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

Question 1

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

Answer 1

Angiotensin II

Question 2

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

Answer 2

The basolateral surface of renal cells

Question 3

True/False.

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

Answer 3

False.

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

Question 4

Angiotensin II primarily acts on ___ receptors.

AT2 receptors are primarily involved in:

Answer 4

AT1;

renal development

Question 5

True/False.

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

Answer 5

True.

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

Question 6

What cell type produces renin?

Answer 6

Juxtaglomerular cells

Question 7

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

Answer 7

Renin production

Question 8

Answer 8

A.

B.

C.

Question 9

Name the four major activating mechanisms for renin secretion.

Answer 9

(First row)

Question 10

Name the three mechanisms for increasing renin secretion.

Answer 10

(Second row)

Question 11

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

Answer 11

(Third row)

Question 12

Answer 12

A.

B.

C.

D.

Question 14

Answer 14

C.

Question 18

Answer 18

C.

Question 19

True/False.

Angiotensin II has many diverse actions.

Answer 19

True.

Question 21

What renal mechanism senses increased renal arteriolar stretch?

What is the result?

Answer 21

Baroreceptors in juxtaglomerulus (calcium channels opened);

inhibition of renin release

Question 23

What effect does increased sympathetic tone have on juxtaglomerular cells?

Answer 23

β₁ activation –> cAMP –> increased renin secretion

Question 24

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

Why?

Answer 24

Decreased renin secretion;

the JG cells interpret this as increased ECF

(maybe mediated via PGE₂)

Question 25

Answer 25

A.

B.

C.

Question 26

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

Why?

Answer 26

Increased renin secretion;

the JG cells interpret this as decreased ECF

(maybe mediated via PGE₂)

Question 29

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

Answer 29

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

Question 30

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

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

Answer 30

Efferent arteriole constriction (with no change in GFR);

it decreases it (mesangial contraction)

Question 31

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

Answer 31

The PCT and DCT

Question 32

What overall effect does angiotensin II have on the GFR?

How?

Answer 32

It maintains it;

efferent arteriole constriction

Question 33

**True/False**. Increases in Na⁺ retention via aldosterone will also result in an increase in K⁺ loss.

Answer 33

True.

Question 34

Answer 34

A.

Question 35

Answer 35

C.

Question 37

Answer 37

A. B. C. D. E.

Question 38

What are the major prostaglandins produced in the kidney?

Answer 38

PGE₂ PGI₂ (prostacyclin) Thromboxane A₂

Question 39

What are the major vasodilating prostaglandins produced by the kidney? What do they dilate?

Answer 39

PGI₂ (prostacyclin), PGE₂; **both** the afferent and efferent arterioles

Question 40

What effect do renal prostaglandins have on GFR? Which arterioles do they affect? How? How do they affect NaCl reabsorption?

Answer 40

Virtually no effect; both afferent and efferent, dilation; decreased

Question 41

When are renal prostaglandins produced? Why?

Answer 41

When ECF and MAP are decreased; to **counteract** angiotensin II, norepinephrine, ADH, etc.

Question 42

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

Answer 42

PGE₂, PGI₂, bradykinin, afferent and efferent; angiotensin II, efferent

Question 43

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

Answer 43

Bradykinin

Question 44

\_\_\_\_\_\_\_\_\_\_\_ digests high-molecular weight ____________ to produce bradykinin.

Answer 44

Kallikrein; kininogen

Question 45

Where is renal kallikrein found?

Answer 45

The renal collecting tubule (late DCT)

Question 48

How does bradykinin exert an effect on the kidney?

Answer 48

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

Question 49

What is a normal blood pressure? What is an elevated blood pressure?

Answer 49

\<120 / \<80 mmHg 120 - 129 / \<80 mmHg

Question 50

What is hypertension stage I? What is hypertension stage II?

Answer 50

**130-139** mmHg SBP OR **80-89** mmHg DBP **≥ 140** mmHg SBP OR **≥ 90** mmHg DBP

Question 51

What BP defines a hypertensive crisis?

Answer 51

≥ 180 mmHg SBP OR ≥ 120 mmHg DBP

Question 52

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

Answer 52

True.

Question 53

What is malignant hypertension?

Answer 53

≥ 200 mmHg SBP and ≥ 100 mmHg DBP

Question 54

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

Answer 54

True.

Question 55

**True/False**. Many monogenetic causes of hypertension have been identified in the kidneys.

Answer 55

True.

Question 56

**True/False**. Sodium excretion has little to do with hypertension reduction in sodium-replete states.

Answer 56

False.

Question 57

**True/False**. Loss of alkali can occur via the kidneys and GI tract.

Answer 57

**True**.

Question 58

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

Answer 58

Alkaline; acidic

Question 59

What is the principal mechanism for renal acid buffering?

Answer 59

Phosphate secretion *(Net acid excretion = titratable acid + NH₄⁺ - HCO₃^-)*

Question 60

**True/False**. Daily renal pH excretion is typically about 70 mEqv of base.

Answer 60

**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)*

Question 61

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

Answer 61

Basolateral co-transport of 3 HCO₃^- to every 1 Na⁺; also, HCO₃^-/Cl^- exchangers

Question 62

How does acetazolamide affect the kidneys?

Answer 62

**Increased HCO₃^- excretion** via blockage of lumen carbonic anhydrase

Question 63

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

Answer 63

All increase reabsorption

Question 64

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

Answer 64

Secrete H⁺, reabsorb HCO₃^-; secrete HCO₃^-

Question 65

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

Answer 65

True.

Question 66

What is the major acid of urine excretion? What is the major buffer of urine excretion?

Answer 66

NH₄⁺; PO₃^-

Question 67

**True/False**. Excretion of NH₄⁺ corresponds exactly with creation of HCO₃^-.

Answer 67

**True**. Both are made from glutamine.

Question 68

**True/False**. Very small increases in plasma K⁺ can be deadly.

Answer 68

**True**.

Question 69

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

Answer 69

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

Question 70

What is the initial defense against hyperkalemia?

Answer 70

Uptake into cells (often via insulin, osmolality, β-adrenergic effects)

Question 71

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

Answer 71

Collecting tubule cells / principal cells

Question 72

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

Answer 72

Tachycardia; hypotension (may be orthostatic); skin turgor (variable); dry mucus membranes (variable)

Question 73

Total body __ determines ECF volume.

Answer 73

Na⁺

Question 74

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?

Answer 74

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)

Question 75

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?

Answer 75

Not much; alkalemia; decrease

Question 76

What happens when plasma Na⁺ levels rise?

Answer 76

ADH is released to increase H₂O reabsorption ## Footnote *(diluting the Na⁺ and maintaining osmolality)*

Question 77

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

Answer 77

Low osmolality; normal BP; lowered plasma Na⁺

Question 78

Do relatively small changes in blood volume affect ADH secretion?

Answer 78

No.

Question 79

What are the three ionic main effects of aldosterone?

Answer 79

Na⁺ reabsorption K⁺ secretion H⁺ secretion