deck_603758 Flashcards
2
Q
Kidney excretion =
A
filtered + secreted - reabsorbed
3
Q
Filtration Fraction =
A
GFR/RPF (about 1/5)
4
Q
properties causing filtration at glomerulus ?
A
elevated capillary hydrostatic pressure more permeable capillary (glomerular cap’s)
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
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
7
Q
Concentration =
A
M/V
8
Q
Total Body Water markers
A
Tritiated water Deuterated water Antipyrine
9
Q
Extracellular fluid markers
A
Inulin Mannitol radioactive Na
10
Q
Plasma fluid markers
A
Evan’s Blue (T-1824) 125I albumin
11
Q
Intracellular Volume =
A
TBW-ECF
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
13
Q
GFR estimated by:
A
inulin clearancealso creatinine clearance reflects GFR
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
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
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
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
18
Q
Plasma Osmolarity Estimation
A
2x[Na] + glucose/18 + BUN/2.8usually about 300mosm/kg
19
Q
Effects on body volumes:Diarrhea
A
Diarrhea (isosmotic):- ECFICF and Osmolarity unchanged
20
Q
Effects on body volumes:Water Deprivation
A
Water Deprivation (hyperosmotic):- Both ECF and ICF+ osmolarity
21
Q
Effects on body volumes:Adrenal insufficiency
A
Adrenal insufficiency (Hyposmotic): - ECF and osmolarity+ ICF
22
Q
Effects on body volumes:Infusion of Isotonic Na
A
Isotonic increase: + ECFUnchanged ICF and Osmolarity
23
Q
Effects on body volumes:NaCl Intake
A
Hyperosmotic increase:+ ECF and Osmolarity- ICF
24
Q
Effects on body volumes:SIADH/drinking lots of water
A
Hyposmotic increase:+ ECF and ICF- Osmolarity
25
Q
GFR =
A
Kf x (Pc - Pbs - oncotic Pc) aka net filtration Pnet filtration usually 6mmhg (45 - 29 - 10)
26
Physiological Regulation of GFR
Pgc --> determined by BP and Resistance of afferent and efferent arterioles
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Constriction of Afferent arteriole
- RPF- Pgc --> - GFRex) symp activation or high Angio II
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Constriction of Efferent arteriole
-RPF+ Pgc --> +GFRex) low Angio II (efferent preference)
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Renal Autoregulations
Maintain RPF during change in BP via afferent and efferent arteriole constrictionMyogenic mechanism --> afferenttubuloglomerular feedback --> afferentAngio II --> efferent
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Renal Failure and types
diminished GFRPrerenalIntrinsicPostrenal
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Prerenal failure
GFR falls due to compromised blood flow/pressure to kidneysex) dehydration, heart failure
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Post renal failure
GFR falls due to obstruction downstream of kidney
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Intrinsic Renal Failure
Decreased GFR from vascular occlusion (Pgc), glomerular damage (Kf), Tubular damage, Nephritis
34
Determinants of Protein Filtration
Size and ChargeIncrease size --> decrease filtrationmore - charge --> decrease filtration
35
Causes of Proteinuria
1. loss of filter charge barrier2. loss of filter size barrier3. proximal tubule disfunction - less reabsorption4. Overload
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Nephrotic Syndrome
Collection of diseases defined by proteinuria, hypoproteinemia, edema, hyperlipidemia
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Proximal tubule
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-
38
Proximal tubule secretion
secretes organic acids and bases2 non specific carriers: 1) Anion carrier 2) cation carrier
39
late proximal tubule
Primary reabsorption of NaCl driven by [Cl] gradient from lumen to blood.transcellular and paracellular transport
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Glomerulotubular Balance
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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Thin descending limb
permeable to water and relatively impermeable to ions --> H2O reabsorption
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Thin ascending limb
impermeable to water; Na reabsorption passively
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Thick ascending limb
active reabsorption of --> Na-2Cl-K pump driven by Na-K primary pumpK+ leakage back into lumen --> + potential drive Mg, Ca paracellular reabsorption
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early distal tubule
impermeable to water; active transport of Na-Cl. Also Na-Ca (into blood) pump.cortical diluting segment
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Intercalated cells
dark cells of collecting ductreabsorb Na; secrete H+
46
Principal Cells
Light cells of collecting ductReabsorb Na; secrete K+
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SGLT transporters
Na-Glucose linked transporterSGLT 2 in Early PCT - 1:1 Na-Sodium ratioSGLT 1 in late PCT - 2:1 Na-Sodium ratio
48
High Plasma glucose effect of filtration, reabsorption and excretion rates
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
Plasma PAH effect on filtration, reabsorption and excretion rates
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
Volume expansion and excretion
Volume expansion over rides glomerularfeedback --> increased excretiondespite increase in GFR, peritubular cap. P increases and oncotic P decreases --> less reabsorption
51
Renal Autoregulation vs Glomerulotubule balance
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
Vasoconstrictors in Kidney
Norepinephrine, Angiotensin II, Endothelin, Thromboxane A2, Adenosine, ADH
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Vasodilators in Kidney
