histopath Flashcards by Shanxi Jen

neurofibroma + pilocytic astrocytoma

neurofibromatosis type I

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schwannoma + meningioma

neurofibromatosis type II

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haemangioblastoma

von hippel lindau

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most frequent brain tumour in adults

secondary metastases

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most frequent brain tumour in children

pilocytic astrocytoma

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most common types of brain tumour in children

pilocytic astrocytoma

2. medulloblastoma

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Pilocytic astrocytoma

20% of CNS tumours <14 yo
often cerebellar, optic-hypothalamic, brain stem
MRI: circumscribed lesion
BRAF mutation

piloid hairy cell
often rosenthal fibres and granular bodies

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piloid ‘hairy’ cell

+/- rosenthal fibres and granular bodies

pilocytic astrocytoma

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astrocytomas eventually become?

glioblastomas

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what is the most aggressive and most frequent brain tumour in adults?

de novo glioblastoma (IDH wildtype)

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a diffuse infiltrating astrocytoma w mutation in the IDH1 or IDH2 gene

diffuse astrocytoma

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what does tumour grade tell us?

survival/ prognosis

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second most common brain tumour in children?

medulloblastoma

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most frequent primary brain tumour in adults?

glioblastoma multiforme (90% de novo 10% secondary progression from astrocytoma)

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brain tumour with round cells w clear cytoplasm (fried eggs) on histology

oligodendroglioma

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what is the 2nd most common primary brain tumour in adults?

meningioma

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senile plaques of beta amyloid protein and neurofibrillary tangles of tau protein

alzheimers

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neuropathology of alzheimer’s disease?

extracellular plaques (senile plaques made of beta amyloid)
neurofibrillary tangles
cerebral amyloid angiopathy leading to neuronal loss and cerebral atrophy

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Beta amyloid proteins cleaved from?

APP

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How are senile plaques formed?

beta amyloid proteins congregate and form insoluble plaques

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parkinsons pathology?

loss of dopaminergic neurons in substantia nigra

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lewy bodies in affected neurons (histology)

Parkinsons
and Lewy body dementia
(pathologically indistinguishable)

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what is the main component of lewy bodies?

misfolded alpha synuclein protein

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tau protein misfolding

picks disease
frontotemporal dementia linked to chr 17
corticobasal degeneration

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Picks disease

fronto temporal atrophy
tau positive Pick bodies
marked gliosis and neuronal loss
balloon neurons

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what is the inheritance of frontotemporal dementia linked to chr 17?

auto dominant

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cerebral oedema

excess accumulation of fluid in brain parenchyma

-> ICP raised

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what produces CSF?

choroid plexus

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hydrocephalus non communicating

obstruction of flow of CSF

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hydrocephalus communication

no obstruction but problems w reabsorption of CSF into venous sinuses

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normal ICP in adult

7-15 mmHg

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consequences of raised ICP

herniation of brain structures

e.g. subfalcine, transtentorial (uncal), tonsillar

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causes of raised ICP

SOL

oedema

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risk factors of stroke

smoking, hypertension, DM, Family history, obesity, past TIAs, peripheral vascular disease, hyperviscosity
arrhythmia e.g. AF

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what is a high pressure structure which may cause massive bleeding? in the brain

arteriovenous malformations

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a well-defined malformative lesion composed of closely packed vessels found in the CNS. a low pressure structure that may lead to recurrent bleeds

cavernous angioma

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rupture of berry aneurysm

sub arachnoid haemorrhage

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where does rupture of berry aneurysm most often occur?

internal carotid artery bifurcation

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thunderclap headache, vomiting, LOC

Sub arachnoid haemorrhage

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what kind of bleed does an arteriovenous malformation cause?

subarachnoid

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what kind of bleed does a cavernous angioma cause

subarachnoid

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most common cause of cerebral infarction

cerebral atherosclerosis

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what pathology do you see on brain infarct?

tissue necrosis
permanent damage in affected area
no recovery

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what pathology do you see on haemorrhage in brain?

bleeding
dissection of parenchyma
fewer macrophages
limited tissue damage
partial recovery

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raccoon eyes

base of skull fracture

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diffuse axonal injury

commonest cause of coma when no bleed
shear and tensile forces affecting axons
midline structures particular affected. e.g corpus callosum

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Causes of large droplet fatty change in liver?

obesity and DM
protein-calorie malnutrition
Total parenteral nutrition
drugs and toxins e.g. alcohol, corticosteroids
metabolic disorders e.g. wilsons
infections e.g. hepatitis c

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causes of small droplet fatty change

alcohol
fatty liver of pregnancy
drugs
toxins
inborn errors of metabolism
Reyes syndrome
infections e.g hepatitis A

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fatty liver hepatitis

hepatocyte ballooning and necrosis
Mallory-Denk bodies
Fibrosis

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Mallory-denk bodies

fatty liver alcoholic hepaitis

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most common causes of acute pancreatitis?

gallstones
alcohol
idiopathic

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how does alcohol lead to acute pancreatitis?

alcohol leads to spasm/ oedema of sphincter of oddi and the formation of protein rich pancreatic fluid which obstructs the pancreatic ducts

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what enzymes are elevated following acute pancreatitis?

serum amylase
serum lipase (more sensitive)

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complications of acute pancreatitis

shock, hypoglycaemia, hypocalcaemia
pancreatic pseudocyst
pancreatic abscess

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what is the most common cause of chronic pancreatitis?

alcohol

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histology of chronic pancreatitis

chronic inflammation with parenchymal fibrosis and loss of parenchyma

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complications of chronic pancreatitis?

malabsorption
diabetes
pseudocysts
carcinoma of pancreas?

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Xray finding of pancreatic calcifications

Chronic pancreatitis

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a cyst lined by fibrous tissue and contains fluid rich in pancreatic enzymes or necrotic material

Pancreatic pseudocyst

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Autoimmune pancreatitis

IgG4 positive plasma cells

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Most common tumour of the pancreas?

ductal carcinoma

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risk factors for pancreatic carcinoma?

smoking
BMI and dietary factors
chronic pancreatitis
diabetes

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most common site of ductal carcinoma

head of pancreas

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courvoisiers’ law: palpable painless gallbladder - most likely?

ductal adenocarcinoma of the pancreas (head)

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MEN1

3Ps
Pancreatic endocrine neoplasms
pituitary adenoma
parathyroid adenoma/ hyperplasia

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complications of gall stones

bile duct obstruction
acute and chronic cholecystitis
acute pancreatitis/ chronic
gall bladder cancer

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most common cause of acute cholecystitis

gall stones

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most common cause of chronic cholecystitis

gall stones

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rokitansky-aschoff sinuses

chronic cholecystitis.

• Diverticula due to long term pressure build up

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most common cause of gall bladder cancer

gall stones

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most common type of gall bladder ca

adenocarcinoma

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oat shaped cells on microscopy - lung ca

small cell carcinoma

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peripheral tumours in lung

adenocarcinoma

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Biopsy of GI tract showing non-caseating granulomas w transmural inflammation

crohns disease

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Biopsy shows villous atropy with crypt hyperplasia and increased intraepithelial lymphocytes

Coeliac disease

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Biopsy showing signet ring cells and linitis plastica (leather bottle stomach)

gastric carcinoma

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most common cause of infective endocarditis in IVDU?

staph aureus

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most common cause of infective endocarditis in normal population?

streptococcus viridans

esp after dental procedures

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ejection systolic murmur, narrow pulse pressure, slow rising pulse

aortic stenosis

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nutmeg liver, haemosiderin macrophages in lungs

left heart failure

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autoimmune complication of MI ~4 wks after. chest pain, fever, pericardial rub

dresslers syndrome

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complications of MI within 1 week

myocardial rupture, valve incompetence, arrhythmias (most commonly VF/ VT)

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cardiac complications of rheumatic fever?

endocarditis
myocarditis
pericarditis
pancarditis
chronic rheumatic heart disease after many years with fibrosis of mitral and aortic valves

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st vitus dance

rheumatic fever

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sydenhams chorea

rheumatic fever

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aschkoff bodies and anitschow cells

rheumatic fever

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rheumatic fever

following group A B-heamolytic streptococci

inflammatory condition affecting connective tissue of heart, joints and CNS

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focal calcification of media of small medium-sized arteries

monckeberg arteriosclerosis

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progressive loss of myocytes

dilated cardiomyopathy

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autosomal dom condition causing mutation in the B-myosin heavy chain

hypertrophic obstructive cardiotrophy

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myocyte hypertrophy and disarray

hypertrophy obstructive cardiotrophy

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5-hydroxyindoleacetic acid producing tumour

carcinoid syndrome

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episodic flushing, abdominal cramps and diarrhoea + right sided valve abnormalities

carcinoid syndrome

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permanent dilation of bronchi and bronchioles secondary to chronic inflammation

bronchiectasis

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bronchial wall destruction and transmural inflammation

bronchiectasis

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Ix of bronchiectasis?

high resolution CT scan

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complications of bronchiectasis

abscess formation
haemoptysis
pulmonary HTN

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F508 mutation

cystic fibrosis

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nests of small round hyper chromatic cells that are fragile and possess nuclear moulding - ‘oat cells’

small cell carcinoma

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Lambert-eaton myasthenic syndrome - which lung ca?

small cell carcinoma

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predominantly central lung ca

small cell ca

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non-small cell ca comprise?

adenocarcinoma
squamous cell ca
large cell ca

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gland forming and mucin vacuoles. lung ca

adenocarcinoma

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lung ca with keratinisation and intracellular prickle desmosomes

squamous cell carcinoma

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peripheral lung cancers

non small cell ca

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CXR showing bat wings (alveolar oedema), Kerley B lines, cardiomegaly, upper lobe diversion of blood vessels and effusions

pulmonary oedema - cardiac cause (e.g. heart failure, mitral stenosis)

