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Renal Physiology Flashcards

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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
Effect of angiotensin 2 on kidney?
Efferent arteriole constriction >> afferent arteriolar constriction >GFR FF >oncotic pressure (PC) Increased re absorption at peritubular capillaries due to increased oncotic pressure and decreased hydrostatic pressure
26
Effect on kidney during a stress response eg. Volume depleted state (>>sympathetic stimulation and ang 2)?
>>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
27
How is ischemic damage prevented in the kidney in stress situations (intense vasoconstriction due to stimulation of sympathetic system and ang 2)
Release of prostaglandins (PGI2 and PGE2) via kidney cause vasodilation and counter vasoconstriction
28
Why is NSAIDs contraindicated in stress situations?
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
29
Why are ACE inhibitors contraindicated in bilateral renal artery stenosis?
Severely compromised GFR->GFR dependent on EA pressure Risk of hyperkalemia
30
Structures of the nephron in the cortex vs. medulla?
Cortex: PCT, renal corpuscle, DCT, beginning of collecting duct Medulla: loop of henle [juxtaglomerular nephrons], terminal part of collecting duct
31
How will you calculate filtered load and excretion in a kidney?
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
32
If filtered load=excreted load what has happened to the substance in the kidney?
No net tubular modification eg. Inulin, mannitol
33
How is net transport rate in a kidney calculated?
Net transport rate=filtration load-excretion load =GFR*Px - V*Ux 0=no change +=re absorption -=excretion
34
Primary active transport vs. secondary active transport?
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
35
How will you calculate filtered load and excretion in a kidney?
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
36
If filtered load=excreted load what has happened to the substance in the kidney?
No net tubular modification eg. Inulin, mannitol
37
If filtered load>excreted load, what has happened to the substance in the kidney?
Re absorption Eg. Glucose, sodium, amino acids
38
If excreted load>filtered load, what has happened to the substance in the kidney?
Secretion eg. PAH, creatinine
39
How is net transport rate in a kidney calculated?
Net transport rate=filtration load-excretion load =GFR*Px - V*Ux 0=no change +=re absorption -=excretion
40
If filtered load>excreted load, what has happened to the substance in the kidney?
Re absorption Eg. Glucose, sodium, amino acids
41
If excreted load>filtered load, what has happened to the substance in the kidney?
Secretion eg. PAH, creatinine
42
How is net transport rate in a kidney calculated?
Net transport rate=filtration load-excretion load =GFR*Px - V*Ux 0=no change +=re absorption -=excretion
43
How will you calculate filtered load and excretion in a kidney?
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
44
If filtered load=excreted load what has happened to the substance in the kidney?
No net tubular modification eg. Inulin, mannitol
45
Factors that determine clearance?
1. Plasma concentration 2. Excretion rate Clearance rate=excretion rate/plasma conc (ml/min)
46
At a conc of PAH such that transport proteins are not saturated, how much of plasma is cleared?
Amount of plasma cleared=RPF 20% filtered PAH is excreted completely, rest 80% entering the peritubular capillaries is secreted
47
At a conc of PAH, such that transport proteins are saturated, how much of plasma is cleared?
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
How is renal blood flow calculated from renal plasma flow? [where, RPF is calculated via PAH clearance]
Renal blood flow=renal plasma flow/1-HCT PAH clearance=90% of RPF b/c some plasma supplied to capsule
49
Other substances that compete with PAH for its protein transporter [organic anion transporter]?
Penicillin Furosemide Acetazolamide Salicylate
50
What is the effect on plasma concentration of increasing the concentration of one out of two a anionic substances secreted via OAT?
Elevation of plasma concentration due to decreased secretion leading to decreased clearance of one substance
51
Drugs that compete for secretion via cationic protein transporters?
``` Atropine Morphine Procainamide Cimetidine Amiloride ```
52
Substance where filtration=0 from kidney?
Protein
53
Substance filtration>excretion from kidney?
Potassium sodium urea
54
Substance filtration=re absorption in kidney?
