R2 Flashcards
Hematuria defination?
Having more than 3 RBC/HPF
Bladder Ca fetcher?
Old person
Painless hematuria
Smoking or industrial exposure
Diet recommendation in Ca-oxalate stone?
1-increase fluid intake
2-Decrease sodium intake(Na will increase urine ca excretion)
3-Normal Ca intake(High ca intake will increase urine Ca level and low ca intake will increase oxalate absorption and secretion in the kidney).
4-High K intake(Increase urine citrate secretion(make ca more soluble)
5-Avoid animal protein(metabolites make the urine acidic–Hypocitreturia–precipitation)
6)-avoid diet with high oxalate(Vit c.chocolate,
peanut, and tea)
7)Thiazides–lower urine Ca level
Calcium stone feaucher?
Radiopaque and Shaped like envelope or dumbbell
Calcium stones most common (80%);
calcium oxalate more common than calcium
phosphate stones.
Can result from ethylene glycol (antifreeze)
ingestion, vitamin C overuse, hypocitraturia
(associated with urine pH), malabsorption(increase free oxalate absorption) (eg, Crohn’s disease).
Cause of nephrotic syndrome?
1-primary
2 secondary
1-primary?
1-FSGS(most common cause in adult especially BA)
2-MCD(common in children)
3-MN(2nd MCC)
2 secondary
1-amyloidosis
2-DM
Risk for FSGS?
1- 1° (idiopathic) 2° to other conditions HIV Obesity Heroin use, Sickle cell disease Interferon treatment, congenital malformations). 1° disease has an inconsistent response to steroids. May progress to CKD.
Sign of Nephrotic syndrome?
Proteinuria > 3.5 mg/dl
Hypoalbuminemia
Hyperlipidemia
Lipiduria
Precipitating factor for HRS?
The factor that led to decrease renal perfusion GI bleeding Vomiting Sepsis Excessive diuretic use SBP
Urinary finding?
FeNA <1 %(urine Na <10 Meq)
no blood,protien or granular cast
What is the initiating factor?
Cirrhosis–Portal HTN–high NO–pheripherial and splanchnic vasodilation–Low renal perfusion–Low GFR–RAAS activation.–further decrease GFR
myoglobin/hemoglobinuria?
Will have positive urine for blood(B/C of Heme) but no RBC.
cause for rhabdomyolysis?
Crush injury
prolonged immobilization
Intense muscle activity(seizure/exertion)
Drug or medication toxicity(statin)
Clinical manifestation?
Muscle pain and weakness Dark urine(myoglobinuria/pigmenturia) \+blood urinalysis/no RBC on microscopy Increase serum K and PO4, decrease serum Ca, increase AST/ALT AKI serum CK > 1000 U/L
Medication that causes Hyperkalemia?
NSBAB (B2 receptor blokage)
ACE and ARB(inhibit aldosterone production)
KSD(amilioride) and trimetoprime–inhibit Na reabsorbtion in CD
Digitalis(inhibit Na/k ATPase)
Cyclosporine-Block aldosterone activity
Heparin–Block aldosterone production
NSAID: Decrease K delivery to the kidney
succinylcholine: promote extracellular K movement by activating AC receptors.
Trimetoprim effect in Rf?
Raise creatinin(inhibit secretion of Cr) Hyperkalemia(inhibit ENAK chanel)
What to do patient with an asymptomatic UTI with a negative deepstick?
urine culture
Does nitrate positivity indicate?
Gram-negative organism mainly enterobacteria (eg. ECOLI) infection–metabolize nitrate to nitrite
Differentiation of IgA nephropathy and PSGN?
Clinically
IgA-More common in adults(20-30), occurs within 5 days URI and will have a recurrence hematuria history.
PSGN: More in children(10-20),occur 10-15 day URI.gross hematuria.
Laboratory?
IgA:normal complement,mesangial IgA deposit
PSGN: Low C3 with subepithelial bump/antiSO and DNAs
Prognosis?
IgA: good, sometimes progress to RPGN and NS
PSGN: Good in children, CKD in adult
complement level in lupus nephritis?
low C3 and C4
Renal vein thrombosis sign and symptom?
Flank pain
Hematuria
Left varicose vein dilation
Risk factor?
Renal Ca
Nephrotic syndrome
Trauma
Why NS have hypercoagulability risk?
Loss of protein S & C, plasminogen & antithrombin III
Platelet activation and high serum fibrinogen level
Membranoproliferative glomerulonephritis fetcher?
Is a nephritic syndrome that often co-presents with nephrotic syndrome. I.e patient will have nephrotic range proteinuria with haematuria.
Classified as type I and II
Both types: mesangial ingrowth GBM splitting “tram-track” on H&E and PAS E stains.
Type I?
May be 2° to hepatitis B or C infection.
May also be idiopathic.
Subendothelial IC deposits with granular IF
Type II?
Is associated with the C3 nephritic factor (IgG autoantibody that stabilizes C3 convertase persistent complement activation C3 levels).
Intramembranous deposits also called dense deposit disease
CKD-specific factor related to CV complication?
Anemia
Vascular calcificaion
Uremia and dialysis–oxidative stress–atherosclerosis and impaired vascular NO synthesis
CV cases account for 50% of death among CKD
Drug-induced interstitial nephritis fetcher?
common in cephalosporins, penicillin, and sulphonamide
fever, arthralgia, and rash are a major symptom
eosinophilia,eosinophiluria,WBC cast,haematuria and sterile pyuria
discontinuation of the drug is the major Tx.
what is normal post-void urinary volume?
<50 ml
clinical feucher of analgesic nephropaty?
associated with long term analgesic (e.g aspirin)usage
usually asymptomatic
chronic tubulointerstitial nephritis
haematuria due to papillary necrosis
Diagnosis?
Elevated creatinine with urinalysis showing hematuria or sterile pyuria.
Can have mild proteinuria(,1.5 mg/day)
Trace proteinuria
Bilateral small kidney with papillary calcification on CT
painless hematuria, sterile pyuria, trace protein, and WBC cast indicate?
Non-glomerular disorder
like tubulointerstitial and urinary tract lining.
Hypomagnesemia?
common electrolyte abnormality in alcoholics
present as refractory hypokalemia(b/G magnesium helps in K absorption in the kidney)
How hypophosphatemia patient present?
common in alcoholics weakness rhabdomyolysis paraesthesia respiratory failure
calciurine inhibitors(cyclosporine and tacrolimus) adverse effect?
have vasoconstrictive effect
HTN
AKI
CKD
CIN AKI?
reversible
due to efferent and afferent arteriole constriction
CIN CKD?
Irriversible
Due to progresive RFT decline
Ischemia and drug related parenchymal injury can be the cause