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respiratory distress syndrome aka surfactant deficiency aka?

hyaline membrane disease

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extrinsic allergic alveolitis

long-term exposure to inhaled allergen leads to pulmonary fibrosis

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mucus gland hypertrophy, goblet cell hyperplasia/ metaplasia, mucosal oedema

chronic bronchitis

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CREST syndrome

calcinosis
raynauds
oesophageal dysmotility
sclerodactyly
telangiectasia

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pathogenesis of systemic sclerosis

excessive release of PDGF -> widespread fibroblast activation and multi organ fibrosis

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‘onion skinning’ of microvasculature (intimal thickening due to chronic fibrosis)

systemic sclerosis

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most sensitive antibodies to SLE?

anti-ds DNA

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cytology of tissues reveals haematoxylin bodies

SLE

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LE cells visible on microscopy- macrophages that have phagocytosed a haematoxylin body

SLE

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apple-green birefringence using polarised light and Congo red stain

amyloidosis

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what amyloid is derived from IgG light chains? and assoc w myeloma

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amyloid assoc w alzheimers

beta amyloid

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amyloid derived from serum amyloid assisted protein and assoc w inflammation

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pANC assoc w?

microscopic polyangitis

eosinophilic granulomatosis with polyangiitis (churg-strauss)

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microscopic polyangitis?

a small vessel vasculitis
triggered by microorganisms and drugs
affecting the skin, heart, brain and kidneys

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histology of affected vessels include fibrinoid necrosis that leads to fragmented neutrophilic nuclei within vessel walls

microscopic polyangitis

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difference between myasthenia graves and dermatomyositis?

sparing of the ocular muscles

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heliotrope rash and gottron papules

dermatomyositis

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dermatomyositis ix

raised creatine kinase levels

anti Jo1

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dry eyes dry mouth

sjogrens

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positive Schirmers test

sjogrens

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immune mediated destruction of the lacrimal and salivary glands

sjogrens

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arteritis w no pulses and low BP in arms and cold hands

takayasu arteritis

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degeneration of substantia nigra and locus coeruleus of the basal ganglia, loss of dopaminergic neurons

parkinsons

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Lewy bodies made of?

alpha synuclein

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subarachnoid haemorrhages assoc w which conditions?

Polycystic kidney disease
coarctation of the aorta
fibromuscular dysplasia

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histology along the CNS include active (containing lymphocytes and macrophages) and inactive (reduced myelin and nuclei) plaques

multiple sclerosis

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optic neuritis, intranuclear ophthalmoplegia (disruption of medial longitudinal fasciculus) and cerebellar signs + spasticity and weakness of limbs

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downs assoc w which dementia?

alzheimers

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damage to the middle meningeal artery

extradural haemorrhage

assoc w severe trauma and fracture to pterion

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extradural haemorrhage assoc w severe trauma and fracture to pterion, which artery affected?

middle meningeal artery

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skip lesions and fistulae, transmural inflammation

crohns

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complications of crohns

thickening of bowel wall leading to bowel obstruction

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extra intestinal manifestations of crohns

arthritis 
uveitis 
stomatitis
pyoderma gangrenosum
erythema nodosum

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metaplastic columnar epithelial cells in the oesophagus

barrett’s oesophagus

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barrett oesophagus increased risk of ?

adenocarcinoma of the oesophagus

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main causes of peptic ulcers

h pylori
NSAIDs
zollinger- Ellison
smoking

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chronic gastritis risk of ?

carcinoma

MALT lymphoma

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what is cirrhosis?

diffuse fibrosis of the liver w abnormal architecture (nodules of regenerating hepatocytes) + intra and extrahepatic shunting of blood

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what cell is repsonsible for fibrosis in liver?

stellate cell activation -> deposit collagen

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nodules of regenerating hepatocytes + haphazard blood supply (shunting and portal hypertension)

cirrhosis

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what gene is implicated in Wilsons?

ATP7B gene

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Mutation in ATP7B gene

Wilsons disease

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inheritance on wilson’s

autosomal recessive

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Wilsons

multi-organ copper accumulation
-> cirrhosis, behavioural changes, depression, psychosis,
parkinsonism, seizures and dementia
cardiomyopathy

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kayser- Fleischer rings

wilsons

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haemochromatosis inheritance?

auto recessive

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what gene is involved in haemochromatosis?

HFE gene

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HFE gene

haemochromatosis

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golden- brown haemosiderin deposition in the parenchyma in many organs

haemochromatosis

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Perl’s Prussian blue stain +

haemochromatosis

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what organs are involved in haemochromatosis?

liver (cirrhosis)
heart (cardiomyopathy), skin (bronzed pigmentation), pancreas (diabetes)
gonads (atrophy and impotence)

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most common liver malignancy

hepatocellular carcinoma

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aflatoxin malignancy

hepatocellular carcinoma

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alpha fetoprotein marker of malignancy?

hepatocellular carcinoma

germ cell tumours

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BHCG malignancy marker?

choriocarcinoma

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dense accumulation of lymphocytes around bile ducts creating granulomas and total destruction of ducts

primary biliary cirrhosis

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anti mitochondrial antibodies

PBC

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risk factors of developing cholangiocarcinoma

Primary sclerosing cholangitis
parasitic liver fluke infection
exposure to medical imaging contrast media

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PBC assoc with which autoimmune condition?

sjogrens syndrome

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emphysema in lungs and cirrhosis - deficiency in?

alpha1- antitypsin

lack of inhibition of neutrophil proteases -> destruction of tissues

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biopsy of bile ducts showing periductal fibrosis that eventually invades the lumen causing concentric onion ring fibrosis

primary sclerosing cholangitis

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pemphigoid

deep- dermoepidermal junction. autoimmune deep bullous condition
nikolskys sign NEGATIVE. cause bullae do not rupture easily.

eosinophils recruited to site which destroys the elastic fibres

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IgG (+C3) binding to hemi-desmosomes in the dermoepidermal junction the skin

pemphigoid

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pemphigus

superficial blisters. nikolsky sign positive.

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IgG binding to desmosomes in the intra epidermal region resulting in acantholysis

pemphigus

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pemphigus which layer is affected

intra epithelial

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pemphigoid which layer is affected

subepithelial.

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Steven Johnsons syndrome

severe form of erythema multiforme
involving mucosal surfaces
characterised by epidermal necrosis

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auspitz sign (pinpoint bleeding when rubbing lesion)

psoriasis

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salmon pink plaques with silver white scale

psoriasis

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psoriasis nail changes?

onycholysis

pitting

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epidermal dysplasia secondary to sunlight - presents as brown-red warty lesion w sandpaper consistency

actinic keratosis

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solar elastosis, focal parakeratosis on histology

actinic keratosis

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actinic keratosis may progress to?

squamous cell carcinoma

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subtypes of malignant melanoma?

lentigomaligna, acrallentigious, superficial spreading, nodular

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squamous carcinoma in situ

bowens disease

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herald patch

pityriasis rosea

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rodent ulcers

basal cell carcinoma

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pearly, raised, ulcerated, telangiectasia. skin lesion

basal cell ca

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red cell and white cell casts, haematuria

nephritic syndrome

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1-4 days after resp/ GI infection - frank haematuria

IgA nephropathy

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IgA nephropathy aka

bergers disease

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deposition of IgA immune complexes in glomeruli

IgA nephropathy

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most aggressive Glomerulonephritis - end stage renal failure in days to week

rapidly progressive (crescentic) glomerulonephritis

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most common viral cause of rapidly progressive glomerulonephritis

Hep B

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causes of rapidly progressive glomerulonephritis

type 1: anti GBM antibody (goodpastures)
type 2: immune complex mediated e.g. SLE
type 3: lack of immune complex e.g. Wegeners or microscopic poluangitis

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wegeners’ rapidly progressive glomerulonephritis pattern of deposition on fluorescence microscopy

absent/ scant immune complex deposition

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green/ white discharge from breast

duct ectasia

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microcalcification of well defined lesion in breast

ductal carcinoma in situ

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leaf like/ artichoke like appearance on histology. rapidly growing tumour

phyllodes tumour

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peau d’orange, paget’s disease of the breast, nipple retraction, tethering, lymphadenopathy

features of invasive carcinoma

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polyostotic fibrous dysplasia + cafe au lait spots + precocious puberty ?

McCune-Albright Syndrome

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lytic lesions in the epiphyses -> characteristic soap bubble appearance on Xray

giant cell tumour

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histology showing multinucleate giant osteoclasts with surrounding ovoid and spindle cells

giant cell tumour

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looser zones (pseudo fractures)

osteomalacia

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soap bubble osteolysis + shepherds crook deformity

fibrous dysplasia

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cotton wool calcification - often in the hands (X-ray)

enchondroma (Ends sounds like hands)

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painful bone neoplasm, common in children, Xray reveals radiolucent central nidus and sclerotic rim pattern

osteoid osteoma

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cartilage capped bony outgrowth typically in long bones

osteochondroma

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non-caseating granulomas + Schaumann and asteroid bodies on histology (multisystem disease)

Sarcoidosis

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Bilateral hilar lympadenopathy + insidious SOB, cough, chest pain, night sweats

Sarcoidosis

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Ix showing high Ca, high ACE, high ESR

Sarcoidosis

Ca high due to Vit D hydoxylation by activated macrophages
ACE blood levels increase as the cells surrounding granulomas produce increased amts of ACE

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multisystem disorder caused by abnormal folding of proteins that are deposited as amyloid fibrils in tissues, disrupting their normal function

amyloidosis

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primary amyloidoisis

deposition of amyloid L protein
assoc w multiple myeloma
Plasma cells produce amyloid!

