Physiology: Renal

Front 1

Ideal Stats: BP/HR/RR/pOx?

Back 1

BP 120/70
HR 70
RR 12
pOx 99%

Front 2

Ideal Stats: pH/ PCO2/ PaO2?

Back 2

pH 7.4
PCO2 40
PaO2 90

Front 3

Ideal Stats: Na/ K/ Cl/ HCO3/ BUN/ Cr

Back 3

Na 140
K 4
Cl 102
HCO3 24
BUN 15
Cr 1

Front 4

what is renal clearance Cx?

Back 4

Cx = Ux*V/Px
(urine conc*urine flow rate/plasma conc)

Front 5

RBF = ?

Back 5

RBF = RPF/(1-hct)

Front 6

what are the 3 barriers for glomerula filtration?

Back 6

1. fenestrated cap. endothelium (size barrier)
2. glom. basement membrane, fused with podocytes in a matrix of collagen IV, fibronectic and heparan sulfate (neg charge barrier -> repels albumin)
3. epithelial layer of podocyte foot processes (pedicels)

Front 7

what happens when charge barrier is lost in glomerulus?

Back 7

nephrotic syndrome -> albuminuria, hypoproteinemia, edema

Front 8

GFR = ?

Back 8

GFR = K [(Pgc - Pbs) - (pi_gc - pi_bs)]
P - hydrostatic pressure
pi - oncotic pressure (high pi = high [protein])

Front 9

what does C_inulin approximate?

Back 9

inulin is neither secreted or abs -> C_inulin = GFR
(also approx = C_creatinine cos creatinine is only partially secreted)

Front 10

what does C_PAH approximate?

Back 10

All PAH is actively secreted in proximal tubule -> C_PAH = RPF

Front 11

what is tubuloglomerular (TG) feedback?

Back 11

high GFR -> high [NaCl] in DCT ->
sensed by macula densa ->
secrets ATP and adenosine ->
vasoconstriction of afferent arteriole to decrease GFR

Front 12

where are baroceptors to sense BP?

Back 12

cardiac atria, pulm. vasculature, carotid sinus, aortic arch, juxtaglomerular apparatus, CNS, liver

Front 13

what is FF?

Back 13

FF = GFR / RPF

Front 14

what is the effect of AngII on renal corpuscle?

Back 14

preferentially constricts eff vs aff arteriole -> de. RPF, in. GFR -> in. FF

Front 15

where is glucose reabsorbed?

Back 15

proximal tubule.

Front 16

what is normal plasma [glucose]?
at what level does glucosuria begin (threshold)?
at what level is glucose transport saturated?

Back 16

normal - 90 mg/dL
glucosuria - 200 mg/dL
saturate - 350 mg/dL

Front 17

where are amino acids reabs?

Back 17

proximal tubule

Front 18

what is a normal FF?

Back 18

15 - 20%

Front 19

what is the effect of nausea, emesis and pain on the kidneys?

Back 19

induces ADH release -> in. water reabs -> hypoosmo / hyponatremia

Front 20

where is ADH made and secreted?

Back 20

made in hypothalamus, secreted in post. pituitary

Front 21

what triggers release of ADH?

Back 21

1. (mainly) increased plasma osmolarity (by osmoreceptors in ant. hypothalamus)
2. decreased volume (receptors in venous circulation) and BP (baroceptors in arterial circulation)
3. nausea, emesis, pain

Front 22

what is the relation between volume and osmolarity in ADH response?

Back 22

low vol/BP -> higher [ADH] for same osmolarity

Front 23

what comes first: thirst or release of ADH?

Back 23

ADH

Front 24

effects of ADH?

Back 24

1. (main) in. water reabs (via in. aquaporins insertion in CD
2. in. act. of NKCC, NCC, ENaC (contribute to osmotic gradient)
3. in. permeability to urea (osmo gradient)

Front 25

what is diabetes insipidus?

Back 25

1. central - ADH cannot be made/secreted
2. nephrogenic - CD resistant to ADH

Front 26

what cells in the kidney make EPO?

Back 26

endo cells of peritubular capillaries
(JG cells also secret them)

Front 27

[tubular fluid]/[plasma] of which ion increases along proximal tubule?

