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Principles Of Physiology And Pharmacology > Kidney > Flashcards

Kidney Flashcards

1
Q

Kidney functions

A

Excretion (urea, Uric acid, creatinine, urobilinogen, metabolites of hormones, foreign chemicals)
Body fluid composition (volume regulation, osmoregulation, ph)
Endocrine

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2
Q

Renal capsule is made of

A

Glomerulus + Bowman’s/renal corpuscle

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3
Q

Layers and characteristics of renal corpuscle

A
  1. Fenestrated capillary endothelium (leaky af)
  2. Basement membrane (lamina densa, interna rara, externa rara; fixed polyanions-> negative charge -> cations filter faster
  3. Podocytes (foot processes interdigitate-> filtration slits; nephrin and podocin are important proteins)
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4
Q

Path of filtrate in nephron

A

Glomerulus -> Bowman’s space-> pct -> proximal straight tubule (MEDULLA)-> descending thin limb -> ascending thin limb -> thick ascending limb -> dct (CORTEX) -> cd

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5
Q

Nephron types

A
  1. Cortical (85%): in outer 2/3 of cortex; short LOH

2. Juxtamedullary (15%): in inner 1/3 of cortex; Long LOH

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6
Q

Juxtaglomerular apparatus location and parts

A
  1. Juxtaglomerular cells (around afferent arterioles)
  2. Mesangial cells (in between glomerulus and dct)
  3. Macula densa (between loh and dct)
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7
Q

Percentage of plasma in glomerulus filtered

A

20%

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8
Q

Infection, damage to glomerulus and high bp can cause

A

Proteinuria
Haemoglobinuria
Haematuria

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9
Q

Gfr definition and factors affecting

A

Volume of fluid filtered from glomeruli per minute

Dependent on: starling forces/ sa/ permeability of capillaries

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10
Q

Starling forces pressures and values; net glomrrular filtration pressure

A

Hydrostatic: capsular pressure towards interface=15mmhg; hydrostatic pressure towards interface=60mmhg
Oncotic: pressure away at glomerular end = 29mmhg; away at capsular end=0mmhg
Net pressure= (60-15)-(29-0)= 16mmhg

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11
Q

What happens to hydrostatic pressure gradient and gfr when aa/ea constricts or dilates

A

Aa dilate-> hydrostatic pressure gradient increases-> gfr increases
Aa constrict-> hydrostatic pressure decreases-> gfr decreases
Ea dilate-> hydrostatic pressure decreases-> gfr decreases
Ea constricts-> hydrostatic pressure increases -> gfr increases

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12
Q

How is sa of filtration interface changeable

A

Mesengial cells have actin -> innervated by sns -> bp drops-> contraction of actin -> decreased sa

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13
Q

Glucose reabsorption

A

Luminal: sglt
Basolateral: glut
Na/k atpase

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14
Q

Aa reabsorption

A

In proximal tubule

6 na dependent

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15
Q

Secretion of organic anions in prox tubule; why aren’t they filtered

A

Bound to protein in blood, not filtered
Basolateral: OAT1/3 (in exchange for dicarboxylate) ; na/dc antiporter maintains dc conc; na/k atpase maintains na conc
Luminal: Pri AT

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16
Q

Secretion of organic cations , eg

A

Basolateral: oct2

Luminal : mate antiporter (exchange h+); OCTN

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17
Q

Clearance definition and formula

A

Volume of plasma cleared of a substance in a give. Time

Clearance = [urine] x [volume of urine per min] / [plasma]

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18
Q

How is GFR measured and why use these substances

A

Inulin/ creatinine (but overestimate as it is slightly secreted in pct)
Freely filtered, Not secreted, not reabsorbed, not metabolites, easily measured

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19
Q

clearance Values for substances reabsorbed/neither reabsorbed Nor secreted/ secreted

A

Reabsorbed <120ml/min
Neither reabsorbed Nor secreted 120ml/min
Secreted >120ml/min

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20
Q

Measuring effective renal plasma flow

A

Use PAH, it is filtered and completely secreted but not reabsorbed
Completely removed from blood that passes through kidneys
An underestimate as some blood to kidneys flows through perirenal fat region, not processed by nephrons

