Ch5.Renal and Acid Base physiology Flashcards

(90 cards)

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
Na is reabsorbed by countertransport via what mechanism in the proximal tubule?
Na-H exchange **which is linked directly to the reabsorption of filtered HCO3
26
What is the mechanism of carbonic anhydrase inhibitors?
diuretics that act in the early proximal tubule by inhibiting hte reabsorption of filtered HCO3 **acetazolamide
27
In the late proximal tubule, Na is reabsorbed with what ion?
Cl
28
which portion of the nephron is the target of loop diuretics? and what is the mechanism of action?
Thick ascending loop of Henle --inhibit Na-K-2CL cotransporter
29
Which portion of the nephron is impermeable to water?
Thick ascending loop of henle **diluting segment and distal tubule
30
What is the site of action of thiazide diuretics?
distal tubule
31
How does the distal tube reabsorb Na?
Na-Cl cotransporter
32
What are the two specialized cell types of the late distal tubule and collecting duct?
Principle cells alpha intercalated cells
33
What is the function of the principle cells of the distal tubule and collecting duct?
-reabsorb Na and H2O -secrete K
34
What is the mechanism of action of aldosterone on principle cells of the distal tubule and collecting duct?
-increases Na reabsorption and increases K secretion
35
What is the mechanism of action of antidiuretic hormone on the principle cell?
increases H20 permeability **directs the insertion of aquaporin 2 channels in the luminal membrane
36
What part of the nephron do K sparing diuretics work?
on the principle cells of the distal tubule and collecting duct **to decrease K secretion
37
What is the function of alpha intercalated cells?
secrete H (sitmulated by aldosterone) reabsorb K (by H-Katpase)
38
What are causes of shifts of K out of cells causing hyperkalemia?
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
What are causes of shifts of K into cells causing hypkalemia?
insulin beta-adrenergic agonists alkalosis (exchange of intracellular H for extracellular K) hyposmolarity (H2O flow sinto the cells: K diffuses in with H2O)
40
Which parts of the nephron are responsible for K regulation?
alpha-intercalated cells (reabsorption) and principle cells (secretion) of the distal tubule and collecting ductW
41
How do alpha intercalated cells reabsorb potassium?
H,K-ATPase in the luminal membrane
42
How do principle cells secrete potassium?
**variable --depends on factors such as dietary K, aldosterone, acid-base status and urien flow rate
43
Aldosterone has what effect on K at the kidneys?
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
What are causes of increases distal K secretion?
hyperaldosteronism High-K diet alkalosis Thiazide diuretics (increase urine flow rate) loop diuretics (inc urine flow rate) luminal anions (inc lumen negativity)
45
What are causes of decreased distal K secretion?
Low-K diet hypoaldosteronism acidosis K-sparing diuretics
46
What acid base status decreases K secretion?
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
What is the acid base status that increases K secretion?
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
How do loop and thiazide diuretics increase K secretion?
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
Spironolactone MOA
antagonists of aldosterone --K-sparing diuretic
50
What percentage of filtered urea is reabsorbed in the proximal tubule by simple diffusion?
50%
51
What sections of the nephron are impermeable to urea?
distal tubule cortical collecting ducts outer medullary collecting ducts
52
What hormone stimulates a facilitated diffusion transporter for urea in the inner medullary collecting ducts?
ADH
53
Where is the highest reabsorption of phosphate occur within the nephron?
85% of filtered phosphate is reabsorbed in the PCT by Na-phospahte cotransport
54
What hormone inhibits phosphate reabsorption?
parathyroid hormone **activating cAMP, and inhibiting Na phosphate cotransport
55
90% of the filtered calcium is reabsorbed in what segments of the nephron?
PCT and thick ascending limb
56
What is the effect of loop diuretics on Ca reabsorption at the kidney?
cause increased urinary Ca excretion **can treat hypercalcemia
57
magnesium is reabsorbed in what segment of the nephron?
proximal tubule thick ascending limb of the LOH and distal tubule
58
In the thick ascending limb, Magnesium competes with what ion for reabsorption?
