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Basic Physician's Training Monash > Renal > Flashcards

Renal Flashcards

1
Q

Causes of HAGMA

A 
C Cyanide, CO
A Alcohols – ethanol
T Toluene
M Methanol, metformin
U Uraemia
D DKA
P Paracetamol, paraldehyde 
I Isoniazid, Iron
L Lactate
E Ethylene glycol
S Salicylates, sepsis
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2
Q

Causes of NAGMA

A 
NAGMA - USED CARP
U Ureteric fistula
S Small bowel fistula
E Extra Chloride
D Diarrhoea
C Carbonic anhydrase inhibitors 
A Addison’s
R RTA
P Pancreatic fistula
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3
Q

Causes of metabolic alkalosis

A 
C Contraction (dehydration)
L Liquorice (diuretic), laxative abuse
E Endocrine (Conn’s, Cushing’s)
V Vomiting, GI loss (villous adenoma)
E Excess alkali (antacids)
R Renal (Bartter’s), severe K depletion
P Post hypercapnia
D Diuretics
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4
Q

Histopathological finding in BK nephropathy

A

Cytopathic changes (intranuclear basophilic viral inclusions)
Tubulitis
SV40 stain

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5
Q

Biopsy finding in minimal change disease

A

Effacement of podocytes on electron microscopy (minimal change on light microscopy)

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6
Q

Biopsy finding in FSGS

A

Focal areas of sclerosis, suPAR (soluble plasminogen activating receptor)

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7
Q

Biopsy finding in Membranous Nephropathy

A

Thickened basement membrane, anti PLA2R in primary (immune complexes)

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8
Q

Biopsy finding in IgA Nephropathy

A

Mesangial deposits that stain for IgA

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9
Q

Biopsy finding in Lupus Nephritis

A

Mild mesangial proliferation through to cresenteric GN, wire loops, subendothelial

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10
Q

Biopsy finding in post streptococcal GN

A

Subepithelial hump like deposits, hypercellularity of mesangial and endothelial cells, subendothelial deposits of IgG, IgM, C3, C4, C5-9

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11
Q

Biopsy finding in pauci-immune GN

A

Crescents, segmental necrotising GN, granulomas in GPA, none in MPA or EGPA

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12
Q

Biopsy finding in cryoglobulinaemia

A

Mixed cryoglobulinaemia: immune complex mediated inflammatory disease
Mostly MPGN: endocapillary proliferation, subendothelial and intraluminal CGs, Ig, complement, granular dense subendothelial deposits with ‘fingerprint’ like appearance

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13
Q

Biopsy finding in anti GBM

A

Crescentic, non-proliferative GN, linear IgG glomerular basement membrane staining

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14
Q

Biopsy finding in AIN

A

Interstitial oedema, marked interstitial infiltrate (predominantly T cells and monocytes), tubulitis
Eosinophilia

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15
Q

Features of Renal Tubular Acidosis Type 1

A 
Impaired ability to excrete H+ in distal convoluted tubule
urine pH >5.5
renal calculi
hyperchloraemic acidosis
low-normal serum potassium
plasma bicarbonate <15
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16
Q

Features of Renal Tubular Acidosis Type 2

A 
Impaired ability to absorb HCO3 in proximal tubule
urine pH <5.5
no renal calculi
hyperchloraemic acidosis
low-normal serum potassium
plasma bicarbonate usually >15
17
Q

Features of Renal Tubular Acidosis Type 4

A 
Decreased secretion of aldosterone or decreased effect
urine pH <5.5
no renal calculi
hyperchloraemic acidosis
high serum potassium
plasma bicarbonate usually >15
18
Q

Causes of Renal Tubular Acidosis Type 1

A

SLE, Sjogrens, Nephrocalcinosis (primary hyperPTH), amphotericin B, obstructive

19
Q

Causes of Renal Tubular Acidosis Type 2

A

Multiple myeloma, acetazolamide, Fanconi syndrome, vitamin D deficiency

20
Q

Causes of Renal Tubular Acidosis Type 4

A

Aldosterone deficiency (primary, secondary), aldosterone resistance, drugs: NSAIDs, ACEI, ARB, spironolactone, trimethoprim

21
Q

Clinical utility of anti PLA2R

A

Sensitivity 78% Specificity 99% for primary Membranous Nephropathy

22
Q

Thrombospodin domain 7A (THDS7A)

A

Found in 2 - 5% of patients with primary membranous nephropathy

23
Q

NPHS2 - podocin

A

Familial FSGS

no response to steroids

24
Q

NPHS1 - nephrin

A

Congenital nephrotic syndrome

25
Q

Secondary causes of FSGS

A 
Obesity
Heroin abuse
HIV (African American)
Malignancy
Loss of renal mass
26
Q

Is there a role for immunosuppression in IgA nephropathy

A

No.

Stop IgAN study - no change in progression

27
Q

Secondary causes of membranoproliferative GN

A 
Hepatitis C +/- mixed cryoglobulinaemia
SLE
Hepatitis B
SBE
Malaria
Thrombotic microangiopathies
28
Q

Defect in TTP

A

Deficiency in ADAMTS13 (metalloproteinase)

29
Q

Diagnostic criteria for autosomal dominant polycystic kidney disease

A

Ultrasound criteria for diagnosis (uptodate)
Age 15 - 29: >/= 3 cysts, unilateral or bilateral
Age 30 - 39: >/= 3 cysts, unilateral or bilateral
Age 40 - 59: >/= 2 cysts in each kidney
Age >60: >/= 4 cysts in each kidney

30
Q

Genetic defect in PCKD

A

PKD 1

  • polycystin 1 on chromosome 16
  • more cysts
  • earlier age
  • earlier ESRD (median at age 50s)

PKD 2

  • polycystin 2 on chromosome 4
  • more indolent
  • later ESRD (median at age 70s)
31
Q

Urine Na level in pre-renal disease

A

Urine Na < 20 mmol/L

32
Q

Cyclosporin

MOA and SE

A

Calcineurin inhibitor
inhibits IL-2 generation
Nephrotoxic, diabetes, hyperlipidaemia, aHUS, hirsutism, gum hyperplasia

33
Q

Tacrolimus

MOA and SE

A 
Calcineurin inhibitor
inhibits IL-2 generation
Binds to FK-BP
More hyperglycaemia
Neurotoxicity, aHUS, alopecia
34
Q

Mycophenolate

MOA and SE

A

Reversible inhibitor of inositol monophosphate dehydrogenase in purine synthesis (G1 arrest)
Myelosupression, higher risk of CMV, teratogenic, diarrhoea

35
Q

Azathioprine

MOA and SE

A 
Purine analogue 
Safe in pregnancy
Bone marrow suppression
Skin malignancy
Increased MCV
36
Q

Prednsiolone

MOA and SE

A

Inhibits genes that code for cytokines - IL1, IL2, TNF gamma, etc
Hyperglycaemia, AVN, osteoporosis, Cushing’s

37
Q

Sirolimus/Everolimus

MOA and SE

A

mTOR inhibitors

Hyperlipidaemia, affects healing, non-nephrotoxic, anti-malignancy, causes oedema

38
Q

Basiliximab

MOA and SE

A 
Anti IL2 (CD25) - lowers rates of rejection
Safe, can cause hypersensitivity
39
Q

ATG (anti-thymocyte globulin)

MOA and SE

A

Polyclonal anti-lymphocyte globulin
Increased risk of infection/malignancy
serum sickness, leukopenia, hypotension, fevers

Basic Physician's Training Monash (16 decks)

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