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ENDOREPRO MODULE > Lecture > Flashcards

Lecture Flashcards

0
Q

What are three physiological actions of the thyroid hormones, T3 and T4?

A

1) Growth and Development of Children
2) Calorigenesis
3) Metabolism of fats, carbs and proteins.

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1
Q

Thyroid hormones T3 and T4 do what do LDL receptors?

A

Increase the expression of LDL receptors on hepatocytes, thus reducing the level of cholesterol in the body.

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2
Q

What is the drug of choice to treat hypothyroidism?

A

Sodium levothyroxine T4 (Synthroid, Levothroid)

Caution: Older patients may have coronary artery disease. increase the dose ofo T4 slowly over time. Excessive levothyroxine replacement MAY increase risk of osteoporosis.

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3
Q

Sodium liothyronine, T3:

When do you give this drug?

A

Used for myxedema coma, given by IV, can be given orally prior to surgery

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4
Q

Thyroid USP

A

Dried, defatted thyroids from pig and sheep, unpredictable strength.

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5
Q

Why is T4 treatment favorable to T3 treatment?

A

T4’s half life is 7 days vs. 1 day for T3.

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6
Q

Toxic Nodular adenoma?

A

Plummer’s Disease

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7
Q

What are three drugs that treat for hyperthyroidism?

MOA?

A 
Thioamides:
    Propylthiouracil (PTU)
    Methimazole
Carbimazole
All act by inhibiting thyroid peroxidase
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8
Q

What patient population should you be very careful in using thioamides with?

A

Caution in pregnancy!!

Both PTU and methimazole cross placenta, but PTU less so, so use the lowest dose possible!

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9
Q

What drugs do you use to treat “Thyroid Storm”

A

–Treat immediately with propranolol or atenolol. Patient can be treated long term with thioamides, 131I, or surgery.
Lugol’s solution (10% KI & 5% I2) can also be given to quiet the thyroid gland. It diminishes the vasculature of the thyroid & therefore useful before thyroidectomy. Wolff–Chaikoff Effect.

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10
Q

The best treatment for a pregnancy woman with Graves’ disease would be…?

A

lowest possible dose of PTU

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11
Q

Radioactive Iodine (131I):

A
  • Iodide actively taken up by the thyroid gland.
  • In theory, in the case of toxic nodular adenoma of the thyroid, the adenoma takes up the 131I while the quiescent normal tissue takes up less.
  • In practice, 131I usually destroys most the thyroid. However, the patient can be placed on levothyroxine replacement therapy for life.
  • CAUTION! Never use 131I during pregnancy!
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12
Q

Look at chart of drugs to treat hypohyper!

A

djf

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13
Q

The synthesis of 1,25 (OH)2 D3…

A

involves PTH regulated hydroxylation of 25 OHD3 in the 1 position in the kidney…

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14
Q

Treatment for hypoparathyroidism?

A

They need the active form! Not just regular diet or sunlight because they are not producing enough PTH to convert Vit D into the active form so…
1,25(OH)2D3 and dietary calcium supplement

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15
Q

Treatment for Pseudoparathyroidism?

A

Treatment - 1,25(OH)2D3

Usually an issue with the Gs receptor (low, abnormal, absent) so you have high PTH but low Ca2+, and 1,25(OH)2D3 is low.

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16
Q

Treatment for Ricketts?

A

Increase PTH, high Ca2+ removal from bones. The body wants Calcium! So, -> Bones become soft.

•Treatment - sunlight, food supplemented with vit. D2 or D3 (milk, bread, cereals)

D3 is low and so you have low active form of VitD

17
Q

How do you treat Paget’s Disease?

A

•Treatment - Calcitonin (porcine or salmon) injections.
–Or orally active bisphosphonates such as
•sodium etidronate
•alendronate (daily and once-a-week)
•risedronate (daily and once-a-week)
•pamidronate
•ibandronate (once a month; generic form available)
•zoledronic acid (once a year iv infusion)

18
Q

Postmenopausal Osteoporosis

A 
Estrogen + progesterone
Raloxifene (SERM)
Bisphosphonates
Teriparatide
Denosumab
19
Q

Pharm Treatment for Primary Hyperparathyroidism

A

Cinacalcet, a calcium mimetic. Binds Ca-sensing receptor in parathyroid gland

20
Q

How do you treat drug induced osteopenia?

A

•Treatment - Administer vitamin 25(OH)D3, D2, or D3

21
Q

Embryology of the fetal adrenal

A

cortex from mesenchyme

medulla from neural crest cells

22
Q

What are the 4 dominant mechanisms of secretory control of ACTH?

