Term
|
Definition
TBW is 60% body weight
40% body weight is ICF, 20% is ECF
25% of ECF is blood plasma, 75% is interstitium
45% of blood plasma is RBC's, 55% is plasma |
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Term
| Calculation of plasma volume |
|
Definition
V = amt/conc
Known amt of labeled albumin is injected into blood and concentration is measured. V can then be calculated |
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Term
| Calculation of blood volume |
|
Definition
| Vplasma (previously calculated) can be multiplied by (1-Hct) to get blood volume |
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|
Term
| Measurement of ECF volume |
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Definition
| Measured with substances that cross capillaries but not cell membranes (inulin) |
|
|
Term
| Measurement of interstitial fluid volume |
|
Definition
V_ECF - V_plasma
Calculated with inulin and albumin/Hct, respectively |
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Term
| Measurement of ICF volume |
|
Definition
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|
Term
|
Definition
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|
Term
Isotonic volume expansion
Cause, effect on D-Y diagram |
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Definition
Caused by NaCl infusion
Extends ECF volume without affecting osmlarity (same height, but wider) |
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Term
Hypertonic volume depletion
Cause, effect on D-Y diagram |
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Definition
Sweating
Shrinks both ECF and ICF. Raises osmolarity (taller and thinner) |
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Term
| Go through hypertonic volume depletion and water volume expansion examples |
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Definition
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|
Term
Water volume expansion
Cause, effect on D-Y diagram |
|
Definition
Drinking water
Widens both ECF and ICF, and shortens osmolarity (short and wide) |
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|
Term
Sweating then replenishing with water
Effect on D-Y diagram |
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Definition
| Same total volume (width), but bigger ICF portion and lower Osm (height) |
|
|
Term
Disorders:
Isosmotic volume depletion and expansion |
|
Definition
Depletion: Hemorrhage, plasma loss through burns
Expansion: Edema, renal Na retention |
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|
Term
Disorders:
Hypotonic volume depletion and expansion |
|
Definition
Deplation: Renal loss of NaCl (lack of aldosterone)
Expansion: Excess H2O ingestion, too much ADH |
|
|
Term
Disorders:
Hypertonic volume depletion and expansion |
|
Definition
Depletion: Sweating, diabetes, alcohol
Expansion: Intake of hypertonic fluids |
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Term
|
Definition
C = UV/P
U is urine concentration, P is plasma concentration, and V is urine flow |
|
|
Term
|
Definition
| Inulin is freely filtered, and neither secreted nor reabsorbed. Therefore, clearance is equal to GFR |
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|
Term
| Substance whose clearance can be used to calculate RPF |
|
Definition
PAH is freely filtered and completely secreted. Therefore, C_PAH equals 'effective RPF'
10-15% of plasma does not enter glomerulus, so this number can by multiplied by 1.1 for a more accurate result |
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Term
| Components of glomerulus filtration barrier |
|
Definition
Fenestrated endothelium
Basal lamina with glycoproteins and proteoglycans that are (-) charged
Podocytes make filtration slits between foot processes |
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Term
| Molecular size and filterability |
|
Definition
<7k: freely filterable
7k-70k: Partially filtered, depending on charge
>70k: not filterable |
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|
Term
Factors preventing or allowing protein filtration
Examples of each |
|
Definition
Prevented: Large and (-) charge. e.g. Albumin
Allowed: Small, e.g. Mb (causes kidney damage), Hb (somewhat), glucagon, PTH, gastrin, ANP |
|
|
Term
| Filtration of small lipid-soluble molecules |
|
Definition
| Not filtered because become bound to albumin |
|
|
Term
| Proteins that build up in blood with renal failure |
|
Definition
| ANP, PTH (small, normally filtered) |
|
|
Term
Cystatin C
Properties, utility |
|
Definition
Small, freely filtered
Used to estimate GFR. Better than Cr because depends less on sex, race, musculature |
|
|
Term
| Filtration fraction equation |
|
Definition
|
|
Term
|
Definition
GFR = (U_In/P_In)*V
Clearance of inulin
GFR = Kf x NFP
Kf is filtration coefficient (hydraulic permeability x surface area)
NFP is net filtration pressure (Starling forces) |
|
|
Term
Utility of creatinine
How its used, limitations |
|
Definition
Produced at relatively constant rate
Freely filtered, not reabsorbed, small amount secreted (offset by procedure which overestimates P_Cr)
Because measuring urine is impractical, blood concentration is estimator. P_Cr is inversely proportional to GFR.
