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Endo / Repro > Day 1, 3 > Flashcards

Day 1, 3 Flashcards

1
Q

What are the regulatory factors in the release of TH and where do they act?

A

T3 and T4 act at the hypothalamus and Pituitary to down regulate TRH and TSH, respectively.

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2
Q

What is the most sensitive test for thyroid function?

A

TSH

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3
Q

What are the reasons for hypothyroid signs and symptoms?

A

Decr. BMR: Decrease in ATPase

Decr. SNS: Decrease in catacholamines

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4
Q

What drug class causes hypothyroidism?

A

Antipsychotics (lithium)

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5
Q

What is a concern for maternal iodide deficiency?

A

Congenital hypothyroidism

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6
Q

What is the most common type of hypothyroidism?

A

Hashimotos

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7
Q

What is the classic triad for Graves?

A

Goiter, Thyrotoxicosis, Opthalmopathy

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8
Q

What are the underlying causes of hyperthyroid signs and symptoms?

A

Incr. BMR from increase ATPase production

Incr. SNS activity from incr. catacholamines

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9
Q

What is the pathogenesis of Graves’ disease?

A

Autoantibodies against TSH receptors –> increase T3 and T4 production and release in the thyroid.

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10
Q

What are the effects of T3 and T4 in regards to cholesterol levels?

A

Reduction by increasing the liver LDL receptors

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11
Q

What is the primary enzyme in the production of T3 and T4?

A

Thyroid peroxidase

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12
Q

What is the DoC for hypothyroidism?

A

Levothyroxine is a T4 sythetic

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13
Q

What is the usual demographic for hyperthyroidism?

A

Older women with a personal or family history of Autoimmune

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14
Q

What is the second leading cause of hyperthyroidism?

A

Toxic nodular adenoma

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15
Q

What is the usual morphology of a Graves’ goiter?

A

Diffuse bilateral hot spots

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16
Q

What is the drug class and DoC used for Graves?

A

Thioamines, Methimazole

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17
Q

What is prescribed to pregnant Graves patients?

A

PTU

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18
Q

What is the first drug given in a thyroid storm?

A

Beta blocker - atenolol or propranolol

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19
Q

What are the 3 actions of PTH?

A

Incr. osteoclast activity via stimulation of blasts
Increase 1, 25 Vit D –> incr. Ca++ absorption
Increase Ca++ reabsorption in kidney

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20
Q

What two structures inhibit PTH release?

A

Ca++ and 1, 25 (OH)2D3

21
Q

What is the pathway for Vit production?

A

http://ajprenal.physiology.org/content/289/1/F8

22
Q

Where does PTH act in the Vit D pathway?

A

Increased 1a-hydroxylase in proximal tubules

23
Q

What is the pathology of pseudohypoparathyroidism?

A

Gs protein deficiency

24
Q

What is the class of drugs and the DoC for treating Paget’s?

A

Bisphosphonates (Alendronate)

25
Q

What are the two drugs preferred in the treatment of postmenopausal Osteoporosis?

A

Raloxifene (SERM)

26
Q

What is the suffix for bisphosphonates?

A

“…dronate”

27
Q

When is PTU used?

A

1st trimester hyperthyroidism (e.g. Graves’)

28
Q

What is the use and MoA of Denosumab?

A

Postmenopausal Osteoparosis, RANK-L Ab – downregulates osteoclasts

29
Q

What is the use and MoA of Levothyroxine?

A

Hypothyroidism, TH analogue

30
Q

What are the embryologic origins of the cortex and medulla of the adrenal gland?

A

Cortex: Mesenchyme
Medulla: Neural crest

31
Q

What supplies the blood to the adrenal gland?

A

aorta, phenic, and renal arteries

32
Q

What are the three zones of the adrenal cortex and their products?

A

Zona glomerulosa: aldosterone
Zona fasiculata: cortisol
Zona reticulata: androgens

33
Q

Where is epi synthesized, what enzyme is used, and what cofactor is required?

A

Phenolethynolamine N-methyltransferase (PNMT)

34
Q

What is the function of Cortisol?

A

Glucocorticoid, mobilzes glucose and ffa

35
Q

What is the function of aldosterone?

A

Mineralcorticoid, stimulates Na reabsorption

36
Q

What is the function of dehydroepiandrosterone sulfate?

A

Androgen, sex hormones

37
Q

Draw out the synthesis of

A

http://www.nature.com/nrendo/journal/v5/n9/fig_tab/nrendo.2009.148_F1.html

38
Q

What is the rate limiting and committed step in steroid synthesis in the adrenal cortex?

A

Desmolase

39
Q

What is the effect of cortisol on the body?

A

Similar to fasting state

40
Q

What are the 5 pathologies associated with excess cortisol?

A 
Primary Cushing's - adrenal
Secondary Cushing's - pituitary
Tertiary Cushing's - hypothalamus
Ectopic ACTH - lung and GI neoplasm
Iatrogenic
41
Q

What is the “heavy hitter” cortisol-based drug?

A

Dexamethasone

42
Q

What is the difference between Cushing’s Syndrome and Disease?

A

Syndrome: No negative feedback set point
Disease: Set point is too high

43
Q

A normal result of what test will exclude Cushing’s?

A

Low-Dose Dexamethasone Suppression

44
Q

What are the ACTH levels after the dexamethasone test in Cushing’s caused by: Adrenal Tumor, Ectopic ACTH Syndrome, and Cushing’s Disease?

A

Undetectable
Elevated
Normal to elevated

45
Q

What is the physiology of the dexamethasone test?

A

http://www.webmd.com/a-to-z-guides/overnight-dexamethasone-suppression-test

46
Q

What is the physiology behind hypocortisolemia skin bronzing?

A

Incr ACTH –> melanocyte activation via melanotropin

47
Q

What is Addison’s Disease?

A

Hypocortisolism (opposite of Cushing’s)

48
Q

What are the three types of hypocotisolemia?

A

Primary: Adrenal destruction (Addison’s)
Secondary: Pituitary doesn’t make ACTH
Tertiary: Hypothalamus doesn’t produce CRH

Endo / Repro (15 decks)

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