Renal/Urology Flashcards

1
Q

Features of Nephrotic syndrome?

4 things

A

Hyperlipidaemia
Oedema
Hypoalbuminaemia
Proteinura

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2
Q

What are features of Nephritic syndrome?

Pharaoh

A
Proteinuria - sub nephrotic range
Haematuria
Azotaemia
RBC casts
Anti-Strep titres
Oliguria
Hypertension
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3
Q

Protein leakage occurs in ___

A

Nephrotic syndrome - leads to leaky filter and podocyte dysfunction

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4
Q

Nephritic syndrome has _____ blocking the filter

A

Antibodies blocking the filter and leading to Inflammation

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5
Q

Three complications of Nephrotic syndrome which lead to the fourth complication?

A

Infection (cellulitis)
Hypercoaguable state (PE, DVT)
Intravascular volume collapse and shock (third spacing)

Leads to CKD

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6
Q

4 Nephritic syndromes?

A

IgA nephropathy
Post Strep GN
Anti-GBM
Pauci-immune GN

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7
Q

5 Nephrotic Syndromes:

A
Minimal change disease
FSGS
Membranous nephropathy
Diabetic nephropathy
Amyloid nephropathy
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8
Q

Nephrotic syndrome affecting childhood?

A

Minimal change - 90% of cases

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9
Q

Management of Minimal change disease?

Mx of complications?

A

Steroids

Oedema - salt restriction, ,daily weight, Diuretics (with albumin)
Infections - Prophylactic Phenoxymethylpenicillin
Thrombotic risk: Apsirin

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10
Q

Segmental sclerosis on Light Microscopy.

Immunofluorescence: weakly positive for IgM and C3

A

FSGS

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11
Q

What is benign nephrosclerosis?

A

Renal changes associated with hypertension causing hyaline arteriosclerosis

Kidneys are atrophic and have a diffuse granular surface

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12
Q

What is primary Vesicoureteric reflux?

A

Due to anatomical impairment:
a ureter did not grow long enough during the child’s development in the womb, the valve formed by the ureter pressing against the bladder wall does not close properly, so urine refluxes from the bladder to the ureter and eventually to the kidney; typically unilateral

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13
Q

What is secondary VUR?

A

Blockage in the urinary tract causes an increase in pressure and pushes urine back up into the ureters; typically bilateral

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14
Q

Hypertension in youth, renal impairment can lead to reflux nephropathy (small scarred kidneys) due to chronic _____

A

Pyelonephritis

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15
Q

VUR with torturous ureter with moderate dilation,blunting of fornices but preserved papillary impressions

Which grade?

A

Grade 4

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16
Q

Diagnosis of VUR?

A
  1. U/S

2.

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17
Q

What are the causes of Primary FSGS?

A

Minimal change disease progression

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18
Q

Secondary causes of FSGS:

A

Podoctye injury (inflammation, toxins) or prior nephron loss (reflux nephropathy, Htn, nephrosclerosis)

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19
Q

Mx of FSGS (Primary vs Secondary)

A

Primary: Prednisolone or consider cyclosporine or tacrolimus

Secondary: Ace-i to lower intraglomerular pressure

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20
Q

Which GN is related to Hepatitis B, paraneoplastic syndrome of melanoma, Gold

A

Membranous GN

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21
Q

Auto-antibodies to M-type Phospholipase A2 receptor

A

Membranous GN

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22
Q

Most common nephrotic syndromes in non-DM adults?

A

Membranous nephropathy

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23
Q

GBM thickening and spikes on silver stain on light microscopy

A

Membranous GN

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24
Q

Mx of Membranous GN?

A

Steroids and cyclosporin

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25
Q

Rule of thirds for Membranous GN?

A

1/3 - experience spontaneous remission
1/3- persistent proteinuria and a reduced but stable renal function
1/3 will lose renal function and result in end stage renal failure

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26
Q

Pathophysiology in Diabetic nephropathy?

A

Initially hyper perfusion and renal hypertrophy, then thickening of GBM and mesangial volume expansion, then microalbuminuria (WHICH IS REVERSIBLE)

then over proteinuria (Which is irreversible)

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27
Q

Kimmelstiel-Wilson lesion/nodule on light microscopy:

A

Diabetic nephropathy

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28
Q

Deposition of insoluble inappropriately folded proteins (with altered secondary structures causing it to fold into _____________):

A

Beta pleaded sheets

  • Condition is Amyloidosis
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29
Q

Presentation of Amyloidosis (3):

A

Presents as proteinuria (amyloid kidneys), restrictive cardiomyopathy, neurological deficits (peripheral neuropathy, carpal tunnel syndrome), pale and waxy appearance and diffuse enlargement of organs (hepatosplenomegaly, macroglossia, etc.), cutaneous ecchymoses (“raccoon eyes”)

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30
Q

Management of Amyloidosis?

