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Step 2 CK renal > R3 > Flashcards

R3 Flashcards

1
Q

Things to do in patients with LUTS and BBH?

A

Urinalysis
Serum PSA(asses risk of PCa)
serum creatnin especially in a patient who has another risk for RF like HTN and DM
Renal ultrasound: especially when they have raised Cr(AKI) —-used to assess the presence of hydronephrosis/other obstraction cause and planing for catheterization.

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2
Q

Cystoscopy use in BPH?

A

Used to assess bladder for signs of chronic obstruction.

But indicated only if the patient fails initial managment.

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3
Q

Indication for prostate biopsy inpatient with prostatic enlargement?

A

asymmetric enlargement
Having nodule/nodularity
persistent PSA elevation > 4ng/dl

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4
Q

How we now cause anion gap metabolic acidosis?

A

to see associated clues like osmolar GAP

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5
Q

Presence of Osmolar GAP indicate?

A

Methanol(Blindness)
Ethylin Glycol(Urinary Ca oxalate crystal)
Propylene Glycol

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6
Q

Osmolar GAP calculation?

A

Measured serum osmolarity - Calculated serum osmolarity

Normal is < 10

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7
Q

Calculated serum osmolarity?

A

2xNa + Glucose/18 + BUN/2.8

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8
Q

Hyperglycemia + Urine Ketone?

A

DKA

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9
Q

Uremia(rise in BUN)

A

AKI

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10
Q

Hypoperfusion?

A

Lactic acidosis

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11
Q

Drugs?

A

Salicylates (early Respiratory alkalosis)
Isoniazid
Iron

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12
Q

Anion Gap metabolic acidosis cause?

A

MUDPILES

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13
Q

The benefit of ACE/ARB in DM?

A

the slow progress of diabetic nephropathy( DN is evidenced by raise in urine albumin/Cr ratio)
By lowering Glomerular Hyperfiltration(caused by raise in glomerular CHP in the disease process)–Which prevents the risk of glomerular capillary sclerosis(DN).

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14
Q

SGLT-2 inhibitors(canaglifinozine) benfit in DM?

A

lower the progress of DN by an unknown mechanism.

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15
Q

progression of DN?

A

First 5 years-Glomerular HyperthrophyRise in GFR
5-15 year(incipient DN)–mesangial expansion, GBM thickening, and arteriolar hyalinosis—moderate Proteinuria and HTN
>15 years (overt DN)–mesangial nodule/KWN/ and tubulointerstitial fibrosis–overt proteinuria(NS) and reduced GFR

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16
Q

Renal and electrolyte complication of anorexia nervosa?

A

Decrease urine concentrating ability
Dehydration
Electrolyte depletion

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17
Q

analgesic nephropathy>

A

MCC of drug-induced CKD
Common in older women
Combination increase more risk
2-3 Kg ingestion of indexed drug required
Papillary necrosis and tubulointerstitial nephritis is the pathogenesis
Microscopic haematuria, Sterile pyuria(reduced kidney concentrating capability), Mild proteinuria(NS in advanced disease)
HTN, polyuria, and flank pain
Increase risk of premature aging, atherosclerosis VD, and UT cancers.

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18
Q

Clues that indicate amyloidosis as a cause of nephrotic syndrome?

A

Presence of chronic inflammatory disease(MC: RA)
Enlarged kidney
Enlarged Liver
Amyloid stain by congo red
Amyloid deposit in BM, BV, and interstitium(may be seen as thin fibrils by E.Microscopy)
apple green birefringence by polarized light

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19
Q

Hyalinosis of the afferent and efferent artery will be seen in?

A

Hypertensive nephropathy

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20
Q

Screening for diabetic nephropathy?

A

randome urine albumin/Cr ratio

can detect >30mg/g protinuria erlier

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21
Q

Factor increase DN risk?

A

Long-standing(5-10 year) DM
Presence of other microvascular complication
Uncontrolled HTN
Poor Glycemic control

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22
Q

Protinuria coplication?

A

Increase risk of CV mortality

Increase risk of macrovascular complication

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23
Q

Metabolic S/E of thiazides?

A

Hyperglycemia(impair insulin production and impair pheripherial glucose uptake)_-mostly by chlorthalidone but have a CV mortality benefit.
High triglyceride and LDL
Hyponatremia.hypokalemia and hypomagnesemia
Hypercalcemia
Hyperuricemia (impair UA excretion)–Gout

24
Q

Cause of AKI in the transplanted kidney?

A 
Acute transplant rejection
BK vires reactivation
Pyelonephritis
Calcineurin inhibitor toxicity
urethral obstruction
25
Q

Acute transplant rejection?

A

Occur in first 6 month
Arteritis (endothelial edema) and lymphocyte infiltration of the intima and tubulointerstitial pattern
Due to T mediated response to antigen in graft
Usually asymptomatic
Present as fever, decrease UO, and graft tenderness
Occurrence decrease by the immunosuppressant
Usually reversible with high dose IV glucocorticoids but needs immunosuppressant dose increament after

26
Q

BK virus?

