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Path > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Basic anatomy of the kidney

A

Thick fibrous outer capsule
Then cortex - contains glomeruli
Internally is the medulla - tubules and collecting ducts that drain urine into pelvis and collects into ureter

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2
Q

Micro anatomy of the kidney

A 
Renal artery divided into branches - interlobar arteries
This branches to arcuate arteries (run between vortex and medulla) 
End arteries (interlobular) run to kidney surface and give rise to afferent arterioles
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3
Q

Fontana stain

A

Positive for melanin

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4
Q

Congo red stain

Apple green birefringence

A

Amyloid

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5
Q

Prussian blue stain

A

Positive for iron

Haemochromatosis

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6
Q

Cd45 positive cells

A

Lymphoid cells

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7
Q

Cytokeratin stain used for

A

Epithelial marker

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8
Q

Complications of MI

A

Contractile dysfunction - cardiogenic shock
CCF - due to ventricular dysfunction
LV infarct - mitral regurgitation
Cardiac rupture of: ventricular wall (haemopericardium), septum (left to right shunt, VSD), papillary muscle (MR)
Ventricular aneurysm - usually 4 weeks after MI (causing persistent ST elevation)

Arrhythmia
VF (in first 24h) common cause of death
90% develop arrhythmia post MI

Pericardial
Early peri infarc associated pericarditis
Pericardial effusion +/- tamponade
Dressers syndrome - chest pain, fevers and effusion weeks-months after MI
Fibrinous pericarditis

Mural thrombus - embolization

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9
Q

Chest pain, fevers and effusion week-months after MI

A

Dressler’s syndrome

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10
Q

Post MI immediate histology

A

Normal

CK-MB also normal

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11
Q

6-24 hours after MI histology

A

Loss of nuclei
Homogenous cytoplasm
Necrotic cell death

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12
Q

Histology 1-4days after MI

A

Infiltration of polymorphs then macrophages (clears up debris)

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13
Q

5-10 days after MI histology

A

Removal of debris

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14
Q

1-2 weeks post MI histology

A

Granulation tissue
New blood vessels
MyoFibroblasts
Collagen synthesis

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15
Q

Weeks-months post MI histology

A

Strengthening

Decellularising scar tissue

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16
Q

Charcot Leyden crystals
Curshman spirals

Which condition
Where
What are they

Pathology

A

Asthma
Bronchus

Degenerating eosinophils
From shedding epithelium

SM hypertrophy
Excess mucus
Inflammation

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17
Q

Dilation of the airways
Mucus gland hyperplasia
Goblet cell hyperplasia
Mild inflammation

What condition

Complications

A

Chronic bronchitis

chronic cough productive of sputum for at least 3 months over at least 2 consecutive yars

Repeated infections
Resp failure, reduced exercise tolerance
Increased lung cancer risk (independent of smoking)

Chronic hypoxia results in PULMONARY HTN AND RHF
= aka cor-pulmonale
- Peripheral oedema
- Hepatosplenomegaly
- Raised JVP
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18
Q

Permanent dilation of the bronchi with scarring

Complications

A

Bronchiectasis

Recurrent infections
Haemoptysis
Pulmonary htn
Amyloidosis (as producing excessive amyloid A protein)

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19
Q

Alpha - antitrypsin deficiency
Dyspnoea cough

Condition and histology

Other cause

A

Emphysema

Loss of alveolar parenchyma distal to the terminal bronchiole - honeycomb appearance

Due to smoking, (Centrilobular) Alpha-1 antitrypsin deficiency (panacinar)
Rarely IVDU, connective tissue

Complicatons:
Bullae - PNEUMOTHORAX
Resp failrue
Pulmonary HTN and RHF

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20
Q

Causes of bronchiectasis

A

Inflammatory

  • post infection
  • immunodeficiency (hypogammoglbulinaeia) or secondary
  • obstruction
  • post inflammatory (aspiration)
  • Secondary to bronchiolar disease and interstitial fibrosis
  • systemic disease
  • Asthma