Back 27

Cl
(K increases very slight; Na stays constant at 1)

Front 28

how is [K] mainly regulated?

Back 28

via Na/K ATPase

Front 29

where is K mostly stored in body?

Back 29

muscles, also liver and rbc
(also as temp storage between ingestion and excretion, as excitable tissue is very sensitive to [K] cos [K] determines Vm)

Front 30

does acidosis tend to move K intracellular or extracellular?

Back 30

EXTRA

Front 31

does alkalosis tend to move K intracellular or extracellular?

Back 31

INTRA

Front 32

does tissue injury tend to move K intracellular or extracellular?

Back 32

EXTRA

Front 33

does insulin tend to move K intracellular or extracellular?

Back 33

INTRA

Front 34

does catechols tend to move K intracellular or extracellular?

Back 34

INTRA

Front 35

does ALDOSTERONE tend to move K intracellular or extracellular?

Back 35

INTRA (in. ENaC -> in. Na/K ATPase activity -> in. {K]i)

Front 36

How is K reabsorbed?

Back 36

Unregulated:
75% PCT (mostly paracellular)
15% TAL (NKCC and paracellular)
Regulated:
secreted or reabs depending on body need; reg by ALDO

Front 37

what ion is mainly responsible for water balance

Back 37

Na (TF/P stays relatively constant)

Front 38

where is ALDO made?

Back 38

adrenal cortex

Front 39

where is renin released?

Back 39

macula densa in JG (part of DCT)

Front 40

what triggers renin release?

Back 40

de. BP/volume (main)
de. Na delivery to DT
in. sympathetic tones

Front 41

what does renin do?

Back 41

cleaves angiotensinogen to angiotensin I; AngI -> AngII by ACE (in lung capillaries)

Front 42

where is AngII made?

Back 42

lung capillaries (by ACE)

Front 43

what's the effect of AngII?

Back 43

(restore GFR and increase BP)
1. preferentially constrict eff vs aff -> in. GFR
2. in. release ALDO from adrenal cortex
3. in. release ADH from post. pituitary
4. stim. Na transport throughout PT, TAL, DCT, CD
5. stimulates hypothalamus -> thirst

Front 44

what does ALDO do?

Back 44

in. Na reabs, in. K secretion, in. H secretion
1. (main) in. ENaC in CD
2. in. Na/K ATPase (-> in. apical K efflux)
3. in. NCC in DCT

Front 45

what triggers ALDO release?

Back 45

1. de. volume (via AngII)
2. in. [K] (K potent stimulus for direct adrenal release)

Front 46

what is fractional excretion (FE)?

Back 46

FEx = (Ux*V/Px) / (Ui*V/Pi)
i: inulin (creatinine also ok)

Front 47

what does macula densa do?

Back 47

(found in JGA, part of DCT) Na sensor

Front 48

what do mesangial cells do?

Back 48

(b/w glom capillaries confined by glom. basement membrane)
1. secret ECM, PGs, cytokines
2. phagocytic
3. contract to regulate GFR

Front 49

what happens when blood pH >7.5?

Back 49

low [H], more unbound albumin, more Ca++ becomes bound to alb instead -> low free [Ca] -> tetany, de. seizure threshold.
(free Ca conc very sensitive to changes in pH)

Front 50

what are the kidney's endocrine functions?

Back 50

1. EPO when hypoxic (endo cells of peritubular capillaries)
2. convert 25-OH-D3 to 1,25-(OH)2-D3 (calcitriol) by 1-alpha-hydroxylase (activated by PTH)
3. JG cells secret renin
4. secretion of PGs that vasodilate aff. arteriole -> in. GFR

Front 51

what are some common kidney failure symptoms?

Back 51

HTN, vol depl, high K, low HCO3 (acidosis), low Ca, high phos, anemia (low EPO)

Front 52

plasma pH = ?

Back 52

blood H buffered by H2CO3:
CO2 + H2O <-> H2CO3 <-> HCO3 + H
pH = pK + log [HCO3]/[CO2]
pK = 6.1
[CO2] = solubility of CO2 (0.03) x Pco2 (~40 normal)

Front 53

low pH, high pCO2, high HCO3, what's wrong?

Back 53

respiratory acidosis

Front 54

high pH, low pCO2, low HCO3, what's wrong?

