renal Flashcards
1
Q
embryology
A
- Pronephros - week 4 –> degenerates
- Mesonephros– functions as interim kidney for 1st trimester then contributes to male genital system
-
Metanephros – permanent
- ureteric bud gives rise to collecting system (ureters, pelvises, calyces and CDs)
- metanephric mesenchyme interacts with ureteric bud –> gives rise to nephron (glomerulus, Bowman’s space, prox tubule, LH + DCT)
- ureteropelvic junction is last to canalize – most common site of obstruction (hydronephrosis) in infant
2
Q
- fluid compartments
- Renal clearance
- GFR
- RPF
A
- total body water = 60% total body mass –> 2/3 intracellular; 1/3 extracellular –> 3/4 interstitial + 1/4 plasma
- Cx= UxV/Px (V = urine flow rate)
- Cinor Ccreatinine (normal GFR = 100 mL/min)
- In + Cr are freely filtered neither reabsorbed or secreted
- CPAH
- PAH is both filtered and actively secreted in the proximal tubule
3
Q
- Filtration Fraction
- filtered load
- excretion rate
- Reabsorption rate
- Secretion rate
A
- FF = GFR/RPF (normal = 20%)
- Filtered load = GFR x Px
- Excretion rate= V x Ux
- Reabsorption = filtered load - excretion rate
- Secretion = excretion - filtered
4
Q
- PCT
- Thick descending limb of LH
- Thick ascending limb of LH
A
- reabsorbs all of the glucose and aa (via Na-dependent cotransporters) + most of HCO3, Na (65-80%), Cl, PO4, K+ and H20
- isotonic absorption
- generates + secretes NH3
- ATII and CAI work here
- concentrating segment
- passively reabsorbs H2O (impermeable to Na)
- diluting segment
- actively reabsorbs Na, K and Cl (impermeable to H2O)
- paracellular reabsorption of Ca and Mg
- loops work here
5
Q
- Early DCT
- Collecting Tubule
A
- actively reabsorbs Na, Cl (urine is most hypotonic here)
- thiazides work here
- reabsorbs Na in exchange for K+ and H+ excretion
- aldo regulates insertion of Na channels (spironolactone compete with aldo and amiloride and triamterene antag Na channel)
- ADH acts at V2 receptor –> insertion of aquaporin channels in medullary segment of CD
6
Q
- Fanconi syndrome
- Bartter syndrome
- Gitelman syndrome
- Liddle syndrome
A
- reabsorptive defect in PCT –> may result in metabolic acidosis
- reabsorptive defect in tALH –> hypokalemia and metabolic alkalosis with hypercalciuria
- reabsorptive defect in DCT –> hypokalemia and metabolic alkalosis
- increased Na reabsorption in distal and collecting tubules –> HTN, hypokalemia
the kidneys put out FaBulous Glittering Liquid
7
Q
RAAS
A
- JG cells secrete renin –> angiotensinogen –> angiotensin I –> angiotensin II (via ACE in lungs) –> angioII:
- vascular smooth muscle –> vasoconstriction
- constrict efferent arteriole of glomerulus –> increase FF
- stimulate aldo secretion from adrenal gland
- stimulate ADH secretion from post pit.
- increased PCT Na/H activity
- stimulates hypothalamus –> thirst
- ANP released in response to atriall stretch checks RAAS –> vasorelaxation of afferent arteriole via cGMP –> increases GFR and decreases renin
8
Q
- shifts K+ out of cell
- shits K+ into cell
A
- digitalis, hyperosmolarity, insulin deficiency, cell lysis, Acidosis (H+ exchanges for K+), beta adrenergic antagonist
- insulin, alkalosis, B-adrenergic agonist
9
Q
- Metabolic acidosis
- metabolic alkalosis
- respiratory acidosis
- respiratory alkalosis
A
- low bicarb –> low PCO2 (hyperventilation response)
- AG: Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates (late) (MUD PILES)
- non-AG: hyperalimentation, Addison, RTA, diarrhea, acetazolamide, spironolactone, saline infusion
- hi bicarb –> high PCO2 (hypoventilation response)
- loops, vomiting, antacid use, hyperaldosteronism
- hi PCO2 –> hi bicarb (increased renal bicarb reabsorption)
- hypovent: airway obstruction, acute lung disease, chronic lung disease, opiods, sedatives, resp mm fatigue
- low PCO2–> low bicarb (decreased renal reabsorption)
- hypervent: hysteria, hypoxemia, salicylates (early), tumor, PE
10
Q
RTA
- type 1
- type 2
- type 4
A
- distal; pH > 5.5; hypokalemia – defect in alpha intercalated cells of CD to secrete H+ –> new bicarb not regenerated
- proximal; pH < 5.5; hypokalemia – defect in PCT bicarb reabsorption
- hyperkalemic, pH < 5.5 – hypoaldosteronism, aldo resistance or K+ sparing diuretics
11
Q
- Mannitol
- Acetazolamide
- loops
A
- osmotic diuretic; act on PCT
- use: high intracranial/intraocular P
- CAI; act on PCT
- use: glaucoma, metabolic alkalosis, altitue sickness (hypervent –> resp alkalosis)
- Furosemide
- act on tALH – inhibit Na/K/2Cl transported
- Loops lose Ca
- otoxicity, hypokalemia, nephritis, hyperuricema, sulfa all
- use ethacrynic acid in sulfa allx
12
Q
- Thiazides
- K+ sparing diuretics
- ACEI
A
- act on DCT – inhibit Na/Cl contransporter
- use for idiopiopathic hypercalciuria (prevent Ca stones) and osteoporosis (retain Ca)
- toxicity: hypokalemia, hypercalcemia, met alkalosis, hyperuricemia, hyperlipidemia, hyperglycemia
- act on CD
- spironolactone = aldo-dependent – antiandrogen effects
- triamterene and amiloride block Na channel induced by aldo
- use in HTN, CGH, diabetic nephropathy, prevent unfavorable heart remodeling
- toxicity: increased Cr (decrease GFR), hyperkalemia, teratogen, cough, angioedema