Congenital

  • CF
  • primary ciliary dyskinesia
  • hypogammaglobulinemia
  • yellow nail syndrome
  • young’s syndrome
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21
Q

Rhinosinusitis
Azoospermia
Bronchiectasis

A

Young’s syndrome

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22
Q

Honeycomb lung

A

Interstitial Lung disease

- all have at end stage

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23
Q

FEV1/FVC <0.7
SOB
End inspiratory crackles
Cyanosis, pulmonary HTN and cor-pulmonale

A

Restrictive lung disease

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24
Q

Broad categories of causes of interstitial lung disease

A

Fibrosis
Granulomatous
Eosinophilic
Smoking related

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25
Q

Collection of histiocytes, macrophages +/- multi-nucleate giant cells

A

Granuloma

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26
Q

What is extrinsic allergic alveolitis

A

Immune mediateevlung disorders caused by prolonged exposure to inhaled organic antigen —> widespread alveolar inflammation

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27
Q

Histology of extrinsic allergic alveolitis

A

Polyploid plugs of loose connective tissue within alveoli/bronchioles - granuloma formation and organising pneumonia

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28
Q

Male smoker
Proximal bronchi cavitating lesion seen in lungs. Pt has hypercalcaemia, haemoptysis and weight loss

What type of tumour
Histology

A

SCC (30-50%)

Histology: keratinisation, intercellular prickles (desmosomes)

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29
Q

Female non smoker. Hx of weight loss, dyspnoea and hemoptysis

Peripheral lesions seen on CXR and possible Mets.

Type of lung cancer
Histology

A

Adenocarcinima (20-30%)

Histology: glandular differentiation
Cytology: cells containing mucin vacuoles
Molecular: EGFR mutations

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30
Q

Smoker. Cushingoid. Proximal weakness. Lack of co-ordination.

Type of lung cancer
Associated conditions
Where does it arise from
Mutations

A

Small cell lung cancer (20-25%) - strong relationship to smoking
Ectopic ACTH
Lamberton-Eaton
Cerebellar degeneration

Arises from neuroendocrine cells

P53 and RB1 mutations

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31
Q

P53/ RB1 mutations
Lung cancer?

Prognosis and why

A

Small cell carcinoma

Poor prognosis as
- early Mets to adrenal, liver and brain
Despite chemo sensitive

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32
Q

4 weeks after MI

Persistent ST elevation

A

Aneurysm

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33
Q

flushing, diarrhoeah, bronchoconsriction

A

carcinoid syndrome
serotonin neoplastic syndrome
- lung, ovary, testes, bowel tumours

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34
Q

EGFR mutation lung cancer

A

adenocarcinoma

TK inhibitor therapy

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35
Q

What does a Kras mutation in lung cancer tell you

A

Adeno/squamous carcinoma
Poor prognosis
No response to TK inhibitor

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36
Q

What does a ERCC1 mutation in lung cancer tell you

A

Non small cell lung cancer

Poorer response to cisplatin

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37
Q

Lung cancer staging

A

T(T1-4)
N(0-2)
M(0-1)

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38
Q

What is mesothelioma

A

Arising from parietal or visceral pluera and spreads widely in pleural space
Associated with extensive pleural effusion, chest pain and dyspnoea

  • In asbestos related - long latent period of 25-45 years
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39
Q

Large pulmonary thrombo-embolism that straddles the main pulmonary arterial trunk at its bifurcation

  • Name
  • What does it lead to?
A

Saddle embolus

Acute cor pulmonale
Cardiogenic shock
Death
If >60% of pulmonary bed occluded

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40
Q

What is a wedge infarct

A 
Pulmonary infarction (commonly after PE)
Repeated infarctions can cause pulmonar HTN
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41
Q

