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3b_Boards - SketchyPharm > (5) GI & Endo: Thyroid etc (3.1-3.4) > Flashcards

(5) GI & Endo: Thyroid etc (3.1-3.4) Flashcards

1
Q

What cell type is responsible for iodine uptake and thyroid hormone production?

A

What cell type is responsible for iodine uptake and thyroid hormone production?

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2
Q

How is iodide transported into the thyroid follicular cell?

A

Na+/I- symporter

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3
Q

Where is thyroglobulin found?

A

Thyroid follicu-LAIR lumen

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4
Q

Name 3 functions of thyroid peroxidase

A

(1) Oxidation of I- → I2
(2) Organification of thyroglobulin
(3) Coupling of iodinated tyrosine residues

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5
Q

In what compartment is thyroid hormone cleaved off of thyroglobulin?

A

Follicular cell’s cytoplasm

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6
Q

Is T3 or T4 more potent?

A

T3

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7
Q

What enzyme converts T4 to T3 in the peripheral tissues?

A

5’ deiodinase

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8
Q

Broadly, what can we attribute the symptoms of hyperthyroidism to?

A

↑ β-adrenergic receptors

(⇒ Hypermetabolic and hyperadrenergic state)

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9
Q

Which thyroid disorder causes exophthalmos?

A

Graves disease

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10
Q

Adverse Effects (3) : I131 ablation therapy

A

(1) Hypothyroidism
(2) Exacerbation of hyperthyroidism
(3) Exacerbation of Graves ophthalmopathy
* (Exacerbation of ophthalmopathy MOA: Rapid reduction in thyroid hormone ⇒ ↑ TSH ⇒ Binds pre-adipocytic fibroblasts ⇒ ↑ Glycosaminoglycan and adipose deposition)*

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11
Q

MOA: Propylthiouracil

A

(1) Inhibits TPO
(2) Inhibits 5’ deiodinase

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12
Q

MOA: Methimazole

A

Inhibits TPO

(TPO: thyroid peroxidase enzyme; involved in iodide oxidation & organification)

(Methimazole is 10x more potent than Propylthiouracil and is usually the DOC. The exception is in FIRST trimester of pregnancy)

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13
Q

MOA: β-blockers (in treating hyperthyroidism)

A

(1) β-blocker
(2) Inhibit 5’ deiodinase

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14
Q

MOA: Glucocorticoids (in treating hyperthyroidism)

A

Inhibits 5’ deiodinase

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15
Q

Which pharmacologic treatment of hyperthyroidism is particularly effective against Graves’s ophthalmopathy?

A

Glucocorticoids

(Glucocorticoids induce lymphocyte apoptosis and ∵ ↓ production of autoantibodies ⇒ ↓ Fibroblast proliferation ⇒ ↓ Ophthalmopathy)

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16
Q

Treatment: Thyroid storm

A

(1) β-blockers
(2) Methimazole
(3) Glucocorticoids
* (Methimazole preferred over PTU∵ of increased efficacy)*

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17
Q

Adverse Effects (3) : Propylthiouracil (unique from methimazole)

A

(1) Hepatotoxicity
(2) Maculopapular rash
(3) ANCA-associated vasculitis

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18
Q

Name 3 adverse effect that Propylthiouracil and Methimazole share

A

(1) Agranulocytosis
(2) Aplastic anemia
(3) Drug-induced lupus

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19
Q

Treatment: Hypothyroidism (in a first-trimester pregnant woman)

A

Propylthiouracil

(Methimazole is contraindicated in the first trimester due to teratogenicity, whereas PTU is contraindicated in second and third trimester due to risk of hepatotoxicity)

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20
Q

Name a T4 analog

A

Levothyroxine

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21
Q

Treatment: Radioactive iodine exposure

A

Anions

(Such as perchlorate, pertechnetate, and thiocyanate which inhibit the Na+/I- symporter)

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22
Q

Suffix: Biphosphonates

A

“-dronate”

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23
Q

Biphosphonates have a chemical structure similiar to what molecule?

A

Pyrophosphate

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24
Q

Name 3 ways biphosphonates affect osteoclasts

A

(1) Inhibit bone adherence
(2) Inhibit recruitment/development
(3) Induce apoptosis

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25
Q

Other than osteoporosis, what can biphosphonates be used to treat?

A

(1) Hypercalcemia
(2) Paget’s Disease
* (Note: Calcitonin has similar indications, but is the second line)*

26
Q

Adverse Effects (3) : Biphosphonates

A

(1) Corrosive esophagitis
(2) Osteonecrosis of jaw
(3) Hypocalcemia

27
Q

What is the mechanism of estrogen therapy in the treatment of osteoporosis?

A

Inhibit osteoclast precursor development

28
Q

What drug is an estrogen agonist in bone but antagonist in the breast and uterus?

A

Raloxifene

29
Q

How does parathyroid hormone stimulate osteoclasts?

A

↑ RANKL on Osteoblasts

(⇒ Osteoclast activation)

30
Q

MOA: Denosumab

A

anti-RANKL antibody

31
Q

Does calcitonin bind receptors on osteoclasts or osteoblasts?

