Needs work Flashcards
UC severity classification
Montreal classification
Mild:
- <4 stools
- no systemic symptoms (fever, weight loss)
- normal ESR
Moderate:
- > 4 stools
- some systemic symptoms (fever, anaemia, abdo pain)
- no weight loss
Severe:
- > 6 stools
- systemic features (fever, tachycardia, anaemia, abdo pain)
- elevated ESR
Define pyuria and sterile pyuria
pyuria is defined as the presence of 10 or more white cells per cubic millimeter in a urine specimen, 3 or more white cells per high-power field of unspun urine, a positive result on Gram’s staining of an unspun urine specimen, or a urinary dipstick test that is positive for leukocyte esterase.1 Sterile pyuria is the persistent finding of white cells in the urine in the absence of bacteria, as determined by means of aerobic laboratory techniques (on a 5% sheep-blood agar plate and MacConkey agar plate).
Viral hepatitis clinical features
A -symptomatic in 70% -acute onset (1 month) -lasts 2 months -faecal oral -rarely fulminant -never chronic or cancer -vaccine outcome -cholestatic (prolonged jaundice) -relapsing
B
- baby making, babies and blood
- DNA virus
acute
- insidious/acute onset (2 months)
- 70% asymptomatic
- resolution within 3-4 months
- rarely fulminant (more with coinfection)
- ongoing fibrosis and detectable HBV DNA despite seroconversion
chronic
- 90% of neonatal
- 5% of adult acute
- polarteritis nodosa
- membranous GN
- aplastic anaemia
- associated with hepatic cancer
D
- Chronic Hep B with sudden decline/severe Hep B with demographic features
- often fulminant
- chronicity dependent on Hep B clearance
- some association with hepatic cancer
C
- blood borne and sexual
- acute lasts 3-4 months
- approx 90% develop chronic
- 30% develop cirrhosis
- high rate of cancer
- extrahepatic in chronic = LLAMP (lichen planus, lymphoma, auto-antibodies, mixed cryoglobinaemia, porphyria cutanea tarda)
E
- same as A but usually asymptomatic
- faecal oral, endemic
- acute onset of 1 month
- lasts approx 2
- can be fulminant and cholestatic
- doesn’t progress to chronicity or cancer
Hep A, D, C virology
HEP A
Anti-HAV IgM
- lasts approx 3 months
- represents acute
Anti-HAV IgG
- lasts indefinitely
- represents past infection
- protected from re-infection
HEP D
- defective RNA virus
- requires HBsAg for envelope
- co-infection and super-infection (change from donor to recipient HBsAg)
- delta antigen present in serum briefly following infection then intra-hepatocyte
acute
- HBsAg positive
- anti-HBc IgM positive
- may have serum delta antigen or HDV RNA or anti-HDV
chronic
-total anti-HDV
HEP C
- RNA virus
- antibodies do not provide protection
- HCV RNA within days of exposure, persists for duration of infection
- RNA levels don’t correlate with prognosis
Medical conditions with bleeding
you can CHAALK it up to:
- Cancer
- Alcohol
- Autoimmune (SLE)
- Liver disease
- Kidney disease (uraemia)
MRI brain mass
Primary brain tumour:
- low grade glioma (no uptake)
- high grade glioma (heterogeneous uptake)
- meningioma (homogeneous uptake)
- primary CNS lymphoma (homogeneous)
Metastatic tumour (homogenous):
- breast
- lung
- melanoma
Vascular: infarct -cortical emboli -venous thrombus (bleeding, oedema) haemorrhage (subacute intraparenchymal) anamoly -cavernous malformation -AV malformation -posterior reversible leukoencephalopathy syndrome
Infection:
- granuloma
- progressive multifocal leukoencephalopathy (JC virus)
- abscess
Inflammatory:
- demyelination (MS)
- autoimmune encephalitis (para/non neoplastic)
DDx for bone lesion
COPIIED
- congestion (vertebral venous)
- osteiod osteoma
- pagets
- infarct
- island
- enchondroma
- dysplasia (fibrous)
Define nephritic syndrome
Characterised by glomerular inflammation (glomerulonephritis) resulting in haematuria, red blood cell casts and dysmorphic RBCs, variable degrees of proteinuria (can be nephrotic range) and pyuria. Often have renal insufficiency (decreasing GFR and azotemia/uremia) leading to HTN and oedema.
Diabetic nephropathy ddx
Both proteinuria and oedema suggest glomerular disease.
