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Anatomy > Renal physiology > Flashcards

Renal physiology Flashcards

1
Q

Bowman’s capsule

A

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

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2
Q

Mesangium

A

contains contractile cells between loops that regulate glomerular filtration

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3
Q

Renal interstitium

A

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

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4
Q

Functions of kidneys

A

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

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5
Q

Renal artery pathway

A

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

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6
Q

Afferent arterioles

A

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

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7
Q

Efferent arterioles

A

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

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8
Q

Function in cortical nephrons

A

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

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9
Q

Function in medullary nephrons

A

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

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10
Q

Main triggers and place of renin release

A

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

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11
Q

Causes of poor renal blood perfusion

A

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

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12
Q

Blood flow regulation

A

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

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13
Q

Myogenic response

A

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

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14
Q

Tubuloglomerular feedback mechanism

A

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

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15
Q

Angiotensin II variable effects on renal blood flow

A

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

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16
Q

Prostaglandins on renal blood flow

A

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

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17
Q

Dopamine on renal blood flow

A

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

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18
Q

Renal sympathetic nerves

A

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

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19
Q

Very high ADH

A

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

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20
Q

Renal filtration apparatus

A

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

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21
Q

Advantages of serum CrCl over inulin

A

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

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22
Q

Disadvantages of serum CrCl over inulin

A

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

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23
Q

BUN plasma level advantages over plasma creatinine

A

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

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24
Q

BUN plasma level disadvantages over plasma creatinine

A

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

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25
Q

Cystatin C plasma levels advantage over creatinine

A

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

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26
Q

Cystatin C plasma level disadvantage over creatinine

A

expensive, less widely available and complex tests

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27
Q

Filtration fraction

A

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

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28
Q

Increase of filtration fraction caused by

A

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

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29
Q

Nephrotic syndrome

A

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

30
Q

Nephritic syndrome

A

disruption of glomerular filtering membrane by inflammation, proteinuria

31
Q

Causes of hyponatremia

A

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

32
Q

Causes of hypernatremia

A

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

33
Q

Symptoms of hyponatremia/hypernatremia

A

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

34
Q

Aldosterone

A

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

35
Q

ANP

A

acts by inhibiting Na reabsorption at inner medullary collecting ducts

36
Q

Renal sympathetic nerves effects on Na

A

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

37
Q

Why does Na transport in proximal tubule

A

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

38
Q

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

A

loop diuretics, stimulated by ADH

39
Q

principal cell channels an effects

A

ENaC inhibited by K sparing diuretics, stimulated by aldosterone

40
Q

Factors that effect ADH release

A

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

41
Q

Inercalted cell

A

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

42
Q

Proximal convoluted tubule summary of characteristics

A

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

43
Q

Distal nephron

A

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

44
Q

Causes for hypokalemia

A

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

45
Q

Causes for hyperkalemia

A

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

46
Q

hyperphosphatemia is mainly due to

A

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

47
Q

Renal phosphate reabsorption

A

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

48
Q

Causes of hypocalcemia

A

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

49
Q

Causes of hypercalcemia

A

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

50
Q

Calcium reabsorption

A

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

51
Q

PTH effects on Ca

A

inc Ca reabsorption and dec urinary excretion

52
Q

Thiazide diuretic effect on Ca

A

inc Ca reabsorption and dec urinary excretion

53
Q

Loop diuretic effect on Ca

A

decrease Ca reabsorption and inc urinary excretion

54
Q

Magnesium body balance

A

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

55
Q

Mag renal absorption

A

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

56
Q

Shift K+ to outside of cells

A

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

57
Q

Shift K+ into cell

A

Inc ECF pH, insulin, epinephrine, hypoosmolality

58
Q

Bladder control cascade

A

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

59
Q

Sympathetic effects of micturation

A

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

60
Q

Parasympathetic effects of micturation

A

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

61
Q

Uric acid

A

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

62
Q

acid urine

A

ketoacidosis, starvation, diarrhea

63
Q

basic urine

A

kidney failure, UTI, vomiting

64
Q

Effects of ADH on Urine production

A

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

65
Q

General approach of determining shift of H2O

A

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

66
Q

in regards to osmolarity, water goes which direction

A

towards the lower osmolarity

67
Q

Isoosmotic volume expansion

A

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

68
Q

Hyperosmotic volume expansion

A

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

69
Q

Hypoosmotic volume expansion

A

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

70
Q

isoosmotic volume contraction

A

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

71
Q

Hyperosmotic volume contraction

A

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

72
Q

Hyposmotic volume contraction

A

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

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