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Endocrinology > Pharm 38 - Adrenal, Thyroid, Pancreas > Flashcards

Pharm 38 - Adrenal, Thyroid, Pancreas Flashcards

1
Q

Identify the three main steroid products of the adrenals

A
  1. Cortisol - aka hydrocortisone
  2. Aldosterone - Primary mineralocorticoid
  3. Androgens (DHEA, DHEA-S, androsterone)
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2
Q
  1. primary physiologic glucocorticoid
  2. primary mineralocorticoid hormones

(name the primary pharmacologic congener of each)

A
  1. Primary physiologic glucocorticoid: Cortisol (pharmacologic congener: hydrocortisone)
  2. Mineralocorticoid hormone: aldosterone (pharmacologic congener: aldosterone)
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3
Q

Primary drug to treat Addison’s disease

A

hydrocortisone

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4
Q

Drug to treat Addison’s disease related HTN

A

Fludrocortisone

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5
Q

Dosing regiment to treat Addison’s

A

a. Dosing regimen involves trying to mimic the body’s normal physiologic levels and patterns of glucocorticoid secretion
i. Need low levels at bedtime
ii. Highest levels 1-2 hours before waking
iii. Fluctuates up and down throughout the day
iv. Stressful events: Require doubling of the dosages

Thus: give 2/3 of dose in AM and 1/3 at HS

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6
Q

Addison’s disease dosing adjustments need to occur…

A
  • During:
    1. stressful events
    2. sickness
    3. emotional stressors
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7
Q

Of the thyroid hormones, which is physiologically active?

Physiologically inactive?

A

Active: T3
Inactive: T4

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8
Q

Of the thyroid hormones, which is more abundant?

Less abundant?

A

More abundant: T3

Less abundant: T4

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9
Q

1/2 life of T3

A

one day

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10
Q

1/2 life of T4

A

seven days

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11
Q

drug used in combo with levothyroxine for individuals that do not convert T4 to T3 very well

A

liothyronine

also never used alone for thyroid supplementation

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12
Q

PREFERRED thyroid supplement in patients

A

Levothyroxine

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13
Q

Thyroid drug that is not as active as liothyronine

A

Levothyroxine

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14
Q

thyroid drug converted to T3 in peripheral circulation

A

Levothyroxine

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15
Q

Levothyroxine 1/2 life

A

5 to 7 days

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16
Q

Two goals of HYPERthyroidism treatment

A
  1. Goal one: suppress thyroid hormone synthesis

2. Goal two: suppress the beta adrenergic symptoms seen in hyperthyroidism

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17
Q

How is goal 1 of HYPERthyroidism treatment handled?

A

Thyroid hormone suppression is achieved through the pharmacologic agent propylthiouracil (PTU).

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18
Q

Propylthiouracil (PTU) is what kind of a drug

A

thyroid synthesis inhibitor

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19
Q

Propylthiouracil (PTU):

1/2 life / dosing

A

short 1/2 life that requires TID dosing

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20
Q

Propylthiouracil (PTU): full benefits are acheived…

A

in 6 to 12 months

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21
Q

How is goal 2 of HYPERthyroidism treatment handled?

A

Beta blockers! They stop the beta adrenergic symptoms that are seen with hyperthyroidism.

22
Q

Describe the role of beta-blockers for symptomatic treatment of HYPERthyroidism.

A

They prevent the beta adrenergic symptoms that are seen with hyperthyroidism.

Symptoms controlled include: tachycardia, tremor, anxiety, other symptoms.

23
Q

Drug of choice for symptomatic treatment of HYPERthyroidism

A

propanolol
labetalol
metoprolol

24
Q

Role of beta-blockers for symptomatic treatment of HYPERthyroidism and PREGNANCY:

  • duration of dose
  • drugs of choice
A

a. Short term or occasional use is okay during pregnancy
i. Do not want to use in long term pregnancy HTN control
b. Long term use is associated with growth retardation
c. drugs: labetalol, metoprolol

25
Q

Describe the particular importance and reason to screen for and closely monitor HYPOthyroidism during pregnancy.

A

a. In first trimester
i. Can result in permanent neuropsychologic deficits in the child
ii. Thyroid hormone production generally increases during pregnancy in response to hcg

26
Q

Describe potential concerns with thyroid synthesis inhibitors during pregnancy.

A

Category D for pregnancy: readily cross the placenta.