A

Osteoclasts

32
Q

How does Calcitonin reduce serum calcium?

A

(1) Inhibits osteoclasts
(2) ↓ Renal Ca2+ reabsorption

33
Q

Name two hormones which upregulate RANKL

A

(1) PTH
(2) Calcitriol

34
Q

Name two mechanisms of negative feedback on PTH

A

(1) ↑ Ca2+
(2) ↑ Calcitriol
* (A rare instance where ↑ intracellular Ca2+ inhibits exocytosis)*

35
Q

What effect does the RANK-RANKL interaction have on osteoclasts?

A

(1) Differentiation
(2) Activation
* (RANKL is upregulated by PTH, whereas osteoprotegrin is upregulated by Calcitriol)*

36
Q

What effect does PTH have on osteoblasts?

A

Maturation of pre-OB → OB

(The net effect of PTH is bone resorption. Vit. D also stimulates OB maturation)

37
Q

What effect does PTH have on renal electrolyte handling?

A

(1) ↑ Ca2+ reabsorption
(2) ↑ PO42- excretion

38
Q

Name 3 ways PTH elevates serum [Ca2+]

A

(1) Activates osteoclasts
(2) ↑ Renal Ca2+ reabsorption
(3) Activates Vitamin D

39
Q

MOA: Teriparatide

A

PTH analog

40
Q

Identify an important physiologic distinction between Teriparatide and endogenous PTH

A

(1) Teriparatide: Net bone formation
(2) Parathormone: Net bone resorption
* (Pulsatile Teriparatide ⇒ bone formation. Constant dosing would likely instead lead to bone resorption)*

41
Q

Indication: Teriparatide

A

Osteoporosis

42
Q

What are the source(s) of Vitamin D3?

A

(1) Dairy products
(2) UVB radiation
* (Vit. D3 = Cholecalciferol. The 3 of Vit. D3 to remember Cholecalciferol starts with the third letter of alphabet)*

43
Q

What are the source(s) of Vitamin D2?

A

Plants

44
Q

Describe how dietary Vitamin D is converted into the active form

A

(1) 25-hydroxylated in the liver
(2) 1-hydroxylated in the kidney
* (∴ Calcitriol would be indicated over Vit. D2/D3 in the setting of renal/liver disease)*

45
Q

What effect does Calcitriol have on renal electrolyte handling?

A

(1) ↑ Ca2+ reabsorption
(2) ↑ PO42- reabsorption

46
Q

What effect does Calcitriol have on GI electrolyte handling?

A

(1) ↑ Ca2+ reabsorption
(2) ↑ PO42- reabsorption

47
Q

Indication: Topical Vit. D

A

Psoriasis

(Vit. D plays an important role in T-cell homing to skin ∴ topical Vit. D exerts immunomodulatory effects)

48
Q

Name 2 endocrine etiologies of hypocalcemia treated with Calcitriol

A

(1) Hypothyroidism
(2) Hypoparathyroidism

49
Q

MOA: Cinacalcet

A

Activates CaSR in parathyroid gland

  • (CaSR = calcium-sensing receptor)*
  • (⇒ reduced secretion of PTH and ∴ is helpful against renal osteodystrophy secondary to CKD)*
50
Q

Indication: Cinacalcet

A

Hyperparathyroidism

51
Q

MOA: Sevelamer

A

Reduces absorption of PO42- in GI tract

(It is a non-absorbable oral formulation)

52
Q

Indication: Sevelamer

A

Hyperphosphatemia

(Secondary to chronic kidney disease)

53
Q

Suffix: Glucocorticoids

A

“-sone”

54
Q

Where is the glucocorticoid receptor found?

A

Cytoplasm

55
Q

What inflammatory enzyme do glucocorticoids inhibit?

A

Phospholipase A2

(By upregulating Lipocortin = Annexin)

56
Q

What transcription factor do glucocorticoids inhibit?

A

NF-κB

(∴ Inhibiting production of inflammatory cytokines and activation of B and T cells)

57
Q

How do glucocorticoids prevent leukocyte migration?

A

Inhibit adhesion molecules

(∴ Also increase WBC count ∵ fewer WBCs are attached to endothelium and more are freely floating in blood)

58
Q

What cell type are glucocorticoids most effective at inducing apoptosis in?

A

TH

(Induce apoptosis of B-cells, T-cells, and eosinophils)

59
Q

Name 5 metabolic effects of glucocorticoids

A

(1) Insulin resistance
(2) ↑ Gluconeogenesis
(3) ↑ Glycogenesis
(4) ↑ Proteolysis
(5) ↑ Lipolysis

60
Q

Name 4 physical symptoms of Cushing’s syndrome

A

(1) Moon facies
(2) Central adipose tissue
(3) Muscle wasting
(4) Skin thinning

61
Q

What CNS effects can glucocorticoids cause?

A

Psychosis

62
Q

What electrolyte abnormality can glucocorticoids cause?

A

Hypokalemia

(Due to mineralocorticoid effects)

3b_Boards - SketchyPharm (32 decks)

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