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secondary amyloidosis

Amyloid formed from serum amyloid A (an acute phase protein) -> secondary to inflammation/ chronic infections

e.g. RA, IBD, TB, IVDU

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haemodialysis associated amyloidosis

deposition of beta2-microglobulin

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familial amyloidosis assoc w which condition?

familial Mediterranean fever

AA Amyloid, predominant renal deposition

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what organs are usually implicated in amyloidosis? + most common

kidney most common- nephrotic syndrome

heart- heart failure, cardiomegaly, conduction defects
liver/spleen - hepatosplenomegaly
tongue- macroglossia
neuropathies

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scalp tenderness, temporal headache, jaw claudication, raised ESR

temporal arteritis

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giant cell arteritis assoc w?

polymyalgia rheumatica

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giant cells + granulomatous transmural inflammation + narrowing of the lumen on histology of vessel

giant cell arteritis

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IgA mediated vasculitis, assoc w preceding URTI in children. palpable purpuric rash

henoch Schonlein purpura

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henoch Schonlein purpura

preceding URTI
palpable purpuric rash
glomerulonephritis
colicky abdo pain
arthritis
orchtiis

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HSP mx

analgesia

supportive

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p-ANCA antibodies against?

myeloperoxidase

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what does microscopic polyangiitis present w?

renal-pulmonary

pulmonary haemorrhage
glomerulonephritis

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what does chrug- Strauss aka eosinophilic granulomatosis w polyangiitis present w?

asthma, allergic rhinitis
eosinophilia
later systemic involvement

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pulmonary haemorrhage
glomerulonephritis

pANCA +

microscopic polyangiitis

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asthma, allergic rhinitis
eosinophilia

pANCA +

churg- strauss

eosinophilic granulomatosis w polyangiitis

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what is the treatment for wegeners?

also for churg-strauss

cyclophosphamide

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saddle nose, epistaxis

pulmonary haemorrhage, glomerulonephritis

wegeners

gPA

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cANCA

wegeners

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cANCA against?

anti proteinase 3

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what does Wegener’s comprise of?

saddle nose, epistaxis

pulmonary haemorrhage, glomerulonephritis

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heavy smoker, 30 yr old, w pain and ulceration of toes and fingers. corkscrew appearance on angiogram

thromboangitis obliterans

Buerger’s disease

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thromboangitis obliterans

usually heavy smokers\
men <35 years

pain and ulceration of toes and fingers. corkscrew appearance on angiogram

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microaneurysms on the angiography “beading” “rosary sign”

polyarteritis nodosa

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polyarteritis nodosa associ w which underlying infection?

Hep B

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polyarteritis nodosa

medium vessel necrotising arteritis involving kidneys and other organs but spares the lungs

“rosary sign” beading on angiography

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connective tissue disease. ANA Immunofluorescence staining pattern for dermatomyositis and polymyositis

speckled pattern

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what type of hypersensitivity in SLE?

Type III

immune complex deposition

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SLE HLA association?

HLA DR3

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SLE autoantibodies

anti nuclear antibodies (ANA)
anti - dsDNA
Anti-smith
anti-histone (drug induced)

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What SLE antibody is most specific? (best true -ve)

anti-smith

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what SLE antibody is most associated with drug-induced SLE?

anti-histone Ab

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connective tissue disease. ANA Immunofluorescence staining pattern for systemic sclerosis?

nucleolar pattern

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Kidney histology: ‘wire loops’ due to Immune complex deposition. + thickened pink glomerular capillary loops

SLE

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what heart complication is most associated with SLE?

Libman Sacks endocarditis

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SLE effect on kidneys

deposition of immune complexes on kidney basement membrane -> thickening of BM

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Malar rash

SLE

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onion skin thickening of arterioles + increased collagen in skin and organs

Systemic sclerosis (limited/ diffuse)

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anti-centromere ab

Limited scleroderma

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anti-topoisomerase ab

diffuse scleroderma

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anti-scl70 ab

diffuse scleroderma

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increased collagen in skin and organs + inflammation within or around muscle fibres

diffuse scleroderma

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scleroderma + pulmonary fibrosis

diffuse scleroderma

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CREST + microstomia + pulmonary hypertension + only skin distal to elbows and knees affected

Limited scleroderma

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anti - JO1 antibody recognises which cellular protein?

tRNA synthetase

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anti-scl70 antibody recognises which cellular protein?

DNA topoisomerase

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dermatological emergency where sheets of skin detach + nikolsky sign +ve. triggered by drugs e.g. anticonvulsants

stevens Johnsons syndrome

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Steven Johnsons syndrome vs toxic epidermal necrolysis

TEN >30% body surface involvement

SJS <10% body surface involvement

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what drugs can trigger Stevens johns syndrome?

anticonvulsants, sulfonamide antibiotics

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salmon pink rash (herald patch) arrives first followed by oval macule in Christmas tree distribution

pityriasis rosea

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pityriasis rosea

appears after viral illness. remits spontaneously

salmon pink rash (herald patch) arrives first followed by oval macule in Christmas tree distribution

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atypical melanocytes growing horizontally into epidermis and vertically into dermis

malignant melanoma

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pagetoid spread of melanocytes “buckshot appearance”

malignant melanoma

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Malignant melanoma most impt prognostic factor?

breslow thickness

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malignant melanoma subtype most often occurring on palms, soles and sublingual areas

acral lentiginous melanoma

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malignant melanoma subtype most often occurring in the younger age group, can occur anywhere

nodular malignant melanoma

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malignant melanoma subtype - irregular borders with variation in colour

superficial spreading

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malignant melanoma subtype - occurs on sun exposed areas of elders caucasians. flat, slowly growing black lesion

lentigo maligna melanoma

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central area of ulceration w raised rim. pearly surface and often with telangiectasia. on the skin

basal cell carcinoma

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atypia/ dysplasia throughout epidermis, nuclear crowding and spreading though basement membrane into dermis

squamous cell carcinoma

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rough, sandpaper like scaly lesions on sun-exposed areas

actinic / solar / senile keratoses

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solar elastosis / parakeratosis

actinic keratosis

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rough plaques look stuck on , waxy

seborrhoeic keratosis

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rapidly growing dome shaped nodule which may have a necrotic crusted centre. grows over 2-3 wks and clears spontaneously. with similar histology to SCC

keratoacanthoma

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intraepidermal squamous cell carcinoma in situ

bowens disease

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flat red scaly patches on sun exposed skin but BM still intact

Bowens disease

SqCC in situ

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coeliac skin manifestation

dermatitis herpetiformis

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itchy vesicles on extensor surfaces of elbows, buttocks. due to IgA Abs binding to BM and causing sub epidermal bullae

dermatitis herpetiformis

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Histology of skin shows micro abscesses which coalesce to form sub epidermal bullae. due to neutrophil and IgA deposits at tips of dermal papillae

dermatitis herpetiformis

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intraepidermal bullae

pemphigus

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sub epidermal bullae with eosinophils and linear deposition of IgG and C3 along BM

pemphigoid

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what are the two infections assoc w erythema multiforme?

HSV

Mycoplasma

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What are the few drugs that could cause erythema multiforme?

NSAIDs
sulphonamides
ALlopurinol
penicillin
phenytoin

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lesions with mother of pearl sheen with fine white network on their surface (wickam’s striae) usually on inner surface of wrists and oral mucous membranes

lichen planus

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wickam’s striae

lichen planus

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inner surface of wrist. histology showing hyperkeratosis with saw toothing of Crete ridges

lichen planus

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psoriasis koebner phenomenon

lesions form at sites of trauma

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Type IV T cell mediated hypersensitivity reaction. Cells in plaque have increased proliferation rate. Histology shows parakeratosis, “test tubes in a rack” appearance, and Munro’s microabscesses

Psoriasis

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Psoriasis what type of hypersensitivity reaction?

Type IV T cell mediated

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guttate psoriasis

rain drop plaque distribution. often 2 weeks post strep throat

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2 wks prior had strep throat, now has rain drop plaques.

guttate psoriasis

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Histology: parakeratosis, test tubes in a rack appearance- clubbing of rite ridges, munro’s microabscesses

psoriasis

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what type of hypersensitivity is contact dermatitis

type IV

GI polyps + multiple osteomas (bony outgrowths attached to normal bone) + epidermoid cysts

Gardner Syndrome

Multiple enchondromas - syndrome?

Olliers syndrome

multiple enchondromas + haemangiomas

Maffuci’s syndrome

Codman’s triangle + sunburst appearance on Xray + elevated ALP

Osteosarcoma

Most common bone tumours in children

osteosarcoma

Ewing’s sarcoma

sheets of small round cells in histology. CD99 +ve. t(11;22) translocation. Bone

Ewing’s sarcoma

malignant chondrocytes on histology. Xray showing lytic lesion with fluffy calcification. affects the axial skeleton mainly.

chondrosarcoma

negatively birefringent crystals

gout

what crystals are usually found in the affected gouty joint?

needle shaped urate crystals

swan neck and boutonniere deformities. symmetrical arthropathy, with radial deviation of wrist and ulnar deviation of fingers.

rheumatoid arthritis

what inflammatory cytokines are implicated in joint destruction in rheumatoid arthritis?

