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T1 - Phase 1 - Integrated (II) > Pulm/Renal - Physiology - Renal Hormones; Hypertension; Acid-Base Balance > Flashcards

Pulm/Renal - Physiology - Renal Hormones; Hypertension; Acid-Base Balance Flashcards

1
Q

What is the major mediator of the effects of the renin-angiotensin system?

A

Angiotensin II

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2
Q

Besides the pulmonary circulation, where is another location where ACE is located?

A

The basolateral surface of renal cells

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3
Q

True/False.

Most angiotensinogen is produced by the PCT, but some is also produced in the liver.

A

False.

Most angiotensinogen is produced by the liver, but some is also produced in the PCT.

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4
Q

Angiotensin II primarily acts on ___ receptors.

AT2 receptors are primarily involved in:

A

AT1;

renal development

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5
Q

True/False.

A fraction of bodily angiotensin II can be produced completely within the kidney without any hepatic or pulmonary or circulatory involvement.

A

True.

Some angiotensinogen is produced in the renal interstitium, and ACE can be found on the basolateral epithelial surface.

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6
Q

What cell type produces renin?

A

Juxtaglomerular cells

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7
Q

What is the rate-limiting factor of the renin-angiotensin system?

A

Renin production

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8
Q
A

A.

B.

C.

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9
Q

Name the four major activating mechanisms for renin secretion.

A

(First row)

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10
Q

Name the three mechanisms for increasing renin secretion.

A

(Second row)

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11
Q

What happens in the juxtaglomerular cells for renin to be secreted?

A

(Third row)

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12
Q
A

A.

B.

C.

D.

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14
Q
A

C.

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18
Q
A

C.

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19
Q

True/False.

Angiotensin II has many diverse actions.

A

True.

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21
Q

What renal mechanism senses increased renal arteriolar stretch?

What is the result?

A

Baroreceptors in juxtaglomerulus (calcium channels opened);

inhibition of renin release

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23
Q

What effect does increased sympathetic tone have on juxtaglomerular cells?

A

β1 activation –> cAMP –> increased renin secretion

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24
Q

What effect does an increase in NaCl delivery to the macula densa have on the juxtaglomerular cells?

Why?

A

Decreased renin secretion;

the JG cells interpret this as increased ECF

(maybe mediated via PGE2)

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25
Q
A

A.

B.

C.

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26
Q

What effect does a decrease in NaCl delivery to the macula densa have on the juxtaglomerular cells?

Why?

A

Increased renin secretion;

the JG cells interpret this as decreased ECF

(maybe mediated via PGE2)

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29
Q

Name the major functions of angiotensin II in the following systems: renal, adrenal, blood vessels, heart, intestines, CNS, PNS.

A
  1. Renal: Reduce RBF, increase NaCl reabsorption
  2. Adrenal: Aldosterone release
  3. BV: Vasoconstriction
  4. Heart: Cardiac contractility
  5. Intestine: NaCl + H2O reabsorption
  6. CNS: Thirst, salt appetite, ADH release
  7. PNS: Sympathetic activity
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30
Q

What effect (if any) does angiotensin II have on the renal arterioles?

What effect (if any) does angiotensin II have on the Kf?

A

Efferent arteriole constriction (with no change in GFR);

it decreases it (mesangial contraction)

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31
Q

What parts of the nephron are stimulated to reabsorb NaCl by angiotensin II?

A

The PCT and DCT

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32
Q

What overall effect does angiotensin II have on the GFR?

How?

A

It maintains it;

efferent arteriole constriction

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33
Q

True/False.

Increases in Na+ retention via aldosterone will also result in an increase in K+ loss.

A

True.

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34
Q
A

A.

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35
Q
A

C.

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37
Q
A

A.

B.

C.

D.

E.

38
Q

What are the major prostaglandins produced in the kidney?

A

PGE2

PGI2 (prostacyclin)

Thromboxane A2

39
Q

What are the major vasodilating prostaglandins produced by the kidney?

What do they dilate?

A

PGI2 (prostacyclin), PGE2;

both the afferent and efferent arterioles

40
Q

What effect do renal prostaglandins have on GFR?

Which arterioles do they affect? How?

How do they affect NaCl reabsorption?

A

Virtually no effect;

both afferent and efferent, dilation;

decreased

41
Q

When are renal prostaglandins produced?

Why?

A

When ECF and MAP are decreased;

to counteract angiotensin II, norepinephrine, ADH, etc.

42
Q

What hormone(s) promote(s) renal arteriolar dilation? Which arterioles?

What hormone(s) promote(s) renal arteriolar constriction? Which arterioles?

A

PGE2, PGI2, bradykinin,

afferent and efferent;

angiotensin II,

efferent

43
Q

Along with prostaglandin production, renal __________ helps counteract angiotensin II.

A

Bradykinin

44
Q

___________ digests high-molecular weight ____________ to produce bradykinin.

A

Kallikrein;

kininogen

45
Q

Where is renal kallikrein found?

A

The renal collecting tubule (late DCT)

48
Q

How does bradykinin exert an effect on the kidney?