Prostglandins (NSAIDS inhibit), NO, Dopamine, Bradykinin
54
Carbonic Anhydrase inhibitor
Proximal tubule diuretic inhibiting Na reabsorption
55
Loop Diuretic
Thick ascending limb diuretic inhibiting Na reabsorption --> most potent
56
Thiazides
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
K+ sparing diuretics
Diuretic acting at principal cells --> inhibits Na reabsorption leading to decreased K+ excretion
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High Pressure baroreceptors
carotid/aortic and renal barorecepters in arteriole circulationdetect blood volume delivery -> effective circulating volumeinitiate changes in Na and fluid retention
59
Low pressure baroreceptors
cardio/pulmonary baroreceptors on venous sideinitiate ANP and BNP if need be... over-riden by high pressure receptors (particularly in heart failure)
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Effective circulating volume
portion of ECF volume in arteries and perfusing tissues
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Reduced ECF volume -->
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)
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Natriuretic factors (list)
ANP, BNP, Urodilatin, Dopamine, Bradykinin, Prostaglandins (inhibit ADH action on CD), NO... essentially vasodilators
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ACE Inhibitor
blocks angiotensin coversion from I to II
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Angiotensin receptor blocker
inhibits aldosterone stimulation, but angiotensin II still active
65
Angiotensin II effects
- 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
aldosterone effects
increase Na reabsorption of principle cells in CD -> increase K+ secretion- more Na-K ATPase on Principle cells
67
Causes of K+ into cell
InsulinaldosteroneBeta-agonistsnorepinephrinSNSalkalosis
68
Causes of K+ out of cell
Hyperosmolarityexercisecell lysisacidosis (except diarrhea, organic, renal tubular, resp acidosis)
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amount of K+ left when reached DT
13%
70
K+ intake =
excretion
71
Ways K+ excreted
1. urine2. feces3. sweating
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Site of K+ adjustment
Collecting Duct via principal (K+ secretion) and intercalated (K+ reabsorption) cells
73
factors influencing K+ secretion
DietAldosterone -> increases secretiontubular flow rateacid-base status: acidosis -> - secretion
74
Phosphate reabsorption, filtration and excretion
normal plasma levels are near Tm for reabsorption -> increase plasma Phos -> reabsorption plateaus and excretion increases80-95% reabsorbed
75
Causes Excretion of Phos
PTH -> PO4 linked to Ca in bones -decreases reabsorb in PCTAcidosis -> PO4 acts as acid transporter to excretion (H2PO4 not reabsorbed)
76
Increases Ca Reabsorption
PTH (in distal nephron)metabolic acidosis (via PTH)Hyperphosphatemia (via PTH) Vit D metabolitesThiazide diuretic
77
causes of alkalosis
volume contractionhyperaldosteronevomiting (metabolic)diuretics (metabolic)
78
free water clearance =
V - (Uosm x V)/Posmif - then water retentionif + then water excreted
79
Fractional Delivery (FDx) =
(TFx/Px)/(TFi/Pi)if 1 in bowmans space, then freely filtered like inulinthis equation compares a substance filtration to inulin
80
corticopapillary osmotic gradient
- 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
Counter current multiplier
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
urea trapping
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
ADH effects
- 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
ADH release signals
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
decrease ADH secretion
cold, alcohol, obviously normal volume and osmolarity
86
Osmotic diuresis
glucosemannitol
87
Diabetes insipidus types and effect
secretory - no ADH secretionNephrogenic - ADH doesn't stimulatepolyuria -> plasma volume decreases -> plasma osmolarity increases
88
urine buffering
phosphate and ammonia
89
Henderson Haselbalchs equn.
pH = pka + log (HCO3/.03 x PCO2)
90
bicarbonate reabsorption
99.9% in PCTH+ is recycled in mechanism of HCO3- reabsorptionIf alkalosis -> HCO3 filtered saturates reabsorption mechanism -> HCO3 excreted
91
Volume contraction alkalosis
- increased reabsorption due to starling forces- renin - angio - aldost -> stim PCT Na-H pump -> increased HCO3 reabsorption
92
Acid excretion
- H+ secreted from intercalated cells -> H+ binds with PO4 or NH3 -> excreted- results in new HCO3 reabsorbed
93
Type B intercalated cells
secreted HCO3opposite of alpha intercalated cells
94
base excretion
- saturation of reabsorption in PCT -> HCO3 excretion- HCO3 excreted by B intercalated
95
Ammonium-H+ trapping
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
net acid excretion =
titratable acid + NH4 excretion - HCO3 excretion
97
Metabolic acidosis
Primary: decrease HCO3Compensatory: decrease PCO2Renal correction: H+ excretion, HCO3 syn. and reabsorption
98
metabolic alkalosis
primary: increase HCO3compensatory: increase PCO2renal correction: HCO3 excretion
99
Respiratory acidosis
Primary: Increase PCO2 (slight HCO3 increase)Compensatory: Increase HCO3, increase H+ excretion (via NH3 and PO4)
100
respiratory alkalosis
primary: decrease PCO2 (slight decrease HCO3)compensatory: decrease HCO3, decrease H+ excretion
101
anion gap =
Na - (HCO3 + Cl)helps diagnose type of metabolic acidosis
102
increase anion gap metabolic acidosis
diabetes mellituslactic acidosischronic renal failurealcohol
103
normal anion gap matabolic acidosis
diarrheacarbonic anhydrase inhibitors Renal tubular acidosisammonium chloride
104
Base Excess
quantitative index of metabolic excursion - resp. disturbances dont change - metabolic compensation for resp. disturbance does not change
