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Year 1: 09. CPR Exam 2 > Lecture 11: Endocrinology > Flashcards

Lecture 11: Endocrinology Flashcards

1
Q

Where is ADH made?

A

Supraoptic nucleus of the hypothalamus

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2
Q

What triggers ADH secretion?

A

Low blood pressure
Low blood volume
High osmolality
Dehydration

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3
Q

Where is low blood pressure sensed?

A

Cardiac and aortic baroreceptors

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4
Q

Where is low blood volume sensed?

A

Atrial stretch receptors

-less stretch can trigger

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5
Q

Where is high osmolality sensed?

A

Hypothalamic osmoreceptors

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6
Q

What is the secretion of ADH most sensitive to?

A

Plasma osmolality changes

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7
Q

How does ADH affect blood vessels?

What receptors recognize ADH?

A

Vasoconstriction –> increases blood pressure and volume

-V1 receptors

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8
Q

How does ADH affect kidneys?

What receptors recognize ADH?

A

Increases absorption of water –> increases blood pressure and volume
-V2 receptors

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9
Q

How does ADH work?

A

1) ADH is recognized by V2 receptors on basolateral side principal cells on DCT or collecting duct
2) Aquaporin 2 channels are placed on apical membrane to reabsorb water
3) Water enters blood via aquaporin 3 channels on basolateral side

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10
Q

What happens to a person who is dehydrated?

A

1) Hypothalamus releases ADH to reabsorb water.

2) Urine becomes more concentrated

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11
Q

What happens to a person who is over-hydrated?

A

1) ADH is released less

2) Kidneys remove more water

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12
Q

What is diabetes insipidus?

A

No effect of ADH on renal collecting duct

-frequent urination and thirst

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13
Q

What is the difference between central and nephrogenic diabetes insipidus?

A

Central: damage to pituitary gland and cannot release ADH
Nephrogenic: ADH released normally but kidneys cannot respond to ADH

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14
Q

How does administration of exogenous vasopressin differentiate central and nephrogenic diabetes insipidus?

A

Central: Urine osmolarity will increase since ADH is working properly on kidneys
Nephrogenic: Urine osmolarity stays the same because kidneys do not respond to any forms of ADH

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15
Q

Describe SIADH (Syndrome of inappropriate ADH secretion).

A

Excessive secretion of ADH –> increased water retention

  • hyperosmolarity of urine is increased
  • ADH still not inhibited
  • can be caused by small cell lung carcinoma or issue with posterior pituitary
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16
Q

Where is aldosterone made?

A

Adrenal cortex

17
Q

What is aldosterone released in response to?

A

Low sodium levels or increased potassium levels

Low blood pressure

18
Q

How does aldosterone work?

A

1) Aldosterone is recognized by cytoplasmic receptors on principal cells at DCT or collecting duct
2) New protein pumps are secreted on apical side to secrete potassium and increase sodium intake
3) On the basolateral side, Na+/K+ ATPase pumps pushes sodium into the blood

19
Q

What does angiotensin II promote?

A

Increased sodium reabsorption
Increased ECF volume
Increased thirst
Increased TPR

20
Q

Describe primary adrenal insufficiency.

A

Both cortisol and aldosterone secretion is low

-does not respond properly to ACTH or renin

21
Q

Describe secondary adrenal insufficiency.

A

Cortisol production is low but angiotensin-aldosterone axis still exists

22
Q

ANP and BNP respond to ____ blood pressure.

A

High blood pressure

23
Q

Where is ANP found?

A

Myocytes of atria

24
Q

How does ANP work?

A

Increases excretion of NaCl and water by kidneys

-reduces BP

25
Q

How does BNP work?

A

Reduces reabsorption of NaCl and water in collecting duct

26
Q

What does urodilatin do?

A

Inhibits NaCl and water reabsorption in medullary portion of collecting duct to decrease blood pressure

27
Q

Natriuretic peptides induce _____ of afferent arterioles and _____ of efferent arterioles of the glomerulus.

A

Natriuretic peptides induce vasodilation of afferent arterioles and vasoconstriction of efferent arterioles of the glomerulus.

28
Q

How does the body respond to increased sodium intake?

A

Decreased sympathetic activity and RAAS
Increased ANP
Decreased oncotic pressure of capillaries

29
Q

What are causes of hyperkalemia?

A 
Insulin Deficiency
 β2-adrenergic antagonists
α-adrenergic agonists
Acidosis
Hyperosmolarity
Cell lysis
Exercise
30
Q

What are causes of hypokalemia?

A 
Insulin
B2-adrenergic agonists
α-adrenergic antagonists
Alkalosis
Hyposmolarity
31
Q

How does insulin affect potassium levels?

A

Insulin stimulates potassium uptake

-prevents hyperkalemia

32
Q

How does 17α-hydroxylase deficiency affect potassium levels?

A

Decrease potassium levels

33
Q

How does 21β-hydroxylase deficiency affect potassium levels?

A

Increase potassium levels

34
Q

How does 11β-hydroxylase deficiency affect potassium levels?

A

Decrease potassium levels

Year 1: 09. CPR Exam 2 (24 decks)

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