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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
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
26
Cystatin C plasma level disadvantage over creatinine
expensive, less widely available and complex tests
27
Filtration fraction
percentage of plasma that is filtered through the glomerular capillary membrane to become glomerular filtrate
28
Increase of filtration fraction caused by
[albumin] peritubular inc, (pi)c in peritubular capillary inc, Na reabsorption inc
29
Nephrotic syndrome
disruption of glomerular filtering membrane w/out inflammation, marked proteinuria >3.5g/d, small dec in GFR, edema, hypoalbuminemia, lipiduria, hyperlipidemia
30
Nephritic syndrome
disruption of glomerular filtering membrane by inflammation, proteinuria
31
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
32
Causes of hypernatremia
dehydration, diuretics (if secrete more H2O than Na not common)
33
Symptoms of hyponatremia/hypernatremia
confusion, drowsiness, muscle weakness, seizures; weakness, sluggishness, very high levels- confusion, paralysis, coma, seizures
34
Aldosterone
produced in zoma glomerulosa of adrenal cortex, triggered by Ang II, K+, main function is salt retention (reabsorbs Na and secretes K)
35
ANP
acts by inhibiting Na reabsorption at inner medullary collecting ducts
36
Renal sympathetic nerves effects on Na
reduce GFR and RBF, but inc FF, renin released, overall dec sodium excretion
37
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
38
Na/K/2CL cotransporter is inhibited/secreted by
loop diuretics, stimulated by ADH
39
principal cell channels an effects
ENaC inhibited by K sparing diuretics, stimulated by aldosterone
40
Factors that effect ADH release
inc: cellular dehydration, hypovolemia, pain, trauma, emotioinal stress, nausea, fainting, anesthetics, nicotine, morphine, ang II dec: ethanol and ANP
41
Inercalted cell
Alpha- secretion of protons, reabsorb K, beta- secrete bicarb, important for acid/base balance
42
Proximal convoluted tubule summary of characteristics
high transport capacity, high H2O permeability, low transepithelial gradients, leaky tight junction, coarse control
43
Distal nephron
low transport capacity, low H2O permeamility, high transepithelial gradients, tight tight junctions, fine control
44
Causes for hypokalemia
hyperaldosteronism, acute renal failure, CRF, diuretics, GI fluid loss, sx: inc insulin production, fatigue, confusion, muscle weakness, cramps, arrythmias
45
Causes for hyperkalemia
Addison's, kidney failure, K retaining diuretics; sx: arrythmias, usually fatal >10
46
hyperphosphatemia is mainly due to
low PTH (pth inhibits na-phosphate cotransport), renal failure or drugs, extremely rarely due to food
47
Renal phosphate reabsorption
60-70%% lost in PCT, 15% lost in PST, 5-20% in urine (acts as buffer)
48
Causes of hypocalcemia
widespread infection, low PTH, Vit D def; sx: weakness, paresthesias, confusion, seizures, chvostec's sign, long QT
49
Causes of hypercalcemia
bone CA, high PTH sx: slight inc no symptoms, moans (constipation, nausea), stones (kidney), groans (confusion, memory loss) and bones (aches)
50
Calcium reabsorption
67% in PCT, 25% in ALH, 8% in DCT, 5% in collecting duct, .5-2% in urine
51
PTH effects on Ca
inc Ca reabsorption and dec urinary excretion
52
Thiazide diuretic effect on Ca
inc Ca reabsorption and dec urinary excretion
53
Loop diuretic effect on Ca
decrease Ca reabsorption and inc urinary excretion
54
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
55
Mag renal absorption
30% in PCT, 60% in TALH, 5% in DCT, 5% in urine
56
Shift K+ to outside of cells
dec ECF pH, digitalis, O2 lack, hyperosmolality, hemolysis, ingection, inschemia, trauma
57
Shift K+ into cell
Inc ECF pH, insulin, epinephrine, hypoosmolality
58
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
59
Sympathetic effects of micturation
inhbition of SM detruso, wall relaxed, stimulation of SM in bladder neck area-- internal sphincter closed
60
Parasympathetic effects of micturation
stimulationof SM detrusor-- wall contracted, inhibition of SM in bladder neck-- internal sphincter open
61
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
62
acid urine
ketoacidosis, starvation, diarrhea
63
basic urine
kidney failure, UTI, vomiting
64
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
65
General approach of determining shift of H2O
identify change in ECF, change in osmolarity, identify H2O movement
66
in regards to osmolarity, water goes which direction
towards the lower osmolarity
67
Isoosmotic volume expansion
large intake of isotonic volume, fluid is added to plasma, ECF: vol inc, osm unchanged; ICF: vol and osm unchanged
68
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
69
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
70
isoosmotic volume contraction
hemorrhage, burns; fluid lost from plasma and then repleted from interstitial fluid; ECF: vol dec, osm unchanged; ICF: vol/osm unchanged
71
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
72
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

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