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physiology Flashcards

1
Q

Total body water (TBW) - proportion

A

60% of body mass

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2
Q

Non water mass (NWM) - proportion

A

40% of body mass

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3
Q

total body water mass and non water mass if Body mass is 70kg

A
  • total body water –> 60% of body mass = 42kg = 42L

- non water mass –> 40% of body mass = 28kg

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4
Q

Total body water (TBW) is divided to … (and proprotions)

A
  1. extracellular fluid (ECF) –> 1/3

2. intracellular fluid (ICF) –> 2/3

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5
Q

extracellular fluid (ECF) in a body mass 70kg

A

1/3 of 60% body mass –> 20% of body mass –> 14kg

–> 28L

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6
Q

intracellular fluid (ICF) in a body mass 70kg

A

2/3 of 60% body mass –> 40% of body mass –> 28kg

–> 28L

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7
Q

extracellular fluid (ECF) vs intracellular fluid (ICF) according to proportion in body mass

A 
extracellular fluid (ECF) --> 20%
intracellular fluid (ICF) --> 40%
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8
Q

extracellular fluid (ECF) is divided to (proportions and L in body mass 70 kg)

A
  1. interstitial fluid –> 75% ECF –> 10.5 kg –> 10.5 L

2. plasma –> 25% ECF –> 3.5kg –> 3.5 L

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9
Q

RBC volume

A

2.8 L (part of intracellular fluid)

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10
Q

blood conistis of (and volumes)

A

RBCs (2.8.L) and plasma (3.5L) –> 6.2 L

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11
Q

Normal HCT (calculation and alternative calculation)

A

RBC volume/blood volume = 2.8/6.2 = 45%

altenatively –> HCT(%) = 3X(Hb) in g/dL

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12
Q

Plasma volume can be measured by

A

radiolabeling albumin

or Evans blue (it binds albumin)

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13
Q

Extracellular volume can be measured by

A

inulin or manitol, or sulfate

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14
Q

osmolarity is the

A

measure of solute concentration, defined as the number of osmoles (Osm) of solute per litre (L) of solution

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15
Q

osmolarity - normal range

A

285-295 mOsm/kg H2O

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16
Q

Glomerular filtration barrier is responsible for

A

filtration of plasma according to size and net charge

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17
Q

Glomerular filtration barrier is composed of (and role of every component)

A
  1. fenestated capillary endothelium –> SIZE BARIER
  2. fused basement membrane with heparan sulfate –> NEGATIVE CHARGE AND SIZE BARRIER
  3. epithelial layers consisting of podocyte foot processes –> NEGATIVE CHARGE BARRIER
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18
Q

Glomerular filtration barrier - components for size barrier and components for charge barrier

A

size: 1. fenestated capillary endothelium 2. fused basement membrane
charge: 1. fused basement membrane 2. epithelial layers consisting of podocyte foot processes

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19
Q

Charge barrier is lost in ….(and clinical presentation)

A

nephrotic syndrome –> 1. albuminuria 2. hypoproteinemia

3. generalized edema 4. hyperlipidemia

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20
Q

renal clearance - definition

A

volume of plasma from which the substance is completely cleared per unit (from renal)

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21
Q

renal clearance - calculation

A 
Cx=Ux.V/Px
CX=Clearance of x (ml/min)
Ux=urine concentration of x (mg/ml)
Px=plasma concentration of X (mg/ml)
V=urine flow rate (ml/min)
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22
Q

if renal clearance equals/smaller/bigger than GFR

A

Cx smaller: if smaller net tubular reabsorption of X
Cx bigger: net tubular secretion of X
Cx=GFR: no net secretion or reabsorption

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23
Q

Inulin clearance can be used to … (why)

A

caclulate GFR because it is freely filtered and is neither reabsorder nor secreted

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24
Q

Glomerular filtration rate (GFR) estimates

A

how much blood passes through the glomeruli each minute.

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25
Q

GFR calculation

A

GFR = inulin clearance = (Urine concentration of inulin x urine flow rate) / plasma concentration of inulin = Starling equation

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26
Q

Normal GFR =

A

100ml/min

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27
Q

Starling equation

A 
GFR= Kf ((Pgc - Pbs) - (πgc-πbs)) 
gc: glomerular capillary
bs: Bowman space 
Kf: filtration constant  
πbs = 0
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28
Q

creatinine clearance - clinical relevance

A

it is an approximate measure of GFR –> slightly overestimates GFR because creatinine is moderaterly secreted by renal tubules

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29
Q

chronic kidney disease - GFR measure

A

incremental reductions in GFR define the stages of chronic kidney disease

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30
Q

creatinine serum concentration

A

0.6-1.2mg/dL or 53-106μmol/L

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31
Q

Effective renal plasma flow (eRPF) is used to

A

calculate renal plasma flow (RPF) and hence estimate renal function.

