RENAL Flashcards
What are the embryologic sources of renal system?
Pro nephrons degenerates 4 week
Mesonephros male genital contribution
Metanephros uerteric bud until collector tubes // metanephric mesenchyme (mesoderm) until distal convoluted tubule
What’s POTTER sequence ?
Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted skin Extremity defects Renal failure (in utero)
Genetic defects related whit Horseshoe kidney ?
ANEUPLOID DEFECTS
down, Edwards, Patau, turner…
What’s the clearance Ecuation?
Cx = UxV/Px
Cx GFR: net tubular secretion of X.
Cx = GFR: no net secretion or reabsorption.
What’s the GFR Ecuation?
GFR = Uinulin × V/Pinulin
What are the effective renal plasma flow And renal blood flow?
eRPF = UPAH × V/PPAH = CPAH.
RBF = RPF/(1 − Hct).
What’s filtration fraction and filtered load?
Filtration fraction (FF) = GFR/RPF. Normal FF = 20%.
Filtered load (mg/min) = GFR (mL/min)× plasma concentration (mg/mL).
Actions of NSAIDs and ACE inhibitors in bowman capsule
NSAIDs ⬇️GFR ⬇️RPF ↔️FF (afferent 🚫)
ACE inhibitors ⬇️GFR ⬆️RPF ⬇️FF (efferent ✅)
Calculation of reabsorption and secretion rate(4)
Filtered load = GFR × Px.
Excretion rate = V × Ux.
Reabsorption = filtered – excreted.
Secretion = excreted – filtered.
How is the glucose clearance?
∼ 200 mg/dL, glucosuria begins (threshold)
∼ 375 mg/dL, all transporters are fully saturated (Tm).
What’s Hartnup disease?
neutral aminoaciduria and absorption from the gut tryptophan for conversion to niacin pellagra-like symptoms.
Treat with high-protein diet and nicotinic acid.
Which drugs acts in the 4 diferents nephrons segments?
EARLY PCT
ACE inhibitors 🚫Na/H exchange
ACETAZOLAMIDE 🚫carbonic anidrase
THICK ASCENDING LOOP
Loop diuretics 🚫NA,K,Cl co-transporter
EARLY DCT
Thiazides diuretics 🚫NA,Cl co transporter
⬆️Ca/Na exchanger PTH
COLLECTING TUBULE
Amiloride triamterene 🚫 Na channels
Espironolactone 🚫aldosterone receptores
Whats the fundación of ALDOSTERONE in Collecting Tubule? (1,3. 2,2.)
✅ In principal cells:⬆️ apical K+ conductance, ⬆️Na+/K+ pump, ⬆️ENaC channels ⏩lumen negativity ⏩K+ loss.
✅In α-intercalated cells: ⬆️ H+ ATPase activity⏩⬆️ HCO3−/Cl− exchanger activity.
Whats the función of ADH in Collecting tubule?
✅ADH—acts at V2 receptor⏩ insertion of aquaporin H2O channels on apical side.
Explain renal tubular defects (FaBio Guarnizo Loca)
FANCONI 🚫PCT ⬆️excretion a.a. , glucose, HCO3–, and PO43– metabolic acidosis
BARTTER Affects Na+/K+/2Cl– cotransporter.metabolic alkalosis ⬆️U Ca
GITELMAN Affects NaCl reabsortion DCT Hypokalemia , hypomagnesemia, hypocalsuria ,metabolic alkalosis.
LIDDLE ⬆️Na reabsortion ⬆️TA hypokalemia metabolic alkalosis ⬇️aldosterone tto Amiloride
What’s Syndrome of apparent mineralocorticoid excess?
Hereditary deficiency of 11β-hydroxysteroid dehydrogenase
TOO MUCCH CORTISOL
⬆️mineralocorticoid activity
⬆️TA,hypokalemia,metabolic alkalosis.
What’s the action of ANP BNP?
relaxes vascular smooth muscle via cGMP⏩ ⬆️GFR ⬇️renin
⬆️Na+ filtration with no compensatory Na+ reabsorption
What’s the function of juxtaglomerular aparatus?
JG cells secret RENIN ( B1 receptors ⏩renin) BBs⏩ ⬇️renin
MACULA DENSA sense ⬇️NaCl ⏩adenosine⏩vasoconstriction
Action of PTH to ⬆️ Ca reabsortion
✅1α-hydroxylase
Convert 25-OH D3⏩1,25-(OH)2 D3
Action of ATII
Efferent constriction ⏩⬆️GFR and ⬆️FF but with compensatory Na+ reabsorption
Which situations cause hyperkalemia? DO LAβS.
Digitalis (blocks Na+/K+ ATPase)
HyperOsmolarity
Lysis of cells (e.g., crush injury, rhabdomyolysis, cancer)
Acidosis
β-blocker ⬇️Na+/K+ ATPase
High blood Sugar (insulin deficiency)
What’s the predicted PCO2 from Metabolic Acidosis
Pco2 =1.5[HCO3–]+8±2
Types of renal tubular acidosis (3)
Distal (type 1), urine pH > 5.5 Hypokalemia ⬇️H secretion
Proximal (type 2), urine pH
Ethology of urine Casts (6)
RBC casts glomerulonephritis malignant hypertension
WBC casts acute pyelonephritis transplant resection
Fatty casts (“oval fat bodies”) Nephrotic Syndrome
Granular (“muddy brown”) Acute Tubular Necrosis
Waxy casts CRF
Hyaline casts Non specific