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Principles Of Physiology And Pharmacology > Kidney > Flashcards

Kidney Flashcards

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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
Thick ascending limb Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed
25% Luminal: na/k/2cl symporter; k+ channel Basolateral: Na/k atpase Paracellular: ca2+, mg2+, Na+, nh4+ (k+ channel-> luminal membrane is positively charged)
26
Distal tubule Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed
2-5% Luminal: na/cl symporter Basolateral: Na/k atpase Paracellular: cl- (luminal membrane is negatively charged)
27
Collecting duct Na reabsorption on luminal/basolateral/paracellular; percentage reabsorbed
5% Luminal: na+ Basolateral: Na/k atpase Paracellular: cl- (luminal membrane is negatively charged )
28
How do tight junctions affect tubule permeability
Increase
29
Descending vs ascending limb of LOH
Descending: permeable to water Ascending: impermeable to water
30
medullary interstitial gradient/Counter current multiplier explained, osmolality of blood entering DCT, what maintains gradient
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
Urea recycling; % of urea filtered that is excreted
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
Adh mechanism
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
Osmolar clearance formula and definition
Osmolar clearance = vol of plasma cleared of all osmotically active particles per unit time Urine osmolarity x urine flow rate / plasma osmolarity
34
Free water clearance formula and definition ; | Implication of values
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
Osmoreceptors in hypothalamus
SFO: subformical organ MPN : median Preoptic nucleus OVLT: organum vasculosum terminalis
36
Why is adh so effective
Short half life Rapid release Rapid effect
37
What else controls adh levels other than osmoreceptors
``` Nicotine (stimulates) Nausea (stimulates) Pain (stimulates) Stress (stimulates) Alcohol (inhibits) ```
38
Diabetes inspidus characteristics and types
Types: neurogenic (no adh secreted; congenital/ head injury) Nephrogenic (Inherited mutated aqp 2/ acquired from infection/drug) Characteristics: polyuria; polydipsia; nocturia
39
Osmotic diuresis characteristics and mechanism
Characteristics: polyuria/ polydipsia Mechanism: increased blood glucose-> increased glomerular filtration of glucose-> increased osmolarity of filtrate-> decreased water reabsorption
40
Reabsorption of k+
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
Secretion of k+
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
Hypokalemia + hyperkalemia levels
``` 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
Hypokalemia causes
External losses via GI/skin (severe sweating)/ kidney (high tubular flow or hyperaldosteronism) Redistribution into cells (alkalosis/insulin excess) Inadequate k intake
44
What does aldosterone do , where is it produced
``` 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
What contributes to high tubular flow rates
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
How does alkalosis and insulin excess increase k+ redistribution into cells
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
Hypokalemia signs and symptoms
``` Very Negative rmp Cardiac dysrythmias Muscle weakness Nausea Polyuria ```
48
Hypokalemia treatment
Diet rich in k+ Kcl administration Alkalosis correction K-sparing diuretics
49
Hyperkalemia causes
Decreased external losses: hypoaldosteronism/ drugs/ renal failure Redistribution out of cells: acidosis/lack of insulin/ cell lysis
50
Signs and symptoms of hyperkalemia
High rmp with Long refractory Cardiac dysthymia Muscle weakness and paralysis Nausea
51
Hyperkalemia treatment
Long term: Diuretics Intermediate term: Insulin Short term: Ca iv (stabilise cardiac membrane)
52
How is na content regulated
1. GFR | 2. Na reabsorption
53
SNS control of GFR and renin in response to Low bp
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
Intrinsic control of GFR and purpose
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
Sensors of bp
NaCl concentration receptors in macula densa Baroreceptors in central arteriole tree Baroreceptors in afferent arteriole Baroreceptors in atrium + intrathoracic veins
56
Effector pathways in response to changes in bp, linked to sodium reabsorption
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
Macula densa mechanism
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
How’re angiotensin 2 and aldosterone secreted
Low bp-> plasma angiotensinogen (made by liver) -RENIN-> angiotensin 1 (10 peptide) -ACE-> angiotensin 2 (8 peptide) -> causes aldosterone secretion from adrenal cortex
59
Angiotensin 2 effects
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
Types of natriuretic peptides, origin, when they are produced, effects
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
How h+ is gained
1. Production of acids from metabolism 2. Hypoventilation 3. Loss of bicarbonate in diarrhoea 4. Loss of bicarbonate in pee
62
How is h+ lost
1. Hyperventilation 2. Loss in puke 3. Loss in pee 4. Loss in metabolic activity
63
Ph equation
Ph = pka + lg[hco3-]/[pco2]
64
Normal pco2 & [hco3-] levels
``` Pco2= 5.3kpa [hco3-]= 25mM ```
65
How is bicarbonate reabsorbed , and where , which pumps are involved
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
How is hco3- secreted and where
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
Glutamine and hco3- reabsorption
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
H+ excretion, when does this happen
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
Respiratory acidosis causes and responses
high pco2 Causes : acute (asthma/drugs) ; chronic (copd) Responses : chemical (co2-> hco3-); renal (increases h+ secretion as nh4+; increased hco3- absorption)
70
Metabolic acidosis causes
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
Respiratory alkalosis
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
Metabolic alkalosis
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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