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physiology > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

Osmolarity of interstitium of cortex vs. medulla?

A

Cortex: interstitium isotonic with tubular fluids via capillaries

Medulla: interstitium gradient maintained via slow flow through vasa recta

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2
Q

Why is the medulla more susceptible to ischemic damage as compared to the cortex?

A

Medulla->slow flow of blood via vasa recta->partial pressure of oxygen received is low

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3
Q

Mechanism of filtration at the renal corpuscle?

A

Starling forces-> ultra filtrate resembling plasma enters bowmans space

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4
Q

Processes in auto regulation of renal blood flow?

A
  1. Myogenic response-contraction of sm in response to stretch
  2. Tubuloglomerular feedback(TGF).
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5
Q

Why does tubuloglomerular feedback allow auto regulation of blood flow to kidney?

A

High sodium delivery to macula densa->release of ATP and adenosine->decrease cAMP->vasoconstriction of afferent arteriole->decreased sodium delivery

And low sodium delivery-> vasodilation of afferent arteriole

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6
Q

Arrangement of afferent efferent arteriole within a nephron vs. arrangement of blood supply to all nephrons

A

Within a nephron- connected in series
Nephrons that make up a kidney- arranged in parallel

Flow through a series circuit same at all points of the circuit, any change in 1 point reflected equally at all points

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7
Q

Blood flow through a nephron depends on?

A

Pressure gradient (upstreamP-downstreamP)-> increased-> increased flow

Resistance->increased resistance at any point decreases flow at all points

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8
Q

Changes in pressure gradient and resistance that occur due to arteriolar vasoconstriction?

A

Increased resistance->decreased flow

Upstream pressure increases and downstream pressure decreases

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9
Q

Changes in pressure gradient and resistance with arteriolar vasodilation?

A

Resistance decreases->flow increases

Upstream pressure decreases and downstream pressure increases

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10
Q

Consequences of high glomerular capillary pressure and low peritubular capillary pressure?

A

High glomerular cap pressure>oncotic pressure->filtration

Low peritubular capillary pressure re absorption

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11
Q

Main driving force of filtration vs. driving force of re absorption?

A

Filtration- hydrostatic pressure in glomerular capillaries

Re absorption-oncotic pressure in peritubular capillaries

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12
Q

Factors determining net filtration pressure?

A

=HP (g)-O(g)-HP(b)

O(b)= 0 as there is no filtration of protein into bowmans space

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13
Q

In case of vomiting, diarrhoea, haemorrhaging, one physiologic mechanism that preserves ECF volume?

A

Re absorption of fluids and electrolyte in PCT due to increased oncotic pressure in peritubular capillaries that drives re absorption

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14
Q

What is the physiology behind using thiazide diuretics in a case of diabetes inspidus?

A

ADH receptors non responsive in DI->polyuria and hypernatremia->thiazides->hypernatriuria and increased filtration fraction->increased oncotic pressure in peritubular capillaries->absorption of fluid in PCT

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15
Q

Components of filtration membrane? How do they increase hydraulic conductivity but restrict passage of proteins?

A
  1. Fenestrated endothelial wall of capillaries->negatively charged protein
  2. GBM->negatively charged proteins
  3. Foot processes of podocytes with slit diaphragms

-charged proteins inhibit filtration of protein

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16
Q

GFR in a kidney is determined by what factors?

A
  1. Hydrostatic pressure of glomerular capillaries
  2. SA of the filtering membrane
  3. Permeability of filtering membrane
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17
Q

What materials are not filtered into bowmans space of the kidney?

A

Albumin, lipid soluble substances bound to proteins-eg. Bilirubin and T4

(Lipid soluble unbound subs-eg. Cortisol are filtered)

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18
Q

Clinical signs in case of non inflammatory disruption of filtration membrane as seen in nephrotic syndrome?

A
  1. Proteinuria (>3.5g/day)
  2. Hypoalbuminemia
  3. Edema (decreased oncotic pressure)
  4. Hyperlipidemia (increased free lipid due to decreased binding
  5. Lipiduria (loss of bound lipid)
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19
Q

When is ratio of filtration concentration/plasma concentration =1?

