Renal physiology Flashcards
Bowman’s capsule
epithelial wall of the corpuscle, includes glomerulous and whose basement membrane is continuous with the remainder of the renal tubule
Mesangium
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
Aldosterone
produced in zoma glomerulosa of adrenal cortex, triggered by Ang II, K+, main function is salt retention (reabsorbs Na and secretes K)
ANP
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