Not sensitive to slightly decreased kidney function. Cr appears only if GFR is very low |
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|
Term
|
Definition
Balanced Starling forces
FF is constant GFR directly proportional to RPF. Once RPF increases, FF goes down |
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Term
| Relationship between RPF and FF |
|
Definition
| Linear at first, but as RPF increases, FF decreases |
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|
Term
| Pressure in capillary beds of renal system |
|
Definition
| Pressure much higher in glomerular capillaries than peritubular |
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|
Term
| Effect of increasing only afferent arteriole resistance |
|
Definition
Decreased glomerular capillary pressure
Decreased RPF
Decreased GFR |
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|
Term
| Effect of increasing only efferent arteriole resistance |
|
Definition
Increased glomerular capillary pressure
Decreased RPF
Increased GFR at low R, decrease at high R |
|
|
Term
| Effect of increasing both afferent and efferent arteriole resistance |
|
Definition
| Little to no change in glomerular capillary pressure |
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|
Term
| Most effective regulator of GFR (in terms of vasoconstrition) |
|
Definition
| Afferent vasoconstriction |
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|
Term
| Effect of autoregulation on GFR |
|
Definition
| Keeps pressures relatively constant. At low pressures, however, fails because arteries can dilate only to a certain extent |
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|
Term
| Tubuloglomerular feedback (TGR) |
|
Definition
Macula densa monitors flow of filtrate
Increased flow is sensed by increased NaCl delivery. This causes adenosine/ATP secretion, which (opposite cardiac) causes vasoconstriction of afferent arterioles and decreases GFR |
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|
Term
| Renin-Angiotensin and renal arterioles (2 effects) |
|
Definition
Constricts afferent and efferent arterioles -> decrease RPF and increase FF -> ↑π in peritubular capillaries -> increase reabsorption
Reduces surface area for filtration, thereby causing small reduction of GFR |
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|
Term
| Sympathetic activity and effect on renal arterioles |
|
Definition
Increase sympathetic activity (NE) from decreased baroreceptor firing -> constriction of aff and eff arterioles -> decreased RPF and increased FF -> increase π in peritubular -> increased perfusion to vital organs
Stimulates renin release |
|
|
Term
| Vasoconstrictors of afferent and efferent renal arterioles |
|
Definition
| Myogenic response, TGF, RAA system, sympathetic activity |
|
|
Term
| Vasodilators of afferent and efferent renal arterioles |
|
Definition
|
|
Term
| Stimulation of PGE2 and PGI2 and consequence |
|
Definition
Stimulated by AngII
Acts to limit its effects (vasodilator) |
|
|
Term
| Danger of NSAIDs on kidney |
|
Definition
| If perfusion is low, vasodilation (prostaglandins inhibited by NSAIDs) is needed to increase it |
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|
Term
| Effect of ANP on kidneys (2 effects) |
|
Definition
Vasodilator for arterioles
Inhibits renin -> decreases Na reabsorption |
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Term
| NaCl reabsorption proportion in nephron segments |
|
Definition
PCT: 67%
Loop (TAL): 25%
DCT/ducts: 7% |
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|
Term
| Na reabsoprtion in early PCT |
|
Definition
Na/H exchanger: H combines with HCO3 in lumen to form CO2, which diffuses into tubular cells. Converted back to H and HCO3 (by CA) and H goes out for Na in (Na/H exchanger).
