Associations Flashcards
Low ADAMST13
give dx and treatment
Dx: Thrombotic thrombocytopenic purpura (TTP)
Tx: Plasmapheresis
Basket-weave and lamellated basement membrane (give dx)
Alport syndrome
Brown urine (give dx)
Post-infectious acute glomerulonephritis
c-ANCA, PR-3 (give dx, organ systems involved, and key biopsy finding)
Dx: granulomatosis
Organs: Pulmonary-renal
Biopsy: Crescentic
CLDN-16 and paracellin-1 mutations
give dx and site of mutation
Dx: Familial Hypomagnesemia with Hypercalcuria
Site of mutation: Thick ascending limb of LoH
Coffin lid shape
give dx and preceding circumstances
Dx: struvite kidney stones
Circumstance: usually happens during infection
Congo-red staining with apple-green birefringence under polarized light (give dx)
Amyloidosis
Crescents of fibrin and plasma proteins such as C3b (give biopsy pattern class)
Rapidly progressive (crescentic) glomerulonephritis
Foot process effacement on EM and normal LM/IF (give dx)
Minimal change disease
Envelope shape (give dx)
Calcium oxalate kidney stones
Eosinophilic nodular glomerulosclerosis (give dx)
Diabetic glomerulonephropathy
Kimmelsteil-Wilson nodules (give dx)
Diabetic glomerulonephropathy
Prior epstein barr virus infection (give dx)
Membranoproliferative GN
Frothy urine (give ddx class)
Nephrotic syndromes
Prior group A beta-hemolytic strep infection (give dx and complement levels)
Dx: Acute post-strep GN
Complement level: low
Hepatitis C serology (give dx)
Membranoproliferative GN
“Humps” on EM (give dx)
Acute-post strep glomerulonephritis
IgG, IgM, and C3 deposition on IF (give dx)
acute-post strep glomerulonephritis
Intramembranous deposits on EM (give dx)
Membranoproliferative GN (type II)
Linear IgG staining on IF (give dx and organ involvement)
Dx: Anti-GbM disease
Organ involvement: lungs (if goodpastures)
Low C3/C4 levels (give ddx)
Post-infectious GN, SLE type IV, membranoproliferative GN
Prior lymphomas (give dx)
membranoproliferative GN
Mesangial cell proliferation, variable proteinuria, hypocomplementemia (give dx)
Membranoproliferative GN
Child with periorbital swelling (give dx and tx)
Dx: Minimal change disease
Tx: Corticosteroids
RBC casts (give ddx category)
Glomerulonephritis
Radiolucent kidney stones (give dx and tx)
Dx: uric acid stones
Tx: Alkalinization of urine and allopurinol
Rhomboid/rosette shaped kidney stones (give dx and associated illness)
Dx: uric acid stones
Associated illness: gout
Segmental sclerosis and hyalinosis in some of the glomeruli (give dx)
focal segmental glomerulosclerosis
“spike and dome” pattern of subepithelial deposits along the GBM (give dx)
membranous nephropathy
Staghorn calculi (give dx and associated illness)
dx: struvite stone
associated illness: infection with ureas positive bacteria (like proteus)
Stones following urease positive bacterial infection (give dx)
struvite stone
Starry sky appearance on LM (give dx)
Acute post-strep glomerulonephritis
Subepithelial deposits and effacement of foot processes of podocytes (give dx)
Membranous nephropathy
Subepithelial deposits on EM + recent history of infection (give dx)
Post-infectious glomerulonephritis
Thickened capillary loops and GBM without cellular proliferation (give dx)
Membranous nephropathy
Thrombocytopenia (give dx and accompanying symptoms)
Dx: thrombotic thrombocytopenic purpura
Symptoms: neuro symptoms, fever, anemia
Tram-tracking on silver stain/EM (give dx)
Membranoproliferative GN
Waxy casts (give dx)
ESRD/CKD
WBCs/eosinophils in urine (give dx and possible common drug association)
Dx: allergic interstitial nephritis
Drugs: antibiotics/penicillin
WBC casts (give dx)
Acute pyelonephritis
Wire looping on LM + deposits everywhere on EM (give dx)
Diffuse proliferative glomerulonephritis
Adenosine (made by, target, action, activation signal)
Adenosine Made by: macula densa Target: afferent areteriole Action: vasoconstriction Signal: Increased NaCl flow past macula densa
Aldosterone (made by, target, action, activation signal)
Aldosterone
Made by: Adrenals
Target: alpha-intercalated, principal cells, DCT
Action: increased H+ secretion (H+ ATPase), increased expression of ENaC and Na+ reabsorption
Activated by: Angiotensin II
Angiotensin II (made by, target, action, activation signal)
Angiotensin II
Made by: Liver
Target: Hypothalamus, kidney, glomerulus, artery, adrenals
Action: increase ADH (hypothalamus), increased aldosterone (adrenals), increased Na+/H+ exchange in PCT (to increase solute delivery and down regulate renin release), efferent arteriole constriction (increase GFR)
Activated by: low NaCl, low BP, sympathetic (beta1) activation all via Renin release
FGF23 (made by, target, action, activation signal)
FGF23 Made by: osteocytes Target: kidney, thyroid Action: decreased vitamin D activation, decreased PTH release, phosphaturia Activated by: hyperphosphatemia
PTH (made by, target, action, activation signal)
PTH
Made by: parathyroid
Target: DCT, PCT, bone, GI
Action: increase calcium in blood (also via increased vitamin D activation)
Activated by: low Ca/Mg or high serum phosphate
Renin (made by, target, action, activation signal)
Renin Made by: juxtaglomerular cells Target: Angiotensinogen Action: produce angiotensin I Activated by: decreased NaCl, decreased BP, sympathetic activation (beta1)
Vitamin D (made by, target, action, activation signal)
Vitamin D Made by: kidney Target: Intestine Action: Increased absorption Ca, PO4 Activated by: Decreased Ca and PO4
Bartter’s syndrome mutation (Location, Action, K+, Mg2+, Ca2+, pH)
Bartter’s
Location: TAL
Action: decreased Na/K/2Cl transport, decreased ROMK K+ secretion, or decreased Cl- reabsorption CIC-Kb
K+: low (K+ can’t be reabsorbed)
Mg2+: low (no charge gradient for Mg/Ca)
Ca2+: low (high in urine)
pH: alkalosis (decreased potassium reabsorption is compensated for by increasing H+ excretion in alpha-intercalated cells)
Liddle syndrome mutation (Location, Action, K+, Na+, pH)
Liddle
Location: CCD
Action: decreased responsiveness to renin and aldosterone, leading to chronic activation of these pathways and hypertension
K+: low (to compensate for increased Na+ reabsorption)
Na+: high (because of inability to regulate ENaC)
pH: alkalosis (to compensate for increase Na+ reabsorption)
Loop diuretic (Location, Action, K+, Na+, Mg2+, Ca2+, pH)
Loop diuretic Location: LoH Action: inhibit Na/K/2Cl K+: low Na+: low Mg2+: low (no charge gradient) Ca2+: low (no charge gradient) pH: alkalosis (H+ exchanged for K+ to compensate distally in the nephron)
Thiazide diuretics (Location, Action, K+, Na+, Ca2+, pH)
Thiazide diuretics
Location: Apical DCT
Action: blocks Na/Cl (favoring Na/Ca exchange)
K+: low
Na+: low
Ca2+: very high (blocking Na/Cl exchange favors Na/Ca exchange)
pH: alkalosis (H+ exchange for K+ to compensate distally in the nephron)