Glucose at low conc
55
Substance excretion>filtration in kidney?
Creatinine
56
Substance excretion=plasma conc in kidney?
PAH
57
How is GFR calculated from creatinine clearance?
Creatinine production = creatinine excretion = GFR*plama conc of creatinine Creatinine production=k If GFR >, Px
58
Highest to lowest clearance?
PAH>creatinine>inulin>urea>sodium>glucose=albumin
59
If free water clearance is +/- how does plasma osmolality change?
+free water=hypotonic urine=increased plasma osmolality -free water=hypertonic urine=decreased plasma osmolality
60
How is free water clearance calculated?
=Volume of urine flow- urine osm*V/Posm
61
Why is clearance of sodium very low?
Higher the % of filtered load absorbed, lesser the clearance Almost entire sodium reabsorbed but some is excreted so it does appear in urine
62
What is the effect of aldosterone vs. atrial natriuretic factor on sodium clearance?
Aldosterone-sodium re absorption-decreases sodium clearance Atrial natriuretic factor-sodium diuresis-increases sodium clearance
63
What is the effect of ADH on urea clearance?
Decreases urea clearance since urea excretion is dependent on water excretion
64
Re absorption of sodium in the PT?
2/3rd re absorbed by secondary active transport-Na-K ATPase creates gradient for sodium entry and removal into bloodstream
65
Re absorption of water and electrolytes in PT?
Water, K+ and Cl- follow sodium into PT Osmolality at end of PT=plasma (iso-osmotic) but only 1/3rd filtrate remains
66
Re absorption of glucose and metabolites in PT?
Glucose- via sodium glucose linked transporter 2 (SGLT-2) [2 active transport] Amino acids, peptides, ketone bodies via 2 active transport
67
What drug inhibits SGLT-2 and is used in treatment of DM-2?
Canagliflozin
68
Bicarbonate re absorption in PT?
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
What hormones stimulate the sodium-potassium ATPase pump in the PT?
Angiotensin 2 and aldosterone
70
What hormone stimulates Na-H exchanger in the PT?
Angiotensin 2. Volume depleted states->angiotensin stimulates secretion of H+ and increases re absorption of bicarbonate->prevents loss->contraction alkalosis
71
What type of kidney stones can frequently occur in patients with gout?
Elevated Uric acid in urine, low pH in urine precipitates kidney stones
72
Where is majority of the filtered urate re absorbed?
In the PCT of the kidney
73
Site of action of diuresis due to diabetes mellitus?
PT; glucose transporters saturated and TM reached; glucose freely filtered into PT->pulls water into tubule via osmosis
74
Site of highest concentration of inulin in nephron?
Collecting duct; concentration increases through nephron since water is re absorbed and inulin is not
75
Site of re absorption of water vs. solutes in loop of Henle?
Descending loop- permeable to water; impermeable to solute Ascending loop-impermeable to water; permeable to solute
76
Site of reabsorption of Mg2+ and Ca+ in kidney ATL?
Para cellular pathway in loop of henle; K+ transported back into lumen--> that creates +luminal potential for reabsorption of ca and mg
77
Site of feedback mechanism of ca absorption in loop of henle?
CaSR on basolateral membrane of ATL; inhibits Na-K-Cl reabsorption
78
Site of defect in bartters syndrome?
Genetic mutation Na-K-Cl transporter in ATL-diminished function
79
Site of action of Familial hypocalciuric hypercalcemia?
AD mutated CaSR-non responsive to plasma ca levels Patients also have high levels of PTH because CaSR expressed in parathyroid gland
80
Site of action of loop diuretics?
Na-K-Cl transporter in ATL blocked
81
Site of sodium absorption in DT of kidney?
Na-Cl symport on apical membrane via 2 active transport; gradient maintained by Na-K ATPase
82
Site of Ca absorption in DT? (Site of action of PTH)
Calcium channels regulated by PTH Extruded into peritubular fluid via Ca-ATPase/ 3Na-Ca antiport
83
Site of action of vitamin D?