Net effect is Na and HCO3 reabsorption
Na/Glc exchanger: Na and Glc moved from lumen to tubular cells via cotransporter (slower). This is electrogenic, making lumen negative. |
|
|
Term
Diuretic that acts on early PCT
Mechanism |
|
Definition
Acetazolamide
Inhibits CA, impeding CO2 breakdown and Na/H exchanger (increase urine volume) |
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Term
|
Definition
Na/H exchanger & Cl/An exchanger: Anion pumped out for Cl in. H pumped out for Na in. In lumen, An binds H and HAn diffuses back into lumen. Net result is Na and Cl reabsorption
Paracellular: Cl not reabsorbed in early PCT, so builds up in late PCT. Gradient drives paracellular route out of lumen. Electrogenic (lumen positive) |
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|
Term
|
Definition
Na/Cl/K transporter: Only functions if all spots are filled (K is usually limiting). K leak channel exists so this can remain active. K leakage makes +15 membrane potential.
Paracellular: Membrane potential drives Ca and Mg out of cell |
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|
Term
Diuretic acting on TAL
Mechanism |
|
Definition
Furosemide
Inhibits Na/Cl/K transporter. Most potent diuretic |
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|
Term
| Reabsorption in early DCT |
|
Definition
| Na/Cl cotransporter: Reabsorbs both. |
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|
Term
| Diuretic that acts on early DCT |
|
Definition
Thiazide
Inhibits Na/Cl cotransporter |
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|
Term
| Reabsorption in late DCT and collecting ducts |
|
Definition
Principal cells:
ENaC: Na channel for Na influx
K channel for K efflux
Generates -40 membrane potential
Intercalated cells:
H+ATPase pumps H into lumen |
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|
Term
| Drugs/hormones that act on late DCT/collecting ducts |
|
Definition
Amiloride downregulates ENaC (diuretic)
Aldosterone upregulates ENaC (retention)
ADH increases H2O permeability |
|
|
Term
| Factors that regulate Na reabsorption and what causes their release (4 factors) |
|
Definition
1) RAA system - JG apparatus
2) Natriuretic factors - Low P in pulmonary vein and atrium
3) Sympathetic activity - High P in carotid and aortic baroreceptors
4) ADH - same as ANP |
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|
Term
| Definition of effective circulating volume (ECV) |
|
Definition
| Measures efficiency of tissue perfusion by blood |
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|
Term
| Short vs long-term effects on blood pressure |
|
Definition
Short: Heart and blood vessels -> change in BP
Long: Kidney -> change in Na excretion |
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|
Term
| Starling forces that increase and decrease Na reabsorption |
|
Definition
Increase oncotic or decrease hydrostatic in peritubular favors reabsorption
and vice versa |
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|
Term
| Location of renin production |
|
Definition
| Granular cells (modified smooth muscle cells) of JG apparatus |
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|
Term
| Stimulation of renin secretion |
|
Definition
BP drop sensed by baroreceptors of granular cells
NaCl delivery to macula densa
Sympathetic stimulation (B1) |
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|
Term
|
Definition
B1: Stimulate renin secretion
B2: Stimulates Na/K-ATPase
B2 agonists are bronchodilators |
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|
Term
|
Definition
ANP
Increased NaCl to macula densa
AngII (feedback) |
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|
Term
Aliskiren (Tecturna)
Function |
|
Definition
|
|
Term
-pril drugs
Example, function |
|
Definition
Captopril
ACE inhibitors (BP meds) |
|
|
Term
Function, side effects of bradykinin
Role of ACE |
|
Definition
Vasodilator
ACE breaks it down
Therefore, ACE inhibitors not only stop AngII, but also stop breakdown of vasodilator
