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deck_603758 Flashcards

2
Q

Kidney excretion =

A

filtered + secreted - reabsorbed

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3
Q

Filtration Fraction =

A

GFR/RPF (about 1/5)

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4
Q

properties causing filtration at glomerulus ?

A

elevated capillary hydrostatic pressure more permeable capillary (glomerular cap’s)

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5
Q

cause of reabsorption in the peritubular capillary?

A

high osmotic pressure generated by filtration upstream, and a low hydrostatic pressure generated by high resistance in the efferent arteriole (upstream) lossof fluid due to filtration

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6
Q

fluid breakdown in body

A

60% total weight2/3 = ICF1/3 = ECF of which is 25% plasmaless in obese peoplemore in skinny males

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7
Q

Concentration =

A

M/V

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8
Q

Total Body Water markers

A

Tritiated water Deuterated water Antipyrine

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9
Q

Extracellular fluid markers

A

Inulin Mannitol radioactive Na

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10
Q

Plasma fluid markers

A

Evan’s Blue (T-1824) 125I albumin

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11
Q

Intracellular Volume =

A

TBW-ECF

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12
Q

renal clearance =

A

VOLUME of plasma completely cleared of X per unit time([Ux] x V) / [Px] Ux: urine concentration V: urine flow ratePx: plasma concentration

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13
Q

GFR estimated by:

A

inulin clearancealso creatinine clearance reflects GFR

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14
Q

RPF =

A

PAH clearanceAssumed 100% of PAH is voided from plasma through the kidney via filtration and secretionReality Only 90% of PAH is excreted, so PAH clearance = effective RPF… underestimate of true RPF

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15
Q

Assumption for inulin and GFR

A

inulin is: freely filtered, not reabsorbed, not secreted, not syn via kidney, not degraded by kidney, doesn’t alter kidney function

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16
Q

BUN/Pcr

A

indicates reason for abnormal serum creatinine and BUN<20:1 = dehydration/prerenal failure10:1 with elevated BUN and Pcr = intrinsic renal failure

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17
Q

FEna diagnostic purpose

A

Fractional Excretion of Na values for PR and ATN/ARF have little overlap… best for diagnostic differentiationPR –> low FEnaATN –> higher FEna

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18
Q

Plasma Osmolarity Estimation

A

2x[Na] + glucose/18 + BUN/2.8usually about 300mosm/kg

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19
Q

Effects on body volumes:Diarrhea

A

Diarrhea (isosmotic):- ECFICF and Osmolarity unchanged

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20
Q

Effects on body volumes:Water Deprivation

A

Water Deprivation (hyperosmotic):- Both ECF and ICF+ osmolarity

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21
Q

Effects on body volumes:Adrenal insufficiency

A

Adrenal insufficiency (Hyposmotic): - ECF and osmolarity+ ICF

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22
Q

Effects on body volumes:Infusion of Isotonic Na

A

Isotonic increase: + ECFUnchanged ICF and Osmolarity

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23
Q

Effects on body volumes:NaCl Intake

A

Hyperosmotic increase:+ ECF and Osmolarity- ICF

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24
Q

Effects on body volumes:SIADH/drinking lots of water

A

Hyposmotic increase:+ ECF and ICF- Osmolarity

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25
Q

GFR =

A

Kf x (Pc - Pbs - oncotic Pc) aka net filtration Pnet filtration usually 6mmhg (45 - 29 - 10)

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26
Q

Physiological Regulation of GFR

A

Pgc –> determined by BP and Resistance of afferent and efferent arterioles

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27
Q

Constriction of Afferent arteriole

A
  • RPF- Pgc –> - GFRex) symp activation or high Angio II
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28
Q

Constriction of Efferent arteriole

A

-RPF+ Pgc –> +GFRex) low Angio II (efferent preference)

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29
Q

Renal Autoregulations

A

Maintain RPF during change in BP via afferent and efferent arteriole constrictionMyogenic mechanism –> afferenttubuloglomerular feedback –> afferentAngio II –> efferent

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30
Q

Renal Failure and types

A

diminished GFRPrerenalIntrinsicPostrenal

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31
Q

Prerenal failure

A

GFR falls due to compromised blood flow/pressure to kidneysex) dehydration, heart failure