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32
Q

Effective renal plasma flow (eRPF) can be estimating using … (why)

A

para-aminohippurinc (PAH) clearance because filtration and secretion is nearly 100% excretion of all PAH that enter kidney

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33
Q

Effective renal plasma flow (eRPF) calculation

A

para-aminohippurinc (PAH) clearance = Upah x V/Ppah

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34
Q

renal blood flow (RBF) is the

A

volume of blood delivered to the kidneys per unit time

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35
Q

renal blood flow (RBF) - calculation

A

renal blood flow (RBF) = RPF/(1-Hct)

1-HcT=plasma

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36
Q

eRPF vs true renal plasma flow

A

eRPF underestimates true renal plasma flow slightly

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37
Q

renal filtration fraction - definition

A

is the ratio of the glomerular filtration rate (GFR) to the renal plasma flow (RPF)

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38
Q

Renal filtration fraction - caclulation and normal value

A

FF=GFR/RPF = 20% (normally)

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39
Q

Filtered load calculation

A

Filtered load (mg/min) = GFR(ml/min) x plasma concentration (mg/ml)

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40
Q

effect of NSAID on renal function

A

NSAIDs inhibit prostagladins (that preferentially dilated afferent arteriole and increase RPF and GFR, not the FF)

  • -> constriction of afferent arteriole –> decrease of RPF and GFR, not the FF –> IN LOW RENAL BLOOD SATES
  • -> ACUTE RENAL FAILUE
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41
Q

effect of ACE inhibitors on renal function

A

ACE inhibitors decrease angiotensin 2 (that preferentially constricts efferent arteriole and decrease RPF, increase GFR and increase FF) –> dilation of efferent arteriole –> increas RPF, decreased GFR, so decrease FF)

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42
Q

prostagladins vs angiotensin 2 on renal function

A
  • prostagladins –> preferentially dilated afferet arteriole and increase RPF and GFR, not the FF
  • angiotensin 2 –> inhibits preferentially constricts efferent arteriole and decrease RPF, increase GFR and increase FF
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43
Q

Afferent arteriole constriction - GFR, PRF, FF?

A

GFR: decreased
RPF: decreased
FF: -

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44
Q

efferent arterile constriction - GFR, PRF, FF?

A

GFR: increased
RPF: decreased
FF: increased

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45
Q

increased plasma protein concentration - GFR, PRF, FF?

A

GFR: decreased
RPF: -
FF: decreased

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46
Q

decreased plasma protein concentration - GFR, PRF, FF?

A

GFR: increased
RPF: -
FF: increased

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47
Q

constriction of ureter - GFR, PRF, FF?

A

GFR: decreased
RPF: -
FF: decreased

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48
Q

dehydration- GFR, PRF, FF?

A

GFR: decreased
RPF: decreased
FF: INCREASED

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49
Q

filtration fruction on dehydration?

A

increased

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50
Q

renal - filtration, reabsorption, secretion excretion???

A

aaaa

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51
Q

renal - Filtered load - calculation

A

GFR X plasma concentration

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52
Q

renal - Excretion rate - calculation

A

urine flow rate (ml/min) x urine concentration

53
Q

renal - how to estimate secretion

A

Secretion = excreted - filtered

54
Q

renal - how to estimate urinary excretion

A

urinary excretion = glomerular filtration - tubular reabsorption + Tubular secretion

55
Q

FENa?

A

fractional excretion of sodium

56
Q

fractional excretion of sodium (FENa) - definition?

A

it is the percentage of the sodium filtered by the kidney which is excreted in the urine

57
Q

fractional excretion of sodium (FENa) - calculation

A

Na+ excreted/Na+ filaterd = (urine flow rate x urine concentration of Na+) / (GFR x plasma concentration of Na+) = (urine flow rate x urine concentration of Na+) / (Ucr x V/Pcr x plasma concentration of Na+) =
(Pcr x U Na) / (Ucr x P Na)

58
Q

Glucose clearance - describe

A

Glucose at a normal plasma level is completely reabsorbed in proximal convoluted tubule by Na+/gluocse contrasport

59
Q

glucose in serum in serum (normally)

A

fasting: 70 - 110 mg/dL (3.8-6.1 mmol/L)

2h postpradial: less than 120mg/dL, less than 6.6mmol/L

60
Q

glucose in serum in cerebrospinal fluid (normally)

A

40-70 mg/dL

2.2-3.9 mmol/L

61
Q

glucose in urine - concentrations (in adults)

A

In adults, at plasma glucose of 200 mg/dL –> glucosouria begins. At rate of 375 mg/min, all trasnportes are fully saturated

62
Q

glucosouria is an important clinical clue to

A

diabetes mellitus

63
Q

glucose clearance - splay?