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21
Q

Renal plasma flow value , percentage of plasma in blood, renal blood flow

A

Renal plasma flow= 600ml/min
% plasma = 55%
Renal blood flow= 1100 ml/min

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22
Q

Normal plasma osmolality

A

290 mosm/kg

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23
Q

Sites of sodium reabsorption

A

Most of it : proximal tubule + thick ascending limb

Parts influenced by hormones: distal tubule + cd

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24
Q

Proximal tubule Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed

A

65%
Luminal: Na/h antiporter (NHE3) ; Na/ nutrient symporter
Basolateral: Na/k atpase
Paracellular: cl- (luminal membrane is negatively charged)

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25
Q

Thick ascending limb Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed

A

25%
Luminal: na/k/2cl symporter; k+ channel
Basolateral: Na/k atpase
Paracellular: ca2+, mg2+, Na+, nh4+ (k+ channel-> luminal membrane is positively charged)

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26
Q

Distal tubule Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed

A

2-5%
Luminal: na/cl symporter
Basolateral: Na/k atpase
Paracellular: cl- (luminal membrane is negatively charged)

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27
Q

Collecting duct Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed

A

5%
Luminal: na+
Basolateral: Na/k atpase
Paracellular: cl- (luminal membrane is negatively charged )

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28
Q

How do tight junctions affect tubule permeability

A

Increase

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29
Q

Descending vs ascending limb of LOH

A

Descending: permeable to water
Ascending: impermeable to water

30
Q

medullary interstitial gradient/Counter current multiplier explained, osmolality of blood entering DCT, what maintains gradient

A

Ascending limb pumps out salt-> descending limb loses water in response-> fluid moves-> recalibration-> numbers on descending limb are increasing, decreasing (upwards) on ascending
Vasa recta
Osmolality leaving loh is hypotonic

31
Q

Urea recycling; % of urea filtered that is excreted

A
  1. Pct : passive reabsorption due to solvent drag between cells
  2. LOH: apical secretion due to UT-A2
  3. CD: reabsorption due to UTA1 (luminal side) ; UTA3 (basolateral)
    40%
32
Q

Adh mechanism

A

Adh-> v2 receptor -> camp pathway activated-> vesicles with AQP2 fuse with luminal membrane-> increased water uptake -> water exits at basolateral membrane with AQP3/4

33
Q

Osmolar clearance formula and definition

A

Osmolar clearance = vol of plasma cleared of all osmotically active particles per unit time
Urine osmolarity x urine flow rate / plasma osmolarity

34
Q

Free water clearance formula and definition ;

Implication of values

A

Ability of kidneys to excrete dilute/concentrated urine
Free water clearance= urine flow rate - osmolarity of urine x urine flow rate/plasma osmolarity
=0 isomotic urine
>0 dilute urine
<0 concentrated urine

35
Q

Osmoreceptors in hypothalamus

A

SFO: subformical organ
MPN : median Preoptic nucleus
OVLT: organum vasculosum terminalis

36
Q

Why is adh so effective

A

Short half life
Rapid release
Rapid effect

37
Q

What else controls adh levels other than osmoreceptors

A 
Nicotine (stimulates) 
Nausea (stimulates) 
Pain (stimulates) 
Stress (stimulates) 
Alcohol (inhibits)
38
Q

Diabetes inspidus characteristics and types

A

Types: neurogenic (no adh secreted; congenital/ head injury)
Nephrogenic (Inherited mutated aqp 2/ acquired from infection/drug)
Characteristics: polyuria; polydipsia; nocturia

39
Q

Osmotic diuresis characteristics and mechanism

A

Characteristics: polyuria/ polydipsia
Mechanism: increased blood glucose-> increased glomerular filtration of glucose-> increased osmolarity of filtrate-> decreased water reabsorption

40
Q

Reabsorption of k+

A

PCT: 65% paracellular solvent drag
Thick ascending limb: 30% by k/Na/2cl symporter+paracellular (luminal); k channels + k/cl + na/k atpase (basolateral)
Dct: 5% by k/h antiporter + paracellular (luminal) ; k channels + k/cl + na/k atpase (basolateral)
CD: k/h antiporter (luminal); k channels (basolateral)