Causes coughing and pain |
|
|
Term
-rtan drugs
Example, function |
|
Definition
Losartan
Block AngII receptors instead of ACE
Relieves side effects of bradykinin accumulation |
|
|
Term
|
Definition
Hemodynamic: Vasoconstriction lowers RPF, GFR, and raises FF. Increases oncotic pressure of peritubulars and favors Na reabsorption
Tubular: Increases Na channels and stimulates Na/H exchanger in PCT/TAL
Stimulates thirst
Stimulates aldosterone production |
|
|
Term
| Stimulation of aldosterone |
|
Definition
AngII
High K levels in ZG cells of adrenal cortex (increase K channel activity in late DCT/collecting duct, increasing K excretion. alternate effect from BP)
ACTH from stress (minor) |
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|
Term
|
Definition
Stimulates Na/K-ATPase and ENaC in tubules
K secretion and H secretion as well |
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|
Term
| Effect of sympathetic stimulation directly on tubular system |
|
Definition
Constriction of arterioles and hemodynamic route of Na reabsorption
Binding B1 receptors for renin release
Directly stimulates Na reabsorption on PCT by Na/H exchanger and Na/K-ATPase upregulation |
|
|
Term
|
Definition
Increase aquaporins on DCT and collecting ducts
Increase Na/Cl/K transporter in TAL
Increase ENaC activity in principal cells |
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|
Term
| Type of pathway used by ANP |
|
Definition
|
|
Term
|
Definition
Increase Na excretion through hemodynamic effects (vasodilation, drops FF)
Inhibits renin
Inhibits aldosterone
Inhibits Na transport on tubules |
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|
Term
Equation for fractional excretion of Na
Interpretation of results |
|
Definition
FENa = (Una x Pcr)/(Pna x Ucr) x 100
<1%: Low perfusion (pre-renal disease)
>2%: Acute tubular necrosis (too little reabsorption) |
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|
Term
| Medullary gradient with and without ADH |
|
Definition
With ADH, steep gradient (1200) at deepest part of medulla
Without, only 600 osm |
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Term
| Stimulation of ADH secretion (4 factors) |
|
Definition
Osmoreceptors in brain, outside BBB stimulate thirst and ADH when hyperosmotic.
Stress, pain
AngII |
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|
Term
| Inhibition of ADH secretion (2 factors) |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Crosstalk between volume and osmoregulation |
|
Definition
Decreased ECV (effective circulating volume) increases sensitivity of osmosensors to ADH
Logic is volume decrease will cause water retention regardless of osmolarity |
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|
Term
| Factors that stimulate and suppress thirst |
|
Definition
Stimulate:
Increase in osmolarity (osmoreceptors)
Decrease in volume (baroreceptors)
Dryness of mouth
Inhibits:
Increased water intake by GI tract |
|
|
Term
| Mechanism of coutercurrent multiplier |
|
Definition
Descending limb is permeable to H2O, but not Na (becomes hyperosmotic). TAL is permeable to Na but not H2O (becomes hyposomtic).
Movement of fluid causes hyperosmotic fluid to enter ascending limb.
Process repeats, bottom of medulla becomess hyperosmotic |
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|
Term
| Urea contribution to medullary gradient |
|
Definition
| When ADH present, H2O reabsorption increases urea concentration in cortical collecting ducts. ADH also increases urea permeability. Urea diffuses into interestitium then enters thin ascending limb. Urea impermeable in DCT and CCT, so cannot exit tubule system until medullary collecting duct again. Creates hyperosmotic medulla |
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|
Term
|
Definition
50% reabsorbed in PCT
Mostly paracellular (as H2O reabsorbed, concentration gradient increases)
Some transcellular, via facilitate diffusion |