Primary glomerular disease (My Girlfriend Is Mega Fit):
- Approx. 25% of diabetics have concurrent or isolated other glomerular disease
- minimal change
- glomerulonephritis
- IgA nephropathy
- membranous
- FSGS
Secondary: infective -Hep B/C inflammatory: -amyloidosis neoplastic: -lymphoma -multiple myeloma drugs: -NSAIDS autoimmune: -lupus -cryoglobinaemia
Oedema (CATCH ME)
- cirrhosis
- artery (renal artery stenosis)
- thiazolidinediones
- congestion (venous hypertension)
- heart failure
- myxedema
- enteropathy (protein losing, such as crohn’s)
DDx intrinsic AKI
Glomerular (Mindful Sailors Invest In A Good Anchor):
- membranoproliferative
- SLE
- IgA
- infectious (eg. post strep)
- anti GBM
- good pastures
- ANCA (polyangitis with granulomatosis, microscopic polyangitis, eosinophilic granulomatosis with polyangitis)
Vascular (Some Honest Virgins Admit Masturbating Every Day They Can):
small:
- Scleroderma
- Hypertension (malignant)
- Vasculitis
- Atheroemboli
- Microangiopathies
large:
- Embolus (systemic/renal)
- Dissection (aortic)
- Thrombosis (renal vein)
- Compartment syndrome (abdo)
Tubulointerstitial (Indoor Dogs Should SIT on their MAT)
interstitial nephritis:
- Infections (legonella)
- Drugs (antibiotics, NSAIDs)
- Systemic (sarcoid, srjogens, SLE)
ATN:
- Sepsis
- Ischaemia
- Toxins (vanc, aminoglycosides, contrast)
tubular obstruction:
- Myeloma
- Acyclovir
- Tumor lysis syndrome
DDx reflux nephropathy case
Provisional:
UTI’s + nocturia + HTN = UTO
Childhood Hx = congenital cause
- UPJ obstruction/narrowing
- UVJ obstruction/narrowing
- UVJ reflux
- Uretercele
- Bladder outlet obstruction
- Neurogenic bladder (spina bifida)
DDx:
Acquired:
- most likely functional secondary to anatomic or neurogenic
- carcinoma (kidney, ureter, bladder) = too young
- calculi/papillae = no pain
Vascular:
- nephrosclerosis due to HTN
- renal artery stenosis
Glomerular (nephrotic)
- My Girlfriend Is Mega Fit
- Secondary causes
- Diabetic nephropathy
Tubulointerstitial
- PCKD
- SLE, Srjogens, sarcoid
Pre-renal:
- CCF
- Cirrhosis
Smoking effects on vessel wall
Association between smoking and atherosclerosis well established but mechanism unclear
Damage to endothelium
- sympathetic activation -> increase HR and TPR
- increases LDL and triglycerides, decreases HDL
- free radicals that oxidise LDL
- > impairs endothelium dependent vasodilation (generation of NO)
- impaired prostacyclin production
- elevation of homocysteine also causes vascular damage
-also prothrombotic (decrease tPA, increase tissue factor, elevated fibrinogen and platelet activation)
path uc
Almost always involves the rectum (proctitis), commonly sigmoid (proctosigmoiditis) and up to left colic flexure. Can involve entire colon (pancolitis), with backwash ileitis.
Continuous lesions with sharp demarcation between healthy and diseased tissue.
Macroscopic: In mild disease, mucosa is erythematous with granular appearance (wet sandpaper). In severe disease, it may be haemorrhagic, oedematous and ulcerative (broad based). Regeneration leads to formation of pseudopolyps which may form mucosal bridges. In chronic disease, mucosa may be atrophied with loss of features.
Microscopic: Inflammation (mixed) is confined to mucosa or superficial submucosa. Disorganisation of crypts with crypt abscesses. There may be pseudopyloric or Paneth cell metaplasia. Shallow ulcers may be visible. There may be fibrosis of submucosa. No serositis or granulomas.
path of cd
Can involve any section of alimentary canal. 75% of cases involve small bowel, and of those, 90% involve terminal ileum. Often spares rectum. There may be skip lesions.
Macroscopic: Erythematous, longitudinal (serpinguous) ulcers giving cobblestone appearance. May be deep fissures or sinus tracts that can fistulate. Wall is thickened and there are commonly strictures. Wrapped by mesentary, creeping fat.
Microscopic: Transmural (mixed) inflammation. Disorganised crypts with crypt abscesses. May be pseudopyloric or Paneth cell metaplasia. Deep ulceration/fissures that may perforate bowel wall. Granulomas at any level. Submucosa is fibrotic, muscularis is hypertrophied and there may be serositis.
effects of acidosis
- Fall in pH detected by peripheral (carotid bodies) and central (mainly ventral surface of medulla, but now thought to be scattered throughout hind brain)
- Increase in ventilation, especially tidal volume (Kussmauls breathing)
- Impairs the function of all organs, but cardiovascular system is primarily affected
- Decreased response to catecholamines
- Increase in release of catecholamines may counter some of these effects
- Decreased myocardial contractility
- Decreased conductivity
- Vasodilation of peripheral vessels (hypotension)
- Vasodilation of splanchnic circulation, decreases perfusion
- Likewise, vasodilation of cerebral vasculature and depression of CNS function, with headache, lethargy, stupor –> coma
- Leads to constriction of pulmonary vasculature, decreased compliance and pulmonary oedema
- Decreased enzymatic activity of liver
- Impaired ATP production with decreased glucose uptake and reduction in glycolysis
-Procoagulant effect, associated with intravascular clotting