41
Q

Secretion of k+

A

By principal cells in collecting duct
Luminal: k+ channels (renal outer medullary k+ channel ROMK / ca2+ activated big conductance k+ channel BK) + kcl symporter
Basolateral: Na/k atpase

42
Q

Hypokalemia + hyperkalemia levels

A 
Hypokalemia mild= 3.0-3.5mM
Moderate= 2.5-3.0
Severe= <2.5 
Hyperkalemia mild= 5.5-6.5
Moderate= 6.5-7.5
Severe >7.5
43
Q

Hypokalemia causes

A

External losses via GI/skin (severe sweating)/ kidney (high tubular flow or hyperaldosteronism)
Redistribution into cells (alkalosis/insulin excess)
Inadequate k intake

44
Q

What does aldosterone do , where is it produced

A 
zona glomerulosa
Increases activity of k/Na atpase 
K+ channels 
Na channels 
Altogether enhancing k+ secretion, Na+ reabsorption in dct/cd/gut/sweat glands
45
Q

What contributes to high tubular flow rates

A

Loop diuretics : target thick ascending limb -> inhibits Na/k reabsorption -> inhibits water absorption
Thiazide diuretics: proximal tubule-> inhibits na reabsorption
Transported mutations : inhibit Na+ reabsorption
Osmotic diuresis

46
Q

How does alkalosis and insulin excess increase k+ redistribution into cells

A

Alkalosis: k/h antiporter -> k in h out to buffer ; increased k+ secretion due to electrochemical gradient changes
Insulin excess: insulin increases Na/k atpase activity

47
Q

Hypokalemia signs and symptoms

A 
Very Negative rmp 
Cardiac dysrythmias 
Muscle weakness 
Nausea 
Polyuria
48
Q

Hypokalemia treatment

A

Diet rich in k+
Kcl administration
Alkalosis correction
K-sparing diuretics

49
Q

Hyperkalemia causes

A

Decreased external losses: hypoaldosteronism/ drugs/ renal failure
Redistribution out of cells: acidosis/lack of insulin/ cell lysis

50
Q

Signs and symptoms of hyperkalemia

A

High rmp with Long refractory
Cardiac dysthymia
Muscle weakness and paralysis
Nausea

51
Q

Hyperkalemia treatment

A

Long term: Diuretics
Intermediate term: Insulin
Short term: Ca iv (stabilise cardiac membrane)

52
Q

How is na content regulated

A
  1. GFR

2. Na reabsorption

53
Q

SNS control of GFR and renin in response to Low bp

A

When bp is Low, SNS -> renin release/vasoconstriction of afferent arteriole/ contraction of mesangial cells -> decreased SA of filtration barrier -> decreased GFR -> increased na absorption -> increased bp

54
Q

Intrinsic control of GFR and purpose

A

Maintains constant gfr between bp of 90-200 to protect renal capillaries fro, hypertensive damage
Increased bp-> juxtaglomerular apparatus senses this -> vasoconstriction of afferent arteriole-> gfr does not increase

55
Q

Sensors of bp

A

NaCl concentration receptors in macula densa
Baroreceptors in central arteriole tree
Baroreceptors in afferent arteriole
Baroreceptors in atrium + intrathoracic veins

56
Q

Effector pathways in response to changes in bp, linked to sodium reabsorption

A

Renal sympathetic nerves -> renin release -> increase bp
Direct pressure effect on kidney
RAAS -> increase na reabsorption -> increase bp
ANP-> inhibit enac + renin release -> decreased bp
Dopamine -> synergism with ANP

57
Q

Macula densa mechanism

A

High bp-> increased [nacl] detected-> na/k atpase indirectly brings about formation of adenosine -> adenosine binds to A1 receptors of afferent arteriole-> inhibits renin release + increase [ca] -> afferent arteriole vasoconstricts