+calbindin synthesis-binds to calcium; enhances PTH action on DT
84
Site of action of thiazides?
Blocks Na-Cl symporter-->decreases sodium gradient-->hypercalcemia
85
Site of defect in gitelmans syndrome?
Mutated Na-Cl transporter-->hypokalemic, alkalotic, low urine ca
86
Site of action of sodium absorption in CD?
Epithelial Na channels in luminal membrane of CD via 2 active transport--> gradient maintained by Na-K ATPase [principle cells]
87
Site of action of potassium secretion in CD?
ENaC cause sodium absorption into CD but not chloride--> negative luminal potential-->potassium secretion [principle cells]
88
Site of action of aldosterone in CD?
++ 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
Site of action of ADH in collecting duct
V2 receptors->insertion of aquaporins-> water and urea re absorption [principle cells]
90
Site of action of K+ sparing diuretics/aldosterone antagonists in CD?
ENaC in the CD--> sodium re absorption reduced, potassium excretion diminished
91
Site of defect in liddles syndrome?
Gain of function in ENaC in CD; enhanced sodium re absorption, potassium secretion; hypokalemic, hypertensive and alkalotic
92
Site of action of acid-base regulation in CD?
H-ATPase in luminal membrane of intercalated cells; H+ excreted buffered via HPO4/NH3+ and excreted; bicarbonate re absorbed
93
Defect in distal renal tubular acidosis? (Type 1)
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
Defect in proximal renal tubular acidosis? (Type 2)
Diminished capacity of PT to absorb bicarbonate Fanconi syndrome- defect in proximal tubular transport CA inhibitors
95
Defect in renal tubular acidosis type 4?
Hypoaldosterone Diminished synthesis of H-ATPase for H+ secretion Diabetic nephropathy, RAAS inhibitors, trimethoprim, Addison's disease
96
Renal tubular acidosis with hyperkalemia vs. hypokalemia?
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
Distribution of K in body fluids?
ICF= 150mEq/L ECF=4mEq/L Hyperkalemia= >5mEq/L Hypokalemia=
98
Factors determining K secretion in kidney?
Filtrate flow=increased flow, increased secretion Sodium re absorption=increased, increased secretion due to negative potential created
99
Potassium distribution in case of acidosis vs. alkalosis?
Acidosis=K shift from ICF to ECF=hyperkalemia Alkalosis=K shift from ECF to ICF =hypokalemia
100
Kidney disorders that promote hyperkalemia?
Oliguric kidney disease, chronic kidney disease, hypoaldosteronism (renal tubular acidosis type 4)
101
Transcellular shifts that promote hyperkalemia?
Metabolic acidosis, insulin deficiency, hyperglycaemia, muscle trauma
102
Site of action of epinephrine, aldosterone and insulin in regulation of K levels?
Sodium potassium ATPase stimulation in kidney
103
Kidney factors that promote hypokalemia?
Diuretics, hyperaldosteronism, increased excretion of negative ions, renal tubular acidosis type 1 and 2
104
Transcellular shifts that promote hypokalemia?
Metabolic alkalosis, increase in catecholamines and insulin
105
Defect in pre renal failure type of acute renal failure?
Decreased renal perfusion due to hypovolumia of haemorrhage, diarrhoea, vomiting, congestive heart failure
106
Defect in intrarenal type of acute renal failure?
Tubular dysfunction due to toxins, interstitial nephritis, ischaemia, rhabdomyolysis, sepsis
107
Defect in post renal type of acute renal failure?
Obstruction of outflow from kidney- renal caliculi, enlarged prostate
108
Fractional excretion of Na in prerenal vs. intrarenal vs. post renal type of acute renal failure?
Decreased in pre renal and early post renal: GFR decreased, sodium re absorption increased Increased in intrarenal: tubular dysfunction- no reabsorption of sodium
109
BUN:Cr ratio in prerenal vs. intrarenal vs. post renal type of acute renal failure?
Increased in early post renal and pre renal: due to increased water and therefore urea absorption Decreased in intrarenal due to tubular dysfunction

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