Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

What is the 60-40-20 rule?

A

In terms of % of body weight for the average person:

  • 60% to total body weight is total body water
  • 40% of that total body water is ICF or INside cells
  • 20% of that total body water is ECF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the ratio of plasma and interstitial fluid in the ECF?

A

1/4 of ECF is plasma

3/4 of ECF is interstitial fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What substance is used to measure plasma?

A

Radiolabeled albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What substance is used to measure ECF/Extracellular Volume?

A

Inulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the average osmolality inside and outside of cells?

A

290 mOsm/kg H20

no movement of water in and out of cells at resting concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the major anions and cations in the ICF?

A

K+, protein and organic phosphates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the major anions and cations in the ECF?

A

Na+, HCO3-, Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the function of the glomerular filtration barrier?

A

Responsible for filtration of plasma according to size and net charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the glomerular filtration barrier composed of?

A
  • Fenestrated capillary endothelium (size barrier)
  • Fused Basement Membrane with heparin sulfate (negative charge barrier)
  • Epithelial layer consisting of podocyte foot processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the equation for renal clearance?

A

C = (U x V)/P

C = clearance of X (mL/min)
U = urine concentration of X (mg/mL)
V = urine flow rate (mL/min)
P = plasma concentration of X (mg/mL)

**Clearance will be increased if the kidneys are not functioning properly, also clearance increases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does it mean when C

A

net tubular reabsorption of substance X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does it mean when C > GFR?

A

net tubular secretion of substance X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does it mean when C = GFR?

A

no net tubular reabsorption or secretion of substance X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What substance can be used to calculate GFR and why?

A

Inulin clearance can be used to calculate GFR because it is freely filtered and is neither reabsorbed nor secreted

Creatinine clearance is also an approximate measure of GFR (used more than inulin bc its easier to measure), but it slightly OVERESTIMATES GFR because creatinine is moderately secreted by the renal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the equation used to calculate GFR?

A

GFR = Cinulin = (Uinulin x V) / Pinulin

GFR = K [ (Pgc - Pbs) - (πgc - πbs) ]
**don’t really need to memorize this, just know the concept that the GFR is the difference in hydrostatic pressure between glomerular capillary and bowman’s space minus the difference in oncotic pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the normal value of GFR?

A

100 mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What can be used to estimate the effective renal plasma flow (eRPF)?

A

Para-aminohippuric acid (PAH) clearance because it is both filtered and secreted in the proximal collecting tubule (PCT) resulting in near 100% excretion of all PAH entering kidney

eRPF = amount of plasma flowing through the kidneys per unit time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the equation to calculate effective renal plasma flow (eRPF) and is it an overestimation or underestimation of true renal plasma flow (RPF)?

A

eRPF = (Upah x V) / Ppah = Cpah

eRPF underestimates true renal plasma flow (RPF) by ~10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the equation to calculate renal blood flow (RBF) using renal plasma flow (RPF)?

A

RBF = RPF / (1 - Hct)

normally RBF is double RPF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the equation used to calculate filtration fraction (FF) and what is a normal FF?

A

Filtration Fraction (FF) = GFR/RPF

Normal FF = 20%

(GFR can be estimated using creatinine clearance and RPF can be estimated using PAH clearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the equation to calculate filtered load?

A

Filtered Load (mg/min) = GFR (mL/min) x plasma concentration (mg/mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the effect of prostaglandins on the kidney’s arterioles?

A

Prostaglandins preferentially dilate the AFFERENT arteriole, which increases RPF and increases GFR, so FF stays constant

(don’t forget NSAIDS block prostaglandins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the effect of angiotensin II on the kidney’s arterioles?

A

Angiotensin II preferentially constricts the EFFERENT arteriole, which decreases RPF, but increases GFR, so FF increases

(don’t forget ACE inhibitors block the action of AT II)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens to GFR, RPF and FF (GFR/RPF) when the afferent arteriole is constricted?

A

GFR decreases
RPF decreases
FF no change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What happens to GFR, RPF and FF (GFR/RPF) when the efferent arteriole is constricted?

A

GFR increases
RPF decreases
FF increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens to GFR, RPF and FF (GFR/RPF) when there is an increase in plasma protein concentration?

A 
GFR decreases (bc increase in oncotic pressure)
RPF no change
FF decreases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens to GFR, RPF and FF (GFR/RPF) when there is an decrease in plasma protein concentration?