A

For a freely filtered fluid

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20
Q

What is normal GFR?

A

120ml/min or 180L/day

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21
Q

Normal FF rate for a freely filtered substance?

A

20%

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22
Q

Effect of filtration fraction on oncotic pressure in peritubular capillaries?

A

FF-> expresses the loss of protein free fluid->increased loss->increased oncotic pressure in peritubular capillaries

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23
Q

How does afferent constriction affect FF vs. efferent constriction?

A

Afferent constriction: decreased downstream pressure [HP(g)]=Low GFR; constriction=low RPF, FF=no change

Efferent constriction:increased upstream pressure [HP(g)]=high GFR; constriction=Low RPF, FF=increase

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24
Q

Effects of sympathetic nervous system stimulation on kidney?

A

Afferent arteriolar constriction»efferent arteriolar constriction

FF
>oncotic pressure at peritubular capillaries

Re absorption of fluid at peritubular capillaries due to >oncotic pressure and

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25
Q

Effect of angiotensin 2 on kidney?

A

Efferent arteriole constriction&raquo_space; afferent arteriolar constriction

> GFR
FF
oncotic pressure (PC)
Increased re absorption at peritubular capillaries due to increased oncotic pressure and decreased hydrostatic pressure

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26
Q

Effect on kidney during a stress response eg. Volume depleted state (»sympathetic stimulation and ang 2)?

A

> > constriction of both afferent and efferent arterioles-»FF->increased oncotic pressure in peritubular capillaries->increased re absorption->preservation of fluid

+ADH
+renin release by sympathetic system

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27
Q

How is ischemic damage prevented in the kidney in stress situations (intense vasoconstriction due to stimulation of sympathetic system and ang 2)

A

Release of prostaglandins (PGI2 and PGE2) via kidney cause vasodilation and counter vasoconstriction

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28
Q

Why is NSAIDs contraindicated in stress situations?

A

Release of prostaglandins (PGI2 and PGE2) via kidney cause vasodilation and counter vasoconstriction

Administration of NSAIDs->blocks PG release->ppt renal failure due to intense vasoconstriction

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29
Q

Why are ACE inhibitors contraindicated in bilateral renal artery stenosis?

A

Severely compromised GFR->GFR dependent on EA pressure

Risk of hyperkalemia

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30
Q

Structures of the nephron in the cortex vs. medulla?

A

Cortex: PCT, renal corpuscle, DCT, beginning of collecting duct

Medulla: loop of henle [juxtaglomerular nephrons], terminal part of collecting duct

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31
Q

How will you calculate filtered load and excretion in a kidney?

A

Filtered load=GFR * concentration of solute in plasma

Excreted load=urine volume flow* concentration of solute in urine

Both measured in amount/time i.e mg/min

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32
Q

If filtered load=excreted load what has happened to the substance in the kidney?

A

No net tubular modification eg. Inulin, mannitol

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33
Q

How is net transport rate in a kidney calculated?

A

Net transport rate=filtration load-excretion load

=GFRPx - VUx

0=no change
+=re absorption
-=excretion

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34
Q

Primary active transport vs. secondary active transport?

A

Primary active transport-ATP consumed directly. Eg. Na-K ATPase transporter

Secondary active transport-depends indirectly on ATP as source. Eg. Na-glucose symport in proximal tubule depends on consumption of ATP by Na-K ATPase

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35
Q

How will you calculate filtered load and excretion in a kidney?

A

Filtered load=GFR * concentration of solute in plasma

Excreted load=urine volume flow* concentration of solute in urine

Both measured in amount/time i.e mg/min

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36
Q

If filtered load=excreted load what has happened to the substance in the kidney?

A

No net tubular modification eg. Inulin, mannitol

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37
Q

If filtered load>excreted load, what has happened to the substance in the kidney?

A

Re absorption Eg. Glucose, sodium, amino acids

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38
Q

If excreted load>filtered load, what has happened to the substance in the kidney?

A

Secretion eg. PAH, creatinine

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39
Q

How is net transport rate in a kidney calculated?

