R2 Flashcards

(40 cards)

1
Q

Hematuria defination?

A

Having more than 3 RBC/HPF

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2
Q

Bladder Ca fetcher?

A

Old person
Painless hematuria
Smoking or industrial exposure

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3
Q

Diet recommendation in Ca-oxalate stone?

A

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

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4
Q

Calcium stone feaucher?

A

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).

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5
Q

Cause of nephrotic syndrome?

A

1-primary

2 secondary

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6
Q

1-primary?

A

1-FSGS(most common cause in adult especially BA)
2-MCD(common in children)
3-MN(2nd MCC)

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7
Q

2 secondary

A

1-amyloidosis

2-DM

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8
Q

Risk for FSGS?

A
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.
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9
Q

Sign of Nephrotic syndrome?

A

Proteinuria > 3.5 mg/dl
Hypoalbuminemia
Hyperlipidemia
Lipiduria

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10
Q

Precipitating factor for HRS?

A
The factor that led to decrease renal perfusion
GI bleeding
Vomiting
Sepsis
Excessive diuretic use
SBP
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11
Q

Urinary finding?

A

FeNA <1 %(urine Na <10 Meq)

no blood,protien or granular cast

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12
Q

What is the initiating factor?

A

Cirrhosis–Portal HTN–high NO–pheripherial and splanchnic vasodilation–Low renal perfusion–Low GFR–RAAS activation.–further decrease GFR

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13
Q

myoglobin/hemoglobinuria?

A

Will have positive urine for blood(B/C of Heme) but no RBC.

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14
Q

cause for rhabdomyolysis?

A

Crush injury
prolonged immobilization
Intense muscle activity(seizure/exertion)
Drug or medication toxicity(statin)

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15
Q

Clinical manifestation?

A
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
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16
Q

Medication that causes Hyperkalemia?

A

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.

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17
Q

Trimetoprim effect in Rf?

A
Raise creatinin(inhibit secretion of Cr)
Hyperkalemia(inhibit ENAK chanel)
18
Q

What to do patient with an asymptomatic UTI with a negative deepstick?

A

urine culture

19
Q

Does nitrate positivity indicate?

A

Gram-negative organism mainly enterobacteria (eg. ECOLI) infection–metabolize nitrate to nitrite

20
Q

Differentiation of IgA nephropathy and PSGN?

A

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.

21
Q

Laboratory?

A

IgA:normal complement,mesangial IgA deposit
PSGN: Low C3 with subepithelial bump/antiSO and DNAs

22
Q

Prognosis?

A

IgA: good, sometimes progress to RPGN and NS
PSGN: Good in children, CKD in adult

23
Q

complement level in lupus nephritis?

A

low C3 and C4

24
Q

Renal vein thrombosis sign and symptom?

A

Flank pain
Hematuria
Left varicose vein dilation

25
Risk factor?
Renal Ca Nephrotic syndrome Trauma
26
Why NS have hypercoagulability risk?
Loss of protein S & C, plasminogen & antithrombin III | Platelet activation and high serum fibrinogen level
27
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 Ž GBM splitting Ž “tram-track” on H&E and PAS E stains.
28
Type I?
May be 2° to hepatitis B or C infection. May also be idiopathic. Subendothelial IC deposits with granular IF
29
Type II?
Is associated with the C3 nephritic factor (IgG autoantibody that stabilizes C3 convertase Ž persistent complement activation Ž  C3 levels). Intramembranous deposits also called dense deposit disease
30
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
31
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.
32
what is normal post-void urinary volume?
<50 ml
33
clinical feucher of analgesic nephropaty?
associated with long term analgesic (e.g aspirin)usage usually asymptomatic chronic tubulointerstitial nephritis haematuria due to papillary necrosis
34
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
35
painless hematuria, sterile pyuria, trace protein, and WBC cast indicate?
Non-glomerular disorder | like tubulointerstitial and urinary tract lining.
36
Hypomagnesemia?
common electrolyte abnormality in alcoholics | present as refractory hypokalemia(b/G magnesium helps in K absorption in the kidney)
37
How hypophosphatemia patient present?
``` common in alcoholics weakness rhabdomyolysis paraesthesia respiratory failure ```
38
calciurine inhibitors(cyclosporine and tacrolimus) adverse effect?
have vasoconstrictive effect HTN AKI CKD
39
CIN AKI?
reversible | due to efferent and afferent arteriole constriction
40
CIN CKD?
Irriversible Due to progresive RFT decline Ischemia and drug related parenchymal injury can be the cause