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32
Q

Post renal failure

A

GFR falls due to obstruction downstream of kidney

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33
Q

Intrinsic Renal Failure

A

Decreased GFR from vascular occlusion (Pgc), glomerular damage (Kf), Tubular damage, Nephritis

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34
Q

Determinants of Protein Filtration

A

Size and ChargeIncrease size –> decrease filtrationmore - charge –> decrease filtration

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35
Q

Causes of Proteinuria

A
  1. loss of filter charge barrier2. loss of filter size barrier3. proximal tubule disfunction - less reabsorption4. Overload
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36
Q

Nephrotic Syndrome

A

Collection of diseases defined by proteinuria, hypoproteinemia, edema, hyperlipidemia

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37
Q

Proximal tubule

A

site of most reabsorption –> 2ndary pumps driven by primary Na-K pump. reabsorbs: Na, Glucose, AA’s, phosphate, lactate, early reabsorb of Na couple with HCO3- and late with Cl-

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38
Q

Proximal tubule secretion

A

secretes organic acids and bases2 non specific carriers: 1) Anion carrier 2) cation carrier

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39
Q

late proximal tubule

A

Primary reabsorption of NaCl driven by [Cl] gradient from lumen to blood.transcellular and paracellular transport

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40
Q

Glomerulotubular Balance

A

Increase GFR –> increase reabsorption (compensates for high GFR)driven by: peritubular oncotic pressure rise; Tubular hydrostatic P rise; Peritubular hydrostatic P decrease

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41
Q

Thin descending limb

A

permeable to water and relatively impermeable to ions –> H2O reabsorption

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42
Q

Thin ascending limb

A

impermeable to water; Na reabsorption passively

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43
Q

Thick ascending limb

A

active reabsorption of –> Na-2Cl-K pump driven by Na-K primary pumpK+ leakage back into lumen –> + potential drive Mg, Ca paracellular reabsorption

44
Q

early distal tubule

A

impermeable to water; active transport of Na-Cl. Also Na-Ca (into blood) pump.cortical diluting segment

45
Q

Intercalated cells

A

dark cells of collecting ductreabsorb Na; secrete H+

46
Q

Principal Cells

A

Light cells of collecting ductReabsorb Na; secrete K+

47
Q

SGLT transporters

A

Na-Glucose linked transporterSGLT 2 in Early PCT - 1:1 Na-Sodium ratioSGLT 1 in late PCT - 2:1 Na-Sodium ratio

48
Q

High Plasma glucose effect of filtration, reabsorption and excretion rates

A

Filtration increases linearly with glucose concentrationReabsorption =’s filtration until threshold, then begins to slow until total saturation (Tm) of transporters, then plateauExcretion rate = 0 until threshold, then increases. At Tm excretion rate = filtration rate

49
Q

Plasma PAH effect on filtration, reabsorption and excretion rates

A

Filtration increases linearly with [Plasma]Secretion increases linearly with [plasma] until threshold (transporter saturation), then begins to plateau off.Excretion = filtered load + rate of secretionat threshold, excretion increases parallel to filtration increase

50
Q

Volume expansion and excretion

A

Volume expansion over rides glomerularfeedback –> increased excretiondespite increase in GFR, peritubular cap. P increases and oncotic P decreases –> less reabsorption

51
Q

Renal Autoregulation vs Glomerulotubule balance

A

Renal autoregulation - maintains filtration across wide range of BP’s, by adjusting afferent and efferent arteriole resistanceglomerulotubule balance - alters reabsorption if there is a change in filtration amount

52
Q

Vasoconstrictors in Kidney

A

Norepinephrine, Angiotensin II, Endothelin, Thromboxane A2, Adenosine, ADH

53
Q

Vasodilators in Kidney

A

Prostglandins (NSAIDS inhibit), NO, Dopamine, Bradykinin

54
Q

Carbonic Anhydrase inhibitor

A

Proximal tubule diuretic inhibiting Na reabsorption

55
Q

Loop Diuretic

A

Thick ascending limb diuretic inhibiting Na reabsorption –> most potent

56
Q

Thiazides

A

Early distal tubule diuretic inhibiting Na reabsorption Treatment for nephrogenic Diabetes insipidus –> decreases dilution of urine and GFR and ECF (increases reabsorption at proximal tubule)increases plasma Ca