A

GFR increases
RPF no change
FF increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What happens to GFR, RPF and FF (GFR/RPF) when the ureter is constricted?

A

GFR decreases
RPF no change
FF decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the equations to calculate filtered load, excretion rate, reabsorption and secretion?

A

Filtered Load = GFR x Px
Excretion Rate = V x Ux
Reabsorption = filtered - excreted
Secretion = excreted - filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What happens to glucose after it is filtered by the kidney?

A

Glucose at a normal plasma level is completely reabsorbed in PCT by Na+/glucose co-transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the threshold for glucose appearing in the urine and what is the concentration at which all transporters are fully saturated?

A

At plasma glucose of ~200 mg/dL, glycosuria begins (threshold)

At ~375 mg/dL all transporters are fully saturated (Tm)

*Also, normal pregnancy may decrease the ability of PCT to reabsorb glucose and amino acids leading to glycosuria and aminoaciduria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What happens to amino acids after they are filtered by the kidney?

A

Na+-dependent transporters in the PCT reabsorb amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Hartnup disease and what are its clinical manifestations?

A

Deficiency of neutral amino acid (eg. tryptophan) transporters in proximal renal tubular cells and enterocytes –> neutral aminoaciduria and decreased absorption from the gut

With decreased tryptophan, there is decreased conversion to niacin leading to pellagra-like symptoms (3Ds):

Dermatitis (erythematous skin lesions)
Diarrhea
Dementia

Useful to check tryptophan in the urine and can treat with high protein diet and nicotinic acid

34
Q

What gets reabsorbed in the early PCT?

A
  • Contains brush border
  • Reabsorbs all glucose and amino acids and most HCO3-, Na+, Cl-, PO43-, K+ and H20
  • ISOTONIC absorption
  • Generates and secretes NH3, which acts as a buffer for secreted H+
  • 65-80% of Na+ reabsorbed here
35
Q

What are the main transporters located on the lumenal side of the early PCT?

A
  • Na+/glucose or Na+/AA exchangers
  • Na+ and H+ exchanger (CO2 diffuses across the membrane and HCO3- gets reabsorbed on the other side)
  • Cl- and Base- exchanger
36
Q

What inhibits the Na+/PO43- cotransporter in the early PCT?

A

PTH –> leads to phosphorus excretion

37
Q

What stimulates the Na+/H+ exchanger in the early PCT?

A

Angiotensin II stimulates the Na+/H+ exchanger increasing Na+, H2O and HCO3- reabsorption (permitting contraction alkalosis)

38
Q

What is the function of the thin descending loop of henle and what gets reabsorbed?

A
  • Passively reabsorbs H20 via medullary hypertonicity
  • This segment is IMPERMEABLE to Na2+
  • Concentrating segment that makes urine hypertonic
39
Q

What is the function of the thick ascending loop of henle and what gets reabsorbed?

A
  • Reabsorbs Na+, K+ and Cl-
  • Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through (+) lumen potential generated by K+ back leak
  • This segment is IMPERMEABLE to H20
  • Makes the urine less concentrated as it ascends
  • 10-20% of Na+ reabsorbed in this segment
40
Q

What is the major transporter on the luminal side of the thick ascending loop of henle and what drug inhibits it?

A

Na+, K+ and 2Cl- cotransporter

Inhibited by loop diuretics (furosemide)

41
Q

What is the function of the early distal convoluted tubule and what gets reabsorbed?

A
  • Reabsorbs Na+, Cl-
  • Makes urine most dilute (hypotonic)
  • 5-10% Na+ reabsorbed
42
Q

What is the major transporter on the luminal side of the early distal convoluted tubule and what drug inhibits it?

A

Na+ and Cl- cotransporter

Inhibited by thiazide diuretics

43
Q

What small molecule increases Ca2+/Na+ exchange in the early distal convoluted tubule?

A

PTH, which increases Ca2+ reabsorption

44
Q

What gets reabsorbed in the collecting tubule?

A

Reabsorbs Na+ in exchange for secreting K+ and H+

3-5% of Na+ reabsorbed

45
Q

What is the function of ADH and in which cells does it act in the collecting tubule?

A

ADH acts at the V2 receptor which stimulates the insertion of aquaporin channels on the apical side of principal cells

46
Q

What is the function of Aldosterone and in which cells does it act in the collecting tubule?