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|
Term
| Portion of RPF that goes to vasa recta |
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Definition
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|
Term
| Function of hairpin loop in vasa recta |
|
Definition
| Vessels turn around from medulla to go back to cortex. If they exited directly from medulla, would send out very hyperosmotic blood, due to equilibration with interstitium. Returning to cortex allows absorption of water and only slightly hyperosmotic blood |
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|
Term
H2O clearance equation
Interpretation |
|
Definition
C_H2O = Vu (1 - Uosm/Posm)
Positive means urine osmolarity is less than blood plasma
When negative, it is more than plasma |
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Term
| Hyposmosis in marathon runners |
|
Definition
| Fluid and Na lost in sweat. Replenished with water, but ECF compartment still hypovolemic. Hypovolemia will inhibit ADH effect and fluid cannot be concentrated. Effect can be severely hyposmotic plasma |
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Term
Primary hyperaldosteronism
Effect on body |
|
Definition
Overstimulation of Na/K-ATPase and K and Na channels in collecting duct
Increased BP, decreased plasma [K], increased pH, decreased renin
Plasma [Na] is normal because water will follow Na reabsorption |
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Term
| Secondary hyperaldosteronism |
|
Definition
Hypovolemia (fluid loss) causes high renin/AngII levels
Decreased BP because aldosterone cannot fully compensate for fluid loss
OR
Renal artery constriction causes high renin/AngII levels
Increased BP because fluid loss is apparent, not real
for both: Decrease plasma [K], increased pH |
|
|
Term
Bartter syndrome
Cause
Effect on: [K], urine volume, ECF volume, plasma aldosterone, blood pH, urinary Ca/Mg
Drug it is similar to |
|
Definition
Caused by mutation that inactivates Na/K/Cl cotransporter, apical K channel, or basolateral Cl channel of TAL
Decreased plasma [K], increased urine, decreased ECF volume, increased aldosterone, increased pH, increased urine Ca/Mg (dysfunctional K channel does not establish (+) membrane potential)
Similar to loop diuretics and furosemide |
|
|
Term
Gitelman syndrome
Cause
Effect on: Urine volume, ECF volume, plasma aldosterone, plasma K, blood pH
Drug it is similar to |
|
Definition
Caused by mutation of Na/Cl cotransporter in early DCT
Increase urine volume, decrease ECF volume, increase aldosterone, decrease K, increase pH
Thiazides |
|
|
Term
Liddle syndrome
Cause
Effect on Na reabsorption, ECF volume, plasma K, aldosterone
Drug it is similar to |
|
Definition
Gain of function mutation of ENaC
Increases Na reabsorption, increases ECF volume, decreased plasma K (increased K driving force), decrease aldosterone
Amiloride |
|
|
Term
Pseudohypoaldosteronism
Cause
Effect on ECF volume, BP, plasma K, aldosterone |
|
Definition
Inactivating mutation of ENaC or aldosterone receptor
Decrease ECF volume, decrease BP, increase plasma K, increase aldosterone |
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|
Term
Central diabetes insipidus
Cause
Effect on urine volume, urine osmolarity, plasma Na |
|
Definition
Lack of ADH production
Increase urine volume, decrease urine osmolarity, increase plasma [Na] but can be normal with drinking |
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|
Term
Nephrogenic diabetes insipidus
Cause
Effect on urine volume, urine osm, and plasma [Na] |
|
Definition
Caused by lack of ADHR or aquaporin. Can be side-effect of lithium
Increases urine volume, decreases urine osm, increases plasma [Na] |
|
|
Term
SIADH
Cause
Effect on plasma Na, urine osm
Treatment |
|
Definition
Excessive ADH (by tumor)
Decreases plasma [Na], increases urine osm
Treated by tumor removal, water restriction, or ADH antagonists |
|
|
Term
Diabetes mellitus
Cause