TNFa

IL6 and IL1 -> induce MMPs and lead to joint destruction

histology shows proliferative synovitis w thickening of synovial membranes, hyperplasia of surface synoviocytes, intense inflammatory cell infiltrate, fibrin deposition and necrosis.

rheumatoid arthritis

what leads to joint destruction in rheumatoid arthritis

chronic inflammation due to inflammatory cytokines -> panes formation (inflamed synovium) -> cartilage and bone destruction

Heberdens nodes and Bouchards nodes

Osteoarthritis

Heberdens (DIPJ)
Bouchards (PIPJ)

what type of fracture shows splintered bone on xray but intact soft tissue?

comminuted

what process is this?

organization of haematoma (pro-callus) -> formation of fibrocartilaginous callus -> mineralisation of fibrocartilagnious callus -> remodelling of bone along weight bearing lines

fracture repair

most common causative pathogen of osteomyelitis in adults?

staph aureus

what causative pathogen is implicated in osteomyelitis in patients with sickle cell disease?

salmonella

what causative pathogen is implicated in osteomyelitis in IVDU patients? (apart from staph aureus)

pseudomonas

whats the most common pathogens causing osteomyelitis in children?

haemophilus influenza

group B strep

Xray changes show mottled rarefaction (decreased density of bone) + lifting of periosteum. Later, showing involucrum (irregular new bone formation) and sequestra.
Acutely unwell patient, with pain, swelling and tenderness of the area.

osteomyelitis

what crystals are usually found in pseudo gout? and what shape?

rhomboid shaped, calcium pyrophosphate crystals

what mx in acute gout?

analgesia

NSAIDS / colchicine

what chronic mx in gout?

allopurinol (xanthine oxidase inhibitor)

decrease alcohol intake and purine intake (sardines/ liver)

what mx in pseudogout?

NSAIDs or intraarticular steroids

Wilsons Disease and HyperPTH predispose to gout or pseudo gout?

pseudogout

DEXA scan shows T score

osteoporosis

why is tetracycline not given to children?

turns immature bone black e.g. teeth

reduced bone mineralization + bone pain/ tenderness + looser’s zones

Osteomalacia

reduced bone mineralization + bowing tibia,, (bowed legs), bone pain, delayed walking, Xray findings of splaying of metaphysis

rickets

Very elevated ALP, normal Ca and phosphate.

Pagets disease

bone pain, micro fractures, mixed lytic and sclerotic lesions affecting the spine, skull and pelvis most frequently

Pagets disease

High Ca + xray shows browns tumours, salt and pepper skull and subperiosteal bone resorption in phalanges.

HyperPTH -> osteitis fibrosa cystica

Brown tumours (cyst-like) + loss of bone mass replaced by fibrous tissues

osteitis fibrosa cystica

what biochemistry is usually seen in primary hyperPTH

PTH is high or inappropriately normal
High Ca, low PO4
High / normal ALP

what cancer commonly produces PTHrP?

paraneoplastic breast cancer/ squamous cell carcinoma

which dementia is pathologically indistinguishable from Parkinson’s disease?

Dementia w lewy bodies

What is the presenting features in Dementia w levy bodies?

psychological disturbances occur early. e.g day to day fluctuations in cognition, visual hallucinations
motor signs of parkinsonism
recurrent falls and syncope

what mx for Alzheimers?

mild-mod: anticholinesterases e.g. Donepezil, Galantamine

mod-severe: memantine

a ventricular brain tumour, causing hydrocephalus

ependymoma

most common pathogens in a neonate with bacterial meningitis?

GBS
E coli
Listeria

most common pathogens in a neonate with viral meningitis?

echovirus
coxsackie virus
mumps virus
HIV

most common pathogen(s) in a young child (1 month to 6 years) with bacterial meningitis?

streptococcus penumoniae

h. influenza (reduced since vaccinations)

most common pathogens in young adults and adolescents with bacterial meningitis

neisseria meningitidis

strep pneumoniae

most common cause of bacterial meningitis in elderly

strep pneumoniae

gram - bacilli e.g. e coli

Turbid CSF, predominantly polymorphs, low glucose, high protein

bacterial meningitis

clear CSF, predominantly lymphocytes, normal glucose, normal protein

viral meningitis

Opalescent (cob web) CSF, predominantly lymphocytes, low glucose, high protein

TB meningitis

most common vascular territory affected in a stroke?

middle cerebral artery

Mx for stroke:

aspirin +/- dipyridamole
thrombolytics if <3h from event
+/- carotid endarterectomy

Long term: treat HTN, lipids and anticoagulation

what medication is indicated in combination with aspirin to prevent stroke in those who have had a TIA/ previous stroke?

dipyridamole

triple assessment in breast cancer?

breast examination, mammogram/USS, FNA & cytology / Biopsy

single most important prognostic factor in breast cancer?

status of axillary lymph nodes

this breast lesion is mostly benign, but can be aggressive therefore excised with wide local excision/ mastectomy. usually relatively big/ palpable mass.

Phyllodes tumour

presents as painless breast mass. has the feel of a firm malignant lump so quite worrying for the patient. completely benign, may be caused by trauma, radiotherapy, surgery

fat necrosis

painful red breast, fever, during lactation/ breastfeeding

acute mastitis

what organism usually causes acute mastitis?

staph aureus via cracks in nipple

mx of acute mastitis?

continued expression of milk
antibiotics flucloxacillin
surgical drainage if abscess formed

recurrent subareolar abscesses. histology showing keratinising squamous epithelium. common in smokers and not assoc w lactation.

periductal mastitis

poorly defined palpable periareolar mass w thicc white/ green nipple secretions. can cause breast pain. cytology of discharge shows proteinaceous material and inflammatory cells.

Duct ectasia

granulomatous inflammation and dilation of large breast ducts. with proteinaceous material and inflammatory cells on cytology

duct ectasia

breast lumpiness that fluctuates with menstrual cycle. can lead to calcification that gets picked up on mammography

fibrocystic disease/ fibroadenosis

breast mouse. most common benign tumour. rubbery, freely mobile mass. changes in response to hormones thus increase in size during pregnancy and calcify after menopause

fibroadenoma

breast: central scarring surrounded by proliferating glandular tissue in stellate pattern

radial scar

bloody discharge. no lump. not seen on mammogram. benign tumour

duct papilloma

hard fixed lump, pagers disease, nipple retraction, peau dorange

breast carcinoma

what is the earliest morphological precursor to low grade ductal carcinoma in situ?

flat epithelial atypia (4x risk of developing BrCa)

histological grading of breast ca involves which 3 things?

assessment of nuclear pleomorphism, mitotic activity and tubule formation

what is the risk of developing breast cancer from this histological finding? in situ lobular neoplasia

7 x risk

what is the risk of developing breast cancer from this histological finding? flat epithelial atypia

4 x risk

what is the risk of developing breast cancer from this histological finding? usual epithelial hyperplasia

1.5-2x risk

area of microcalcifications on mammogram. may have lump/ pagets disease of the nipple.

ductal carcinoma in situ

what is the most common breast carcinoma?

invasive ductal BrCa

incidental finding on biopsy where cells lack adhesion protein E cadherin. No microcalcifications. RF for subsequent breast carcinoma

lobular carcinoma in situ

which receptor does trastuzumab act on?

HER2 Receptor

what receptors have to be positive for tamoxifen to work? (breast cancer)

Oestrogen receptor, progesterone receptor

ER/PR +ve Breast ca Mx?

Tamoxifen

HER2+ve Breast ca mx?

herceptin/ trastuzumab

which type of breast cancer is typically ER/PR/HER2 -ve, has a v poor prognosis. shows sheets of atypical cells with lymhocytic infiltrate and stains positive for CK5/6/14. + many mets?

basal like carcinoma

HPV proteins E6 and E7 bind and inactivate which two tumour suppressor genes, leading to cervical cancer?

retinoblastoma (E7) and p53 (E6)

dysplasia at transformation zone result of infection by which HPV subtypes?

HPV 16, 18, 33

Risk factors of CIN/ Cervical Ca?

early age at first intercourse
multiple partners
multiparity
smoking
HIV or immunosuppression
COCP

Meigs syndrome

pleural effusion + ascites + benign ovarian fibroma

which ovarian tumour produces oestrogen?

causing breast enlargement, irregular menstrual cycle, endometrial/br ca

granulosa-theca cell tumour

which ovarian tumour produces androgens?

causing symptoms like virilisation (hirsutism, deepened voice, enlarged clitoris) and defeminisation (breast atrophy)

sertoli-Leydig cell tymour

HCG plasma protein. Which tumour?

choriocarcinoma

mature tissues seen in tumour (skin, hair, teeth, bone, cartilage). benign

dermoid cyst. mature teratoma

AFP assoc w which ovarian tumour?

germ cell tumours. (immature teratomas)

which is the most common type of malignant ovarian tumour?

serous cystadenocarcinoma

associated with pseudomyxoma peritonei

mucinous cystadenocarcinoma

2nd most common type of malignant ovarian tumour?

mucinous cystadenocarcinoma

malignant ovarian tumour derived from surface epithelium, psammoma bodies common.

serous cystadenocarcinoma

endometriosis is a risk factor for what type of ovarian cancer?

endometrioid ovarian ca

and clear cell carcinoma

ovarian cancer: abundant clear cytoplasm, hobnail appearance, rare but malignant w poor prognosis, assoc w endometriosis

clear cell ovarian ca

VIN assoc w which HPV subtype

Risk factors of Endometrial carcinoma

increased exposure to oestrogen: early menarche, late menopause, tamoxifen, nulliparity, PCOS, obesity
DM, HTN

fibroid - what is it?

leiomyoma
benign tumour of smooth muscle origin
causes heavy bleeding, painful periods, pressure effects (urinary frequency, tenesmus), subfertility

adenomyosis - what is it?

presence of ectopic endometrial tissue deep within the myometrium
causes heavy bleeding, painful periods, deep dyspareunia

most common causes of Pelvic Inflammatory Disease

chlamydia trachomatis
neisseria gonorrhoea

TB and shistosomiasis are common causes in some parts of the world

deep dyspareunia, fever, adnexal tenderness and cervical excitation. + RUQ pain and peri-hepatic adhesions

Fitz Hugh Curtis syndrome

RUQ from peri hepatitis and peri hepatitis adhesions

PID complications:

Fitz hugh curtis
adhesions leading to infertility/ risk of ectopic pregnancy
tubo ovarian abscess
chronic pelvic pain
plical fusion

how does endometriosis occur?

implantation from retrograde menstrual flow of endometrial cells

metaplastic transformation of coelomic epitherlial cells

vascular or lymphatic dissemination of endometrial cells

fixed retorverted uterus, with chocolate cysts and brown “powder burn” nodules on laparoscopy

endometriosis

Polycystic Kidney Disease pattern of inheritance?