Non thrombotic emboli examples

A

BM, amniotic fluid, tumour, air, foreign body

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42
Q

PE cause

A

95% caused by DVT

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43
Q

Risk factors for PE/DVT

A 
Female
Immobility
Cardiac disease
cancer
Primary and secondary hypercoaguable states 
(Virchow's triad)
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44
Q

Define pulmonary HTN

A

Mean pulmonary arterial pressure of >25mmHg at rest

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45
Q

Pulmonary HTN classification

A

According to aetiology

1) PAH (idiopathic, hereditary, drugs, associated with congenital heart disease)
2) Pulmonary HTN associated with left heard disease
3) Pulmonary HTN due to lung disease
4) Chronic thromboembolic pulmonary HTN
5) Pulmonary HTN with unclear multifactoral mechanisms

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46
Q

Complications of Pulmonary HTN

A

RHF
Nutmeg liver
Peripheral oedema

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47
Q

What is nutmeg liver

A

Venous congestion of organs

Due to pulmonary HTN

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48
Q

Intra alveolar fluid, iron laden macrophages

A

Pulmonary oedema

- Cause is Left heart failure

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49
Q

Lung expanded, firm, plum-coloured , airless
Cause
Clinical presentation

A

Diffuse alveolar damage

ARDS adults - infection, aspiration, trauma
HMD (hyaline membrane disease) neonates - insufficient surfactant production in prems

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50
Q

Normal oesophagus histology

A

Proximal 2/3 squamous
Squamo-columnar junction/z-line
Distal 1/3 columnar

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51
Q

GORD histopath

A

Reflux of gastric acid content

Consequences 
Ulceration (muscularis proposal)
- haemorrhage, perforation
Granulation tissue
- fibrosis, structures
Barretts oesophagus
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52
Q

Barrett oesophagus histopath

Stages

A

Columnar lines oesophagus

Re-epithelialisation by metaplastic columnar epithelium

1) gastric metaplasia
2) intestinal metaplasia (goblet cells too)

Can lead to adenocarcinoma:
Metaplasia - dysplasia - cancer

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53
Q

Adenocarcinoma oesophagus histopath

A

Invading basement membrane unlike dysplasia
Associated with Barrett

Risk factors: smoking, obesity

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54
Q

SCC of oesophagus

Associations
Where in oesophagus

A

Etoh and smoking
Afro carribean

Middle and lower oesophagus
Poor prognosis -early spread

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55
Q

Oesophageal varices define
Cause
Histology
Management

A

Engorged dilated veins

Cirrhosis/portal htn

Thrombosed variceal focus

Emergency endoscopy - sclerotherapy/banding

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56
Q

Acute gastrits causes

A

Aspirin/NSAIDs
Corrosives
Alcohol
Acute H pylori

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57
Q

Chronic gastritis causes

A

H pylori (Antral usually)
AI - pernicious anaemia
Smoking, etoh

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58
Q

Gastric ulcer

Symptoms

Risk factors

Complications

A

Breach through muscularis mucosa into submucosa

Worse with food (unlike duodenal

H.pylori
Smoking
NSAID
Elderly

Anaemia
Perforation (erect CX)
Malignancy

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59
Q

Investigating gastric ulcer

A

Biopsy for H.pylori status

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60
Q

Tumors of the stomach

A

95% adenocarcinoma

Rest
MALT
Neuroendocrine
SCC
GIST
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61
Q

H Pylori eradication

A

Triple therapy
PPI
Clarithromycin
Amox or metro

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62
Q

Gastric lymphoma

A

Chronic antigen stimulation - chronic inflammation by H.pylori
- B cell (marginal zone) lymphoma

H pylori eradication if limited to stomach
- will go away

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63
Q

Duodenitis, duodenal ulcer and H.pylori

Risk factors

A

Increased acid production spills into duodenum. Chronic inflammation and gastric metaplasia with helicobacter infefctoion. LOSS OF GOBLET CELLS = gastric metaplasis