Back 54

respiratory alkalosis

Front 55

low pH, low pCO2, low HCO3, what's wrong?

Back 55

metabolic acidosis

Front 56

high pH, high pCO2, high HCO3, what's wrong?

Back 56

metabolic alkalosis

Front 57

what are the defenses against H+?

Back 57

1. HCO3 and other buffers
2. respiratory accomodation (in. pH -> de. ventilation -> in. CO2)
3. renal excretion

Front 58

where and how is bicarbonate reclaimed?

Back 58

in PCT, (80% reclaimed)
1. carbonic anhydrase (apical and cytoplasmic)
2. apical NHE3 (Na/H exchanger)
3. basolaterol Na/HCO3 exchanger
(net effect: Na and HCO3- reabs, H recycled)

Front 59

what are the major filtered buffers for H+ in urine? (titratable acidity)

Back 59

1. phosphate (major), pKa ~ 6.8, mostly protonated in urine (pH decreases as it goes from PCT to DCT to CD)
2. creatinine, pKa ~ 4.8
3. uric acid, pKa ~5.8

Front 60

where is ammonium produced in response to increased pH?

Back 60

in PCT, cells take up glutamine and break down to HCO3, aKGA and NH4,
1. NH4+ goes to lumen (either diffuse as NH3, or through NH4/Na exchanger), NH4+ impermeable in lumen, buffers H+ (proton trapping)
2. , HCO3 go to blood (basolat. Na/HCO3 symport)

Front 61

what triggers NH4+ production?

Back 61

1. de. serum pH
2. in. Pco2
3. vol. depl. (NE/Epi, glucocorticoids, AngII)

Front 62

what is the effect of catechols (epi, NE) on NH4 production?

Back 62

increases

Front 63

how does body deal with acidosis?

Back 63

mainly by increasing NH4+ production, also by inserting more H-ATPase on IC cells in CD

Front 64

how does body deal with alkalosis?

Back 64

PCT:
de. HCO3 transport
de. NH4+ syn (de. uptake and metab of GLN)
CD:
de. H+ secretion
convert alpha-IC to beta-IC

Front 65

does beta intercalated cells in CD secret or reabs HCO3?

Back 65

secret
alpha: apical H-ATPase, basolat. HCO3/Cl exchanger
beta: reverse, secrets HCO3

Front 66

how much blood is filtered a day?

Back 66

~180L/day, only ~0.8L as urine

Front 67

what is the effect of sympathetics (NE/epi) on renal BP?

Back 67

alpha1 adrenoceptors -> constriction of afferent arteriole -> de. renal BP

Front 68

what is the effect of endothelin on renal BP?

Back 68

vasoconstriction -> de. BP

Front 69

what factors trigger renal vasodilation?

Back 69

PGs (counter balance for effects of vasoconstriction by AngII and sympathetics)
also via NO (present at basal level to blunt vasoconstriction response):
stretch (myogenic response)
ACh
histamine
bradykinin

Front 70

what is the effect of NSAIDs on renal BP?

Back 70

NSAIDs -> de. PGs -> exaggerated response to AngII and sympathetics -> super vasoconstriction -> renal hypotension

Front 71

what does ANP do? how is it produced?

Back 71

released by atrial myocytes upon stretch
ANP -> vasodilation of aff and vasoconstriction of eff -> in. GFR;
ANP inhibits renin and aldo secretion

Front 72

what is BNP?

Back 72

brain natriuretic peptide, but released by ventricular myocytes, similar to ANP

Front 73

sketch flow of blood in kidneys

Back 73

renal artery -> interlobar a. -> arcute a. (boundary of cortex and medulla) -> interlobular a. -> aff arteriole -> glom -> eff -> peritubular cap (cortex) -> vasa recta (medulla)

Front 74

if a person sweats a lot, what happens to his plasma osmolarity?

Back 74

decreases; sweat is hypoosmotic (more water is lost than salt)

Front 75

what happens to free [Ca] with hyperventilation?

Back 75

decreases; hyperventilate -> de. CO2 -> in. pH (lower [H]) -> less positive charge bound to albumin -> more Ca bound to albumin instead

Front 76

50% of circulating Ca is bound to what?

Back 76

albumin (not free)

Front 77

how is Ca stored?