57
Q

K+ sparing diuretics

A

Diuretic acting at principal cells –> inhibits Na reabsorption leading to decreased K+ excretion

58
Q

High Pressure baroreceptors

A

carotid/aortic and renal barorecepters in arteriole circulationdetect blood volume delivery -> effective circulating volumeinitiate changes in Na and fluid retention

59
Q

Low pressure baroreceptors

A

cardio/pulmonary baroreceptors on venous sideinitiate ANP and BNP if need be… over-riden by high pressure receptors (particularly in heart failure)

60
Q

Effective circulating volume

A

portion of ECF volume in arteries and perfusing tissues

61
Q

Reduced ECF volume –>

A
  1. increase Symp –> decrease GFR; increase Na+ reabsorption (PT)2. decrease ANP -> decrease GFR; increase Na+ reabsorption (CT)3. increase oncotic pressure -> Increase Na+ reabsorption4. increase renin-angiotensin-aldosterone -> increase Na+ reabsorption (PT and CD)
62
Q

Natriuretic factors (list)

A

ANP, BNP, Urodilatin, Dopamine, Bradykinin, Prostaglandins (inhibit ADH action on CD), NO… essentially vasodilators

63
Q

ACE Inhibitor

A

blocks angiotensin coversion from I to II

64
Q

Angiotensin receptor blocker

A

inhibits aldosterone stimulation, but angiotensin II still active

65
Q

Angiotensin II effects

A
  • vasoconstriction of afferent and efferent arterioles (only efferent in low amounts) -> decrease GFR- systemic vasoconstriction -> increase BP- increases Na-H exchanger in PCT -> increase Na reabsorption- increase thirst- stimulates aldosterone
66
Q

aldosterone effects

A

increase Na reabsorption of principle cells in CD -> increase K+ secretion- more Na-K ATPase on Principle cells

67
Q

Causes of K+ into cell

A

InsulinaldosteroneBeta-agonistsnorepinephrinSNSalkalosis

68
Q

Causes of K+ out of cell

A

Hyperosmolarityexercisecell lysisacidosis (except diarrhea, organic, renal tubular, resp acidosis)

69
Q

amount of K+ left when reached DT

70
Q

K+ intake =

71
Q

Ways K+ excreted

A
  1. urine2. feces3. sweating
72
Q

Site of K+ adjustment

A

Collecting Duct via principal (K+ secretion) and intercalated (K+ reabsorption) cells

73
Q

factors influencing K+ secretion

A

DietAldosterone -> increases secretiontubular flow rateacid-base status: acidosis -> - secretion

74
Q

Phosphate reabsorption, filtration and excretion

A

normal plasma levels are near Tm for reabsorption -> increase plasma Phos -> reabsorption plateaus and excretion increases80-95% reabsorbed

75
Q

Causes Excretion of Phos

A

PTH -> PO4 linked to Ca in bones -decreases reabsorb in PCTAcidosis -> PO4 acts as acid transporter to excretion (H2PO4 not reabsorbed)

76
Q

Increases Ca Reabsorption

A

PTH (in distal nephron)metabolic acidosis (via PTH)Hyperphosphatemia (via PTH) Vit D metabolitesThiazide diuretic

77
Q

causes of alkalosis

A

volume contractionhyperaldosteronevomiting (metabolic)diuretics (metabolic)

78
Q

free water clearance =

A

V - (Uosm x V)/Posmif - then water retentionif + then water excreted

79
Q

Fractional Delivery (FDx) =

A

(TFx/Px)/(TFi/Pi)if 1 in bowmans space, then freely filtered like inulinthis equation compares a substance filtration to inulin

80
Q

corticopapillary osmotic gradient

A
  • osmolar gradient of interstitial fluid of kidney- established by loop of henle counter current multiplier and urea trapping- maintained by vasa recta counter current exchange- allows ability to concentrate urine
81
Q