Duodenal ulcer More common than gastric ulcer
Pain relieved by food, worse at night + WHEN STOMACH EMPTY
Biopsy: neutrophils

H.pylori, Smoking, NSAID, Young

Anaemia
Perforation (erect CX)

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64
Q

Duodenal disease

A 
Ulcer
Immunosuppressive
- CMV
- cryptosporidisis 
Giardia lamblia 
Whippes disease
Coeliac - MALT (Tcell)

Paeds

  • atresia
  • Stenosis
  • Hirschsprung
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65
Q

Coeliac histopath

A

Vilous atrophy
Crypt hyperplasia
Lymphocyte infiltration

10% get lymphoma

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66
Q

Cause of ischaemic colitis

A

arterial or venous occlusion
Small vessel disease
Low flow states
Obsruction

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67
Q

Typical areas of ischamic colitis

A

Splenic flexure: SMA to IMA transition

Rectosigmoid IMA to internal ileac

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68
Q

Which type of IBD does smoking worsen?

A

Chron’s

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69
Q

MZ twin conordance in IBD

A

Chron’s 50%

UC 15%

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70
Q

Histopath chron’s

A 
Mouth to anus
Skip lesions - cobblestone appearance
First lesion - aphthous ulcer - deep rosethorn ulcer
Non caseating granluomas
Transmural inflammation
Fistula/fissure common
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71
Q

UC histopath

A

Extends proximally from rectum continuously
Small bowel not affected unless ‘backwash ileitis’
Mucosa only
No granulomas/fistulas/fissures/strictures

Can get pseudopolyps

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72
Q

IBD presentation

A

Chron’s: Intermittent diarrhoea, pain and fever

UC: More bloody diarrhoea, mucus. Crampy abdo pain relieved by defecation.

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73
Q

IBD extra-GI manifestations

A

Anaemia - stomatitis
Eyes: uveitis, conjunctivitis
Skin: erythema nodosum/multiforme, clubbing, pyoderma gangrenosum
Joints: Migratory polyarhropathy of large joints, sacroilitis, myositis, ankylosing spondylitis
Liver: PSC (UC), pericholangitis

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74
Q

Chron’s complications

A

Fissures/fistula
Strictures (requiring resection)
Abscess
Perforation

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75
Q

UC complications

A

Severe haemorrhage
Toxic megacolon
30% require colectomy within 3 years
Adenocarcinoma (20-30X risk)

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76
Q

Chron’s management

A

Mild: Pred
Severe attack: IV hydrocortisone, metronidazole

Additional: Azathioprine, methotrexate, infliximab

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77
Q

UC management

A

Mild: Pred + mesalazine (5ASA)
Moderate: Pred + mesalazine + steroid enema bd
Severe: Admit, nbm IV fluid, IV hydrocortisone, rectal steroids

For remission: All 5ASA (1st line), azathioprine (2nd line)

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78
Q

Carcinoid syndrome manifestations

Treatment

A

Bronchoconstriction
Flushing
Diarrhoea

Octreotride (somatostatin analogue)

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79
Q

Types of non-neoplastic polyps

A 
Hamartamous polyp (juvenile, peutz jegher)
Hyperplastic - folds of mucosa grown to much - benign - seen at 50-60yo
Inflammatory - psuedopolyps in UC
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80
Q

Multiple polyps, hyperpigmentation, freckles around mouth, palms and soles

Condition
Management

A

Peutz-Jegher syndrome (AD)

Increased risk of intussusception and malignancy
- regular GI, pevlis and gonadal surveillance

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81
Q

Risk factors for colon/rectum cancer

A

Size >4cm
Proportion of villous component
Degree of dysplastic change

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82
Q

Colon adenoma

Symtoms

A

Benign dysplastic lesions
- precursors to most adenocarcinomas (most remain benign) - takes 10 years