58
Q

How’re angiotensin 2 and aldosterone secreted

A

Low bp-> plasma angiotensinogen (made by liver) -RENIN-> angiotensin 1 (10 peptide) -ACE-> angiotensin 2 (8 peptide) -> causes aldosterone secretion from adrenal cortex

59
Q

Angiotensin 2 effects

A
  1. Aldosterone secretion
  2. Increased na+ reabsorption from PT (binds to AT1 receptors-> stimulates NHE3 + Na/k-atpase)
  3. Vasoconstriction of small arterioles
  4. Thirst (binds to osmoreceptors)
  5. ADH release (binds to osmoreceptors)
60
Q

Types of natriuretic peptides, origin, when they are produced, effects

A

Produced when heart is stretched
ANP (atrium)
BNP (ventricle)
Natriuretic: inhibits ENaC + renin release + aldosterone production; synergism with dopamine to inhibit na/k atpase
Diuretic: inhibit adh release
Hypotensive: vasodilation + dilates afferent arterioles

61
Q

How h+ is gained

A
  1. Production of acids from metabolism
  2. Hypoventilation
  3. Loss of bicarbonate in diarrhoea
  4. Loss of bicarbonate in pee
62
Q

How is h+ lost

A
  1. Hyperventilation
  2. Loss in puke
  3. Loss in pee
  4. Loss in metabolic activity
63
Q

Ph equation

A

Ph = pka + lg[hco3-]/[pco2]

64
Q

Normal pco2 & [hco3-] levels

A 
Pco2= 5.3kpa 
[hco3-]= 25mM
65
Q

How is bicarbonate reabsorbed , and where , which pumps are involved

A

In tubular epithelial cells,
H2O + co2 -> h2co3 -> H+ + Hco3-
Hco3- goes into bs; H+ into lumen by NHE3/H+ atpase/ H+K+ atpase
Luminal H+ combines with filtered hco3- -> h2co3-> h20 + co2 -> passive diffusion into cells
At PCT/ascending LOH/ cd type A

66
Q

How is hco3- secreted and where

A

Cd type b
In tubular cell, co2+h2o -> h2co3-> h+ +hco3-
H+ to blood by h+ atpase
Hco3- to lumen by hco3-/cl antiporter PENDRIN

67
Q

Glutamine and hco3- reabsorption

A

Acidosis-> liver produces glutamine -> gln enters tubular cell by glutamine-aa exchanger (LAT2)on basolateral side; na/gln symporter on luminal side-> nh4 + hco3- -> hco3- reabsorbed ; nh4 excreted by nh4/na antiporter

68
Q

H+ excretion, when does this happen

A

H+ excreted when no more filtered hco3- is present

H20+ co2-> h2co3 -> h+ + hco3- -> hco3- reabsorbed
H+ excreted into Lumen and combines with nonbicarbinate buffer -> excreted OR excreted as H+

69
Q

Respiratory acidosis causes and responses

A

high pco2
Causes : acute (asthma/drugs) ; chronic (copd)
Responses : chemical (co2-> hco3-); renal (increases h+ secretion as nh4+; increased hco3- absorption)

70
Q

Metabolic acidosis causes

A

Low hco3-
Causes : true hco3- deficit (diarrhea/ renal tubular acidosis) ; h+ gain (nh4cl administration/ lactic acidosis)
Responses: chemical ( increased ph-> increased h+ -> hco3- decreases -> pco2 rises) ; respiratory (hyperventilation) ; renal (increased h+ excretion as nh4+, increased hco3- reabsorption)

71
Q

Respiratory alkalosis

A

Low pco2
Causes: hypoxic simulation (altitude ) ; excessive respiratory drive (fever)
Responses: chemical (h+ and hco3- drop) ; renal (decreases h+ secretion-> not all hco3- reabsorbed-> Hco3 in pee)

72
Q

Metabolic alkalosis

A

High Hco3
Causes: alkali ingestion / vomiting (H loss)/ aldosterone (stimulates H+ atpase)
Responses: chemical (hco3- and h+ drop by a bit) ; respiratory (hypoxia and co2 stimulate respiration) ; renal (decreased h+ secretion -> hco3- excretion)

Principles Of Physiology And Pharmacology (4 decks)

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