Counter current multiplier

A

produces corticomedullary osmolar gradient- ascending limb pumps Na into interstitium (Na-2Cl-L pump) -> osmolarity increases- descending limb equilibrates with higher interstitial osmolarity- descending limb fluid (now with higher osmolarity) flows to ascending limb- ascending limb pumps Na out -> further increasing osmolarity… cycle continues till about 6-800 and urea trapping causes rest of gradient

82
Q

urea trapping

A

adds to corticomedullary osmolar gradient when ADH present- distal tubule and upper collecting duct reabsorb water, but impermeable to urea -> [urea] increases- ADH makes distal CD permeable to urea- urea flows down [ ] gradient into interstitiumsome taken back up by thin descending and remains in cycle

83
Q

ADH effects

A
  • increase water permeability of distal tubule and collecting duct- Increase Na-2Cl-K pump in ascending tubule- Increase UT 1 transporters of distal collecting duct -> increase interstitial [urea]
84
Q

ADH release signals

A
  1. increased plasma osmolarity -> detected by osmoreceptors in brain more sensitive than volume receptors- Decreased plasma volume -> detected by arterial and atrial baroreceptors less sensitive but larger effect when triggered- other stim: pregnancy, stress
85
Q

decrease ADH secretion

A

cold, alcohol, obviously normal volume and osmolarity

86
Q

Osmotic diuresis

A

glucosemannitol

87
Q

Diabetes insipidus types and effect

A

secretory - no ADH secretionNephrogenic - ADH doesn’t stimulatepolyuria -> plasma volume decreases -> plasma osmolarity increases

88
Q

urine buffering

A

phosphate and ammonia

89
Q

Henderson Haselbalchs equn.

A

pH = pka + log (HCO3/.03 x PCO2)

90
Q

bicarbonate reabsorption

A

99.9% in PCTH+ is recycled in mechanism of HCO3- reabsorptionIf alkalosis -> HCO3 filtered saturates reabsorption mechanism -> HCO3 excreted

91
Q

Volume contraction alkalosis

A
  • increased reabsorption due to starling forces- renin - angio - aldost -> stim PCT Na-H pump -> increased HCO3 reabsorption
92
Q

Acid excretion

A
  • H+ secreted from intercalated cells -> H+ binds with PO4 or NH3 -> excreted- results in new HCO3 reabsorbed
93
Q

Type B intercalated cells

A

secreted HCO3opposite of alpha intercalated cells

94
Q

base excretion

A
  • saturation of reabsorption in PCT -> HCO3 excretion- HCO3 excreted by B intercalated
95
Q

Ammonium-H+ trapping

A

Glutamine metabolized to NH4 and HCO3 in PT -> NH4 to blood -> reabsorbed in ascending tubule -> changes to NH3 in interstitium -> NH3 to CD -> NH3 bind H+ -> excretion

96
Q

net acid excretion =

A

titratable acid + NH4 excretion - HCO3 excretion

97
Q

Metabolic acidosis

A

Primary: decrease HCO3Compensatory: decrease PCO2Renal correction: H+ excretion, HCO3 syn. and reabsorption

98
Q

metabolic alkalosis

A

primary: increase HCO3compensatory: increase PCO2renal correction: HCO3 excretion

99
Q

Respiratory acidosis

A

Primary: Increase PCO2 (slight HCO3 increase)Compensatory: Increase HCO3, increase H+ excretion (via NH3 and PO4)

100
Q

respiratory alkalosis

A

primary: decrease PCO2 (slight decrease HCO3)compensatory: decrease HCO3, decrease H+ excretion

101
Q

anion gap =

A

Na - (HCO3 + Cl)helps diagnose type of metabolic acidosis

102
Q

increase anion gap metabolic acidosis

A

diabetes mellituslactic acidosischronic renal failurealcohol

103
Q

normal anion gap matabolic acidosis

A

diarrheacarbonic anhydrase inhibitors Renal tubular acidosisammonium chloride

104
Q

Base Excess

A

quantitative index of metabolic excursion - resp. disturbances dont change - metabolic compensation for resp. disturbance does not change

M:1 year (19 decks)

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