SGU Physiology - Renal

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EPO (erythropoietin)

hormone: glycoprot, dec PO2 -> fibroblasts secrete in renal interstitium -> inc RBCs => people w/ renal failure dev anemia

principal cells

2/3 of distal tubule/collecting duct, cells for Na/H2O balance (Ald action)

intercalated cells

1/3 of the cells in the distal tuble/collecting duct, for acid/base bal

cortical nephrons

85% of nephrons, have a short LOH + PCT

juxtamedullary nephron

15% of nephrons, have a long LOH + vasa recta, have greater filtration, reabs, "salt-conserving"

180 liters

norm daily GFR

RBF (renal blood flow)

Upah*V/Apah, est w/ PAH, 20% CO = 1L/minute = 350mL/minute/100g, which is 7x that of brain

RPF (renal plasma flow)

(1-Hct)RBF = UpahV/Ppah = Cpah, 687 mL/min

nephrin

bridges gap betw GBM podocyte foot procs, defect in Congenital Nephrotic Syndrome

GFR (glomerular filtration rate)

Puf Kuf = ultrafiltration P ultrafiltration coeff, Kuf = permability * SA, est w/ Insulin or Creatinine

myogenic mechanism

GFR autoreg: distend afferent arteriole -> open non-spec cation chans -> depol -> VGCa2+ open -> contract smooth mm -> inc R -> restore Q to norm

TGF (tubuloglomerular feedback)

GFR autoreg: inc NaCl to macula densa (how it senses inc flow) -> inc ATP -> adenosine -> A1 on afferent arteriole -> vasoconstrict

A1

adenosine R: aff. arteriole vasoconstrict

A2

adenosine R: metabolic vasodilation

clearance

UxV/Px = volume of plasma rendered free of a subst in 1 min = amt subst per min / []subst in pl

Gault-Cockcroft Forumula

GFR = (140-age)weight/([Cr]pl72)

ERPF (effective renal plasma flow)

use PAH Cl to calc RPF through functional nephrons

FF (filtration fraction)

GFR/ERPF

FL (filtered load)

GFR*Pz

Excretion Rate (ER)

Uz*V

FE (fractional excretion)

ER/FL = UzV/(GFR*Pz)

Tm (transport maximum)

where reabs curve asymptotes

renal threshold

[] where excr (vs reabs) is first recorded

splay

weird filter/reabs lines due to nephron heterogeneity

familial renal glycosuria

clinical: SGLT2 muts

cystinuria

clinical: AR -> dibasic AA carrier mut => kidney stones

Hartnup's disease

neutral AR -> AA carrier mut => pellagra s/s

acetzolamide

drug: dec CA => dc Na/HCO3- transport -> metab acidosis -> inc resp

NHE3

exchanger: Na/H+ in proximal tubules

Fanconi Syndrome

clinical: excr everything w/out reabs => acidosis + polyuria

Bartter's Syndrome

clinical: mut NKCC2, ROMK, or CLC-Kb of TALH -> waste NaCl, lose lots of Ca2+ + Mg

Gittelman's syndrome

clinical NCCT muts -> hyperkalemia, hyperchloremia, alkalosis

liddle's syndrome

clinical: ENaC GoF mut -> Na+ hypertension

PHA (pseudohypoaldosteronism)

clinical: ENaC LoF mut -> hypovolemic, dec ability to excrete K+

thiazide diuretics

drug: diuretics that act on Na/Cl cotransporter of DCT, inc Ca2+ reabs -> hypercalcemia, kyperkalemia

loop diuretics

drug: diuretics that act on NKCC in LoH, Tx for CHF, edema, renal failure

potassium sparing diuretics

drug: diuretics that act on CD

glomerulotubular balance

reg NaCl reabs by bal betw GFR + tubular reabs

increase

action of AII, NE, Ald, ADH on Na+ reabs

decrease

action of Dopa, PGE2, ANP, and NO on Na+ reabs

AII (NE)

inc Na+ reabs in PCT by inc NHE3, inc NaKATPase -> inc transcellular reabs

ADH (AVP)

inc Na+ reabs in TALH by inc NKCC2, ROMK, cation transport, imp for countercurrent mult sys

Aldosterone

inc Na+ reabs in principal cell of CD by inc ENaC, ROMK, NA/K ATPase => also inc K+ secr

ANP (atrial natriuretic peptide)

dec Na+ reabs in prinicpal cell of CD by dec ENaC

V1

ADH receptor for vasoconstriction on vasc smooth mm

V2

ADH receptor for water retention on TALH, CD -> inc cAMP, ins AQP2 vesicles into apical memb, inc transporters (NKCC2, ROMK)

TALH

"diluting seg" since undergoes NaCl reabs

facultative

water reabs under control of ADH

obligatory

water reabs in prox nephron NOT ADH controlled

diabetes insipidus

clinical: bad ADH reg -> polydipsia, polyuria, Central = PosPit ADH rel prob, Nephrogenic = kidney V2 prob, Psychogenic = mental prob

effective circulating volume (ECV)

the "fullness" of circ

11-HSD (11-hydroxysteroid dH)

enzyme: converts glucocorticoids to inactive metabolites

magnesium

second most abund intracellular cation (after K+), 65% reabs in LoH, 25% in PT (reverse of Na+ + Ca2+ handling)

paracellin

paracellular Mg2+ channel in TALH, affected by loop diuretics

CaR (extracellular Ca2+ sensing Receptor)

senses fall in [Ca2+]free, ionized -> G protein -> PTh -> PTH

alkaline phosphate

HPO42-, 80% of phosphate

phosphate

ion: 80% reabs in PCT (Na/P cotransport), PTH dec reabs

3.5-5.5 mEq/L

normal [K+]

alpha-intercalated cells

respond to low [K+]pl -> inc H/K-ATPase -> inc [H+] => acidemia

6.8-7.8

limits of ECF pH compatible w/ life

7.38-7.42

normal reg pH range

CO2

volatile acid (~15kmMols produced per day)

non-volatile

aka fixed or metabolic acids, includes organic acids, P + S acids

buffer

any subst that can rev bind H+ ions

buffering power

# mols of strong acid in 1 L of sltn to reduce pH by 1 OR mols of strong B added to 1 L of sltn to inc pH by 1

NBC (Na Bicarbonate Cotransporter)

Na+ + 3 HCO3- cotransporter on basolateral PCT memb, uses HCO30 from action of cyto CA

beta-intercalated cells

cells in CD that have apical Cl-/HCO3- exchangers active in response to inc pH, minor fx in rel to amt of HCO3- that is reabs, filtered, or created

volume contraction alkalosis

dec ECV -> metabolic alkalosis

base excess

amt of strong HA or B (mEq/L) to titrate pH of 100% ox bl to 7.4 @ 37 dec C @ 40mm Hg, norm range = -2 to + +2, (<-2 = metab acidosis, > +2 = metab alkalosis)

anion gap

[Na+] - ([Cl-] + [HCO3-]), norm = 8-16mmol/L (> 18 = unmeas anions, oft in metabolic acidosis), metab acidosis w/ norm anion gap found in hyperchloremia (due to HCO3-/Cl- exch)

35-45 mmHg

norm PaCO2 range (< = resp alkalosis, > = resp acidosis)

22-28

norm HCO3- range (< = metab acidosis, > = metab alkalosis)

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