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Step 2 CK renal > R2 > Flashcards

R2 Flashcards

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
Q

Risk factor?

A

Renal Ca
Nephrotic syndrome
Trauma

26
Q

Why NS have hypercoagulability risk?

A

Loss of protein S & C, plasminogen & antithrombin III

Platelet activation and high serum fibrinogen level

27
Q

Membranoproliferative glomerulonephritis fetcher?

A

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
Q

Type I?

A

May be 2° to hepatitis B or C infection.
May also be idiopathic.
Subendothelial IC deposits with granular IF

29
Q

Type II?

A

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
Q

CKD-specific factor related to CV complication?

A

Anemia
Vascular calcificaion
Uremia and dialysis–oxidative stress–atherosclerosis and impaired vascular NO synthesis
CV cases account for 50% of death among CKD

31
Q

Drug-induced interstitial nephritis fetcher?

A

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
Q

what is normal post-void urinary volume?

A

<50 ml

33
Q

clinical feucher of analgesic nephropaty?

A

associated with long term analgesic (e.g aspirin)usage
usually asymptomatic
chronic tubulointerstitial nephritis
haematuria due to papillary necrosis

34
Q

Diagnosis?

A

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
Q

painless hematuria, sterile pyuria, trace protein, and WBC cast indicate?

A

Non-glomerular disorder

like tubulointerstitial and urinary tract lining.

36
Q

Hypomagnesemia?

A

common electrolyte abnormality in alcoholics

present as refractory hypokalemia(b/G magnesium helps in K absorption in the kidney)

37
Q

How hypophosphatemia patient present?

A 
common in alcoholics
weakness
rhabdomyolysis
paraesthesia
respiratory failure
38
Q

calciurine inhibitors(cyclosporine and tacrolimus) adverse effect?

A

have vasoconstrictive effect
HTN
AKI
CKD

39
Q

CIN AKI?

A

reversible

due to efferent and afferent arteriole constriction

40
Q

CIN CKD?

A

Irriversible
Due to progresive RFT decline
Ischemia and drug related parenchymal injury can be the cause

Step 2 CK renal (5 decks)

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