A

Aldosterone acts on mineralocorticoid receptor which increases the mRNA and protein synthesis

In prinicpal cells: increases apical K+ conductance, increases Na+/K+ pump, increases ENAC channels leads to lumen negativity and increased K+ lost

In alpha-intercalated cells: increased H+ ATPase activity leading to increased HCO3-/Cl- exchanger activity

47
Q

What is a mnemonic to remember the order of the renal tubular defects?

A

Think: “The kidneys put out FABulous Glittering LiquidS”

FAnconi syndrome is the first defect (PCT)
Bartter syndrome is next (thick ascending loop of henle)
Gitelman syndrome is after Bartter (DCT)
Liddle syndrome is last (collecting tubule)
Syndrome of apparent mineralocorticoid excess (collecting tubule)

48
Q

What is Fanconi Syndrome?

A
  • Generalized reabsorptive defect in PCT: associated with increased excretion of nearly all amino acids, glucose, HCO3- and PO43-
  • May result in metabolic acidosis (proximal renal tubular acidosis
  • Causes include hereditary defects (eg. Wilson’s disease, tyrosinemia, glycogen storage disease), ischemia, multiple myeloma, nephrotoxins/drugs (eg. expired tetracycline, tenofovir), lead poisoning
49
Q

What is Bartter syndrome, what transporter does it affect and what is the result?

A
  • Reabsorptive defect in thick ascending loop of henle; autosomal recessive
  • Affects Na+/K+/2Cl- cotransporter
  • Results in hypokalemia and metabolic alkalosis with hypercalciuria
50
Q

What is Gitelman syndrome, what transporter does it affect and what is the result?

A
  • Reabsorptive defect of NaCl in DCT; autosomal recessive
  • Less severe than Bartter syndrome (bc less Na+ is reabsorbed from the DCT than the thick ascending loop)
  • Leads to hypokalemia, hypomagnesmia, metabolic alkalosis, hypocalciuria
51
Q

What is Liddle syndrome, what is the result clinically and what is the treatment?

A
  • Gain of function mutation leading to increased Na+ reabsorption in collecting tubules (increased activity of Na+ channel)
  • Autosomal DOMINANT
  • Results in hypertension, hypokalemia, metabolic alkalosis, and decreased aldosterone
  • Treatment = amiloride
52
Q

What is the syndrome of mineralocorticoid excess?

A
  • hereditary deficiency of 11 β hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineral corticoid receptor containing cells before cortisol can act on the mineralocorticoid receptors
  • excess cortisol in these cells from the enzyme deficiency leads to increased mineralocorticoid receptor activity, which leads to hypertension, hypokalemia, metabolic alkalosis
  • LOW serum aldosterone levels
53
Q

What is one way to acquire syndrome of mineralocorticoid excess?

A

Glycyrrhetic acid (present in licorice), which blocks the enzyme 11 β hydroxysteroid dehydrogenase

54
Q

What happens to the concentration of inulin along the PCT?

A

Tubular inulin increases in concentration steadily –> even though the amount stays the same, water is being reabsorbed, which increases the concentration of inulin along the PCT

55
Q

Which substances on the osmolarity vs. percent distance along the PCT represent net secretion?

A
  • PAH

- Creatinine

56
Q

Which substances on the osmolarity vs. percent distance along the PCT represent net reabsorption?

A

Urea, Cl-, K+, Na+, HCO3-, amino acids, glucose

57
Q

Which three things trigger the release of renin from the kidney?

A
  1. Decreased BP (JG cells)
  2. Decreased Na+ delivery (macula densa cells)
  3. Increased sympathetic tone (β1 receptors)
58
Q

What does renin do?

A

Converts angiotensinogen from the liver into angiotensin 1

59
Q

What converts angiotensin I into angiotension II and where does this occur?

A

ACE converts AT I into AT II in the lungs and kidney

also causes bradykinin breakdown

60
Q

What are the six effects of angiotensin II and what are their downstream effects?

A
  1. Acts on AT II receptor, type 1 (AT1) on vascular smooth muscle causing vasoconstriction, which increases BP
  2. Constricts the efferent arteriole of glomerulus, which increases FF to preserve renal function (GFR) in low volume states
  3. Releases aldosterone from the adrenal glands, which increases Na+ channel and Na+/K+ pump insertion in principal cells; enhances K+ and H+ excretion by way of principal cell K+ channels and alpha-intercalated cell H+ ATPases –> creates favorable Na+ gradient for Na+ and H20 reabsorption
  4. Releases ADH from the posterior pituitary, which increases aquaporin insertion in principal cells –> H20 reabsorption
  5. Increases PCT Na+/H+ activity leading to Na+, HC03- and H20 reabsorption (can permit contraction alkalosis)
  6. Stimulates the hypothalamus –> thirst
61
Q

How does ANP and BNP affect the renin-angiotensin-aldosterone system?

