Mangiarua - Hormonal Regulation Flashcards

1
Q

What causes the release of renin from the granular cells in the juxtaglomerular apparatus ?

A

Decreased blood pressure,

Decreased extracellular volume

Decreased Na and Cl

Decreased Tubular fluid volume

Increased sympathetic stimulation

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2
Q

What is the end effect of renin ?

A

Increase blood pressure

Thru angiotensin -> aldosterone

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3
Q

Where is angiotensin converting enzyme located ?

A

In the lung

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4
Q

Half life of angiotensin II

A

1-3 minutes

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5
Q

How does sympathetic stimulation affect renin secretion?

A

Stimulates renin secretion by

Direct effect to beta-1 adrenergic receptors

Also decreased flow in macula densa

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6
Q

The major renal prostaglandin ?

A

PGE2

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7
Q

Where are kidney prostaglandins synthesized ?

A

Medullary and cortical collecting tubules (main location)

Glomerular and vascular endothelium

Renomedullary cells

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8
Q

What increases the synthesis of renal prostaglandins ?

A

Vasoconstrictors (angiotensin II, ADH, norepinephrine)

Prostaglandins are local vasodilators, so. They work to counter these

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9
Q

What does the infusion of PGE2 or I2 result in ?

A

Natriuresis and diuresis

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10
Q

Where is ADH formed ?

A

Supraoptic and paraventricular nuclei of the hypothalamus

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11
Q

ADH is rapidly metabolized by the liver and kidneys . What is its half life ?

A

15-20 minutes

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12
Q

What happens when ADH stimulates V2 receptors ?

A

V2 receptors *in principal cells). Cause an increase in water reabsorption

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13
Q

What happens when ADH stimulates V1 receptors.

A

There is a renal and systemic vasoconstriction

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14
Q

Disorder characterized by insatiable thirst and by excretion of large amounts of diluted urine as much as 25 L/day

A

Diabetes insipidus

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15
Q

Type of diabetes insipidus characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in kidney

A

Nephrogenic diabetes insipidus

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16
Q

Diabetes insipidus caused by decreased secretion of ADH

A

Central diabetes insipidusq

17
Q

What can cause the release of aldosterone ?

A

Primary regulation; increased angiotensin II

Increased plasma potassium (this is very sensitive)

Increased level of ACTH

18
Q

Aldosterone will be released in response to a(n) _________ in plasma potassium

A

Increase

19
Q

Aldosterone increases Na and Cl reabsorption and increases K+ and H+ secretion by promoting protein synthesis for what transporters where?

A

Na aand K channels in the luminal side

Na-K-ATPase enzymes in the basolateral border

20
Q

Explain aldosterone escape

A

Prolonged treatment w/ mineralcorticoids/aldosterone results in brief period of salt retention, that only lasts a few days

Effect on K excretion is sustained thru/o treatment period

Escape due to rise in ECF volume which effectively decreases Na reabsorption in proximal tubule

21
Q

Half life of atrial natriuretic peptide?

A

2-4minutes

22
Q

What causes the release of atrial natriuretic peptide ?

A

Hypervolemic states causing atrial stretch

23
Q

What are the renal effects of atrial natriuretic peptide?

A

Inhibit Na reabsorption in the proximal tubule and cortical and medullary collecting ducts

Inhibit ADH dependent water reabsorption

Hyperfiltration - vasodilation of preglomerular arteries (increase GFR and FF)

Inhibit renin releases which decreases angiotensin II formation

24
Q

What are the extrarenal effects of atrial natriuretic peptide ?

A
  1. Vasorelaxation
  2. Centrally stop the release of ADH (vasopressin)
  3. Inhibit aldosterone biosynthesis in the adrenal gland
25
Q

Production of the active form of vitamin D is stimulated by release of parathyroid hormone due to a fall in calcium and by hypophosphatemia

What is the action of this mature vitamin D/

A

Increase intestinal absorption of Calcium and phosphate

Decrease release of PTH

Increase bone resorption

Increase calcium reabsorption in the kidney