Ch20 Flashcards

1
Q

What is diuresis?

A

Urination

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2
Q

What is nocturnal enuresis indicative of?

A

Insufficient ADH

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3
Q

What part of the nephron does ADH act on?

A

Collecting duct

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4
Q

In the absence of ADH is urine dilute or concentrated?

A

Dilute

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5
Q

How does vasopressin elicit a response?

A

Binds to membrane receptor on basolateral side of collecting duct epithelium. Receptor activates cAMP second messenger system and AQP2 is inserted into apical membrane

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6
Q

Does increasing plasma OsM induce or inhibit ADH secretion?

A

Induce

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7
Q

What ion transporter is in the ascending loop of Henle?

A

NKCC
Transports Na+, K+, 2Cl-

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8
Q

What is the primary action of aldosterone?

A

Renal sodium reabsorption

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9
Q

How does aldosterone elicit a response? In what cell type?

A

After binding to the intracellular receptor in the P cell, new protein channels and pumps are made and inserted into the membrane. On the apical side these channels and pumps reabsorb Na+ and secrete K+. On the basolateral side new Na+,K+ ATPases push Na+ into the blood and pull K+ from the blood.

On existing channels and pumps aldosterone increases efficiency

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10
Q

What 3 stimuli regulate aldosterone release? Which is the primary?

A
  1. Hyperkalemia stimulate aldosterone secretion
  2. Increased osmolarity inhibits aldosterone secretion
  3. Tropic effect of ANG II (primary control)
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11
Q

Where is angiotensinogen produced? What stimulates it?

A

Made in the liver

No stimulus needed, constitutively produces

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12
Q

What enzyme converts angiotensinogen into ANG I? Where is it made and what stimulates it?

A

Low BP stimulates the JG cells to make the enzyme renin

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13
Q

What converts ANG I into ANG II? Where is it made?

A

ACE (angiotensin converting enzyme) is made by the endothelium in the lungs

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14
Q

What is the effect of ANG II on the arterioles?

A

Vasoconstriction

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15
Q

What is the effect of ANG II on the CVCC?

A

Increased cardiac response (higher CO)

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16
Q

What is the effect of ANG II on the hypothalamus?

A

Release of vasopressin

Increase in thirst

17
Q

What is the effect of ANG II on the adrenal cortex?

A

Release of aldosterone to increase Na+ resorption (and hence water resorption)

18
Q

What cardiac hormone is antagonistic to the RAAS pathway?

A

Atrial natriuretic peptide (ANP)

19
Q

What stimulates ANP secretion and from where?

A

Stretch receptors in the atria when BP is too high

20
Q

What does ANP do and how?

A

It lowers BP by
1. Increasing GFR by making more available surface area for filtration (idk how)
2. Decreases NaCl and water reabsorption in the collecting duct
3. ANP inhibits renin, aldosterone, and ADH release
4. Stimulates parasympathetic system

Net result is increase naturesis and diuresis

21
Q

Does acidosis result in neuron hyperexcitability or hypoexcitability? Alkalosis?

A

Acidosis: Hypoexcitability
Alkalosis: hyperexcitability

22
Q

What is the first line of defense against pH changes?

A

Buffers (HCO3-)

23
Q

What 2 ways is HCO3- reabsorption regulated in the proximal tubule?

A
  1. H+ is combined with HCO3- in the lumen, forming CO2 that diffuses into the epithelial cell. The CO2 is again separated into H+ and HCO3-. The luminal Na+ and cellular H+ are exchanged. The ceullar Na+ and cellular HCO3- are both delivered to the blood.
  2. Glutamine is metabolized in the epithelium into NH4+ and aKG. The NH4+ is exchanged for luminal Na+. The cellular HCO3- gradient is used to pump HCO3- and Na+ into the blood
24
Q

What cell type functions in resolving acidosis?

25
What cell type functions to resolve alkalosis?
Type B
26
How is acidosis regulated in the kidney? What secondary condition can result?
As HCO3- acts as a buffer the resulting CO2 diffuses into the type A epithelial cell. The CO2 is again separated and the cellular H+ is exchanged for luminal K+, but also just pumped out with an ATPase. The cellular HCO3- is pumped out with the chloride shift and the cellular K+ just leaks into the plasma. Hyperkalemia can result
27
How is alkalosis regulated in the kidney? What secondary condition can result?
CA in the ype B epithelium makes excess HCO2- and H+. The cellular HCO3- is exchanged for luminal Cl- in the chloride shift. Cellular H+ is exchanged for plasmic K+, but also just pumped out with an ATPase. The cellular K+ leaks into the lumen. This can result in Hypokalemia