A

Net transport rate=filtration load-excretion load

=GFRPx - VUx

0=no change
+=re absorption
-=excretion

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40
Q

If filtered load>excreted load, what has happened to the substance in the kidney?

A

Re absorption Eg. Glucose, sodium, amino acids

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41
Q

If excreted load>filtered load, what has happened to the substance in the kidney?

A

Secretion eg. PAH, creatinine

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42
Q

How is net transport rate in a kidney calculated?

A

Net transport rate=filtration load-excretion load

=GFRPx - VUx

0=no change
+=re absorption
-=excretion

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43
Q

How will you calculate filtered load and excretion in a kidney?

A

Filtered load=GFR * concentration of solute in plasma

Excreted load=urine volume flow* concentration of solute in urine

Both measured in amount/time i.e mg/min

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44
Q

If filtered load=excreted load what has happened to the substance in the kidney?

A

No net tubular modification eg. Inulin, mannitol

45
Q

Factors that determine clearance?

A
  1. Plasma concentration
  2. Excretion rate

Clearance rate=excretion rate/plasma conc
(ml/min)

46
Q

At a conc of PAH such that transport proteins are not saturated, how much of plasma is cleared?

A

Amount of plasma cleared=RPF

20% filtered PAH is excreted completely, rest 80% entering the peritubular capillaries is secreted

47
Q

At a conc of PAH, such that transport proteins are saturated, how much of plasma is cleared?

A

Once proteins are saturated, excretion rate of PAH parallels filtration rate of PAH as secretion is constant

But, before TM is reached ER=SR+FR
After TM is reached xER=xFR (where x is change)

Therefore plasma clearance

48
Q

How is renal blood flow calculated from renal plasma flow? [where, RPF is calculated via PAH clearance]

A

Renal blood flow=renal plasma flow/1-HCT

PAH clearance=90% of RPF b/c some plasma supplied to capsule

49
Q

Other substances that compete with PAH for its protein transporter [organic anion transporter]?

A

Penicillin
Furosemide
Acetazolamide
Salicylate

50
Q

What is the effect on plasma concentration of increasing the concentration of one out of two a anionic substances secreted via OAT?

A

Elevation of plasma concentration due to decreased secretion leading to decreased clearance of one substance

51
Q

Drugs that compete for secretion via cationic protein transporters?

A 
Atropine 
Morphine 
Procainamide
Cimetidine
Amiloride
52
Q

Substance where filtration=0 from kidney?

A

Protein

53
Q

Substance filtration>excretion from kidney?

A

Potassium sodium urea

54
Q

Substance filtration=re absorption in kidney?

A

Glucose at low conc

55
Q

Substance excretion>filtration in kidney?

A

Creatinine

56
Q

Substance excretion=plasma conc in kidney?

A

PAH

57
Q

How is GFR calculated from creatinine clearance?

A

Creatinine production = creatinine excretion = GFR*plama conc of creatinine

Creatinine production=k
If GFR >, Px

58
Q

Highest to lowest clearance?

A

PAH>creatinine>inulin>urea>sodium>glucose=albumin

59
Q

If free water clearance is +/- how does plasma osmolality change?

A

+free water=hypotonic urine=increased plasma osmolality

-free water=hypertonic urine=decreased plasma osmolality

60
Q

How is free water clearance calculated?

A

=Volume of urine flow- urine osm*V/Posm

61
Q

Why is clearance of sodium very low?

A

Higher the % of filtered load absorbed, lesser the clearance

Almost entire sodium reabsorbed but some is excreted so it does appear in urine

62
Q

What is the effect of aldosterone vs. atrial natriuretic factor on sodium clearance?

A

Aldosterone-sodium re absorption-decreases sodium clearance

Atrial natriuretic factor-sodium diuresis-increases sodium clearance

63
Q

What is the effect of ADH on urea clearance?

A

Decreases urea clearance since urea excretion is dependent on water excretion

64
Q

Re absorption of sodium in the PT?

A

2/3rd re absorbed by secondary active transport-Na-K ATPase creates gradient for sodium entry and removal into bloodstream

65
Q

Re absorption of water and electrolytes in PT?

