Clinical Medicine - Condition Summary Tables
All conditions in a table, organised by system and subsequently what you would expect to find on history, examination, investigation and management according to Australian guidelines.
ALL systems are included.
Glomerulonephritis
Anatomy
1. Fenestrated Epithelium
a. Prevents RBC’s from passing into the urine
2. Glomerular Basement Membrane
a. Prevents large proteins and RBC’s from passing into
the urine
3. Slit diaphragm between epithelial podocytes
a. Prevents medium proteins from passing into the urine
b. Podocytes are -ively charged which prevents medium
proteins from passing through as they are -ively
charged and repel each other
General Principle: Inflammatory/immune complexes are most
likely to affect the fenestrated epithelium, which means RBC’s will
leak out in the urine, causing haematuria.
a. Inflammatory/immune complexes GN’s will present with
nephritic syndrome
, Nephrotic Syndrome - Damage to podocyte slit membranes results in protein leaking into the urine to cause heavy proteinuria
(>3.5g/day).
a. Major protein lost is albumin resulting in hypoalbuminaemia and albuminuria
b. Hypoalbuminaemia leads to extravascular fluid expansion and non-gravity dependent oedema
c. To make more protein, liver works in overdrive and creates a large amount of lipids too leading to hypertriglyceridaemia
d. Anti-coagulation ATIII is also lost which result in an increased clotting risk; hypercoaguable state
e. Immunoglobulins are also lost which result in immunosuppression
f. Non-proliferative, inactive urine sediment i.e no RBC’s or WBC’s unless there is a superimposed infection
g. Minimal Change Disease, FSGS, Membranous Nephropathy, Amyloidosis, Diabetic Nephropathy, MCGN (also known as
membranoproliferative GN)
Minimal Change Focal Segmental Membranous Diabetic Nephropathy Membranoproliferative
Disease Glomerulosclerosis Nephropathy GN
Epi: most common GN Epi: Most common GN in Epi: most common Ax of Epi: Diabetics, leading Ax of Ax: immune complex
in children Hispanics African Americans; nephrotic syndrome in ESRD in high income deposition resulting in tram-
Ax: Idiopathic, may be adults > children adults countries track appearance
due to infection, Ax: Idiopathic, heroin use, Ax: Primary – anti-PLA2R Ax: High serum glucose leads Presentation: Mixed
Hodgkin’s HIV infection, sickle cell Ab; secondary – Hep B, to glycosylation of the nephrotic-nephritic
lymphoma or NSAID’s disease hep C, malaria, syphilis vascular BM. The efferent presentation, but mostly
Pathology: Pathology: and solid tumours, SLE, arteriole is more affected that nephrotic
a. LM: No a. LM: Focal (only some or drugs (NSAIDs or afferent i.e resulting in Pathology:
changes; glomeruli) & segmental penicillin), hyaline casts glomerular hyperfiltration a. IF: +ive as due to
unable to see (only some parts of the Pathology: Presentation: retinopathy, immune complex
effacement glomeruli) affected a. LM: Diffuse neuropathy, IHD, stroke, PVD deposition
b. IF: -ive as no b. IF: -ive; may be IgM, C1, thickened Pathology: Types:
immune C3 deposits in sclerotic glomerular capillary a. LM: Thick glomerular 1. Subendothelial –
component regions loops in BM walls with HIV/HCV
c. EM: effacement c. EM: effacement of b. IF: granular pattern Kimmelstiel-Wilson 2. Intramembranous –
of podocyte podocyte foot processes of stain due to nodules, PAS + silver C3
foot processes phospholipase A2 staining Buzzwords: poor response
Ab to steroid, progressed to CKD
Tx – prednisolone, c. EM: Granular
good prognosis subepithelial
deposits of IgG and
Buzzwords: C3 – spike and
Hodgkin’s Lymphoma, dome appearance
remits with Tx: RAAS inhibitors,
corticosteroids prednisolone (poor
response), other
immunosuppressants e.g
Tx – prednisolone (poor cyclosporine, tacrolimus
response), other Often progresses on ESRD
immunosuppressants e.g if untreated
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