Autosomal dominant

what gene is involved in polycystic kidney disease?

85%- PKD1 gene on chr 16

15%- PKD2 gene on chr 4

common causes of chronic renal failure:

diabetes
glomerulonephritis
hypertension and vascular disease
reflux nephropathy 
polycystic kidney disease

large multicystic kidneys with destroyed renal parenchyma, liver cysts, and berry aneurysms

Polycystic Kidney Disease

what gene is involved in Polycystic kidney disease, where liver cysts are also seen?

PKD1 gene

on chromosome 16
encoding polycystin-1

Polycystic Kidney Disease presentation

haematuria, flank pain, UTI.

usually due to cyst complications such as cyst rupture, cyst infection and cyst haemorrhage

what is the categorization of lupus nephritis?

Class I- minimal mesangial lupus nephritis
Class II- mesangial proliferative lupus nephritis
Class III - focal lupus nephritis
Class IV- diffuse lupus nephritis
Class V- membranous lupus nephritis
Class VI- advanced sclerosing

lupus nephritis histology showing immune complexes but no structural alteration. Which class?

Class I- minimal mesangial lupus nephritis

lupus nephritis histology showing immune complexes and mild/ mod increase in mesangial matrix and cellularity. which class?

Class II- mesangial proliferative lupus nephritis

lupus nephritis histology showing active swelling and proliferation in < 50% of glomeruli

Class III - focal lupus nephritis

lupus nephritis histology showing involvement of >50% of glomeruli

Class IV- diffuse lupus nephritis

lupus nephritis histology showing subepithelial immune complex deposition

Class V- membranous lupus nephritis

lupus nephritis histology showing complete sclerosis of >90% of glomeruli

Class VI- advanced sclerosing

most common type of renal carcinoma

clear cell carcinoma

Golden yellow tumours with haemorrhagic areas. Histology shows nests of epithelial cells with clear cytoplasm set in a delicate cappilary vascular network.
Most common type of renal carcinoma. Well differentiated.

clear cell carcinoma

friable brown tumours, most common in dialysis- associated cystic disease. Histology shows epithelial tumours with papillary/ tubopapillary growth pattern. Whch type of renal carcinoma?

Papillary carcinoma

Solid brown tumours in the kidney. Histology shows sheets of large cells with distinct cell borders and thick walled vasculature. “pale, eosinophilic cells”

chromophobe (aka pale) renal carcinoma

risk factors of renal carcinoma

smoking
obesity
HTN
unopposed oestrogen
heavy metals
CKD

clinical features of Renal carcinoma

palpable mass
haematuria
costovertebral pain

most common malignant childhood renal tumour, presents commonly with painless abdo mass. Histology shows undifferentiated ‘small blue round cells’

nephroblastoma wilms tumour

acute renal failure chemical features

metabolic acidosis
hyperK
hyperPO4
fluid overload
HTN
low Ca
Uraemia

pre renal causes of acute renal failure

caused by renal hypoperfusion

e.g.
hypovolaemia
sepsis
burns
renal artery stenosis

renal causes of acute renal failure

acute tubular necrosis (commonest)
acute glomerulonephritis
thrombotic microangiopathy

post renal causes of acute renal failure

obstruction to urine flow

stones, tumours, prostatic hypertrophy, retroperitoneal fibrosis

Thrombotic Thrombocytopenia Purpura (TTP) features?

pentad of features

fever
low platelets
MAHA
Neuro impairment
Kidney impairment

haemolytic uraemic syndrome features?

Triad

Haemolytic anaemia
Uraemia
low Pl

HUS vs TTP: differences in where thrombi occur

HUS: thrombi generally confined to kidneys
TTP: thrombi throughout circulation esp in CNS

assoc with diarrhoea caused by E coli O157 with outbreaks caused by children visiting petting zoos. toxin produced targets renal epithelium causing?

Haemolytic Uraemic Syndrome

signs of haemolysis

increased Bilirubin, reticulocytes, LDH
decreased Hb
fragmented RBCs on blood film

most common cause of acute pyelonephritis

e coli

fever chills, flank pain, leucocytosis, +/- frequency, dysuria, haematuria + White cell casts in urine

acute pyelonephritis

causes of chronic pyelonephritis

urine reflux- reflux nephropathy

chronic obstruction- renal calculi, posterior urethral valves

Elderly man on long-term NSAIDS/ paracetamol. Symptoms of HTN, anaemia, proteinuria and haematuria

chronic interstitial nephropathy

analgesic nephropathy

hypersensitivty reaction. days after taking drug (ABx, nsaids, diuretics) causing fever, skin rash, haematuria, proteinuria and eosinophilia.

acute interstitial nephritis

muddy brown granular casts + histology showing necrosis of short segments of tubules, oedema fluid between tubules

acute tubular necrosis
aka

acute tubular injury

most common cause of acute renal failure

acute tubular necrosis

causes of acute tubular necrosis

nephrotoxin- drugs, (NSAIDs, gentamicin), radiographic contrast agents, myoglobin, heavy metals
ischaemia- burns, septicaemia

1-3 wks after strep throat infection or impetigo

haematuria, proteinuria and oededma. raised ASOT titre

post streptococcal glomerulonephritis

most common pathogenic trigger for post strep glomerulonephritis

strep pyogenes.

a group A alpha haemolytic strep

post strep glomerulonephritis- what do you see on ix?

raised anti-streptolysin O titre

decreased C3

1-2 days after upper respiratory tract infection, frank haematuria, or asymptomatic microscopic haematuria

IgA nephropathy
(berger disease)

causes by IgA immune complexes in the glomeruli

granular deposition of IgA and complement in mesangium on kidney histology + frank haematuria

IgA nephropathy

most aggressive glomerulonephritis- can cause end stage renal failure in days to weeks

rapidly progressive (crescentic) glomerulonephritis

Goodpastures syndrome with pulmonary haemorrhage and haematuria. with sudden oliguria and renal failure.

Type 1 crescentic glomerulonephritis (aka rapidly progressive GN)

SLE, sudden oliguria and renal failure. light microscopy shows crescents in kidneys.

Type 2 crescentic GN

saddle nose, pulmonary haemorrhage and haematuria with sudden onset oliguria and renal failure requiring dialysis

Type 3 crescentic GN (rapidly progressive)

Pattern of deposition of IgG in glomerular BM seen in Goodpastures

Linear

Pattern of deposition of IgG immune complexes on glomerular BM/ mesangium in SLE/ Ig A nephropathy, post infectious GN

granular

nephritic syndrome + sensorineural deafness + eye disorders (lens dislocation, cataracts) in a young adolescent (5-20 yrs old)

Alports syndrome

Alports syndrome - mutation in what?

type IV collagen alpha 5 chain

What is the inheritance of alports syndrome?

x linked

asymptomatic microscopic haematuria. automosal dominant pattern - runs in the family. renal function normal

benign familial haematuria

thin basement membrane disease

in thin basement membrane disease, aka benign familial haematuria, what is the mutation in?

type IV collagen alpha 4 chain

what is the filtration barrier made of? in the kidney

fenestrated endothelium
basement membrane (Type IV collagen)
podocytes (w foot processes)

what is the innermost layer (1st layer) of the filtration barrier?

fenestrated endothelium

what is the outermost layer (last layer) of the filtration barrier?

podocytes (w foot processes)

what is nephrotic syndrome characterised by?

proteinuria (>3g/24h) + hypoalbuminaemia + oedema

+hyperlipidaemia + hypercoagulable state (lostt of ATIII) + increased risk of infection (loss of Ig)

swelling of ankles and eyelids + frothy urine

nephrotic syndrome

most common cause of nephrotic syndrome in children?

minimal change disease

most common cause of nephrotic syndrome in adults?

focal segmental glomerulosclerosis

then membranous

light microscopy showing focal and segmental consolidation and scarring, hyalinosis.

focal segmental glomerulosclerosis

light microscopy showing diffuse glomerular basememnt membrane thickening

membranous glomerular disease

diffuse glomerular BM thickening + Kimmelsteil Wilson nodules

diabetes

what drug is associated with haemorrhagic cystitis?

cyclophosphamide

Commonest cause of cystitis

E coli

tx of acute cystitis?

trimethoprim / nitrofurantoin

what is the most common bladder tumour?

transitional cell tumour

risk factors of transitional cell tumours

smoking, industrial exposure to aromatic amines

painless haematuria, frequency, urgency + smoker of 50 pack year

transitional cell carcinoma

diagnosis of transitional cell carcinoma

cystoscopy and biopsy

bladder tumour associated w shistosomiasis

squamous cell carcinoma

difficulty urinating (terminal dribbling, hesitancy), retention, frequency, nocturia, frequent UTIs. hyperplasia mediated by dihydrotestosterone.

benign prostatic hyperplasia

tx of benign prostatic hyperplasia

TURP

5a reductase inhibitors

what is the most common form of prostate cancer?

adenocarcinoma

risk factors of prostate cancer

** family history
age
hormonal and environmental influences. e.g. diet- red meat

most common malignant tumour in men?

prostate cancer

precursor lesion of prostate cancer?

prostatic interstitial neoplasia

Diagnosis and Grading of prostate cancer?

diagnosis by history, examination, PSA >4ng/ml

Grading by Gleason score

severe colicky pain in flank to groin, haematuria

urinary calculi

complications of renal stones

obstruction - post renal acute renal failure

recurrent UTIs

most common testicular tumour

seminoma (resembles germ cells)

biggest risk factor of germ cell cancer (testicular cancer)

cryptorchidism

undescended testes

in gout/ rapid cell turnover, what types of renal stones are formed

uric acid

mx of large renal stones

removed by endoscopic/ percutaneous methods

shock wave lithotripsy

hyper calcaemia - what types of renal stones are formed

calcium oxalate

large staghorn calculi – usually what types of stone would contribute to this

magnesium ammonium phosphate (triple stones)

what pattern of inheritance in haemochromatosis?

autosomal recessive

what pattern of inheritance in wilson’s disease?

autosomal recessive

what pattern of inheritance in alpha 1 antitrypsin deficiency?

autosomal dominant

ix shows increased Iron, increased ferritin, high transferrin saturation and reduced Total iron binding capacity. + bronzing of skin, hepatomegaly with micronodular cirrhosis, hypogonadis, psuedogout

haemochromatosis

mutated HFE gene

haemochromatosis

mutated ATP7B gene

wilsons disease

Rhodanine stain

for copper in wilsons disease

stains golden brown

Cirrhosis, parkinsonism, psychosis, kayser fleischer rings. microscopy shows mallory bodies and fibrosis. rhodanine stain +ve.

wilsons disease

in wilsons disease, ix?

low serum copper
high urinary copper
low serum caeruloplasmin (cu binding protein)

alpha 1 antitrypsin - where is it normal synthesized?

hepatocytes

alpha 1 antitrypsin deficiency presentation?