A

Water, K+ and Cl- follow sodium into PT

Osmolality at end of PT=plasma (iso-osmotic) but only 1/3rd filtrate remains

66
Q

Re absorption of glucose and metabolites in PT?

A

Glucose- via sodium glucose linked transporter 2 (SGLT-2) [2 active transport]

Amino acids, peptides, ketone bodies via 2 active transport

67
Q

What drug inhibits SGLT-2 and is used in treatment of DM-2?

A

Canagliflozin

68
Q

Bicarbonate re absorption in PT?

A

80% re absorbed->bicarbonate+H->H2CO3->CO2+H2O via CA enzyme

CO2 diffuses across cell; reverse reaction occurs->H+ pumped back into tubule via antiport and bicarbonate re absorbed

69
Q

What hormones stimulate the sodium-potassium ATPase pump in the PT?

A

Angiotensin 2 and aldosterone

70
Q

What hormone stimulates Na-H exchanger in the PT?

A

Angiotensin 2.
Volume depleted states->angiotensin stimulates secretion of H+ and increases re absorption of bicarbonate->prevents loss->contraction alkalosis

71
Q

What type of kidney stones can frequently occur in patients with gout?

A

Elevated Uric acid in urine, low pH in urine precipitates kidney stones

72
Q

Where is majority of the filtered urate re absorbed?

A

In the PCT of the kidney

73
Q

Site of action of diuresis due to diabetes mellitus?

A

PT; glucose transporters saturated and TM reached; glucose freely filtered into PT->pulls water into tubule via osmosis

74
Q

Site of highest concentration of inulin in nephron?

A

Collecting duct; concentration increases through nephron since water is re absorbed and inulin is not

75
Q

Site of re absorption of water vs. solutes in loop of Henle?

A

Descending loop- permeable to water; impermeable to solute

Ascending loop-impermeable to water; permeable to solute

76
Q

Site of reabsorption of Mg2+ and Ca+ in kidney ATL?

A

Para cellular pathway in loop of henle; K+ transported back into lumen–> that creates +luminal potential for reabsorption of ca and mg

77
Q

Site of feedback mechanism of ca absorption in loop of henle?

A

CaSR on basolateral membrane of ATL; inhibits Na-K-Cl reabsorption

78
Q

Site of defect in bartters syndrome?

A

Genetic mutation Na-K-Cl transporter in ATL-diminished function

79
Q

Site of action of Familial hypocalciuric hypercalcemia?

A

AD mutated CaSR-non responsive to plasma ca levels

Patients also have high levels of PTH because CaSR expressed in parathyroid gland

80
Q

Site of action of loop diuretics?

A

Na-K-Cl transporter in ATL blocked

81
Q

Site of sodium absorption in DT of kidney?

A

Na-Cl symport on apical membrane via 2 active transport; gradient maintained by Na-K ATPase

82
Q

Site of Ca absorption in DT? (Site of action of PTH)

A

Calcium channels regulated by PTH

Extruded into peritubular fluid via Ca-ATPase/ 3Na-Ca antiport

83
Q

Site of action of vitamin D?

A

+calbindin synthesis-binds to calcium; enhances PTH action on DT

84
Q

Site of action of thiazides?

A

Blocks Na-Cl symporter–>decreases sodium gradient–>hypercalcemia

85
Q

Site of defect in gitelmans syndrome?

A

Mutated Na-Cl transporter–>hypokalemic, alkalotic, low urine ca

86
Q

Site of action of sodium absorption in CD?

A

Epithelial Na channels in luminal membrane of CD via 2 active transport–> gradient maintained by Na-K ATPase

[principle cells]

87
Q

Site of action of potassium secretion in CD?

A

ENaC cause sodium absorption into CD but not chloride–> negative luminal potential–>potassium secretion

[principle cells]

88
Q

Site of action of aldosterone in CD?