Usually asymptomatic
Bleed/anaemia

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83
Q

1000 adenomatous polyps. Condition

Prognosis
Genetics

A

Familial adenomatous polyposis
>100polyps is diagnostic

100% develop cancer in 10-15yrs
APC tumour suppressor gene - Chr 5q21 in 70%

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84
Q

Condition similar to FAP

Differences

A

Gardner’s syndrome

Extra intestinal manifestations too

  • Osteomas of skull and mandible
  • Epidermoid cysts
  • desmoid cysts
  • Dental caries
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85
Q

Young (<50yo) bowel cancer proximal t splenic flexure

Condition

A

Hereditary non-polyposis colorectal carcinoma/Lynch syndrome

Early age
AD mutations in DNA mismatch repair genes
Carcinomas usually in right colon
Extra-colonic cancers - endometrium, prostate, breast, stomach

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86
Q

Colorectal carcinoma

Type of cancer
Age
Location in bowel

A

Adenocarcinoma in 98%
60-79
45% in rectum

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87
Q

Colorectal carcinoma risk factors

A

Diet, lack of exercise, obesity, familial syndromes, IBD

NSAIDs protective (COX-2 overexpressed in 90%)

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88
Q

Investigation bowel cancer

A

Proctoscopy, sigmoidoscopy, colonoscopy, barium enema, bloods
CT/MRI
CEA (monitor disease)

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89
Q

Staging colorectal carcinoma

A

Dukes
A) Limited to mucosa (5yr survival >95%)
B1) Extending into muscularis propria
B2) Transmural invasion
C1) Extending into muscularis propria with lymph nodes
C2) Transmural invasion with lymph nodes
D) Distant metastasis (5yr survival <10%)

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90
Q

Right hemicolectomy for cancer located where

A

Caecum, ascending colon and proximal transverse

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91
Q

Extended right hemicolectomy for cancer located where

A

Transverse colon

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92
Q

Left hemicolectomy for cancer located where

A

Descending colon and distal transverse

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93
Q

Sigmoid colectomy for cancer located where

A

Sigmoid

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94
Q

Anterior resection for cancer located where

A

> 1-2cm above anal sphincter

- allows preservation of anal sphincter

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95
Q

Adomino-perinal resection for cancer located where

A

<1-2cm above anal sphincter

- associated with permanent colostomy

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96
Q

Pancreatic carcinoma types
Location
Risk factors

A 
Ductal adenocarcinoma (85%)
Also can have acinar cell cancers

Head of pancreas

Smoking, diet, FAP, HNPCC, diabetes, chronic pancreatitis

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97
Q

Painless jaundice, weight loss, steatorrhoea

A

Pancreatic carcinoma

- Jaundice if obstructing common bile duct

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98
Q

Prognosis of pancreatic ductal carcinoma

A

5 year survival ~ 5%

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99
Q

Ca 19-9

A

Pancreatic tumour marker

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100
Q

Severe epigastric pain radiating to back
Relieved by sitting forward
Vomiting

A

Acute pancreatitis

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101
Q

Histology it acute pancreatitis

A

Coagulative necrosis

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102
Q

Complications of acute pancreatitis

A

Pseudo cyst, abscess

Shock, hypoglycaemia, hypocalcaemia

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103
Q

Chronic pancreatitis causes

A

80% alcohol
Haemochromatosis
Duct obstruction: gall stones, CF, tumours
Autoimmune (IgG4) - gG4-POSITIVE PLASMA CELLS–>Tx with steroids

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104
Q

Epigastric pain radiating to back, weight loss, steatorrhoea, DM

A

Chronic pancreatitis

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105
Q

Histology chronic pancreatitis

A

Fibrosis and loss of exocrine tissue (atrophy of acinar cells)
- not of duct cells
Duct dilation, secretions, calcification

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106
Q

Complications of chronic pancreatitis

A

Pseudocyst
Diabetes
Pancreatic cancer
Malabsorption

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107
Q

Structural unit of the liver

A

Hepatic lobule - 1-2mm hexagon
In the centre are terminal branches of the hepatic vein (centrilobular vein)

Angles of hexagon formed by portal tracts

  • bile duct
  • portal vein
  • hepatic artery
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108
Q

Significance of liver zones

A

1) near portal tract (periportal hepatocytes) have rich blood supply
2) hepatocytes grow up
3) centrilobular hepatocytes bear terminal hepatic vein - more metabolically active

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109
Q

Portal tract with no bile duct

A

Indicates bile duct disease going on

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110
Q

Liver functions

A 
Metabolism
Hormone metabolism
Bile synthesis 
Protein synthesis
Storage
Immune function
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111
Q

Metabolic function of the liver

A

Involved in glycolysis, glycogen storage, glucoses synthesis , amino acid synthesis, fatty acid synthesis makes, drug metabolism

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112
Q

Hormone metabolism by the liver

A

Activation of vit D
Conjugation and secretion of steroid hormones
Peptide hormone metabolism (GH, PTH, insulin)

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113
Q

Bile synthesis by liver

A

600-1000ml daily

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114
Q

Protein synthesis by liver

A

All proteins except gamma globulins

- Notable albumin, fibrinogen and coagulation factors

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115
Q

Storage function of liver

A

Large amounts: Glycogen, vitA, D, B12

Small amounts: Vit K, folate, iron and copper

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116
Q

Immune function of the liver

A

Antigens from gut arrive via portal circulation

Phagocytosed by Kupffer cells

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117
Q

Liver cirrhosis definition

A

1) Whole liver hepatocyte necrosis
2) Fibrosis - deposition of collagen
3) Nodules of regenerating hepatocytes
4) Distortion of liver vasculature - intra and extra hepatic shunting

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118
Q

Extrahepatic shunting of blood through?

A

Oesophageal varices
Caput medusae
Retroperitoneal space

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119
Q

Causes of liver cirrhosis

A

3 main

1) Alcoholic liver disease
2) Non-alcoholic fatty liver disease
3) Chronic viral hepatitis (B+/-D and C)

Autoimmune, Biliary (PBC, PSC), Genetic, Drugs (methotrexate)

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120
Q

Genetic causes of liver cirrhosis

A 
Haemochromatosis (HFE gene, Chr6)
Wilson disease (ATP7B gene Chr 13)
Alpha-1 antitrypsin deficiency (A1AT)
Galactosaemia
Glycogen storage disease
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121
Q

Cirrhosis classification

A

Micronodular (<3mm)
- caused by alcohol, biliary tracy disease

Macronodular (>3mm)
- caused by viral, Wilson, alpha-1 antitrypsin deficiency)

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122
Q

Causes of portal hypertension >10-12mmHg leading to venous system dilation and collateral vessel formation

A

1) pre-hepatic: Portal vein thrombosis (factor V leiden)
2) Hepatic
- Pre-sinusoidal - schistomsomiasis, PBC, Sarcoid
- Sinusoidal: Cirrhosis
- Post sinusoidal - Veno-occlusive disease
3) Post hepatic: Budd-Chiari syndrome, idiopathic, thrombophilia, OCP, leukaemia, compression by renal tumour, HCC, radiotherapy

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123
Q

Budd chiari syndrome

A

Abdominal pain
Ascites
Liver enlargement

124
Q

Treatment of the collateral vessels formed by portal HTN

A

Thrombolytic
Treat underlying cause
TIPS (transjugular intrahepatic portosystemic shunt)

125
Q

Alcoholic liver disease patterns and order

A

1) Fatty liver
2) Alcoholic hepatitis
3) Alcoholic Cirrhosis

126
Q

What is fatty liver

Macroscopic features
Microscopic features

A

First stage of alcoholic liver disease

Large, pale, yellow and greasy liver

Steatosis - fat droplets in hepatocytes
Chronic exposure –> fibrosis

Fully reversible if alcohol avoided

127
Q

What is alcoholic hepatitis

Macroscopic features
Microscopic features

A

Stage 2 of alcoholic liver disease

Large, fibrotic liver

In zone 3:
Hepatocyte ballooning and necrosis due to accumulation of fat, water and proteins
Mallory bodies
Fibrosis
Seen acutely after heavy drinking. Ranges from asymptomatic to fulminant liver disease