AT1A accumulates in hepatocytes where it is synthesized -> hepatitis and cirrhosis
emphysema due to lack of AT1A in the lungs

liver stained with periodic acid schiff shows intracytoplasmic inclusions

alpha 1 antitrypsin deficiency

intracytoplasmic inclusions are the accumulated A1AT unable to be secreted by the hepatocytes

Alpha 1 antitrypsin deficiency Ix?

low serum A1AT

absent alpha-gobulin band on electrophoresis

Tx of wilsons disease

lifelong penicillamine (cu chelating agent)

tx of haemochromatosis

venesection

desferrioxamine

inflammation and obliterative fibrosis of extrahepatic and intrahepatic bile ducts

primary sclerosing cholangitis

ERCP showing beading of the bile duct - multi focal stricture formation with dilation of preserved segments

primary sclerosing cholangitis

Primary scleroising cholangitis associated with?

ulcerative colitis

Primary scleroising cholangitis increases risk of which cancer?

cholangiocarcinoma

PSC assoc with which auto antibodies?

pANCA
anticardiolipin in 66%
antinuclear antibodies in 53%

autoimmune inflammatory destruction of medium sized intrahepatic bile ducts. histology: bile duct loss with granulomas

primary biliary cirrhosis

antibodies associated with primary biliary cirrhosis

anti mitochondrial antibodies

Primary biliary cirrhosis presentation

fatigue, pruritus, abdo discomfort.
xanthelasma, steatorrhoea, vit D malabsorption, inflammatory arthropathy

can tx w ursodeoxycholic acid

Primary biliary cirrhosis Ix?

high Alkphos
high cholesterol
high IgM
late high Br

autoimmune hepatitis antibodies?

Type 1:
anti nuclear antibodies
anti smooth muscle,
anti actin
anti soluble liver antigen

Type 2:
antil-LKM (liver kidney microsomal)

acute hepatitis histological features?

spotty necrosis

hepatic steatosis in non alcoholic, obese individual with hyperlipidaemia/ metabolic syndrome

non alcoholic fatty liver disease

non alcoholic steatohepatitis

steatosis: fatty infiltration
hepatitis

can progress to cirrhosis

fat droplets in hepatocytes, but still fully reversible if alcohol avoided

large, pale, yellow and greasy liver

fatty liver

hepatocyte ballooning and necrosis
mallory-denk bodies
fibrosis

alcoholic hepatitis

fatty liver turns into shrunken non fatty, brown liver. micronodular cirrhosis

alcholic cirrhosis.

what causes portal hypertension?

prehepatic: portal vein thrombosis
hepatic: cirrhosis
posthepatic: budd-chiari syndrome

where do collateral vessels form in portal hypertension?

oesophageal varices
rectum
anterior abdominal wall -> caput medusae
retroperitoneum
diaphragm

portal hypertension tria of?

ascites
splenomegaly
varices e.g oesophageal

what staging system is used to indicated prognosis in liver cirrhosis

modified childs pugh score

scores based on ascites, encephalopathy, bilirubin, albumin, prothrombin time

hepatocyte necrosis, fibrosis (showing collagen in liver), nodules of regenerating hepatocytes, disruption of liver architecutre

cirrhosis

causes of macronodular regeneration of hepatocytes

viral hepatitis, Willsons disease, alpha 1 antitrypsin deficiency

causes of micronodular regeneration of hepatocytes

alcoholic hepatitis, biliary tract disease

what cell is responsible for the fibrosis seen in liver cirrhosis?

stellate cells

chronic inflammation causes activation of stellate cells in the space of disse. They become myofibroblasts -> initiating fibrosis by deposition of collagen

complications of cirrhosis

portal hypertension
hepatic encephalopathy
hepatocellular carcinoma

benign liver tumour associated with OCP, presents with abdo pain/ intraperitoneal bleeding

hepatic adenoma

which zone in the liver receives more blood rich in nutrients and oxygen

zone 1. near the portal tract

which vitamins are stored in the liver

vitamins A, D, B12 and K

MEN2A

2Ps, 1 M

Parathyroid, Medullary thyroid, Phaeochromocytoma

MEN2B

1P 2M
Phaeochromocytoma + medullary thyroid + mucosal neuroma

+ marfanoid habitus

neuroendocrine tumour assoc w hypoglycaemic attacks

insulinoma

neuroendocrine tumour assoc with recurrent peptic ulceration

zollinger- ellison

neuroendocrine tumour assoc w diarrhoea

VIPoma

Vasoactive intestinal peptide

CA19.9

Pancreatic Carcinoma

Pancreatic Carcinoma tumour marker

CA 19.9

what are the endocrine functions of the pancreas?

alpha cells - glucagon
beta cells - insulin
delta cells - somatostatin

what are the exocrine secretions of the pancreas?

lipases, proteases, amylases

fasting hyperglycaemia, HTN, central obesity, dyslipidaemia, microalbuminaemia

metabolic syndrome

what is the most sensitive serum marker of acute pancreatitis?

serum lipase

Colorectal cancer tumour marker

CEA carcinoembryonic antigen

Carcinoembryonic antigen (CEA)

colorectal cancer

What staging is used in colorectal cancer

Duke’s staging

multiple polyps in colon, mucocutaneous hyperpigmentation, freckles around mouth, palm and soles.

peutz jeghers syndrome

aut dominant

sterile fibrin and platelet vegetations present on cardiac valves, more commonly affected L sided H valves (mitral> aortic). absence of inflammation or bacteria. Assoc w numerous diseases, esp advanced stage malignancy. recurrent emboli

non bacterial thrombotic endocarditis.

non bacterial thrombotic endocarditis?

sterile fibrin and platelet vegetations present on cardiac valves (usually mitral)

absence of inflammation or bacteria.

Assoc w numerous diseases, esp advanced stage malignancy. & recurrent emboli

fever, new onset murmur, changing murmur, blood cultures +, Roth spots, laneway lesions, Osler’s nodes

Infective endocarditis

Libman-sacks endocarditis assoc w?

SLE

cystic medial necrosis: affects the aorta, causing focal degeneration of the elastic tissue and muscle fibres in the media, w accumulation of basophilic ground substance

assoc w?

aortic dissection

aortic dissection assoc w which syndrome?

Marfans

After an MI, histology is normal. (CK-MB also normal)

how long ago was the MI?

under 6 hours

After an MI, histology shows loss of nuclei in the myocardial cells, homogenous cytoplasm, necrotic cell death. how many hours after the MI is it?

6 - 24 hours

After an MI, histology shows infiltration of polymorphs then macrophages (to clear up the debris). Debris is present and the cytoplasm is homogeneous so that it is difficult to see the outlines of the myocardial fibres. How long after the MI is it?

1-4 days

After an MI, histology shows removal of debris. how long after the MI is it?

5-10 days

after an MI, histology shows myofibroblasts, angioblasts, macrophages. The area undergoes repair and a classic young scar with new capillaries is seen with early collagenization. how long after the MI is it?

1-2 weeks

after an MI, histology shows strengthening of the area with formation of a decellularizing scar tissue. how long after the MI is it?

weeks to months

polymyositis vs dermatomyositis?

both have the same muscle components involved

dermatomyositis has the accompanied skin features - periorbital oedema and heliotrope rash + gottrons papules

also polymyositis tends to have a positive electromyogram result compared to dermatomyositis

mutation in gene coding for alpha synuclein and mostly free of Lewy bodies on histology. + parkinsonism

what condition?

familial Parkinsons Disease

in Multiple sclerosis, histology shows oedema and macrophages, indicated of an inflammatory diorder of the CNS< with some myelin breakdown. Reactive astrocytosis present. What kind of plaque is this?

early chronic active plaque

in Multiple sclerosis, histology shows complete loss of myelin. Some macrophages with contain myelin debris and there will be often very mild perivascular inflammation at this stage with enlarged perivascular spaces. what kind of plaque is this?

late chronic active plaque

in multiple sclerosis, histology shows complete loss of myelin w the absence of macrophages. what kind of plaque is this?

chronic inactive plaque

In multiple sclerosis, histology shows nearly complete remyelination as a thin myelin with some scattered macrophages and a mild microglial up regulation. what kind of plaque is this?

shadow plaque

in multiple sclerosis, histology shows minor changes e.g. oedema and often difficult to recognize. what kind of plaque is this?

active plaque

in Alzheimers disease, where is brain atrophy most prominent? (which parts of the brain)

hippocampus (earliest change)

and frontal lobe

what parts of the brain shows cerebral atrophy in Huntington’s disease?

caudate nucleus and putamen

Papp- Lantos bodies (glial cytoplasmic inclusion bodies) in brain

Multiple system atrophy

in H pylori associated gastritis, which part of the stomach is most severely affected?

pyloric antrum

Gastritis most severe in the pyloric antrum. what is the most likely cause?