27
Q

thyroid synthesis inhibitors

A

methimazole

propylthiouracil (PTU)

28
Q

methimazole and pregnancy

  1. what’s it cause?
  2. when to use?
A
  1. What’s it cause: Fetal abnormalities

2. drug of choice for hyperthyroidism during second and third trimesters

29
Q

PTU and pregnancy

  1. what’s it cause?
  2. when to use?
A
  1. Liver toxicity
  2. Drug of choice for hyperthyroidism during or just prior to first trimester of pregnancy. Also used to treat thyroid storm in pregnant women.
30
Q

Most notorious drug for causing thyroid disorders

A

amiodarone: causes:

  1. Hyperthyroidism: May increase synthesis and release of thyroid hormone
  2. Hypothyroidism: Esp. in patients with preexisting thyroid disease
31
Q

amiodarone drug class

A

Class III anti-dysrhythmic:

  • K+ channel blocker
  • blocks Na+, Ca++
  • blocks adrenergic alpha and beta receptors
32
Q

Other drugs that cause thyroid disorders

A
  1. GI drugs: ones that alter cations/bind to things in the GI tract (acid suppressants, acid neutralizers, sucralfate)
  2. Lithium (painless thyroiditis)
  3. warfarin
33
Q

Alpha cells of the pancreas (20% of islet mass) secrete (2)

A

glucagon*

proglucagon

34
Q

Beta cells of the pancreas (70-75% of islet mass) secrete (4)

A

insulin*
C-peptide
proinsulin
amylin

35
Q

Amylin is co-secreted with ___ from the ___ cells as well

A

Amylin is co-secreted with insulin from the beta cell as well

36
Q

Delta cells of the pancreas (3-5% of islet mass) secrete

A

somatostatin

37
Q

Somatostatin causes

A

widespread inhibition of endocrine and exocrine functions of the pancreas, gallbladder, and gut

					- When somatostatin is released from the hypothalamus, it inhibits growth hormone and TSH
						- Inhibits LH, PTH, calcitonin, serotonin
38
Q

When released by the pancreatic delta cells, somatostatin functions to…

A

Regulate secretion from alpha and beta pancreatic cells to stop their secretory functions.

This inhibits the release of gastrin and histamine secretion from the G cells in the stomach to slow/stop digestion when the gastric pH is < 2

39
Q

G cells of the pancreas (1% of islet mass) secrete

A

gastrin

40
Q

F cells of the pancreas (1% of islet mass) secrete

A

pancreatic polypeptides that are used as a tumor marker to diagnose/monitor pancreatic endocrine tumors

41
Q

L cells of the intestines secrete

A

proglucagon (a glucagon-like peptide) that becomes a glucagon-like peptide “GLP” that is used for T2DM treatment

42
Q

7 steps to insulin secretion and how the beta cell acts as a glucose sensor

A

1) Increased blood glucose enters the beta cell
2) The beta cell metabolizes this glucose to create ATP
a) This causes a rise in the ratio of ATP : ADP
3) The increased ratio causes inactivation of the K+ channel
4) Depolarization of the cell membrane ensues and…
5) Ca2+ channels open and the cell is flooded with Ca2+
6) Intracellular Ca2+ levels increase
7) Increased Ca2+ levels lead to an exogenous release of insulin by the beta cell

43
Q

Describe the release of glucagon by the alpha-cell, and how it acts as a counter-regulatory glucose sensor.

A

In low glucose levels:

1) ATP levels fall in the alpha cell
2) K+ gated channels CLOSE
3) Cell membrane depolarizes
4) Ca2+ channels open and the cell is flooded with Ca2+
5) Cells exocytosis the stored glucagon granules to provide energy to the body

44
Q

Basal physiologic serum insulin levels

A

1) Even when fasting, insulin is secreted around the clock at low levels
a) Results in a low plasma insulin concentration

45
Q

Prandial physiologic serum insulin levels

A

ii. During a meal, there is a sudden increase in glucose that stimulates a surge of insulin 10+ times it’s basal level
1) This occurs in 3-5 minutes
2) Insulin levels start to decrease after about ten minutes
3) 15 - 20 minutes post prandial, if glucose levels continue to rise, insulin levels start to increase again parabolically

46
Q

What does insulin do in the body?

A

Insulin functions in fatty acid synthesis, protein synthesis, glycogen synthesis, cell growth and survival, and amino acid and electrolyte transport

47
Q

Insulin effects on the liver

A

i) Allows for storage of glucose as glycogen

ii) Excess glucose is converted into fatty acids

48
Q

Insulin effects on the muscle

A

i) Muscles cannot use glucose without insulin

ii) Insulin is necessary for entry of glucose into muscles

49
Q

Insulin effects on adipose tissue

A

Converts glucose to glycerol for use with triglycerides

50
Q

Effects of insulin deficiency on fatty acid metabolism

A

1) Adipose tissue lipase is activated and increases levels of free fatty acids in the plasma
a) These are used for cellular energy
b) Also functions to increase cholesterol and triglyceride synthesis in the liver
c) Excess free fatty acid breakdown
i) Leads to ketones and ketoacidosis

51
Q

Effects of insulin deficiency on protein metabolism

A

1) Protein synthesis stops, catabolism of proteins increases, and plasma amino acid levels increase
2) Excess AAs are burned for energy or used for gluconeogenesis
3) Urea levels increase in the urine
4) Muscle wasting, weakness, and organ dysfunction can follow

52
Q

A1C indications (2)

A

i. Dx tool for DM

ii. Monitor DM patients glycemic goals

Endocrinology (11 decks)

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