Effect on urine volume, Na and K excresion, ECF volume |
|
Definition
Glucose exceeds tubular threshold and enters urine
Increases urine volume, increases Na and K excretion, vastly decreases ECF volume |
|
|
Term
| Two types of glucose transport in PCT |
|
Definition
Early: SGLT2 transports 1Na/Glucose
Late: SGLT1 transports 2Na/glucose (larger gradient to overcome, most leaves lumen in early PCT) |
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|
Term
| Description of glucose titration curve |
|
Definition
| Early part of curve (physiological range)filtered load and reabsorbed curve are superimposed. Eventually reabsorption rate reaches threshold and more filtered glucose leads to non-zero excretion (300 mg/dL) |
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|
Term
|
Definition
| Gradual approach to Tm (saturation of reabsorption, max rate). Ideal curve is jagged, but difference of each nephron makes it rounded |
|
|
Term
AA reabsorption
Type of transport, distribution by nephron segment |
|
Definition
Either facilitated diffusion or secondary active transport (Na or H, which acidifies urine)
Essentially complete by end of PCT |
|
|
Term
Carboxylate reabsorption
Type of transport, distribution by nephron segment |
|
Definition
Na-coupled cotransporters
Complete by end of PCT |
|
|
Term
Oligopeptide reabsorption
Type of transport, distribution by nephron segment |
|
Definition
H coupled transport of short oligopeptides or degradation to AA
Complete by end of PCT |
|
|
Term
Protein reabsorption
Mechanism, distribution by nephron segment |
|
Definition
Small amount filtered are reabsorpbed by endocytosis
Complete by end of PCT |
|
|
Term
| Hypo and hyperkalemia symptoms |
|
Definition
Hyper: Arrhytmias
Hypo: Muscle weakness, constipation |
|
|
Term
| Quick and slow responses to K+ ingestion |
|
Definition
Quick: Cellular uptake. Though significant compared to ECF [K], insignificant for ICF
Slow: Excretion from kidney |
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|
Term
| Stimulation of K uptake by cells |
|
Definition
Kinetic effect: Increased [K] will increase Na/K-ATPase activity
Insulin stimulates Na/K-ATPase
Ep stimulates Na/K-ATPase (B2 receptor) |
|
|
Term
| Distribution of K+ reabsorption throughout nephron |
|
Definition
PCT: 65% (paracellular)
TAL: 30% (Na/K/Cl, paracellular)
DCT/CD: Minor amounts by intercalated (H/K-ATPase) |
|
|
Term
|
Definition
| Apical K channels in principal cells |
|
|
Term
| Passive regulation of K secretion |
|
Definition
Increased plasma K speeds up Na/K-ATPase
Increased urine flow speeds up K removal from lumen (loop diuretics and thiazide)
Increased tubular Na stimulates Na entry, which depolarizes membrane and increases driving force for K |
|
|
Term
| Hormonal regulation of K secretion |
|
Definition
| Increased plasma [K] directly stimulates aldosterone, which increases K secretion (via increased Na/K-ATPase, ENaC activity, and K channel activity) |
|
|
Term
| Relationship between acid/base balance and K levels |
|
Definition
H/K exchanger is theoretical exchanger (protein not found) that pumps H in for K out
Hypokalemia induces alkalosis: Low K outside increases driving force, and therefore activity, of exchanger. H then enters cell and plasma becomes alkaline. Alkalosis causes hypokalemia by the same mechanism.
Acidosis causes hyperkalemia (and vice versa) but same principle |
|
|
Term
| Methods of increasing K uptake into cells |
|
Definition
| Insulin/glucose, B2 agonists, HCO3 (alkalosis->hypokalemia) |
|
|
Term
| Methods of increasing K removal from body |
|
Definition
Loop diuretics or thiazides (not K-sparing diuretics)
Dialysis |
|
|
Term
|
Definition
Amiloride (ENaC blocker)
Spironolactone (aldosterone antagonist) |
|
|
Term
Symptoms of hypo and hypercalcemia
Reasoning |
|
Definition
Hypo: Hyperreflexia, tetany, laryngospasm
Hyper: Weakness/hyporeflexia, calcification of soft tissues, kidney stones, psychiatric disorders