H pylori associated gastritis

autoimmune chronic gastritis associated w pernicious anaemia in the elderly typically affects which part of the stomach?

stomach body

histology of pancreas showing inflammation with parenchymal fibrosis, loss of pancreatic parenchymal elements and duct strictures with formation of intra pancreatic calculi. (Xray shows the calculi well!)

chronic pancreatitis

what HLA type is associated with T1DM

HLA DR3/ DR4

excessive fluid intake w no orgnanic pathology

psychogenic polydipsia

gastric hypersecretion, multiple peptic ulcers and diarrhoea caused by gastric secreting tumour of the pancreatic G cells

zollinger-Ellison syndrome

which Hepatitis virus is the only DNA virus?

Hep B

continous inflammation extending proximally from rectum. bloody diarrhoea + mucus.

ulcerative colitis

skip lesions, can affect whole GI tract from mouth to anus, most commonly in terminal ileum and caecum. Transmural inflammation and non caseating granulomas, thickened walls of the bowel. Rubber hose wall and cobblestone mucosa

crohns disease

autosomal dominant mutations in DNA mismatch repair genes. Carcinomas in the colon, with polyps quickly progressing to malignancy. assoc w endometrial, ovarian, small bowel, transitional cell and stomach carcinoma as well.

Hereditary non-polyposis colorectal cancer (HNPCC)

autosomal dominant condition caused by mutation in FAP gene. presence of 100s - 1000s of adenomatous polyps

familial adenomatous polyposis

bronchoconstriction, flushing, diarrhoea

carcinoid syndrome

carcinoid syndrome ix?

24 hr urine 5-HIAA (main metabolite of serotonin)

life threatening vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia. tumours of enterochromaffin cell origin.

carcinoid crisis

too much serotonin

mx: octreotide (somatostain analogue)

smoking worsens symptoms in which condition? crohns or ulcerative colitis

crohns

backwash ileitis occurs in ?

ulcerative colitis

ischaemic colitis - what areas tend to be affected

watershed areas like splenic flexure and rectosigmoid

what GI abnormalities are more common in downs?

Tracheooesophageal fistula, Duodenal stenosis/ atresia, imperforate anus, hirschsprungs disease

epigastric pain, worse at night, relieved by food and milk. RF: h pylori, drugs e.g. NSAIDS and aspirin, smoking

Duodenal Ulcer

complications of Duodenal ulcer:

anaemia (IDA)

perforation

What HLA is associated with coeliac?

HLA DQ2 amd DQ8

the most sensitive and specific antibody for coeliac?

anti tissue transglutaminase (IgA)

epigastric pain +/- weight loss, worsened with food, relieved by antacids

Gastric Ulcer

Risk factors: H pylori, smoking, NSAIDs

chronic h pylori infection -> chronic antigenic stimulation -> increases risk of?

ulcer -> Gastric MALToma

complications: bleeding - anaemia, shock. perforation- peritonitis

metaplasia of squamous mucosa in oesophagus to columnar epithelium

Barretts oesophagus

barretts oesophagus assoc with increased risk of which cancer?

oesophageal adenocarcinoma

oesophageal cancer associated with ETOH and smoking, most commonly found in middle 1/3 of oesophagus. Presenting w progressive dysphagia, odynophagia, anorexia and severe weight loss.

Squamous cell oesophageal carcinoma

engorged dilated veins in oesophagus, usually due to portal HTN

oesophageal varices

dilatation of the airways and excess mucus production + chronic cough and sputum . histology showing goblet cell hyperplasia and hypertrophy of mucous glands

chronic bronchtiis

permanent airway dilatation (of bronchi) and scarring. Associated with cystic fibrosis, kartagener’s. chronic cough, purulent sputum.

bronchiectasis

histology showing loss of alveolar parenchyma. airspace enlargement and wall destruction. associated with alpha 1 antitrypsin deficiency, connective tissue disease e.g. Marfans

emphysema

episodic cough, wheezing and dyspnoea. histology shows curschman spirals, eosinophils, carcot-leyden crystals, smooth muscle cell hyperplasia and excess mucus.

asthma

Curshman spirals + Charcot-Leyden crystals on histology

Asthma

emphysema complications

bullae may rupture -> pneumothorax

pulmonary hypertension and cor pulmonale

honey comb lung, end inspiratory crackles, features of restrictive lung disease on spirtometry. progressive patchy interstitial fibrosis.

pulmonary fibrosis

non-neoplastic lung reaction to inhalation of mineral dusts or inorganic particles. usually affects the upper lobe.

pneumoconiosis

Histology showing cogestion -> red hepatization (neutrophilia) -> grey hepatization (fibrosis) -> resolution.
what condition?

lobar pneumonia

Mx of Adenocarcinoma of lung

Anti EGFR drugs (erlotinib)

tyrosine kinase inhibitor

which type of lung cancer is commonly associated with ectopic ACTH secretion (Cushings) and lambert-eaton?

small cell carcinoma

acute onset SOB, pleuritic chest pain, wedge shaped infarct in lung

pulmonary embolus

histology showing intra alveolar fluid + iron laden macrophages. SOB. caused by left heart failure

pulmonary oedema

widespread saddle shape ST elevation on ECG

pericarditis

complications of MI

VF/ VT
ventricular wall rupture (-> haemopericardium)
septal rupture (L to R shunt, VSD)
papillary muscle rupture (mitral regurg - pansystolic murmur)

what is the most common cause of sudden death with MI?

90% of patients develop an arrhythmia following MI

progressive loss of myocytes

dilated cardiomyopathy

SOB, orthopnoea, Paroxymal nocturnal dyspnoea, wheeze, fatigue. Pulmonary oedema.
+ decreased cardiac output

left heart failure

peripheral oedema, ascites, facial engorgement. hepatomegaly.

Right heart failure

myocardial hypertrophy without ventricular dilation. Autosomal dominance. heart is thick walled, heavy, hyper contracting.

hypertrophic obstructive cardiomyopathy

may cause sudden cardiac death in young ppl.

carditis (endocarditis, myocarditis, pericarditis)
arthritis
syndenhams chorea
Erythema marginatum
Subcutaneous nodules

Jones major criteria for Rheumatic Fever

Rheumatic fever

2-4 wks after strep throat infection

carditis, arthritis, sydenhams chorea, erythema marginatum, subcutaneous nodules

fever, raised CRP/ESR

what valve is most commonly affected in rheumatic fever?

mitral

some aortic

Anitschkov myocytes (enlarged macrophages found within granulomas) + Aschoff bodies (granulmoas)
pathognomonic of ?

Rheumatic fever

Tx of rheumatic fever?

Benzylpenicillin

what is the pathogenesis of rheumatic fever?

molecular mimicry

antibodies to streptococcal antigen cross react with myocardial antigens

small warty vegetations found along the lines of closure of valve leaflet - ‘verrucae’

rheumatic heart disease

small, warty vegetations that are sterile and platelet rich. assoc w SLE and anti phospholipid syndrome

libman sacks endocarditis

most common cause of infective endocarditis overall, in those w prosthetic valves, and in IVDU

staph aureus

most common cause of subacute infective endocarditis

strep viridans

usually on damaged heart valves

what are the immune phenomena of infective endocarditis?

roth spots
oslers nodes
heamaturia due to glomerulonephritis

what are the thromboembolic phenomena of infective endocarditis?

janeway lesions
septic abscesses in brain/ lungs/ spleen/ kidney
microemboli
splinter haemorrhages
splenomegaly

what valves are usually involved in infective endocarditis? and in IVDU users?

usually left sided, mitrac and aortic valves

IVDU: right sided valves

collection of histiocytes and macrophages with or without multinucleate giant cells

granuloma

centrally located lung tumours

small cell lung carcinoma

squamous cell lung cancer

what part of the lungs does asbestosis tend to affect

lower lobes

histopathology of spongiosis of epidermis and perivascular chronic inflammatory infiltrate in the dermis

eczema

fracture penetrates skin surface and is also known as an open fracture

compound fracture

bone breaks and the two ends are pushed towards each other

impacted fracture

subchondral sclerosis, subchondral cysts, loss of joint space and osteophytes. (LOSS)

osteoarthritis

bamboo spine

ankylosing spondylitis

circinate balanitis, keratoderma blenorrhagicum

reiters

reactive arthritis

arthritis + erythema chronicum migrans (BIG target)

lyme disease

caused by borrelia burgdorferi

osteomyelitis in big toe is usually secondary to?

diabetic skin ulcer

Histology core biopsy codeof breast tissue. B5=?

Malignant
5a = ductal carcinoma in situ
5b= invasive carcinoma

cysts in patients on dialysis

acquired cystic disease

what does stag horn calculi in the kidney predispose to?

hydronephrosis -> renal scarring and atrophy

what organisms are likely to cause triple stones consisting of magnesium, ammonium and phosphate?

urease-producing organisms e.g. proteus.

basophils are a poor prognostic factor in which haematological malignancy?

chronic myeloid leukaemia

in which part of the nephron do most urinary calculi form?

collecting duct

angina at rest suggesting what % stenosis?

90%

ECG showing ST depression changes in the anterior leads?

there is likely to be obstruction of the left anterior descending artery (left circumflex artery obstruction will involve lateral leads). ST depression is suggestive of subendocardial necrosis due to ischaemia of the inner 1/3 of the heart muscle. (transmural infarction involving all layers will cause ST elevation).

what is the most significant independent risk factor of coronary heart disease?

family history

which subtype of invasive breast cancer forms tubules with low-grade nuclei?

tubular

basal like carcinoma- what cytokeratins?

