Renal- Physiology

Question 1

Renal clearance

Answer 1

Cx = (UxV)/Px = volume of plasma from which the substance is completely cleared per unit time.

Question 2

Effective renal plasma flow (eRPF)

Answer 2

estimated using para-aminohippuric acid (PAH) clearance.

eRPF = UPAH× V/PPAH = CPAH.
Renal blood flow (RBF) = RPF/(1 − Hct).
Plasma volume = TBV × (1 – Hct).

Question 3

Filtration

Answer 3

Filtration fraction (FF) = GFR/RPF.
Normal FF = 20%.
Filtered load (mg/min) = GFR (mL/min) × plasma concentration (mg/mL).

Question 4

Changes in glomerular dynamics

• increase in plasma protein concentration
• Decrease in plasma protein concentration

Answer 4

Decrease GFR

Increase GFR

Question 5

Calculation of reabsorption and secretion rate

Answer 5

Filtered load = GFR × Px.
Excretion rate = V × Ux.
Reabsorption rate = filtered – excreted.
Secretion rate = excreted – filtered.

Question 6

Splay phenomenon

Answer 6

Tm for glucose is reached gradually rather than sharply due to the heterogeneity of nephrons

Question 7

Glucose clearance

Answer 7

Plasma glucose of ∼ 200 mg/dL, glucosuria begins (threshold). At rate of ∼ 375 mg/min, all transporters are fully saturated (Tm).

Question 8

Fanconi syndrome

• Deffect
• Effect
• Etiology

Answer 8

Defect in PCT  excretion of amino acids, glucose,
HCO3, and PO4, and all substances reabsorbed by the
PCT

Proximal RTA, hypophosphatemia, osteopenia

Hereditary defects, ischemia, multiple myeloma,
nephrotoxins/drugs, lead poisoning

Question 9

Bartter syndrome

• Deffect
• Effect

Answer 9

Defect in thick ascending loop of Henle. AR

Metabolic alkalosis, hypokalemia, hypercalciuria

Question 10

Gitelman syndrome

• Deffect
• Effect

Answer 10

Reabsorption defect of NaCl in DCT. AR

Metabolic alkalosis, hypomagnesemia, hypokalemia,
hypocalciuria

Question 11

Liddle syndrome

• Deffect
• Effect

Answer 11

Gain of function mutation in EnaC. AD

Metabolic alkalosis, hypokalemia, hypertension, decrease aldosterone

Question 12

Syndrome of Apparent Mineralocorticoid Excess (SAME)

Answer 12

Hereditary deficiency of 11β-hydroxysteroid dehydrogenase. AR

Metabolic alkalosis, hypokalemia, hypertension low aldosterone; cortisol

Question 13

ANP, BNP

Answer 13

relaxes vascular smooth muscle via cGMP Ž increase GFR, decrease renin.

Dilates afferent arteriole, constricts efferent arteriole, promotes natriuresis.

Question 14

Juxtaglomerular apparatus

Answer 14

Consists of mesangial cells, JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, located at distal end of loop of Henle)

Question 15

Kidney endocrine functions

Answer 15

Erythropoietin

Calciferol (vitamin D) (PCT cells)

Prostaglandins (vasodilates afferent artery)

Dopamine (by PCT cells, promotes natriuresis)
- At low doses, dilates interlobular arteries, afferent
arterioles, efferent arterioles
- At higher doses, acts as vasoconstrictor

Question 16

SHIFTS K+ INTO CELL (CAUSING HYPOKALEMIA)

Answer 16

Hypo-osmolarity

Alkalosis

β-adrenergic agonist

Insulin

Question 17

SHIFTS K+ OUT OF CELL (CAUSING HYPERKALEMIA)

Answer 17

Digitalis
HyperOsmolarity
Lysis of cells
Acidosis
β-blocker}
high blood Sugar (insulin deficiency)
Succinylcholine

DO LABSS

Question 18

Electrolyte disturbances clinical manifestations

• Low Na
• High Na

Answer 18

Nausea and malaise, stupor, coma, seizures

Irritability, stupor, coma

Question 19

Electrolyte disturbances clinical manifestations

• Low K
• High K

Answer 19

U waves and flattened T waves on ECG, arrhythmias, muscle cramps, spasm, weakness

Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness

Question 20

Electrolyte disturbances clinical manifestations

• Low Ca
• High Ca

Answer 20

Tetany, seizures, QT prolongation, twitching
(Chvostek sign), spasm (Trousseau sign)

Stones (renal), bones (pain), groans (abdominal pain), thrones (urinary frequency), psychiatric overtones (anxiety, altered mental status)

Question 21

Electrolyte disturbances clinical manifestations

• Low Mg
• High Mg

Answer 21

Tetany, torsades de pointes, hypokalemia, hypocalcemia (when [Mg2+] < 1.2 mg/dL)

Increase DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

Question 22

Electrolyte disturbances clinical manifestations

• Low PO4
• High PO4

Answer 22

Bone loss, osteomalacia (adults), rickets (children)

Renal stones, metastatic calcifications, hypocalcemia

Question 23

Henderson-Hasselbalch equation

Answer 23

pH = 6.1 + log [HCO3−] / 0.03 PCO2

Question 24

Normal anion gap Metabolic acidosis

Answer 24

HARDASS:
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion

Question 25

Increase anion gap Metabolic acidosis

Answer 25

``` MUDPILES: Methanol (formic acid) Uremia Diabetic ketoacidosis Propylene glycol Iron tablets or INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late) ```

Question 26

Distal renal tubular acidosis (type 1) - Defect - Urine pH and K - Causes - Associations

Answer 26

Inability of α-intercalated cells > 5.5 Urine pH, Decrease K Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune risk for calcium phosphate kidney stones

Question 27

Proximal renal tubular acidosis (type 2) - Defect - Urine pH and K - Causes - Associations

Answer 27

Defect in PCT HCO3– reabsorption excretion of HCO3 – in urine < 5.5 pH, decrease K Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors risk for hypophosphatemic rickets

Question 28

Hyperkalemic tubular acidosis (type 4) - Defect - Urine pH and K - Causes

Answer 28

Hypoaldosteronism or aldosterone resistance < 5.5 pH, Increase K Decrease aldosterone production (eg, diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (eg, K+-sparing diuretics, nephropathy due to obstruction, TMP-SMX)