Firecracker II Flashcards
4 K+ sparing diuretics
Spironolactone
Eplerenone
Amiloride
Triamterene
PTH stimulates the production of [WHAT?] in the kidney which catalyzes the conversion of 25-OH-vitamin D → active 1,25-(OH)2-vitamin D.
1-α-hydroxylase
Remember that hypovolemia and hypokalemia can exacerbate metabolic alkalosis. How?
Hypovolemia → contraction alkalosis
Hypokalemia → transcellular shift of K and H → H+ goes from ECF to ICF to maintain electrical neutrality → alkalosis.
Which side effects of furosemide can exacerbate metabolic alkalosis?
Hypovolemia and hypokalemia
Glomerulonephritis on microscopy
Scarred glomeruli w/ blue staining collagen on trichome in and between glomeruli
Atrophic tubules
Hyaline arteriolsclerosis 2ndary to HTN
Lymphocytic infiltrate
What does aldosterone do?
Na reabsorption and ↑ K secretion in principal cells; also ↑ H secretion in intercalated cells
PKD1 encodes polycystin-1: a transmembrane protein important for
connective tissue cohesion between renal tubular epithelial cells (esp. the distal nephron).
Where is glomerulotubular balance maintained?
PCT!
Glomerulotubular balance maintains a constant fraction (normally 2/3rds, or ~67%) of filtered Na+ and H2O reabsorption in the PCT. It is regulated by Starling forces in the peritubular capillaries
Paraneoplastic syndrome from ectopic hormone production occurs in 20% of RCC patients:
- PTHrP → hypercalcemia
- EPO → polycythemia
- ACTH → ↑ cortisol → Cushing syndrome
- Renin → hypertension
With what is IgA nephropathy associated? (Besides HSP)
- Celiac sprue—IgA-mediated bowel disease (anti-gliadin IgA) & Dermatitis herpetiformis—grouped vesicles on extensor surfaces
What type of infection precedes PSGN?
URI or skin infection with a nephritogenic strain of group A β-hemolytic Streptococcus pyogenes (especially serotype M12, M4, or M1)
How long after the URI/skin infection do you get PSGN?
1-4 weeks to make antibodies (↑ anti-DNAse B) and form immune complexes
What type of hypersensitivity reaction is PSGN?
Type III hypersensitivity in glomeruli (renal tubular function (concentrating ability) remains largely intact)
Where are the immune complexes deposited in PSGN?
Subepithelial (subpodocyte)
What happens immediately after the immune complexes are deposited in PSGN?
Alternative complement activation
Describe alternative complement activation –> glomeruonephritis after subepithelial immune complex deposition in PSGN?
C5a recruits neutrophils → glomerular damage/inflammation with large hypercellular glomeruli due to WBC infiltrate & proliferation of mesangial and endothelial cells
What recruits the neutrophils to the glomeruli in PSGN?
C5a
What cells in the glomerulus proliferate w/ PSGN?
mesangial and endothelial cells (plus WBC infiltrate)
How does an increase in plasma protein affect RBF?
It doesn’t!
How old is the typical patient w/ PSGN?
6-10
Name some URIs and skin infections (dz process not bug!) that could set off PSGN in 1-4 weeks
pharyngitis,
impetigo, erysipelas, scarlet fever
What are the 6 S/Sx of nephritic syndrome present in PSGN?
- Hematuria
- Proteinuria
- Oliguria
- Azotemia
- Mild to moderate HTN
- Periorbital edema
Besides s/sx of nephritic syndrome, child with PSGN presents w/
Sudden development of fever, nausea, malaise,
What does light microscopy of a urine sample show in a patient with calcium oxalate stones?
colorless octahedral crystals (square crossed by a diagonal line in 2-dimensional view).
Describe the gross appearance of a kidney with acute pyelonephritis
Patchy pale abscesses on the cortex and medulla
What happens with increased RAAS and ADH secretion? (3 things)
- efferent arteriole vasoconstrition
- increased reabsorption of urea by ADH
- Increased reabsorption of Na and H2O –> oliguria
1 and #2 causes of chronic glomerulonephritis
- RPGN
2. FSGN
Treatment for cysteine stones?
Hydration and alkalinization of the urine
4 causes of oxalate stone formation in kidney
- hypercalcinuria
- hypocalcemia
- Crohn’s dz
- Ethylene glycol ingestion