A

Intranuclear inclusion
Mixed lymphocyte and neutrophil infiltration
Interesticial nephritis feture

27
Q

Acute Calcineurin inhibitor toxicity?

A

Present as Prerenal AKI(BUN/Cr >20)
the renal biopsy usually unremarkable
due to efferent and afferent renal artery vasoconstriction
Hypertension

28
Q

Urethral obstruction?

A

Due to ureter necrosis–stenosis

Consider in unremarkable renal biopsy

29
Q

familial hypocalciuric hypercalcemia presentation?

A

Usually asymptomatic
Normal high PTH level
High serum ca
Low urine Ca

30
Q

pathogenesis?

A

Autosomal dominant
Defect in Ca sensing receptor in parathyroid and kidney—PT need high serum ca for suppression and kidney increase Ca absorption

31
Q

How to D/T from primary hypertyroidism?

A

PHTS–Will have High urine Ca

Differentiate using urine calcium /cr ratio

32
Q

urine calcium /cr ratio?

A

Ca urine/Ca serum/Cr urine/Cr serum
if <0.01 FHH
if >0.02 FHPT

33
Q

How the other causes like MM, RCC, Sarcoidosis, and it D toxicity?

A

low PTH level

34
Q

managment of renal cyst?

A

Depend on whether benign/malignant

35
Q

when to say benign?

A 
common in old
thin, smooth, regular wall
unilocular
homogenous
no septation
absence of contrast enhancement
usually asymptomatic
36
Q

benign managment?

A

no, follow up needed
ureter stent if there is a sign of obstruction
inspiration if large, painful and infection sign

37
Q

malignant fetcher?

A

biopsy

38
Q

uric acid stone risk factor?

A

Increase UA excretion(MPD and Gout)
Decrease urine PH(chronic diharoa(BC loss) and Dm/metabolic syndrome)
Increase urine consentration (DHN)

39
Q

patophysiology?

A

Acidic urine favours uric acid(insoluble) formation to that of urate(soluble)
supersaturation increase precipitation

40
Q

Clinical menifetation?

A

Radiolucent stone
UAS crystal(rhomboid(rosette) on urine
Uine PH < 5.5

41
Q

Managment?

A

Alkalanise urine by potasium citrate to 6-6.5
Alopirinol for resistant one with hyperuricemia
Low purine diet

42
Q

Renal calcuoi symptom?

A

Intermitent sever flank pain
Intermitent high voulume diuresis(when obstraction relived)
AKI for patient with single kidney
Post diuresis hypokalemia

43
Q

Acid base diserdor and electroyte disturbance in vomiting?

A 
Metabolic alkalosis(loss of H and Increase HCO3 reabsorbtion.
Hypokalemia(GI loss,High aldosteron and intracelular shift due to alkalosis)
Hypocloremia(GI loss)
44
Q

aproch to metabolic alkalosis?

A

asses urine cloride

45
Q

Low urine chloride(saline responsive MA)?

A

vomiting
Ng tube aspiration
diuretic overuse

46
Q

High urine chloride(saline unresponsive)?

A

Normo/hyoertensive—Bartner/Getilman syndrome

Hypertensive—PHA,Cushing disease and ectopic ACTH production?

47
Q

HiV associated nephropathy (HIVAN) CM?

A

Rapidley progresive
Heavy protinuria
AKI
Common in advaced HIV patients
Subseharan are at risk B/C of APOL1 gene mutation
patient may have edema,hematuria and hypertension

48
Q

pathogenesis?

A

Direct infection of tubular and glomerular cell

49
Q

Diagnosis?

A

Collapsing Focal segmental glomerulosclerosis on renal biopsy
Tubuloreticular inclusion on EM

50
Q

managment?

A 
ART
ACE inhibitor(treat protinuri and HTN)
Poor prognosis(develop to CKD eve with theraphy)
51
Q

lab finding in rhabdomyolysis?

A

Hyerkalemia/hyperphosphatemia–release from damaged muscles
Hypocalcemia–Ca deposition in damged muscles
High AST/ALT ration due to high amount of AST in muscle

52
Q

How sedative risk for rhabdomyolysis?

A

Prolonged immobilization

Ischemic muscle injury duto prolonged stay in dependent position.

53
Q

managment of rhabdomyolysis?

A

exesive hydration

NaHCO3 in some cases

54
Q

drug induced rhabdomyilysis?

A 
Direct myotoxicity(statine,fibrates,cholchicine,cocaain and ethanol)
Vasoconstrictive ischemia(Cocain and amphitamine)
Prolonged immobilization(compression ischemia)--sedatives
55
Q

How to improve Survival in ESRD?

A

Transplantation(living donor has more mortality benifit to that of diseased donor)
type(changing) of dialysis have not d/c survavial effect

56
Q

alchol induced myophty?

A

Preferentialy affect lower extremity

cause pain,swelling and weekness

Step 2 CK renal (5 decks)

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