Counterintuitive: Extracellular Ca hyperpolarizes membrane, shifting voltage-gated channels to that higher voltages are needed |
|
|
Term
| Distribution of Ca reabsorption throughout nephron |
|
Definition
PCT: 65% (mainly paracellular)
TAL: 25% (mainly paracellular), PTH regulated
DCT: 8% (mainly transcellular), PTH regulated. Apical is ECaC, basolateral is PMCA and NCX
CD: 1.5 reabsorbed, 0.5% excreted |
|
|
Term
| Effect of PTH on Ca reabsorption in kidney |
|
Definition
| Increases ECaC, PMCA, and NCX, favoring reabsorption |
|
|
Term
| Effects of PTH other than Ca reabsorption in kidney |
|
Definition
Increases D3 formation
Inhibits PO4 reabsorption |
|
|
Term
Primary hyperparathyroidism
Consequences |
|
Definition
Increase in Ca, decrease in PO4 (leads to bone problems)
Increases urine concentration (despite fact that PTH increases Ca absorption), because extra Ca in plasma increases filtered load. CaSR (Ca sensor) on basolateral side of tubular cells directly inhibits Ca reabsorption
Increases urine cAMP (by indiscriminate anion transporters. PTH uses cAMP pathway, so builds up in cells) |
|
|
Term
| Role of CaSR on basolateral tubular cells |
|
Definition
Decreased calcium:
Increased Ca reabsorption, increased D3 formation
Increased Ca:
Opposite effects |
|
|
Term
Familial hypocalciuric hypercalcemia (FHH)
Cause, symptoms |
|
Definition
Loss of function mutation of CaSR, senses as if plasma Ca is low
Increases PTH (form of hyperparathyroidism), thereby increasing Ca reabsorption
Decreases urine [Ca] (opposite primary hyperPTism) |
|
|
Term
| Diuretics that inhibit Ca rabsorption |
|
Definition
Loop diuretics
Reduce transcellular potential gradient, thus inhibiting Ca reabsorption |
|
|
Term
| Diuretics that stimulate Ca rabsorption |
|
Definition
Thiazides (decrease Cl in cell, hyperpolarization)
Amiloride (decrease Na entry, hyperpolarization)
Hyperpolarization increases driving force for Ca to enter cell |
|
|
Term
| Bartter, furosemide, and loop diuretics affect on Ca, K, and H excretion |
|
Definition
Increase Ca excretion
Increase K excretion
Increase H excretion |
|
|
Term
| Thiazide, Gitelman effect on Ca and K excretion |
|
Definition
Increase K excretion
Decrease Ca excretion
Increase H excretion |
|
|
Term
| Amiloride effect on K, Ca and H excretion |
|
Definition
K-sparing
Decreases Ca excretion
Decrease H excretion |
|
|
Term
| Distribution of phosphate reabsorption throughout nephron |
|
Definition
PCT: 80% reabsorbed (Apical: Na/P cotransporter)
Collecting: 10% excreted |
|
|
Term
| Inhibition and stimulation of P reabsorption |
|
Definition
D3: Stimulate P reabsorption in kidney and Ca uptake from gut
PTH: Inhibits reabsorption by blocking Na/P cotransporters |
|
|
Term
| Distribution of Mg reabsorption throughout nephron |
|
Definition
PCT: 15% reabsorbed
TAL: 70% (paracellular)
DCT: 10% (transcellular)
3-5% excreted |
|
|
Term
|
Definition
Familial hypomagnesemia with hypercalciuria and nephrocalcinosis
Mutation of proteins that inhibit reabsorption in TAL. TAL is mostly paracellular so this disease shows paracellular is protein-mediated |
|
|
Term
|
Definition
Hypomagnesemia with secondary hypocalcemia
Mutation that affects Mg channel in DCT (transcellular) |
|
|
Term
|
Definition
Tertiary active transport:
ATP drive Na out and K in. 3Na cotransported with aKG into cells. aKG antiported for PAH (all BL side).
PAH antiported for A- (luminal side) or passed through channel |
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Term
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Definition
Tertiary active transport:
ATP drive Na out and K in (BL). Na antiported for H (apical). Luminal H antiported for cation (apical) |
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Term
| Organic anions secreted by PCT |
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Definition
Penicillin and probenecid. If administered together, less penicillin is needed because both are secreted by same channel.
