
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20
Q

Exophthalmos in Graves disease is associated with what substance buildup?

A

Glycosaminoglycans

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21
Q

What symptom of Graves disease do glucocorticoids not resolve?

A

Exophthalmos

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22
Q

What is the MOA to Methimazole and Propylthiouracil?

A

Inhibit thyroid peroxidase, thereby inhibiting iodine organification

Rx for Graves disease

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23
Q

What is the adverse effect of both Methimazole and PTU?

A

Agranulocytosis

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24
Q

What is an adverse effect of Methimazole?

A

1st trimester teratogen

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25
Q

What is an adverse effect of PTU?

A

Hepatic failure, ANCA vasculitis

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26
Q

What is an additional effect of PTU, beyond inhibiting thyroid peroxidase?

A

Decreases peripheral conversion of T4 > T3

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27
Q

Describe intracellular effects after insulin binds its receptor.

A

Insulin > RTK > protein phosphatase > enzymes

  • Activate glycogen synthase to increase glycogen synth
  • Deactivate fructose 1,6 bis to decrease gluconeogeesis
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28
Q

What is the Rx to decrease sympathetic adrenergic symptoms of thyrotoxicosis?

A

Beta blocker

29
Q

What are 2 effects of beta blockers in thyrotoxicosis?

A

Decrease sympathetic adrenergic drive

Decrease peripheral conversion of T4 > T3

30
Q

What is the effect of Lithium on the thyroid?

A

HYPOthyroidism

- Measure TSH periodically

31
Q

What is the MOA of Canagliflozin, Dapgliflozin?

A

SGLT2 inhibitors
Decrease absorption of glucose in the proximal tubule
Increased urinary loss of glucose

“Floozies lose everything”

32
Q

Anti-androgens: what is the MOA of…

Ketoconazole?

A

Blocks T synthesis at Leydig cells

33
Q

Anti-androgens: what is the MOA of…

Spironolactone?

A

Blocks T synthesis + binding at receptor

34
Q

Anti-androgens: what is the MOA of…

Finasteride

A

Blocks peripheral conversion of T to DHT

35
Q

Anti-androgens: what is the MOA of…

Flutamide

A

Block action at receptor

36
Q

Anti-androgens: what is the MOA of…

Cyproterone

A

Block action at receptor

37
Q

Watery diarrhea
Hypokalemia
Achlorhydria

A

VIPoma, pancreatic tumor

38
Q

What is the Rx for a VIPoma?

A

Octreotide (SST)

39
Q

What is the pathogenesis of poisoning by Amanita Phalloides?

A

Amatoxins bind to RNA pol II and stop mRNA synthesis

Aminata goes by MINA…mRNA
PhaLLoides…pol II

40
Q

Most tissues have X as the first enzymes in the glycolytic pathway, but the pancreas has Y.

A 
X = hexokinase 
Y = glucokinase
41
Q

Which has a higher Km, hexokinase or glucokinase?

A

Glucokinase

- It only works when glucose levels are high

42
Q

Which is more sensitive to feedback inhibition by G6P, hexokinase or glucokinase?

A

Hexokinase

- Glucokinase is not as affected by negative feedback

43
Q

What is the effect of glucokinase in pancreatic beta cells?

A

Coverts glucose > G6P rate limiting step

Results in insulin release!

44
Q

What is the result of mutation to glucokinase?

A

Hyperglycemia and decreased insulin release

45
Q

What are carrier proteins for oxytocin and ADH?

A

Neurophysins

46
Q

What is the result of mutations to neurophysins, carrier proteins for oxytocin and ADH?

A

Decreased ADH, diabetes insipidus

47
Q

What is the Rx for a Pheo?

A

Phenoxybenzamine

48
Q

Increased LFTs with neuro symptoms
Slit lamp test indicated

Diagnosis?

A

Wilson’s Disease

49
Q

Increased LFTs with > 50% transferrin sat
New onset diabetes

Diagnosis?

A

Hemochromatosis

50
Q

What is the cause of Bronze Diabetes?

A

Hemochromatosis

51
Q

Tall, crowded follicular epithelium
Small pseudopapillae project into lumen

Graves or Hashimoto?

A

Graves

52
Q

Lymphocytic infiltrate with lymphoid germ centers
Destruction of thyroid follicles

Graves or Hashimoto?

A

Hashimoto

53
Q

What are the functions of Vitamin D?

A

Increased intestinal absorption of Ca and Phos

Bone resorption and release of Ca and Phos when levels of one or both are low

54
Q

What kind of receptor does glucagon target?

A

GPCR (> cAMP > PKA)

55
Q

What is the cause of paresthesias and muscle weakness in Conn’s Syndrome

A

HypoK paresis

The hyperaldo leads to increased Na+ in and K+ out

56
Q

What is the Rx for Congenital Adrenal Hyperplasia?

A

Low dose corticosteroids

57
Q

What is the pathogenesis of hypercalcemia in Sarcoidosis?

A

T cells are activated in inflammatory response > IFN-g >
1-a-hydroxylase in MACROPHAGES >
Activates vitamin D >
Increased Ca and Phos absorption from gut

58
Q

What is the overall effect of estrogen on thyroid hormone?

A

Estrogen increases thyroid hormone binding globulin

- Will increase overall thyroid hormone but maintain free

59
Q

What are the levels of neutrophils, lymphocytes, monocytes, basophils, and eosinophils with corticosteroid use?

A

Neutrophils INCREASE because of demargination of neutros attached to cell walls

DECREASED: lymphos, monos, basos, eos

60
Q

Describe the intracellular cascade that releases insulin from pancreatic beta cells, starting with glucose.

A 
Glucose enters via GLUT2 >
Generates ATP through Kreb's Cycle >
ATP binds and closes KATP channel >
No more K+ out, so cell depolarizes >
Voltage gated Ca channels open >
Increase in Ca induces INSULIN RELEASE
61
Q

What is the MOA of sulfonylureas and meglitinides in DM?

A

Increase endogenous insulin secretion

ex) Glyburide

62
Q

Thyroid cancer:

Finely dispersed chromatin: “ground glass”
Intranuclear inclusions + grooves
Orphan Annie nuclei
Psammoma bodies (calcifications)

A

Papillary

63
Q

Thyroid cancer:

Polygonal spindle shaped cells
Cytostain for calcitonin
Adjacent amyloid
MEN2

A

Medullary

64
Q

Thyroid cancer:

Pleomorphic cells
Giant cells
Biphasic Spindle cells

A

Anaplastic

65
Q

What is the Rx for DKA?

A

Regular insulin, administered IV for aute DKA

66
Q

How does estrogen impact thyroid binding globulin? What are the levels of TSH and T4?

A

Increases synth of TBG
T4 pool increases but free T4 remains normal
Euthyroid with normal TSH

67
Q

What is the underlying cause of diabetic mononeuroathy of CN III?

A

Ischemia

68
Q

External radiation in childhood increases risk of what in adulthood?

A

Thyroid cancer

69
Q

What is the MOA of Perchlorate + PErtechnate?

A

Competitive inhibitors of iodide uptake in thyroid at the sodium-iodide transporter

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