Ca **hypercalcemia causes an increase in Mg excretion and vice versa
59
What is the response of kidney to water deprivation?
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
What are causes of hyposmotic urine?
low circulating ADH levels -- water intake, central diabetes insipidus OR ADH ineffective --nephrogenic diabetes insipidus
61
What is the stimulus for secretion of PTH?
decreases plasma Ca
62
Wha tis the MOA of PTH at the kidney?
basolateral receptors adenylate cyclase (cAMP)--> urine --dec phosphate reabsorption (early PCT) --INC Ca reabsorption (distal tubule) Stimulates alpha hydroxylase (proximal tubule)
63
What is the stimulus for secretion of ADH?
inc plasma osmolarity dec blood volume
64
What is the MOA of ADH at the kidney?
basolateral V2 receptor Adenylate cyclase cAMP **increase H20 permeability (late distal tubule and collecting ducts of the principle cells)
65
What is the stimulus for secretion of aldosterone?
decreased blood volume (RAAS) INC plasma K
66
What is the MOA of aldosterone at the kidney?
-INC Na reabsorption (ENaC, distal tubule principle cells) -INC K secretion (distal tubule principle cells -INC H secretion (distal tubule alpha intercalated cells)
67
What is the stimulus for secretion of ANP?
increased atrial pressure
68
What is the MOA of ANP at the kidney?
Guanylate cyclase cGMP -- INC GFR --dec Na reabsorption
69
What is the stimulus for secretion of angiotensin II?
decreased blood volume (via renin)What
70
is the MOA of angiotensin II at hte kidney?
INC Na-H exchange and HCO3 reabsorption (proximal tubule)
71
What is the enzyme that catalyzes the reversible reaction between CO2 and water?
carbonic anhydrase
72
What is the major extracellular buffer?
HCO3
73
What is the major intracellular buffers?
organic phosphates proteins (hemoglobin)
74
Reabsorption of the filtered HCO3 primarily occurs at what section of the nephron?
early proximal tubule
75
What are causes of the metabolic acidosis?
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
What are causes of metabolic alkalosis?
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
What are causes of respiratory acidosis?
opiates; sedatives or anesthetics: inhibition of medullary respiratory center airway obstruction: DEC CO2 exchangein lungs COPD: dec CO2 exchange in lungs
78
What are causes of respiratory alkalosis?
pneumonia, pulmonary embolus: hyoxemia causes iNC ventilation rate high altitute: hypoxemia causes iNC ventilation rate
79
What is the site of action of carbonic anhydrase inhibitors?
early proximal tubule
80
What is the mechanism of carbonic anhydrase inhibitors (acetazolamide)?
inhibition of carbonic anhydrase
81
What is the major effect of carbonic anhydrase inhibitors (acetazolamide)?
INC HCO3 excretion
82
What is the site of action of loop diuretics (furosemide)?
thick ascending limb of the LOH
83
What is the MOA of loop diuretics (furosemide)?
inhibition of Na-K-2Cl cotransport
84
What are the major effects of loop diuretics (furosemide)?
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
What is the site of action of the thiazide diuretics (chlorothiazide and hydrochlorothiazide)?
early distal tubule (cortical diluting segment)
86
What is the MOA of hiazide diuretics (chlorothiazide and hydrochlorothiazide)?
inhibition of Na-Cl cotransport
87
What are the major effects of hiazide diuretics (chlorothiazide and hydrochlorothiazide)?
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
What is the site of action of K-sparing diuretics (spironolactone, amiloride, etc)?
late distal tubule and collecting duct
89
What is the MOA of K-sparing diuretics (spironolactone, amiloride, etc)?
inhibition of Na reabsorption, K secretion and H secretion
90
What are the major effects of K-sparing diuretics (spironolactone, amiloride, etc)?
INC Na excretion (small effect) DEC K excretion (using a combination with loop or thiazide diuretics) DEC H excretion