A

melphalan and prednisolone (similar to multiple myeloma), treat CHF

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31
Q

Apple green birefringence on a Congo red stain and polarised light

A

Amyloidosis

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32
Q

GN Secondary to chronic infections such as hepatitis C, autoimmune processes, and monoclonal gammopathies

Immune complex-mediated: immune complex deposition leading to activation of complement

A

Membraoproliferative/Mesangiocapillary GN

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33
Q

Light microscopy: glomerular basement membrane reduplication and increased mesangial and inflammatory cells, “tram tracking”

A

Membranoproliferative GN

34
Q

Wire loop Glomeruli on Histology:

A

Lupus Nephritis

35
Q

MDSOAP BRAIN in Lupus?

A

Malar Rash
Discoid Rash

Serositis: Pleuritis, pericarditis
Oral or nasopharyngeal ulcers (on palate)
Arthritis: non-erosive and non-deforming (prayer’s signs)
Photosensitivity
Blood work: haemolytic anaemia or leukopaenia
Renal: Lupus nephritis
ANA Positive
Immunolic: anti- dsDNA, anti-smith
Neuropsych issues

36
Q

Libman-Sacks endocarditis associated with?

A

SLE

37
Q

Markers for SLE:

A

Anti-nuclear antibodies (ANA), anti-dsDNA, anti-Smith (most specific), anti-histone (drug-induced SLE), C3 and C4 (for monitoring)

38
Q

SLE associated endocarditis, characterised by verrucous valvular vegetations that can be detected on TTE:

A

Libman-Sacks endocarditis

Typically asymptomatic, however the verrucae can fragment and produce systemic emboli, and infective endocarditis can develop on already damaged valves

39
Q

GN occurring during and immediately after (1-2 days) viral upper respiratory tract infection

A

IgA Nephropathy: Caused by an infection triggering IgA production, and subsequent deposition and inflammation in the mesangium

40
Q

GN associated with Asian, Coeliac disease, coke coloured urine:

A

IgA nephropathy

41
Q

Triad for Henoch-Schonlein Purpura:

A
Palpable purpuric/ptechiae rash over buttocks and lower extremity
Arthritis: of large joints with painful oedema 
Abdominal pain (diarrhea)
42
Q

Differentiating HSP from ITP and TTP?

A

HSP has thrombocytosis

43
Q

Immunofluorescence starry sky:

A

Post-infective GN

44
Q

GN typically occurring 2-4 weeks after Group A β-haemolytic M type Streptococcus infections (pharyngitis, scarlet fever, impetigo, etc.)

A

Post-infective GN

45
Q

What age group is Post Strep GN most common in?

A

children aged 4-8yrs

46
Q

Light microscopy: “hump-like” subepithelial, as well as subendothelial and mesangial electron-dense deposits, neutrophils present, can be crescentic if severe:

A

Post infective GN

47
Q

GN occurs due to production of anti-GBM antibodies in response to an unknown stimulus

A

Anti-GBM membrane disease

48
Q

Crescentic Glomerulonephritis on Light microscopy:

A

Anti-GBM GN

49
Q

Linear ribbon-like IgG pattern on Immunofluorescence:

A

Anti-GBM disease

50
Q

Mx of Anti-GBM disease:

A

Plasmapheresis with either prednisolone or cyclophosphamide

51
Q

What is pauci-immune GN?

A

A group of nephritis GN associated with vasculitides:

52
Q

What markers in Granulomatosis with polyangitis?

A

c-ANCA, anti-protinase-3

53
Q

Rhinitis + GN + Eyes affected

Small vessel vasculitis

A

Granulomatosis with polyangiitis

54
Q

Glomerulonephritis (Pauci-immune nephritic syndrome) and lung involvement (haemoptysis) with NO presence of granulomas and p-ANCA positive:

A

Microscopic Polyangiitis

55
Q

3 stages of Churg-Strauss syndrome:

A
  • Allergic stage: asthma, atopy, rhinitis
  • Eosinophilic stage: Eosinophilia (leading to abdominal pain, bleeding)
  • Vasculitis stage (Glomerulonephritis - Pauci-immuni nephritis)
56
Q

p-ANCA positive in _____ and ______

A

Microscopic Polyangiitis and Churg-Strauss Syndrome

57
Q

Three types of GN leading to RPGN:

A

Anti-GBM disease, Immune complex disease, Pauci immune GN

58
Q

What are the most common causes of scrotal swellings in primary care?