A
  • ANP is released from the atria and BNP is released from the ventricles in response to increased volume (stretching myocytes), may act as a “check” on RAAS
  • Relaxes vascular smooth muscle via cGMP which increases GFR and decreases renin
62
Q

What does ADH primarily regulate?

A

Primarily osmolarity (also responds to low volume states)

63
Q

What does aldosterone primarily regulate?

A

Primarily regualtes ECF volume and Na+ content (also responds to low volume states)

64
Q

How does AT II affect baroreceptor function?

A

Limits reflex bradycardia, which would normally accompany its pressor effects, so it helps maintain blood pressure and blood volume

65
Q

Which cells make up the juxtaglomerular apparatus and what do they secrete?

A
  1. Mesangial cells
  2. JG cells (modified smooth muscle of afferent arteriole)
  3. Macula Densa (NaCl sensor, part of DCT)
66
Q

What do JG cells sense/secrete?

A

JG cells secrete renin in response to decreased renal BP and increased sympathetic tone (β1)

β-blockers can decrease BP by inhibiting β1 receptors of the JGA

67
Q

What does the macula densa sense/secrete?

A

Macula dense cells sense a decrease in NaCl delivery to the DCT and secrete adenosine release which causes vasoconstriction

68
Q

What is the effect of prostaglandins in the kidney?

A

Prostaglandins act locally, paracrine secretion vasodilates the afferent arterioles to increase RBF

**NSAIDS block renal protective prostaglandin synthesis (renal papillary necrosis is a commonly tested complication of NSAID use)

69
Q

Where is 1α-hydroxylase produced and what does it do?

A

Produced in PCT cells; it converts 25-OH vitamin D to 1,25-(OH)2 vitamin D (active form)

Stimulated by PTH

70
Q

Where is erythropoietin released and when is it released?

A

Released by interstitial cells in peritubular capillary in response to hypoxia –> stimulates production of RBCs

**COPD patients have chronic hypoxic state, so they tend to have increased levels of EPO

71
Q

What shifts K+ out of cells causing hyperkalemia?

A

Think: “DO LABS”

Digitalis (blocks Na+/K+ ATPase)
HyperOsmolarity
Lysis of cells (eg. crush injury, rhabdomyolysis, cancer)
Acidosis
β-blocker
Sugar…patient with high blood glucose/insulin deficiency

72
Q

What shifts K+ into cells causing hypokalemia?

A

Hypo-osmolarity
Alkalosis
β-adrenergic agonist (increases Na+/K+ ATPase)
Insulin (increases Na+/K+ ATPase)

73
Q

What is the effect of LOW serum Na+?

A

Nausea and malaise, stupor, coma, seizures

**can’t fire APs sufficiently without enough Na+

74
Q

What is the effect of HIGH serum Na+?

A

Irritability, stupor, coma

75
Q

What is the effect of LOW serum K+?

A
  1. U Waves on ECG
  2. flattened T Waves
  3. Arrhythmias
  4. Muscle spasms
76
Q

What is the effect of HIGH serum K+?

A
  1. Wide QRS
  2. Peaked T waves on ECG
  3. Arrhythmias
  4. Muscle weakness
77
Q

What is the effect of LOW serum Ca2+?

A

Tetany, seizures, QT prolongation

78
Q

What is the effect of HIGH serum Ca2+?

A

Stones (renal), bones (pain), groans (abdominal pain), thrones (increased urinary frequency), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria

79
Q

What is the effect of LOW serum Mg2+?

A

Tetany, torsades de pointes, hypokalemia

80
Q

What is the effect of HIGH serum Mg2+?

A
  1. Decreased Deep Tendon Reflexes
  2. Lethargy
  3. Bradycardia
  4. Hypotension
  5. Cardiac arrest
  6. Hypocalcemia
81
Q

What is the effect of LOW serum PO43-?

A

Bone loss, osteomalacia (adults), rickets (children)

82
Q

What is the effect of HIGH serum PO43-?

A

Renal stones, metabolic calcifications, hypocalcemia

Renal (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions