Urology/Nephrology Flashcards
1
Q
Aetiology UTI
A
Simple:
approx. 90% = E. coli
10-15%= sapprophyticus
Complicated (abnormal function or anatomy):
E. coli, pseudomonas, klebseilla, proteus
2
Q
UTI diagnosis vs contamination
A
Diagnosis
->10^3 colony forming units of pathogenic bacteria
Contamination
- squamous epithelial cells
- lactobacilli
- enterococci
- Group B strep
- strep epidermidis
3
Q
pyelonephritis aetiology
A
Most common
-E coli
Other
- klebsiella
- proteus
- pseudomonas
- staph
- > including MRSA
- enterococci
- > considered contaminant for UTI
4
Q
Acute cystitis pharm
A
Avoid
- alkalinising agents
- > reduces efficacy of nitrofurantoin
- ascorbic acid/cranberry juice
- > unproven benefit
Analgesia
-NSAIDs or paracetamol
Antibiotics
- antimicrobial stewardship
- > symptoms will resolve faster with antibiotics
- > symptoms usually resolve within week without antibiotics
- > risk of pyelonephritis without antibiotics is low
- NiTrites
- > nitrofurantoin
- > trimethoprim
5
Q
Define nephritic syndrome
A
- glomerular inflammation (glomerulonephritis) causing
- > haematuria
- > red blood cell casts
- > dysmorphic RBCs
- > pyuria
- variable degrees of proteinuria
- > can be nephrotic range
- decreasing renal function
- > decreasing GFR/increasing creatinine
- > uremia
- complicated by
- > HTN
- > oedema.
6
Q
Define nephrotic syndrome
A
- Core features
- > heavy proteinuria (50mg/kg/day)
- > hypoalbuminaemia
- > peripheral oedema
- Additional
- > HTN
- > lipiduria
- > thrombosis
7
Q
Minimal change overview
A
Epidemiology
- most common cause of nephrotic syndrome in kids
- > congenital disease/infections for kids <1yr
- male predominance in kids but not adults
Aetiology
- primary (idiopathic)
- secondary
- > leukaemia
- > Hodgkins lymphoma
Pathophys
- enhanced glomerular permeability to proteins
- light microscopy
- > no structural changes
- electron microscopy
- > podocyte effacement
Clinical manifestations
- peripheral oedema
- > face, hands and feet
- > progresses over days to weeks
- nausea and vomiting
- recent viral illness
- hx of leukaemia or hodgkins lymphoma
- hypertensive
- respiratory distress (pleural effusion)
Investigations
- urinalysis
- > heavy proteinuria
- > benign sediment (hyaline casts or oval bodies)
- > occasionally haematuria
- > total protein:creatinine >2
- FBC
- > haemoconcentration
- EUCs
- > GFR/creatinine normal
- > dilutional (volume)/pseudonatraemia (hyperlipidaemia)
- Albumin
- > below 3g/dL
- Lipids
- > hyperlipidaemia
- Complement
- > should be normal in MCD
- LFTs
- > screen for hep
- Renal ultrasound
- > normal
- Renal biopsy
- > reserved for refractory/relapsing
Management
- core treatment
- > prednisolone for 6 weeks
- > salt and water restriction
- relapsing or resistant consider
- > high dose corticosteroids
- > renal biopsy (FSGS)
- > tacrolimus
- severe oedema consider
- > frusosemide
- > albumin
8
Q
FSGS background
A
Epidemiology
- most common cause of NS in adults
- male predominance
Aetiology
- primary (most common)
- > idiopathic
- secondary
- > viruses (HIV most common)
- > hyperfiltration (reduced renal mass of any cause)
- > reflux nephropathy
- > drugs (heroin, lithium)
- > obesity
Pathophys
- focal (some glomeruli)/segmental (part of glomerulus)
- > progresses to diffuse and global
- damage to podocytes and apoptosis
- proliferation of mesangium, epithelium, endothelium
- collapse of glomerular tufts
- deposition of collagen and sclerosis
9
Q
Membranous nephropathy background
A
Epidemiology