Glucuronides: What liver conjugates lipophilic substances with so they can be cleared by kidney
cAMP (as in hyperparathyroidism) |
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Term
| Description of PAH titration curve |
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Definition
| For early part of curve, amount secreted is nearly the same as the amount excreted. As concentration increases, secretion reaches a saturation rate and filtered load determines excretion amount |
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Term
| Distribution of HCO3 reabsorption throughout nephron |
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Definition
PCT: 80%. Apical: H transport done mainly by Na/H antiporter (NHE), but also V-type ATPase and H/K-ATPase. BL: Na/3HCO3 (NBC) cotransporter and Cl/HCO3 exchanger (AE)
TAL: 10%. Apical: Mainly NHE, but also V-type
Collecting duct
a intercalated cells: 10% (Apical: V type and H/K ATPase, BL: Cl/HCO)
B intercalated cells: Secrete small amounts of HCO (proteins from a are reversed) |
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Term
H secretion and formation of new HCO
Mechanism, limitations, and ways of dealing with them |
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Definition
H secreted into lumen, causing conversion of more CO2 into HCO3 (transported to interstitium) and H (transported to lumen)
Once tubular fluid reaches pH 4.4, V-types will stop. Titratable acids buffer incoming protons. Once these are overloaded, NH4 can carry the load |
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Term
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Definition
PCT cells break down Gln to NH3 and aKG. NH3 freely diffuses through apical membrane and combines with H in lumen. NH3 can also stay in tubular cells, join with H, and be antiported out of cell as NH4 (by Na).
Each Gln makes 2 NH4 and buffers 2H |
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Term
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Definition
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Term
| What total H excretion equals |
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Definition
=NH4 excretion + titratable acid excretion
=new HCO formation |
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Term
| What total H secretion equals |
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Definition
| = new HCO + reabsorbed HCO |
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Term
| Equation for HCO3 reabsorbed |
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Definition
| HCO3 reabsorbed = (GFR x [HCO3]p) - (V x [HCO3]u) |
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Term
| Effect of carbonic anhydrase inhibitors on blood pH |
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Definition
| Inhibit HCO3 reabsorption -> alkalinize urine -> acidosis |
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Term
| Amiloride effect on blood pH |
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Definition
| Inhibits ENaC -> more positive lumen -> H pump secretes less H -> alkaline urine -> acidosis |
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Term
| Loop diuretics and thiazide effect on blood pH (3 effects) |
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Definition
Make urine more acidic:
1) Induce volume contraction -> RAAS (aldosterone) -> H secretion
2) Enhance Na delivery to tubules -> increase ENaC activity -> more negative lumen -> increase H pump -> increase H secretion
3)K wasting -> hypokalemia -> more H moves into tubular cells (H/K ATPase) -> H secretion |
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Term
Formation of D3
Effect PTH has on process |
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Definition
Hydroxylated at 25 in liver
Hydroxylated at 1 in kidney (by 1a-hydroxylase)
PTH stimulates 1a hydroxylase |
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Term
| Hormones produced in kidneys |
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Definition
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Term
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Definition
| Desired fluid sent countercurrent to patients blood, separated by dialysis membrane |
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Term
| Causes of metabolic acidosis |
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Definition
| Diabetes (ketoacids), lactic acid, diarrhea, kidney failure |
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Term
| Causes of metabolic alkalosis |
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Definition
| Vomiting, loss of H+ (hyperaldosteronism), diuretics |
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Term
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Definition
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Term
| Situation where anion gap is normal but metabolic acidosis is occurring |
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Definition
When conjugate base is also part of AG equation. e.g. HCl: H joins HCO3, so HCO3 is excreted, but Cl is left over and adds as much to the equation as HCO3 subtracted.
Also, with diarrhea NaHCO3 lost, but NaCl conserved to preserve volume. Amount of HCO lost is equal to amount Cl added |
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Term
| Slope of normal blood buffer line of Davenport plot |
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Definition
Buffer capacity (change in HCO / change in pH)
The steeper the slope, the better the buffer |
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Term
| Respiratory acid/alkalosis on Davenport plot |
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Definition
PCO2 isobars of higher value (e.g. 50 mmHg) are to the left of normal isobar (40 mmHg)
Metabolic compensation involves moving up or down the appropriate isobar |
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Term
| Metabolic acid/alkalosis on Davenport plot |
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Definition
Metabolic conditions involve moving up or down 40 mmHg isobar
Respiratory compensation involves moving left or right along a line that is the same slope as the blood buffer line |
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Term
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Definition
| RPF = (Upah x Vu)/(RApah-RVpah) |
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Definition
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Definition
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