Back 77

99% bone
1% intracellular (2nd msg, neurotrans)
0.1% extracellular

Front 78

how is phosphate stored?

Back 78

85% bone
15% intracellular (DNA/RNA, phosphorylation, ATP...)
0.03% extracellular

Front 79

what is hyperparathyroidism?

Back 79

1. primary: unregulated overproduction of PTH (e.g. tumour)
2. usually renal failure -> de. calcitriol -> de. [Ca] -> continuous trigger for high PTH

Front 80

what happens in renal failure in relation to [Ca] and [phos]?

Back 80

de. GFR -> de. phos in urine -> in plasma [Pi] -> in. PTH (to get rid of Pi) renal failure -> de. calcitriol -> low [Ca] -> in. PTH in. resorption from bone to maintain [Ca], but [Pi] ++++
(high [Pi] can lead to Ca:Phos precipitation -> artherosclerosis

Front 81

how is phosphate handled in kidneys?

Back 81

in PCT:
apical Na/Pi symport (inhibited by PTH)
basolat. Pi/A- antiport

also, FGF-23 pulls Na/Pi symporter away from apical surface -> de. Pi reabs.

Front 82

what triggers the release of PTH?

Back 82

major: decreased [Ca] (free, unbound form)
also: increased [Phos] (PTH increases excretion of phos)

Front 83

what are the effects of PTH?

Back 83

1. increase Ca reabs (via Ca channel in DCT)
2. increase calcitriol production by stimulating 1a-hydroxylase
3. increase resorption of Ca and Phos from bone
4. decrease phos reabs from PCT (inhibits apical Na/Pi symporter)

Front 84

how is Ca reabs in kidneys?

Back 84

PCT (unreg): apical Ca channels, basolat. Ca-ATPase, paracellular

TAL (reg): NKCC (recycling of K creates + charge, pushes Ca through apical Ca channels (Ca-ATPase on basolat.) CASR senses Ca -> PKC -> inhibits NKCC -> de. Ca reabs thru channel and paracell.
DCT: apical Ca channel; basolat. CA-ATPase, Na/Ca exchanger
calcitriol increases cytosolic Ca-BP -> improves gradient for Ca uptake thru apical channel
PTH enhances apical Ca channels.

Front 85

what triggers calcitriol (activated vit. D) production?

Back 85

1. PTH (in response to low Ca or high Pi)
2. low Ca
3. low Pi

Front 86

effects of calcitriol?

Back 86

1. increase GI Ca and Pi uptake
2. increase reabs of Ca (by in. Ca-BP in DCT) and Pi from kidneys.
3. increase resorption of Ca and Pi from bone

Front 87

where are NHE3 (Na/H exchangers) found?

Back 87

PCT

Front 88

where is carbonic anhydrase found?

Back 88

PCT

Front 89

where is glucose and aa reabsorbed?

Back 89

PCT

Front 90

where is NKCC found? (Na, 2Cl, K symporter)

Back 90

TAL (recycling of K to lumen creates + charge -> paracellular reabs of + ions)

Front 91

where are Na/Cl symporters found?

Back 91

DCT (thiazide inhibits Na/Cl symporters)

Front 92

where does PTH regulate Ca reabs?

Back 92

DCT (Ca channels apical, Na/Ca antiporter basolat)

Front 93

what type of transporters are found in CD?

Back 93

principle cells: Na (ENaC, in, up by ALDO), K (out), water channels (aquaporins, in, up by ADH)
IC cells: K/H antiport, H-ATPase (apical), HCO3/Cl antiport basolat.

Front 94

where is urea permeable?

Back 94

in CD only; accounts for half of osmotic gradient in medullary interstitium for water reabs.

Front 95

what is countercurrent multiplication?

Back 95

loop shape, urine gets concentrated as it runs through LH.

Front 96

is water permeable in descending thin limb of LH?

Back 96

yes, but Na is NOT

Front 97

is water permeable in tAL?

Back 97

NO (TAL neither)

Front 98

is water permeable in DCT?

Back 98

NO

Front 99

what is a general consequence of nephrotic syndrome?

Back 99

lost of neg charge barrier in nephron -> albumin leaks out to urine -> hypoalbuminemia -> lower combined serum Ca (clinically tested as hypoCa)