CK5/6 and CK14

which subtype of malignant breast cancer produces abundant quantities of extracellular mucin?

mucinous

acute mastitis. what inflammatory cell is likely to be found in high quantities in the tissue?

neutrophil

what proteasome inhibitor to treat multiple myeloma?

bortezomib.

which zone of the hepatic lobule is more susceptible to injury by toxins?

zone 3.

has more mature haptocytes w more enzymes that will convert toxins into active metabolites

how are drugs most likely to affect renal function?

acute interstitial nephritis.

e.g antibiotics, analgesics, diuretics

goodpasture’s syndrome. what molecular target are the antibodies targeted against?

non-collagenous domain of a3 unit of type IV collagen

in thin membrane disease, what molecular target are antibodies targeted against?

a4-unit of type IV collagen

in Alport’s syndrome, what molecular target are antibodies targeted against?

a5-unit of type IV collagen

what renal cell cancer shows pale eosinophilic cells on biopsy?

chromophobe renal cell carcinoma

also seen in benign oncocytoma

what monoclonal antibody can be used to treat haemolytic uraemia syndrome?

eculizumab: anti-C5 antibody

targets the C5 complement of the complement system

bronchiectasis + liver cirrhosis. what stain can be used to detect the intracytoplasmic inclusions?

periodic acid schiff stain.

alpha 1 antitrypsin deficiency.

what does grade indicate about hepatocellular carcinoma?

and stage?

inflammation.

stage- fibrosis.

histopathology coding for breast sample from B1 to B5?

B1 = normal breast tissue. B2 = benign abnormality. B3= lesion of uncertain malignant potential. B4= suspicious of malignancy. B5= malignant (a = DCIS, b= invasive carcinoma)

single most impt prognostic factor for breast cancer?

axillary lymphadenopathy

stap aureus is gram ?, catalase?, coagulase?

triple +. gram +, catalase and coagulase +

subcorneal (upper layer of epidermis) bullae formation. very thin/ superficial bullae.

pemphigus foliaceus

term for intercellular oedema?

spongiosis

term for loss of keratinocyte cohesion

acantholysis

avg turnover rate of keratinocytes?

and what is the average turnover rate in psoriasis?

56 days.
in psoriasis- 7 days.

epidermis gets thicker due to increased turnover of keratinocytes. with small abscesses within epidermis.

• Present in oral cavity as white lines, purply/silvery lines around the wrist/arm.

lichen planus

in lichen planus, where does the reaction occur causing pathology?

Reaction occurs at the basement membrane (dermoepidermal junction) causing death of the basal keratinocytes.

an inflammatory dermatosis, usually a manifestation from other systemic diseases. Ulcer, painful, rolled edge and looks similar to a skin carcinoma . Histology - filled w inflammatory cells. assoc w IBD, sarcoidosis, malignancy

Pyoderma Gangrenosum

Central area of ulceration with rolled edges and pearly white rim around it.

Basal Cell Carcinoma.

Do not metastasise but locally destructive.

rodent ulcer

BCC

Invagination of overlying epidermis within the dermis. The lesion has a layer of epidermis around and is filled with keratin. Once infected, smells pungent and like cheese.

Epidermoid cyst.

smooth, film, with central punctum. doesn’t transilluminate/ not mobile.

which skin cancer has higher rate of recurrence? BCC/SCC?

SCC.
Likelihood of local recurrence is much higher with perineal (nerve cell) invasion as the cancer cells travel down using the nerve cell.

what is responsible for selectivity of the filtration barrier of the kidney?

podocyte slit diaphragm.

Polycystic Kidney Disease- inheritance pattern?

autosomal dominant.

renal failure from 40-70 yrs due to cysts compressing rest of parenchyma -> no functioning nephrons

PCKD assoc w?

liver cysts and berry aneurysms

why does acute tubular injury cause failure of glomerular filtration?

Blockage of tubules by casts
Leakage of fluid from tubules to interstitium reducing flow
secondary haemodynamic changes (as tubule get injured, glomerulus gets signal to decrease GFR)

causes of crescentic glomerulonephritis (rapidly progressive)

Type 1: anti GBM disease
Type 2: immune complex mediated.
Type 3: pauci immune assoc w ANCA

causes of immune complex associated crescentic glomerulonephritis

SLE, IgA nephropathy, post-infectious GN.

Granular IgG immune complex deposition on GBM.

What sort of IgG deposition on glomerular BM in goodpastures syndrome?

Linear

pathology of pauci-immune crescentic Glomerulonephritis?

Usually associated with anti-neutrophil cytoplasm antibodies (ANCA).
These antibodies cause neutrophil activation leading to glomerular necrosis

Mx of crescentic glomerulonephritis

Correct diagnosis and treatment are urgent – aggressive immunosuppression or plasma exchange.
leads rapidly to irreversible renal failure.

renal impairment in diabetics? mesangial expansion + proteinuria followed by nodular sclerosis in the glomerulus

diabetic glomerulosclerosis

Glomeruli look normal apart from effacement of foot processes on EM.

minimal change disease.

glomeruli develop segmental scars. + nephrotic syndrome

focal segmental glomerulosclerosis

microscopic haematuria. familial. autosomal dominant.

thin basement membrane disease.

type IV collage alpha 4 chain mutation.

commonest glomerulonephritis worldwide

IgA nephropathy

complications of GORD

ulceration, haemorrhage, perforation, stricture, Barrett’s oesophagus

inflammation of oesophagus assoc w allergic reaction to food. spasm of the muscle leads to dysphagia.

eosinophilic oesophagitis

tx: steroids + remove allergen

complications of gastric ulcer

bleeding -> anaemia/ shock, perforation leading to peritonitis

where is cortical bone found?

long bones, 80% of skeleton.

appendicular. mainly mechanical and protective.

where is cancellous bone found?

verterbrae and pelvis. axial. mainly metabolic.

glucocorticoid effect on osteoclasts?

Early, transient increase in osteoclast survival, cancellous osteoclasts, bone resorption

glucocorticoid effect on osteocytes

Increased apoptosis -> decreased canalicular circulation -> decreased bone quality

glucocorticoid effect on osteoblasts

Decreased osteoblastogenesis
Increased apoptosis
Early and continual decrease in cancellous osteoblasts, synthetic ability and bone formation

pathogenesis of gall bladder causing acute pancreatitis?

• Gallstone stuck distal to where the common bile duct and pancreatic ducts join leads to: reflux of bile up the pancreatic duct followed by damage to acini with release of proenzymes which then become activated

pancreatic intraductal neoplasia precursor to?

ductal carcinoma

what mutation is highly assoc w ductal carcinoma?

k-ras

why does pancreatic cancer lead to VTE?

mucin produced by cancer cells causes blood to be thicker

histology of rheumatoid arthritis

Proliferative synovitis with 
o	Thickening of synovial membranes (villous)
o	Hyperplasia of surface synoviocytes
o	Intense inflammatory cell infiltrate
o	Fibrin deposition and necrosis

what is the inflamed synovium at the articular surface called?

pannus

pseudgout causes

sporadic, haemochromatosis, hypoMg, low pO4, osteoarthritis, hereditary, traumatic

Familial adenomatous polyposis inheritance pattern?

auto dominant

what gene involved in familial adenomatous polyposis?

APC tumour suppressor gene

on chr5q21

Multiple (100s) adenomas in GI tract + multiple osteomas of skull/ mandible + dental caries + epidermoid cysts, demoed tumours + post surgical mesenteric fibromatoses

Gardners syndrome

Hereditary Non Polyposis Colorectal Cancer HNPCC assoc w which gynae ca

endometrial, ovarian

HNPCC inheritance pattern?

auto dominant

Dukes Staging

o A = confined to wall of bowel
o B = through wall of bowel
o C = lymph node metastases
o D = distant metastases

what makes a vulnerable plaque?

• Lots foam cells, thin fibrous cap, few smooth muscle cells, clusters inflammatory cells

what does the left anterior descending artery supply?

ant wall LV, ant septum, apex

what does the right coronary artery supply?

post wall LV, post septum, post RV

what does the Left circumflex artery supply?

lat LV not apex

myocardial rupture after MI - what is most commonly affected?

free wall most common, septum less common, papillary muscle least common.

what carcinogens does smoke contain?

Polycyclic aromatic hydrocarbons, N Nitrosamines, Nicotine, Phenols, Nickel, Arsenic

what mutation suggests good response to tyrosine kinase inhibitors e.g. erlotinib?

EGFR mutation

what mutation predicts non response to anti EGFR therapy?

k-rase

Cytology of nipple discharge shows proteinaceous material, inflammatory cells only.

Duct ectasia

A benign sclerosing lesion characterised by a central zone of scarring surrounded by a radiating zone of proliferating glandular tissue.

radial scar.

stellate lesions on screening mammograms

most common type of urinary calculus

calcium oxalate

most common renal carcinoma. Grossly appear as golden yellow tumours with haemorrhagic areas.

clear cell renal cell carcinoma

second most common renal carcinoma. Grossly appear as friable brown tumours.

papillary renal cell carcinoma

renal cell tumour. appears as solid brown tumours. 5% of all renal carcinomas.

chromophobe renal cell carcinoma

bilateral metastases composed of mucin producing signet ring cells. most often of gastric origin or breast

krukenberg tumours

sterile fibrin and platelet vegetations on cardiac valves. assoc w advanced stage malignancy. recurrent emboli

non bacterial thrombotic endocarditis.

NBTE - source of thromboembolism to brain, heart, kidneys.

strep agalactiae is an e.g. of?

GBS

what murmur is most consistent with acute rheumatic fever?

mid diastolic murmur at mitral region (mitral stenosis)

what mutation is assoc w poorer response to cisplatin in tx of non small cell lung cancer?

ERCC1

epidermal hyperplasia, increased thickness of stratum spinosum.

acanthosis

thickening of stratum corneum and increased keratin

hyperkeratosis

retention of nuclei in stratum corneum. mode of keratinization

parakeratosis

cellulitis most common cause?

strep pyogenes

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