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Flashcards in Renal physiology Deck (72):

Bowman's capsule

epithelial wall of the corpuscle, includes glomerulous and whose basement membrane is continuous with the remainder of the renal tubule



contains contractile cells between loops that regulate glomerular filtration


Renal interstitium

connective tissue made of fibroblast-like cell, cells that secrete EPO, cells that secrete vasomodulators, macrophages that belong to RES


Functions of kidneys

regulate electrolyte concentrations in ECF, eliminates waste products, special metabolic functions and hormone secretion


Renal artery pathway

renal artery- segmental- interlobar- arcuate- interlobular-afferent arterioles-efferent arterioles- peritubular or vasa recta


Afferent arterioles

20% of plasma water in the afferent arterioles is filtered by the glomerulus


Efferent arterioles

contain blood cells, unfiltered large substances and ~80% of liquid that had been in afferent arterioles


Function in cortical nephrons

delivery of nutrients to epithelial cells and acceptance of reabsorbed and secreted substances


Function in medullary nephrons

follow he loop of henle and serve as osmotic exchanger for production of urine


Main triggers and place of renin release

dec pressure in afferent arteriole, increased renal sympathetic activity; juxtaglomerular cells (granular) and extraglomerular mesangial cells


Causes of poor renal blood perfusion

dec blood volume, movement of fluid from intravascular space to tissue (pancreatitis, peritonitis), decrease circulation (HF), dec GFR (HTN, DM)


Blood flow regulation

important because kidneys are so close aorta, every postural change would cause large change, but have myogenic and tubuloglomerular responses


Myogenic response

blood vessels inc in size in response to pressure inc, the smooth muscle cells of the vasculature contract, Law of LaPlace, wall tension is proportional to distention pressure


Tubuloglomerular feedback mechanism

changes in BP leads to change in GFR, (inc bp- inc GFR), inc capillary hydrostatic pres in peritubular capillaries, which leads to dec reabsorp of Na/ Cl in proximal tubule and inc NaCl delivery to distal tubule, macula densa cells sense high NaCl, response of macula densa facilitates vasoconstricion= autoregulation


Angiotensin II variable effects on renal blood flow

Low angII causes vasoconstriction in afferent (less) and efferent (more)-> dec in RBF, inc in GFR; high angII causes vasoconstriction of afferent and efferent, activates mesangial cells, dec in SA of glomerular capillaries, dec GFR, inc sympathetic, dec in RBF


Prostaglandins on renal blood flow

PGE and PGI are vasodilators acting on afferent and efferent arterioles-> causing a dampening effect on renal vasoconstriction


Dopamine on renal blood flow

at low levels vasodilator for renal arterioles, clinically used as vasoprotector of kidney


Renal sympathetic nerves

sympathetic has no part in autoregulation, but raises MAP at the expenxe of renal blood flow, stimulation inc resistance in afferent and somewhat less in efferent arterioles, dec RBF and GFR


Very high ADH

cause contraction of afferent and efferent arterioles, cause contraction of mesangial cells to dec GFR, extreme response during shock


Renal filtration apparatus

endothelial cells w/ fenestrations of ~ .1um, basal lamina surrounds glomerular cappillaries, epithelial cells with podoctes, that create 25-60 nm wide slits, sieving by size, by charge


Advantages of serum CrCl over inulin

no infusion necessary since creatinine is a product of muscle creatine phosphate


Disadvantages of serum CrCl over inulin

creatinine is secreted less than PT, may not work in severe CRF, may not work w/ drugs that inhibit tubular secretion of creatinine, not every creatinine comes from kidney problem, creatinine may not inc despite renal prob, bilirubin interferes w/ cr, bacteria break down urinary creatinine


BUN plasma level advantages over plasma creatinine

better measurement range, falls and rises faster, slightly more sensitive (BUN can indicate moderate-severe)


BUN plasma level disadvantages over plasma creatinine

not every BUN comes from kidney problems, low BUN has little significance for kidney (liver prob or preg), urea is reabsorbed into blood, then inc w/ vol depletion so GFR is underestimated


Cystatin C plasma levels advantage over creatinine

cysteine proteinase inhibitor that is produced by all nucleated cells, constantly produced and freely filtered by kidneys, not affected by infection, inflammation, neoplastic states, body mass, diet or drugs, more accurate than creatine w/ sudden changes


Cystatin C plasma level disadvantage over creatinine

expensive, less widely available and complex tests


Filtration fraction

percentage of plasma that is filtered through the glomerular capillary membrane to become glomerular filtrate


Increase of filtration fraction caused by

[albumin] peritubular inc, (pi)c in peritubular capillary inc, Na reabsorption inc


Nephrotic syndrome

disruption of glomerular filtering membrane w/out inflammation, marked proteinuria >3.5g/d, small dec in GFR, edema, hypoalbuminemia, lipiduria, hyperlipidemia


Nephritic syndrome

disruption of glomerular filtering membrane by inflammation, proteinuria


Causes of hyponatremia

not enough salt in diet, excreting too much, being overhydrated, IV rehydration, diuretics, high ADH, poorly controlled diabetes, HF, liver failure, kidney disorders


Causes of hypernatremia

dehydration, diuretics (if secrete more H2O than Na not common)