A

is the region of substance clearance between threshold and Tm –> it is due to heterogeneity of nephrons

64
Q

glucose clearance - pregnancy

A

normal pregnancy may decrease ability of proximal convoluted tubule to reabsorb glucose and aminoacids
–> glucosouria and aminoaciduria

65
Q

mechanism that induce glucosouria and aminoaciduria in normal pregnancy

A

normal pregancy may decrease ability of proximal convoluted tubule to reabsorb glucose and aminoacids

66
Q

nephron anatomy (and cortex vs medulla)

A

glomerulus (cortex) –> proximal convoluted tubule (cortex and medulla) –> descending limb loop of Henle (medulla) –> loop of henle (medulla) –> ascending limb of henle (medulla and cortex)–> distal convoluted tubule (cortex) –> collecting duct

67
Q

Nephron physiology - early proximal convoluted tubule structure

A

it contains brush border

68
Q

Nephron physiology - early proximal convoluted tubule - reabsorbs

A

all glucose and aminoacis
most HCO3-, Na+ (65-80%), CL-, PO4, k+, H2O, uric acid, lactate
ISOTONIC ABSORPTION

69
Q

Nephron physiology - early proximal convoluted tubule -secretes

A
  1. secretes H+ (Na-H+ exchange)
  2. secretes NH3 (as a buffer for secreted H+)
  3. base - (CL- - base - exchange)
70
Q

Nephron physiology - early proximal convoluted tubule - reabsorbs Na+ is absorbed via

A
  • cotrnasport with glucose, aminoacids, phosphate and lactate
  • countertrasnport via Na-H+ (linked with HCO3)
71
Q

Nephron physiology - early proximal convoluted tubule - hormones

A
  1. PTH

2. ATII

72
Q

Nephron physiology - early proximal convoluted tubule - PTH

A

It inhibits Na/PO4 cotransport –> increased PO4 excretion

73
Q

Nephron physiology - early proximal convoluted tubule - AT II

A

stimulates Na/H+ exchange –> increased Na+, H2O and HCO3- reabsorption –> permit contraction alkalosis

74
Q

Nephron physiology - early proximal convoluted tubule - basolateral membrane

A
  • Na+/K+ pump

- HCO3 channel

75
Q

Nephron physiology - early proximal convoluted tubule - Carbonic anhydrase - action

A
  • in the cell –> CO2 + H2O –> H + HCO3- –> H+ in the lumen and HCO3 in the blood
  • in the lumen –> H + HCO3- –> CO2 + H2O –> in the cell
76
Q

Nephron physiology - late proximal tubule - action

A

Na+ is reabsorbed with CL-

77
Q

Nephron physiology - thin descending loop of Henle - function

A

passively reabsords H2O via medullary hypertonicity (impermeable to Na+) –> Concentrating segment –>
Makes urine hypertonic

78
Q

Nephron physiology - thick ascending loop of Henle - function

A
  1. reabsorb 1Na+, 1K+ and 2CL- –> K+ is goining either to the blood (basalateral membrane) or back to the lumen
    - -> generates + lumen (K+ backleaking) –> induces paracellular reabsorption of Mg2+ and Ca2+ (to blood)
  2. Impermeable to H2O –> urine less concentrated
  3. CL- is going to the blood (down the electrochemical gradient)
79
Q

Nephron physiology - thick ascending loop of Henle - H2O

A

Impermeable to H2O –> urine less concentrated

80
Q

Nephron physiology - thick ascending loop of Henle - basolateral membrane

A
  1. Na+/k+ pump

2. k+ and CL- channel to their electrochemincal gradient (to the blood)

81
Q

proportion of Na+ reabsorption in proximal convoluted tubule and in thick ascending loop of Henle

A
  • proximal convoluted tubule –> 65-80%

- thick ascending loop of Henle –> 10-20%

82
Q

Nephron physiology - early distal convoluted tubule - function

A
  1. reabsorbs Na/CL- (cotransportation) and Ca2+

2. makes urine fully dilute (hypotonic)