A

By binding B2 receptors –> increase NO, PGE2, and PGI2 secretion

49
Q

What is a normal blood pressure?

What is an elevated blood pressure?

A

<120 / <80 mmHg

120 - 129 / <80 mmHg

50
Q

What is hypertension stage I?

What is hypertension stage II?

A

130-139 mmHg SBP OR 80-89 mmHg DBP

≥ 140 mmHg SBP OR ≥ 90 mmHg DBP

51
Q

What BP defines a hypertensive crisis?

A

≥ 180 mmHg SBP OR ≥ 120 mmHg DBP

52
Q

True/False.

Hypertension can cause (among other effects): stroke, heart attack, retinopathy, peripheral vascular disease, renal failure, left ventricular hypertrophy, congestive heart failure, etc.

53
Q

What is malignant hypertension?

A

≥ 200 mmHg SBP and ≥ 100 mmHg DBP

54
Q

True/False.

Excess salt intake is often accompanied by little-to-no elevation in plasma sodium levels.

55
Q

True/False.

Many monogenetic causes of hypertension have been identified in the kidneys.

56
Q

True/False.

Sodium excretion has little to do with hypertension reduction in sodium-replete states.

57
Q

True/False.

Loss of alkali can occur via the kidneys and GI tract.

58
Q

Loss of ______ (pH) substances often occurs due to diarrhea.

Loss of ______ (pH) substances often occurs due to vomiting or nasogastric tube usage.

A

Alkaline;

acidic

59
Q

What is the principal mechanism for renal acid buffering?

A

Phosphate secretion

(Net acid excretion = titratable acid + NH4+ - HCO3-)

60
Q

True/False.

Daily renal pH excretion is typically about 70 mEqv of base.

A

False.

Daily renal pH excretion is typically about 70 mEqv of acid.

(And a resultant 70 mEqv of carbonic acid created to buffer/replace it)

61
Q

Upon carbonic anhydrase creation of bicarbonate in the PCT cells, what happens to the bicarbonate next?

A

Basolateral co-transport of 3 HCO3- to every 1 Na+;

also, HCO3-/Cl- exchangers

62
Q

How does acetazolamide affect the kidneys?

A

Increased HCO3- excretion via blockage of lumen carbonic anhydrase

63
Q

What effect do angiotensin II, glucocorticoids, and endothelin have on HCO3- renal reabsorption?

A

All increase reabsorption

64
Q

In the collecting tubule and duct, type A intercalated cells do what?

In the collecting tubule and duct, type B intercalated cells do what?

A

Secrete H+, reabsorb HCO3-;

secrete HCO3-

65
Q

True/False.

H+ secretion in the nephron can be through H+/K+ exchange, H+/Na+ exchange, and H+ ATPases.

66
Q

What is the major acid of urine excretion?

What is the major buffer of urine excretion?

A

NH4+;

PO3-

67
Q

True/False.

Excretion of NH4+ corresponds exactly with creation of HCO3-.

A

True.

Both are made from glutamine.

68
Q

True/False.

Very small increases in plasma K+ can be deadly.

69
Q

If a person ingests their daily quantity of potassium in just a few minutes (~100 mEq/day), are they at risk for cardiac complications?

A

No, this ingested K+ is quickly moved to the intracellular fluid

70
Q

What is the initial defense against hyperkalemia?

A

Uptake into cells

(often via insulin, osmolality, β-adrenergic effects)

71
Q

What cell type in the nephron is responsible for K+ secretion?

A

Collecting tubule cells / principal cells

72
Q

What are some easy methods by which you can check for ECF volume depletion in a patient?

A

Tachycardia;

hypotension (may be orthostatic);

skin turgor (variable);

dry mucus membranes (variable)

73
Q

Total body __ determines ECF volume.

74
Q

A patient that has been vomiting presents with a HCO3- of 35 and a K+ of 3.0.

What explains this finding? Why don’t they just urinate out the excess bicarbonate?

How do you treat them?

A

The ECF volume is depleted (regulatory mechanisms are reabsorbing all the Na+, H2O, and HCO3-; Na+ can be in exchange for K+ and H+);

IV saline (correct the ECF depletion and the alkalosis will resolve itself)

75
Q

What effect does Conn’s syndrome usually have on Na+ levels?

What effect does Conn’s syndrome usually have on pH levels?

What effect does Conn’s syndrome usually have on K+ levels?

A

Not much;

alkalemia;

decrease

76
Q

What happens when plasma Na+ levels rise?

A

ADH is released to increase H2O reabsorption

(diluting the Na+ and maintaining osmolality)

77
Q

How would an ADH-secreting small cell carcinoma of the lung present on laboratory findings?

A

Low osmolality;

normal BP;

lowered plasma Na+

78
Q

Do relatively small changes in blood volume affect ADH secretion?

79
Q

What are the three ionic main effects of aldosterone?

A

Na+ reabsorption

K+ secretion

H+ secretion

T1 - Phase 1 - Integrated (II) (23 decks)

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