A

++ of synthesis of ENaC and opening and increases synthesis of Na-K ATPase on basolateral membrane

+H-ATPase of intercalated cells; increases H secretion and bicarbonate absorption; alkalosis

89
Q

Site of action of ADH in collecting duct

A

V2 receptors->insertion of aquaporins-> water and urea re absorption

[principle cells]

90
Q

Site of action of K+ sparing diuretics/aldosterone antagonists in CD?

A

ENaC in the CD–> sodium re absorption reduced, potassium excretion diminished

91
Q

Site of defect in liddles syndrome?

A

Gain of function in ENaC in CD; enhanced sodium re absorption, potassium secretion; hypokalemic, hypertensive and alkalotic

92
Q

Site of action of acid-base regulation in CD?

A

H-ATPase in luminal membrane of intercalated cells; H+ excreted buffered via HPO4/NH3+ and excreted; bicarbonate re absorbed

93
Q

Defect in distal renal tubular acidosis? (Type 1)

A

Inability of distal nephron to secrete and excrete fixed acid

  1. Impairment of transport systems for hydrogen and bicarbonate ions
  2. Increased permeability of luminal mem
94
Q

Defect in proximal renal tubular acidosis? (Type 2)

A

Diminished capacity of PT to absorb bicarbonate

Fanconi syndrome- defect in proximal tubular transport
CA inhibitors

95
Q

Defect in renal tubular acidosis type 4?

A

Hypoaldosterone
Diminished synthesis of H-ATPase for H+ secretion

Diabetic nephropathy, RAAS inhibitors, trimethoprim, Addison’s disease

96
Q

Renal tubular acidosis with hyperkalemia vs. hypokalemia?

A

Hyperkalemia-type 4, aldosterone deficiency; does not synthesise ENaC, decreased K secretion

Hypokalemia-type 1 and 2, increased bicarbonate in urine, diuresis-K loss

97
Q

Distribution of K in body fluids?

A

ICF= 150mEq/L
ECF=4mEq/L

Hyperkalemia= >5mEq/L
Hypokalemia=

98
Q

Factors determining K secretion in kidney?

A

Filtrate flow=increased flow, increased secretion

Sodium re absorption=increased, increased secretion due to negative potential created

99
Q

Potassium distribution in case of acidosis vs. alkalosis?

A

Acidosis=K shift from ICF to ECF=hyperkalemia

Alkalosis=K shift from ECF to ICF =hypokalemia

100
Q

Kidney disorders that promote hyperkalemia?

A

Oliguric kidney disease, chronic kidney disease, hypoaldosteronism (renal tubular acidosis type 4)

101
Q

Transcellular shifts that promote hyperkalemia?

A

Metabolic acidosis, insulin deficiency, hyperglycaemia, muscle trauma

102
Q

Site of action of epinephrine, aldosterone and insulin in regulation of K levels?

A

Sodium potassium ATPase stimulation in kidney

103
Q

Kidney factors that promote hypokalemia?

A

Diuretics, hyperaldosteronism, increased excretion of negative ions, renal tubular acidosis type 1 and 2

104
Q

Transcellular shifts that promote hypokalemia?

A

Metabolic alkalosis, increase in catecholamines and insulin

105
Q

Defect in pre renal failure type of acute renal failure?

A

Decreased renal perfusion due to hypovolumia of haemorrhage, diarrhoea, vomiting, congestive heart failure

106
Q

Defect in intrarenal type of acute renal failure?

A

Tubular dysfunction due to toxins, interstitial nephritis, ischaemia, rhabdomyolysis, sepsis

107
Q

Defect in post renal type of acute renal failure?

A

Obstruction of outflow from kidney- renal caliculi, enlarged prostate

108
Q

Fractional excretion of Na in prerenal vs. intrarenal vs. post renal type of acute renal failure?

A

Decreased in pre renal and early post renal: GFR decreased, sodium re absorption increased

Increased in intrarenal: tubular dysfunction- no reabsorption of sodium

109
Q

BUN:Cr ratio in prerenal vs. intrarenal vs. post renal type of acute renal failure?

A

Increased in early post renal and pre renal: due to increased water and therefore urea absorption

Decreased in intrarenal due to tubular dysfunction

physiology (4 decks)

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