83
Q

Nephron physiology - early distal convoluted tubule - hormones (and action)

A

PTH –> increases Ca+/Na+ exchange on he basolateral membrane –> increases Ca2+ reabsorption

84
Q

Nephron physiology - early distal convoluted tubule - basolateral membrane

A
  • Na+/K+ pump
  • cl channel
  • Na+ /ca2+ exchanger
85
Q

proportion of Na2+ reabsorption in proximal convoluted tubule, in thick ascending loop of Henle, and in early distal convoluted tubule

A
  • proximal convoluted tubule –> 65-80%
  • thick ascending loop of Henle –> 10-20%
  • early distal convoluted tubule –> 5-10%
86
Q

Nephron physiology - collecting tubule - function

A

reabsorbs Na+ in exchange for secreting K+ and H+:

  1. k+ channel to lumen
  2. Na+ channel into cell
  3. H+ ATPase to lumen
  4. H+/K+ pump (H+ to lumen, K+ into cell)
  5. CL/HCO3 exhanger (CL into cells)
  6. aquaporin (H20) channels)
87
Q

Nephron physiology - collecting tubule - type of cells

A
  1. principal cells
  2. α-intercalated cells
  3. β-intercalated cells
88
Q

Nephron physiology - collecting tubule - hormones

A
  1. Aldosterone

2. ADH

89
Q

Nephron physiology - collecting tubule - aldosterone action

A

acts on mineralocorticoid receptor –> mRNA –> proteins synthesis:

  1. in principal cells –> a. increases apical (to the lumen) K+ conductase b. increases Na/K pump (basolateral)
    c. increases epithelial Na+ channel (ENaC) activity –> lumen negatiivty –> K+ secretion
  2. in α-intercalated cells –> lumen negativity –> H+ ATPase activity –> increased H+ secretion –> HCO3-/CL- (Cl in the cell) exchanger activity (in β-intercalated cells)
90
Q

Nephron physiology - collecting tubule - ADH action

A

acts at V2 receptor –> insertion of aquaporin (H20 channels) on apical side

91
Q

Nephron physiology - collecting tubule - function (and which cells)

A

reabsorbs Na+ in exchange for secreting K+ and H+. It also absorb H20:

  1. k+ channel to lumen (principal cells)
  2. Na+ channel into cell (principlal cells)
  3. H+ ATPase to lumen (α-intercalated cells)
  4. H+/K+ pump (H+ to lumen, K+ into cell) ( α-intercalated cells)
  5. CL/HCO3 exhanger (CL into cells) (β-intercalated cells)
  6. aquaporin (H20 channels) (principal cells)
92
Q

Nephron physiology - location of PTH action

A
  1. early proximal convoluted tubule

2. early distal convoluted tubule

93
Q

Nephron physiology - location of ATII action

A

early proximal convoluted tubule

94
Q

Renal tubular defects - types

A
  1. Fanconi syndrome
  2. Bartter syndrome
  3. Gitelman syndrome
  4. Liddle syndrome
  5. Syndrome of apparent minelocorticoid excess
95
Q

Fanconi syndrome - pathophysiology

A

Generalized reabsorptive defect in early proximal convoluted tubule

96
Q

Fanconi syndrome –> …(result in)

A

increased amino acids, glucose, HCO3- and PO4- – Metabolic acidosis (proximal renal tubular acidosis)

97
Q

causes of Fanconi syndrome

A
  1. hereditary defects (Wilson disease, tyrosinemia, glycogen storage disease, cystinosis)
  2. iscemia
  3. multiple myeloma
  4. nephrotoxins/drugs (expired tetracyclines, ifosfamide, cisplatin, tenofovir, lead poisoning)
98
Q

nephrotoxins/drugs that cause Fanconi syndrome

A
  1. ifosfamide
  2. cisplatin
  3. tenofovir
  4. lead poisoning
  5. expired tetracyclines
99
Q

Bartter syndrome - pathophysiology (and result in)

A

Reabsorptive defect in thick ascending loop oh Henle

–> affects Na+/K+/2CL- cotransporter –>

100
Q

Bartter syndrome –> …. (result in)

A
  1. hypokalemia
  2. metabolic alkalosis
  3. hypercalciuria
101
Q

Situation that mimics Bartter syndrome

A

chronic loop diuretic use

102
Q

Loop diuretics - drugs

A

1 Furosemide

  1. Buetanide
  2. torsemide
  3. Ethracrynic acid
103
Q

Bartter syndrome - mode of inheritance

A

AR

104
Q

Gitelman syndrome - pathophysiology

A

Reabsosptive defect in Distal convoluted tubule

105
Q

Gitelman syndrome - Mode of inheritance

A

AR

106
Q

situation that mimics Gitelman syndrome

A

lifelong thiazide diuretics

107
Q

thiazide diuretics: drugs

A
  1. Hydrochlorothiazine
  2. Chlorothalidone
  3. Metolazone
108
Q

Gitelman syndrome –> …. (results in)

