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Gen.Exam.Review > Ch5.Renal and Acid Base physiology > Flashcards

Ch5.Renal and Acid Base physiology Flashcards

1
Q

Total body water is approximately what percentage of body weight?

A

60%

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2
Q

Intracellular fluid is what percentage of total body water?

A

2/3

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3
Q

What are the major cations of ICF

A

K and Mg

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4
Q

What are the major anions of intracellular fluid?

A

protein and organic phosphates
(ATP, ADP, AMP)

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5
Q

extracellular fluid is what fraction of total body water?

A

1/3

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6
Q

What is the major cation of ECF?

A

Na

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7
Q

What are the major anions of ECF?

A

Cl and HCO3

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8
Q

Plasma is what fraction of ECF?

A

1/4
**1/12th of TBW

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9
Q

What are the major plasma proteins?

A

albumin and globulin

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10
Q

Interstitial fluid is what percentage of ECF?

A

3/4

**1/4 if TBW

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11
Q

What is the difference between interstitial fluid and plasma?

A

interstitial fluid has little protein
(it is an ultrafiltrate of plasma)

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12
Q

What is the 60-40-20 rule?

A

TBW is 60% of bwt
ICF is 40% of bwt
ECF is 20% of bwt

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13
Q

What percentage of the cardiac output is renal blood flow?

A

25%

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14
Q

What is the effect of the sympathetic nervous system and angiotensin II on the renal arterioles?

A

Vasoconstriction–> dec in RBF

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15
Q

angiotensin II at low concentrations preferentially constricts which arterioles of the kidney?

A

**constricts efferent arterioles
**protecting GFR

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16
Q

Angiotensin converting enzyme (ACE) inhibitors dilate which arterioles, for what mechanism?

A

–dilate efferent arterioles
– results in dec in GFR
(reduce hyperfiltration and the occurrence of diabetic nephropathy in diabetes mellitus)

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17
Q

Vasodilation of renal arterioles, leading to an increase in renal blood flow is mediated by what hormones/products?

A

prostaglandin E2 & I2
bradykinin
nitric oxide
dopamine

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18
Q

what is the effect of atrial natriuretic peptide (ANP) on the afferent arterioles of the kidney?

A

vasodilation of the afferent arterioles
**lesser extent vasoconstriction of efferent arterioles– INC RBF and GFR

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19
Q

What are the mechanisms for autoregulation of renal blood flow?

A
  1. myogenic mechanism– renal afferent arteriles contract in response to stretch
  2. Tubuloglomerular feedback– INC delivery of fluid to the macula densa– causes constriction of nearby afferent arteriole, increasing resistance to maintain constant blood flow
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20
Q

Where is Na-glucose cotransport performed in the kidney?

A

early proximal tubule

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21
Q

the proximal tubule reabsorbed what percentage of Na and H20?

A

reabsorbs 2/3rds (67%) of the filtere Na and H20

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22
Q

What part of the nephron is the site of glomerulotubular balance?

A

proximal tubule

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23
Q

What substances are reabsorbed at the proximal tubule?

A

Na, H20 with HCO3, glucose, amino acids, phosphate and lactate

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24
Q

In the early proximal tubule, Na is reabsorbed by cotransport with molecules?

A

-glucose, amino acids, phosphate and lactate

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25
Q

Na is reabsorbed by countertransport via what mechanism in the proximal tubule?

A

Na-H exchange
**which is linked directly to the reabsorption of filtered HCO3

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26
Q

What is the mechanism of carbonic anhydrase inhibitors?

A

diuretics that act in the early proximal tubule by inhibiting hte reabsorption of filtered HCO3
**acetazolamide

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27
Q

In the late proximal tubule, Na is reabsorbed with what ion?

A

Cl

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28
Q

which portion of the nephron is the target of loop diuretics? and what is the mechanism of action?

A

Thick ascending loop of Henle
–inhibit Na-K-2CL cotransporter

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29
Q

Which portion of the nephron is impermeable to water?

A

Thick ascending loop of henle
**diluting segment

and distal tubule

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30
Q

What is the site of action of thiazide diuretics?

A

distal tubule

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31
Q

How does the distal tube reabsorb Na?

A

Na-Cl cotransporter

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32
Q

What are the two specialized cell types of the late distal tubule and collecting duct?

A

Principle cells
alpha intercalated cells

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33
Q

What is the function of the principle cells of the distal tubule and collecting duct?

A

-reabsorb Na and H2O
-secrete K

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34
Q

What is the mechanism of action of aldosterone on principle cells of the distal tubule and collecting duct?

A

-increases Na reabsorption and increases K secretion

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35
Q

What is the mechanism of action of antidiuretic hormone on the principle cell?

A

increases H20 permeability
**directs the insertion of aquaporin 2 channels in the luminal membrane

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36
Q

What part of the nephron do K sparing diuretics work?

A

on the principle cells of the distal tubule and collecting duct
**to decrease K secretion

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37
Q

What is the function of alpha intercalated cells?

A

secrete H (sitmulated by aldosterone)
reabsorb K (by H-Katpase)

38
Q

What are causes of shifts of K out of cells causing hyperkalemia?

A

insulin deficiency
beta-adrenergic antagonists
acidosis (exchange of extraclelular H for intracellular K)
hyperosmolarity (H2O flows out of the cells; K diffuses out with H20)
inhibitors of Na-K pump (ie digitalis)
exercise
cell lysis

39
Q

What are causes of shifts of K into cells causing hypkalemia?

A

insulin
beta-adrenergic agonists
alkalosis (exchange of intracellular H for extracellular K)
hyposmolarity (H2O flow sinto the cells: K diffuses in with H2O)

40
Q

Which parts of the nephron are responsible for K regulation?

A

alpha-intercalated cells (reabsorption) and principle cells (secretion) of the distal tubule and collecting ductW

41
Q

How do alpha intercalated cells reabsorb potassium?

A

H,K-ATPase in the luminal membrane

42
Q

How do principle cells secrete potassium?

A

**variable
–depends on factors such as dietary K, aldosterone, acid-base status and urien flow rate

43
Q

Aldosterone has what effect on K at the kidneys?

A

increases K secretion

**mechanism: INC Na entry into the cells across teh l uminal membrane and increased pumping of Na out of the cells by teh Na-K atpase. Stim of the Na-K pump simultatenously increases K uptake into the principle cells, increasing the intracellular K conecntration & driving force for K secretion
**aldosterone also increases the number of luminal membrane K channels

44
Q

What are causes of increases distal K secretion?

A

hyperaldosteronism
High-K diet
alkalosis
Thiazide diuretics (increase urine flow rate)
loop diuretics (inc urine flow rate)
luminal anions (inc lumen negativity)

45
Q

What are causes of decreased distal K secretion?

A

Low-K diet
hypoaldosteronism
acidosis
K-sparing diuretics

46
Q

What acid base status decreases K secretion?

A

Acidosis
– blood contains H, H enters the cell across the basolateral membrane and K leaves the cell. Intracellular K ceoncnetration and driving force for K secretion decrease

47
Q

What is the acid base status that increases K secretion?

A

Alkalosis
–blood contains too little H, therefore H leaves the cell across the basolateral membrane and K enters the cells. The intracellular K concentation adn the driving force for K secretion increase

48
Q

How do loop and thiazide diuretics increase K secretion?

A

INC flow rate through the late distal tubule and collecting ducts that cause dilution fo the luminal K conecntration icnreases hte driving force ofr K secretion
*8Inc Na delivery to teh late distal tubule and collecting ducts

**these diuretics cause hypokalemia

49
Q

Spironolactone MOA

A

antagonists of aldosterone
–K-sparing diuretic

50
Q

What percentage of filtered urea is reabsorbed in the proximal tubule by simple diffusion?

A

50%

51
Q

What sections of the nephron are impermeable to urea?

A

distal tubule
cortical collecting ducts
outer medullary collecting ducts

52
Q

What hormone stimulates a facilitated diffusion transporter for urea in the inner medullary collecting ducts?

A

ADH

53
Q

Where is the highest reabsorption of phosphate occur within the nephron?

A

85% of filtered phosphate is reabsorbed in the PCT by Na-phospahte cotransport

54
Q

What hormone inhibits phosphate reabsorption?

A

parathyroid hormone
**activating cAMP, and inhibiting Na phosphate cotransport

55
Q

90% of the filtered calcium is reabsorbed in what segments of the nephron?

A

PCT and thick ascending limb

56
Q

What is the effect of loop diuretics on Ca reabsorption at the kidney?

A

cause increased urinary Ca excretion
**can treat hypercalcemia

57
Q

magnesium is reabsorbed in what segment of the nephron?

A

proximal tubule
thick ascending limb of the LOH and distal tubule

58
Q

In the thick ascending limb, Magnesium competes with what ion for reabsorption?

A

Ca
**hypercalcemia causes an increase in Mg excretion and vice versa

59
Q

What is the response of kidney to water deprivation?

A

water deprivation
-icnreases in plasma osmolarity
–stimulates osmorepcetors in the anterior hypothalamus
—increases secretion of ADH from posterior pituitary
—-increases water permeability of late distal tubule and collecting duct
—–increases water reabsorption
——iincreases urine osmolarity and decreases urine volume

–>decreases plasma osmolarity toward normal

60
Q

What are causes of hyposmotic urine?

A

low circulating ADH levels
– water intake, central diabetes insipidus
OR
ADH ineffective
–nephrogenic diabetes insipidus

61
Q

What is the stimulus for secretion of PTH?

A

decreases plasma Ca

62
Q

Wha tis the MOA of PTH at the kidney?

A

basolateral receptors adenylate cyclase (cAMP)–> urine
–dec phosphate reabsorption (early PCT)
–INC Ca reabsorption (distal tubule)
Stimulates alpha hydroxylase (proximal tubule)

63
Q

What is the stimulus for secretion of ADH?

A

inc plasma osmolarity
dec blood volume

64
Q

What is the MOA of ADH at the kidney?

A

basolateral V2 receptor
Adenylate cyclase cAMP
**increase H20 permeability (late distal tubule and collecting ducts of the principle cells)

65
Q

What is the stimulus for secretion of aldosterone?

A

decreased blood volume (RAAS)
INC plasma K

66
Q

What is the MOA of aldosterone at the kidney?

A

-INC Na reabsorption (ENaC, distal tubule principle cells)
-INC K secretion (distal tubule principle cells
-INC H secretion (distal tubule alpha intercalated cells)

67
Q

What is the stimulus for secretion of ANP?

A

increased atrial pressure

68
Q

What is the MOA of ANP at the kidney?

A

Guanylate cyclase cGMP
– INC GFR
–dec Na reabsorption

69
Q

What is the stimulus for secretion of angiotensin II?

A

decreased blood volume (via renin)What

70
Q

is the MOA of angiotensin II at hte kidney?

A

INC Na-H exchange and HCO3 reabsorption (proximal tubule)

71
Q

What is the enzyme that catalyzes the reversible reaction between CO2 and water?

A

carbonic anhydrase

72
Q

What is the major extracellular buffer?

A

HCO3

73
Q

What is the major intracellular buffers?

A

organic phosphates
proteins (hemoglobin)

74
Q

Reabsorption of the filtered HCO3 primarily occurs at what section of the nephron?

A

early proximal tubule

75
Q

What are causes of the metabolic acidosis?

A

ketoacidosis– accumulation of beta-OH-butyric acid and acetoacetic acid; INC anion gap

lactic acidosis: accumulation of lactic acid during hypoxia; INC anion gap

chronic renal failure: failure to excrete H and ammonia; INC anion gap

ethylene glycol intoxication: produces glycolic and oalic acids: INC anion gap

diarrhea: GI loss of HCO3; normal anion gap

RTA

76
Q

What are causes of metabolic alkalosis?

A

vomiting: loss of H, leaves Hco3 behind in blood; worsened by volume contraction, hypokalemia; +/- INC ketoacids

hyperaldosteronism: INC H secretion by distal tubule; increased new HCO3 reabsorption

loop or thiazide diuretics; volume contraction alkalosis

77
Q

What are causes of respiratory acidosis?

A

opiates; sedatives or anesthetics: inhibition of medullary respiratory center

airway obstruction: DEC CO2 exchangein lungs

COPD: dec CO2 exchange in lungs

78
Q

What are causes of respiratory alkalosis?

A

pneumonia, pulmonary embolus: hyoxemia causes iNC ventilation rate

high altitute: hypoxemia causes iNC ventilation rate

79
Q

What is the site of action of carbonic anhydrase inhibitors?

A

early proximal tubule

80
Q

What is the mechanism of carbonic anhydrase inhibitors (acetazolamide)?

A

inhibition of carbonic anhydrase

81
Q

What is the major effect of carbonic anhydrase inhibitors (acetazolamide)?

A

INC HCO3 excretion

82
Q

What is the site of action of loop diuretics (furosemide)?

A

thick ascending limb of the LOH

83
Q

What is the MOA of loop diuretics (furosemide)?

A

inhibition of Na-K-2Cl cotransport

84
Q

What are the major effects of loop diuretics (furosemide)?

A

INC NaCL excretion
INC K excretion (INC distal tubule flow rate)
INC Ca excertion
DEC bility to concentrate urine (dec corticpaillary gradient)
dec ability to dilute urine (inhibiton of diluting segment)

85
Q

What is the site of action of the thiazide diuretics (chlorothiazide and hydrochlorothiazide)?

A

early distal tubule (cortical diluting segment)

86
Q

What is the MOA of hiazide diuretics (chlorothiazide and hydrochlorothiazide)?

A

inhibition of Na-Cl cotransport

87
Q

What are the major effects of hiazide diuretics (chlorothiazide and hydrochlorothiazide)?

A

INC NaCL excretion
INC K excretion (INC distal tubule flow rate)
DEC Ca excretion (treatment of idiopathic hyerpcalciuria)
DEC ability to dilute urine (inhibition of cortical diluting segment
NO effect on ability to concentrate urine

88
Q

What is the site of action of K-sparing diuretics (spironolactone, amiloride, etc)?

A

late distal tubule and collecting duct

89
Q

What is the MOA of K-sparing diuretics (spironolactone, amiloride, etc)?

A

inhibition of Na reabsorption, K secretion and H secretion

90
Q

What are the major effects of K-sparing diuretics (spironolactone, amiloride, etc)?

A

INC Na excretion (small effect)
DEC K excretion (using a combination with loop or thiazide diuretics)
DEC H excretion

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