12. CPR Endocrinology Flashcards

1
Q

Where are the cell bodies of the neurons that release ADH? Where do they synapse?

A

Supraoptic nuclei of the hypothalamus then synapse in posterior pituitary

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2
Q

What are triggers for ADH secretion? What is it most sensitive to?

A

Low BP
Arterial stretch due to low blood volume
High osmolality (most sensitive)

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3
Q

What are the main effects of ADH?

A

Raise blood pressure and blood volume via vasoconstriction in blood vessels (V1) and/or increased absorption of water in the kidneys (V2)

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4
Q

What is ADH’s effect on the renal collecting ducts?

A

It binds to V2 receptors then is taken into principal cell. Leads to increased aquaporin-2 on apical surface.

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5
Q

What is another word for hyperosmolarity?

A

Dehydration

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6
Q

Describe central diabetes insipidus and its effects on ADH.

A

Lack of ADH (low plasma ADH). Could result from damage to pituitary and destruction of the hypothalamus. Can be treated with desmopressin (drug that prevents water excretion)

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7
Q

Describe nephrogenic diabetes insipidus and its effects on ADH

A

Kidneys unable to respond to ADH (high plasma ADH). Could result from kidney diseases and drugs like lithium.

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8
Q

What occurs during syndrome of inappropriate ADH secretion (SIADH)?

A

Excessive secretion of ADH. Excessive water retention. Hypoosmolality fails to inhibit ADH release.

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9
Q

What are triggers for aldosterone secretion?

A

Decreased Na+ or increased K+ in blood

Decreased blood volume and/or blood pressure

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10
Q

What is aldosterone’s effect on the renal collecting ducts?

A

It enters principal cells then binds to aldosterone receptor in cytosol. Leads to synthesis of new protein channels and pumps. Results in increased Na+ reabsorption and K+ secretion.

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11
Q

What is the heart’s role in renal NaCl excretion?

A

The atria release ANP when the atria are distended. The ventricles similarly release BNP when distended. Both ANP and BNP are natriuretic peptides that decrease total peripheral resistance and enhance urinary excretion of NaCl and water.

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12
Q

What is the natriuretic peptide released by the kidney? What does it do?

A

Urodilatin. It inhibits NaCl and water reabsorption across the medullary portion of the collecting duct.

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13
Q

What are the main effects of natriuretic peptides related to the control of renal NaCl excretion?

A

Inhibition of renin/aldosterone secretion
Inhibition of ADH secretion
Inhibition of NaCl reabsorption by the collecting duct

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14
Q

What is the role of sympathetics in renal NaCl excretion?

A

They stimulate the reabsorption of NaCl and water by the proximal tubule, thick ascending limb, distal tubule, and collecting duct.

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15
Q

What is the effect of insulin on K+ levels.

A

Insulin stimulates K+ uptake into cells by increasing activity of Na+/K+ ATPase

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16
Q

How does Ca2+ levels effect action potentials?

A

During hypocalcemia, the activation threshold is lower, resulting in increased membrane excitability. This leads to hyperreflexia. (positive Chvostek and Trousseau sign)

17
Q

How are the concentrations of phosphate and calcium related?

A

An increased in phosphate concentration will lead to a decrease in Ca2+ concentration and vice versa.

18
Q

How does acidemia effect Ca2+ concentration?

A

Free ionized Ca2+ goes up because less Ca2+ is bound to albumin

19
Q

How does alkalemia effect Ca2+ concentration?

A

Free ionized Ca2+ goes down because more Ca2+ is bound to albumin. Often accompanied by hypocalcemia.

20
Q

What stimulates PTH secretion?

A

Stimulated by low plasma Ca2+. Leads to increase in plasma Ca2+.

21
Q

What are the effects of PTH on the bones, kidneys, and intestines?

A

Bone: increased bone resorption

Kidney: increased Ca2+ reabsorption and urinary cAMP
decreased phosphate reabsorption

Intestine: increased Ca2+ absorption

22
Q

What is the main circulating (but low activity) form of vitamin D?

A

25-OH-cholecalciferol

23
Q

What is the active form of vitamin D? What enzyme activates it?

A

1,25-(OH)2-cholecalciferol

Activated by 1alpha-hydroxylase

24
Q

What occurs during familial hypocalciuric hypercalcemia (FHH)?

A

Autosomal dominant disorder. Mutation inactivates CaSR in parathyroid glands and parallel Ca2+ receptors in ascending limb of the kidney. This leads to less negative feedback on PTH, increasing blood Ca2+ levels and decreasing urine Ca2+ levels.