A
  1. hypokalemia
  2. hypomagnesia
  3. metabolic alkalosis
  4. hypocalciuria
109
Q

Gitelman syndrome vs Barrter syndrome according to severity

A

Barrter is more severe

110
Q

Liddle syndrome - pathophysiology

A

Gain of function mutation –> increased Na+ reabsorption in collecting tubules (high activity of epithelial channel)

111
Q

situation that mimics Liddle syndrome

A

hyperaldosternism (but aldosterone is nearly undetectable)

112
Q

Liddle syndrome - mode of inheritance

A

AD (gain function mutation)

113
Q

Liddle syndrome –> ….. (result in)

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low aldosterone
114
Q

Liddle syndrome - treatment

A

amiloride

115
Q

Syndrome of Apparent Mineralocorticoid excess - pathophysiology

A

hereditary deficiency of 11β-hydroxysteroid dehydrogenase which normally converts cortisol (can activate mineralocorticoid receptors) to cortizone (inactivate on mineralocorticoid receptors) in cell containing mineralocorticoid receptors –> increased mineralocorticoid activity

116
Q

Syndrome of Apparent Mineralocorticoid excess - manifestations

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low serum aldosterone levels
117
Q

situation that mimics Apparent Mineralocorticoid excess

A

glycyrrhetinic acid (present in licorice) which blocks activity of 11β-hydroxysteroid dehydrogenase

118
Q

licorice, is the root of

A

Glycyrrhiza glabra from which a sweet flavour can be extracted (wide variety of candies or sweets)

119
Q

Apparent Mineralocorticoid excess - treatment

A

coirticosteroids –> decreases endogenous cortisol production –> decrease mineralocorticoid receptor activation

120
Q

Renal tubular defects - types

A
  1. Fanconi syndrome
  2. Bartter syndrome
  3. Gitelman syndrome
  4. Liddle syndrome
  5. Syndrome of apparent minelocorticoid excess
121
Q

Relative concentrations along proximal convoluted tubules - (Tubular fluid)/plasma (smaller, bigger, equals 1)

A

TF/P bigger than 1 –> when solute is reabsorded less quickly than water
TF/P smaller than 1 –> when solute is reabsorded more quickly than water
TF/P=1 –> when solute and water are reabsorbed at the same rate

122
Q

Relative concentrations along proximal convoluted tubules - substance with TF/P=1

A

Na+

123
Q

Relative concentrations along proximal convoluted tubules - substance with TF/P smaller than 1 (explain) (in order)

A

from more negative to 0
1. Glucose
2. aminoacids
3. HCO3
solutes is reabsorded more quickly than water
–> concentration in plasma is bigger than tubule

124
Q

Relative concentrations along proximal convoluted tubules - substance with TF/P bigger than 1 (explain) (in order)

A

from more positive to 0

  1. PAH 2. Creatine 3. inulin 4. urea
  2. CL- 6. k+ water is reabsorbed more quicly than solutes (or solutes secretion –> concentration in tubule is bigger than plasma
125
Q

Relative concentrations along proximal convoluted tubules - substance with TF/P=1

A

Na+

126
Q

Relative concentrations along proximal convoluted tubules - inulin (explain)

A

TF/P is bigger than 1 –> tubular inulin increases in concentration (BUT NOT AMOUNT) along the PCT as a result of water reabsorption

127
Q

Relative concentrations along proximal convoluted tubules - CL- (explain)

A

TF/P is bigger than 1 –> CL- reabsorption occuts at a slower rate than Na+ in early PCT and then matches at the rate of Na+ reabsorption more distally -> thus, its relative concentration increases before it platues

128
Q

Total body water can be measured by

A
  1. Tritiated water
  2. D2O
  3. Antipyrene
129
Q

proportion of Na2+ reabsorption in proximal convoluted tubule, in thick ascending loop of Henle, in early distal convoluted tubule, collecting tubules

A
  • proximal convoluted tubule –> 65-80%
  • thick ascending loop of Henle –> 10-20%
  • early distal convoluted tubule –> 5-10%
  • collecting tubule –> 3-5%

Renal (15 decks)

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