- second most common cause of NS
- rare in kids
Aetiology
- primary (most common)
- > idiopathic
- secondary
- > autoimmune (SLE, srogjens, rheumatoid)
- > neoplastic (bowel, lung, melanoma, lymphoma)
- > infectious (hep A and B)
- > drugs (gold, lithium, NSAIDs)
Pathophys
- unknown
- likely antibodies directed against podocytes/GBM
- complement activation and inflammation
10
Q
Membranoproliferative glomerulonephritis background
A
Epidemiology
-second most common cause of NS in kids
Aetiology
- immune complex mediated (most common)
- > hep B and C
- > SLE
- > lymphoma
- > monoclonal gammopathies
- complement mediated (mostly C3)
- > monoclonal gammopathies
Pathophys
- thickening of GMB
- > deposition of immune complexes/complement
- mesangial proliferation
- double contour capillary walls
11
Q
IgA nephropathy
A
Epidemiology
- almost half of all glomerulonephritis cases
- rare in africans
- peak in child bearing age
Aetiology
- idiopathic (most common)
- secondary
- > liver disease (alcoholic most common)
Pathophys
- depositions of predominately IgA in mesangium
- > also other immunoglobulins and complement
- indistinguishable from HSP
- mesangial hypercellularity
- glomerular sclerosis and fibrosis
12
Q
Lupus nephritis
A
Epidemiology
- most have some evidence of renal involement
- about half with have clinically significant disease
Aetiology (Magic Mikes/Mega Penis/Fucks/Desperate/Mums/ASses -minimal mesangial (i) -mesangial proliferative (ii) -focal (iii) -diffuse (iv) -membranous (v) -advanced sclerosing (vi)
Pathophys
- deposition of anti-double stranded DNA
- subendothelial causes lots of inflammation
- > ii,iii,iv
- subepithelial is less inflammatory
- > v
- class i is just deposition without reaction (rarely seen)
- class vi is healing and fibrosis
13
Q
post streptococcal glomerulonephritis
A
Epidemiology
- most common in developing world
- > relatively rare in developed
- peak incidence in elderly and school aged kids
- male predominance
Aetiology
- post GAS infection
- > approx 10% of pharyngitis
- > approx 25% of skin
Pathophys
- immune complex disease
- light microscopy
- > proliferative glomerulonephritis
- immunofluorescence
- > IgG and C3 deposition (starry sky)
- electron microscopy
- > sub epithelial humps
Clinical manifestations
- antecedent GAS infection
- > up to 3 weeks post pharyngitis
- > longer for skin
- microscopic haematuria to nephritic syndrome
- oedema
- HTN
Investigations
- urinalysis
- > haematuria
- > dysmorphic red cells
- > red cell casts
- > proteinuria (rarely nephrotic)
- > pyuria
- EUCs
- > low GFR
- complement
- > C3 and C4 low
- culture
- > not commonly positive for antecedent GAS infection
- serology
- > anti-streptolysin O (often negative in skin infection)
- > anti deoxyribonuclease B
Management
- if culture/serology postive
- > treat as usually for GAS infection
- if hypertensive
- > fluid and salt restriction
- > consider furosemide
14
Q
Causes glomerulonephritis (nephritic syndrome) child
A
Primary
- IgA nephropathy
- Anti-GMB (rare!)
Secondary (MISHAP)
- membranoproliferative
- IE (rare)
- SLE
- HSP
- ANCA (rare)
- post-strep
15
Q
Causes nephrotic syndrome child
A
Idiopathic
- glomerulonephritis
- > IgA
- > anti-GBM
- bland sediment/no glomerular inflammation
- > MCD
- > FSGS
- > membranous (rare)
Secondary
- glomerulonephritis
- > MISHAP
- MCD
- > leukaemia
- > hodgkins
- FSGS
- > HIV
- > hyperfiltrations
- > reflux
- > drugs
- > obesity
- Membranous (rare)
- > lupus
- > neoplasia
- > drugs
- > hepatitis A and B