A

Epididymal Cysts

59
Q

Where are epididymal cysts located?

A

Found separate to the body of the testicle and found posterior to the testicle

60
Q

A _______ describes the accumulation of fluid within the tunica vaginalis.

A

Hydrocele

61
Q

Hydroceles may develop secondary to…

A

Epididymo-orchitis
testicular torsion
testicular tumours

62
Q

Features of a hydrocele?

A

Soft, non tender swelling of the hemi-scrotum. Usually anterior and below the testicle.
You can get ‘Above’ the mass. TRANSILLUMINATES with a pen torch.

63
Q

A ____ is an abnormal enlargement of the testicular veins.

A

Varocele

64
Q

4 major symptom categories for BPH?

A
  1. Voiding symptoms (obstructive) - hesitancy, dribbling and retaining
  2. Storage symptoms: urgency, frequency, urgency incontinence and nocturia
  3. Dribbling
  4. Complications: UTI, retention, obstructive uropathy
65
Q

Mx options for BPH?

A

Wait
Medication: alpha1 antagonist or 5 alpha reductase inhibitors
surgery - TURP!

66
Q

What medications are used for BPH and what are their side effects?

A
  1. Alpha 1 antagonist - Tamsulosin, alfuzosin
    First line - decrease smooth muscle tone
    Adverse effects - dizziness, postural hypotension, dry mouth, depression
  2. 5 alpha-reductase inhibitors e.g. Finasteride
    Block the conversion of testosterone to dihydrotestosterone which is known to induce BPH
    They reduce size of prostate and hence may take a while to work.
    adverse effects: ED, Reduced libido, ejaculation problems, gynaecomastia
67
Q

Patient with Sepsis present with AKI. What would her blood gases be like and would she be alkalosed or acidotic?

A

She would be acidotic and have reduced HCO3- and hence increased anion gap too.

68
Q

Differentials of a raised anion gap? (TLKR)

A

Toxins (Salicylates, methanol, ethylene glycol)
Lactic acidosis
Ketones (DKA)
Renal failure (increased urate)

others: Metformin, Isoniazid

69
Q

Metabolic acidosis with a normal anion gap (due to loss of bicarbonate or accumulation of H++).
4 DDX?

A

Renal tubular acidosis
Diarrhea
Addison’s disease
Pancreatic fistula

70
Q

Some causes of hyperkalaemia?

A
AKI
Drugs- Spironlactone, ACE inhibitor, ARBS
Metabolic acidosis
Addison's disease
Rhabdomyolosis
Massive blood transfusion
71
Q

Minimal change disease has an association with Atopy and Hodgkin’s Lymphoma - T or F?

A

T

72
Q

In Nephrotic syndrome: Loss of ________, Protein ___& ____ and an associated rise in fibrinogen levels predispose to thrombosis.

A

Loss of antithrombin III, Protein C and S

73
Q

Tibial fracture with fasciotomy after an injury.. the patient probably had ____

A

Compartment syndrome

74
Q

Post op, worsening of renal function with muddy brown casts is suggestive of ____

A

Acute tubular necrosis

75
Q

What is the mode of inheritance of Alport’s syndrome in the majority of cases?

A

X linked dominant

76
Q

What is alport’s syndrome?

A

Congenital defect in the gene which codes for type IV collagen resulting in abnormal glomerular basement membrane.

Presents with a nephritis picture - microscopic haematuria, progressive renal failure and bilateral sensorineural deafness?

77
Q

What is the most common and important viral infection in solid organ transplant recipients?

A

CMV

78
Q

A 60-year-old man presents with visible haematuria for the past three weeks. He has an ache in the left loin but examination is unremarkable other than a LEFT VARIOCELE. He also notes to feeling intermittently hot and sweaty.

A

Renal cell carcinoma

79
Q

What endocrine effects do you get in Renal Cell Carcinoma

A

May secrete eryhtropoetin (Polycythaemic), Parathyroid hormone (Hypercalcaemia), renin, ACTH

80
Q

Classic triad: haematuria, loin pain, abdominal mass

A

Renal Cell carcinoma