Symptoms of hyponatremia/hypernatremia

confusion, drowsiness, muscle weakness, seizures; weakness, sluggishness, very high levels- confusion, paralysis, coma, seizures



produced in zoma glomerulosa of adrenal cortex, triggered by Ang II, K+, main function is salt retention (reabsorbs Na and secretes K)



acts by inhibiting Na reabsorption at inner medullary collecting ducts


Renal sympathetic nerves effects on Na

reduce GFR and RBF, but inc FF, renin released, overall dec sodium excretion


Why does Na transport in proximal tubule

very high ratio of SA to tubular vol, many aquaporin 1 channels apical an dbasolateral, tight junctions permeable to ions


Na/K/2CL cotransporter is inhibited/secreted by

loop diuretics, stimulated by ADH


principal cell channels an effects

ENaC inhibited by K sparing diuretics, stimulated by aldosterone


Factors that effect ADH release

inc: cellular dehydration, hypovolemia, pain, trauma, emotioinal stress, nausea, fainting, anesthetics, nicotine, morphine, ang II dec: ethanol and ANP


Inercalted cell

Alpha- secretion of protons, reabsorb K, beta- secrete bicarb, important for acid/base balance


Proximal convoluted tubule summary of characteristics

high transport capacity, high H2O permeability, low transepithelial gradients, leaky tight junction, coarse control


Distal nephron

low transport capacity, low H2O permeamility, high transepithelial gradients, tight tight junctions, fine control


Causes for hypokalemia

hyperaldosteronism, acute renal failure, CRF, diuretics, GI fluid loss, sx: inc insulin production, fatigue, confusion, muscle weakness, cramps, arrythmias


Causes for hyperkalemia

Addison's, kidney failure, K retaining diuretics; sx: arrythmias, usually fatal >10


hyperphosphatemia is mainly due to

low PTH (pth inhibits na-phosphate cotransport), renal failure or drugs, extremely rarely due to food


Renal phosphate reabsorption

60-70%% lost in PCT, 15% lost in PST, 5-20% in urine (acts as buffer)


Causes of hypocalcemia

widespread infection, low PTH, Vit D def; sx: weakness, paresthesias, confusion, seizures, chvostec's sign, long QT


Causes of hypercalcemia

bone CA, high PTH sx: slight inc no symptoms, moans (constipation, nausea), stones (kidney), groans (confusion, memory loss) and bones (aches)


Calcium reabsorption

67% in PCT, 25% in ALH, 8% in DCT, 5% in collecting duct, .5-2% in urine


PTH effects on Ca

inc Ca reabsorption and dec urinary excretion


Thiazide diuretic effect on Ca

inc Ca reabsorption and dec urinary excretion


Loop diuretic effect on Ca

decrease Ca reabsorption and inc urinary excretion


Magnesium body balance

20% bound to proteins, 80% is filterable in plasma, about 300 mEq/day are filtered and about 90% is reabsorbed, mainly by the thick ascending limb of Henle loop due to voltage difference


Mag renal absorption

30% in PCT, 60% in TALH, 5% in DCT, 5% in urine


Shift K+ to outside of cells

dec ECF pH, digitalis, O2 lack, hyperosmolality, hemolysis, ingection, inschemia, trauma


Shift K+ into cell

Inc ECF pH, insulin, epinephrine, hypoosmolality


Bladder control cascade

bladder filling, mechanoreceptor activation, spinal cord, micturation reflex, detrusor contraction, luminal pressure, decision, pontine micturation center, when yes, detrusor contraction internal sphincter relaxation, then external sphincter relaxation


Sympathetic effects of micturation

inhbition of SM detruso, wall relaxed, stimulation of SM in bladder neck area-- internal sphincter closed


Parasympathetic effects of micturation

stimulationof SM detrusor-- wall contracted, inhibition of SM in bladder neck-- internal sphincter open


Uric acid

the byproduct of purine catabolism, excess leads to kidney stones, prolonged deposit of uric acid is more harmful than the deposit of urea -- gout


acid urine

ketoacidosis, starvation, diarrhea


basic urine

kidney failure, UTI, vomiting


Effects of ADH on Urine production

inc water permeability of late distal tubule and collecting ducts, inc Na/K/2Cl cotransport, enhancing countercurrent multiplication, stimulates urea reabsorption in inner medullary collecting duct, enhancing urea recycling


General approach of determining shift of H2O

identify change in ECF, change in osmolarity, identify H2O movement


in regards to osmolarity, water goes which direction

towards the lower osmolarity


Isoosmotic volume expansion

large intake of isotonic volume, fluid is added to plasma, ECF: vol inc, osm unchanged; ICF: vol and osm unchanged


Hyperosmotic volume expansion

large intake of hypertonic fluid, inc in plasma osmolality, H2O shifts from interstitium into plasma, initial in plasma vol, inc somolality of ECF causes H2O to flow out of ICF; ECF: vol/osm inc; ICF: vol dec, osm inc


Hypoosmotic volume expansion

water intoxication of SIADH; H2O enters plasma, dec plasma osmolality, shift of H2O into interstitial space and dec in osm, dec in interstitial osm causes H2O shift from ECF to ICF; ECF/ICF vol inc, osm dec


isoosmotic volume contraction

hemorrhage, burns; fluid lost from plasma and then repleted from interstitial fluid; ECF: vol dec, osm unchanged; ICF: vol/osm unchanged


Hyperosmotic volume contraction

dec water intake, diabetes; fluid lost from plasma, becomes hyperosmotic, fluid shift from interstial to plasma, rise in interstitial causes fluid shift from ICF to ECF


Hyposmotic volume contraction

adrenal insufficiency, Addison's; fluid and electrolyte lost from plasma, becomes hypoosmotic, H2O shift from ECF to ICF; ECF: vol dec, osm dec; ICF: vol inc, osm dec