A
  1. Negative Feedback Regulation
  2. Episodic (pulsatile) secretion
  3. Diurnal rhythm
  4. Stress
23
Q

How does cortisol act an as anti-inflammatory/immunosuppressive agent?

A
  • Inhibits production of leukotrienes and prostaglandins
  • Inhibits leukocyte adhesion -> neutrophilia
  • Blocks histamine release from mast cells
  • Reduces eosinophils
  • Blocks IL-2 production
24
Q

Cortisol is

BBIIG?

A

B- maintains “B”lood pressure (upregulates alpha-1 receptors on arterioles
B - decreases “B”one formation
I - anti- “I”nflammatory
I- “I” nsulin resistance (diabetogenic)
G - Increase “G”luconeogenesis, lipolysis, proteolysis

25
Q

What molecule is cortisol bound to?

A

Coticosteroid-binding globulin

26
Q

What are regulations of aldosterone secretion?

A
  1. Renin- angiotensin
  2. Serum potassium primarily
  3. ACTH to a lesser degree
27
Q

For a pheochromocytoma, what are the episodic hyperadrenergic symptoms (5 P’s)

A 
Pressure (elevated blood pressure)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor
28
Q

When surgery is not possible to remove a pheochromocytoma, what are some pharmacological options?

A
  1. Alpha blockers (phenoxybenzamine) decrease blood pressure

2. Beta blockers - slow heart rate and contractility

29
Q

A cell responding to a hormone has an immediate increase in intracellular concentrations of cAMP and Ca2+. The hormone to which the cell is responding is MOST LIKELY:

A

Epinephrine -> immediate increase in cAMP mean that it is probably not working through the nucleus.

30
Q

Sectioning of the pituitary stalk will result in:

A

Polyuria, polydipsia and hyperprolactinemia (remove hypothalamic control and prolactins production is uninhibitied)

31
Q

A rapid expansion of the intra-vascular volume by an infusion of 2 liters of isotonic saline will normally be compensated for by:

A

Decrease in angiotensin II production

32
Q

Where is the only source of testosterone in women made? What is it converted to?

A

Zona reticulata; estradiol -> the only source of estrogen for post menopausal women and men.

33
Q

How does the drug cortisone differ from cortisol?

A

Has a carbonyl group at the 11 place instead of the hydroxyl group.

When you inject a patient with a cortisone injection, you are injecting a prodrug and letting it sit in the joint to be converted slowly to cortisol by 11B-HSD1 enzyme. This way you do not have to do daily injections.

34
Q

What syndromes need adrenal steroid replacement therapy?

A

Addison’s Disease

Congenital Adrenal Hyperplasia

35
Q

What is the most common use of glucocorticoids?

A

Anti-inflammatory processes.
Arthritis; rheumatic carditis;
inflammation of the eye, skin bowel, etc.

36
Q

How does prednisone differ from cortisone?

A

Prednisone -> 1,2 double bond
Prednisone is converted to its active form prednisolone in the liver, not the joint like how cortisone is converted to its active form.
Prednisone can be administered orally.

37
Q

Toxicities associated with adrenal steroids?

A 
Pituitary-adrenal suppression
Hypokalemia alkalosis, edema
Hyperglycemia (DM)
increased susceptibility to infection
Inhibition of wound healing
Myopathy
Behavioral Disturbances
Peptic Ulceration (inhibit protection factor from prostaglandins in the stomach)
Cataracts
Growth arrest in children
osteoporosis
various other CUSHINGOID effects
38
Q

Five glucocorticoids.

A 
Prednisone
Hydrocortisone
Triamcinolone
Dexamethasone
Beclomethasone
39
Q

Four approaches to Steroid therapy?

A
  • Replacement (Addison’s; adrenalectomy) - low dose (AM)
  • Suppression (congenital adrenal hyperplasia) – low dose twice (or more) a day
  • Induction (giant cell arteritis; acute phase of nephrotic syndrome) – high dose daily
  • Maintenance – Alternate day (if possible) to minimize immunosuppression and other side effects
40
Q

Glucocorticoid Antagonists?

A

Mifepristone (used to treat hyperglycemia in Cushing Syndrome)
Spironolactone
Eplerenone (more selective mineralocorticoid receptor antagonist

41
Q

Wolff-Chaikoff effect?

A

Reduction in thyroid hormone levels caused by ingestion of a large amount of iodine.
Acutely inhibiting the organification of iodine.
“Iodine-induced hypothyroidism”

ENDOREPRO MODULE (11 decks)

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