128
Q

Alcoholic cirrhosis

Macroscopic features
Microscopic features

A

Last stage of alcoholic liver disease

Yellow-tan, fatty enlarged
Becomes shrunken, non fatty, brown organ

Micronodular cirrhosis
- small nodules and bands of fibrous tissue

129
Q

What is non alcoholic fatty liver disease

Categories

A

Hepatic steatosis in non-alcoholics.
Due to raised BMI, Diabetes

1) Simple steatosis: fatty infiltration, relatively benign
2) Non-alcoholic steatohepatitis (NASH): steatosis and hepatitis (fatty infiltration and inflammation). Can progress to cirrhosis

130
Q

Autoimmune hepatitis associated conditions

Genetic association

Epidemiology

A

Coelia, RA, SLA, thyroiditis, Sjogrens, UC

HLA-DR3

Females, young and postmenopausal

131
Q

Types of autoimmune hepatitis

Treatment
Prognosis

A

1) ANA, anti-SMA, anti-actin
2) Anti-LKM

Immunosuppression until transplant
- but disease returns in 40%

132
Q

What is PBC

Male or female predominant

A

Autoimmune destruction of intrahepatic bile ducts - granulomas = loss of bile ducts

  • -> cholestasis
  • -> slow development of cirrhosis

Female

Ursodeoxycholic acid treatment in early disease

133
Q

Steatorrhoea, pruritus, fatigue, xanthelasma, arthropathy
High ALP, high cholesterol, hyperbillirubinaemia.
Anti-mitochondrial antibody +ve

What is the condition

Histology

Treatment

A

PBC

No bile duct dilation
Intrahepatic bile duct loss with granulomas

Ursodeoxycholic acid tx in early disease
- 25% remission

134
Q

What is PSC

Male or female predominant

A

Inflammation and fibrosis of extrahepatic and intrahepatic bile ducts

  • -> multifocal strictures
  • -> dilation of preserved sements

Male

135
Q

45yo male, UC
High ALP, high p-ANCA

Diagnosis

What will be shown on
US + ECRCP
At risk of

A

PSC

Bile duct dilation
Beading of bile ducts

Cholangiocarcinoma

136
Q

Causes of hepatic granulomas

A

PBC + Drugs

Non specific: TB and sarcoid

137
Q

Most common benign liver tumour

Others

A

Haemangioma

Liver cell adenoma
Bile duct adenoma

138
Q

Rhodanine stain

A

Liver biopsy for dx of Wilson disease

139
Q

Most common malignant liver tumour

A

METS

From Bowel, Breast, bronchus

140
Q

Hepatic adenoma presentation

Management

A

Benign
Abdo pain/intraperitoneal bleeding

Resection if:
Symptomatic
>5cm
No shrinkage when stopping OCP

141
Q

What is a cholangiocarcinoma

Prognosis

A

Adenocarcinoma arising from bile ducts - intra or extra hepatic
Poor prognosis

142
Q

Cholagiocarcinoma causes

A 
PSC
Chronic liver disease
Parasites
Congenital liver abnormalities
Lyn snydrome type 2
143
Q

HCC causes

Investigations

A 
Hep B/C
Alcoholic cirrhosis
NAFLD
Aflatoxin
Androgenic steroids

Alpha feoprotein
US

144
Q

What is alpha-fetoprotein

A

liver tumour marker (HCC)

145
Q

Skin pathology

- layers

A

Epidermis - renews every 15-30days
Dermis: vascular and nerves
Subcutaneous: fatty tissue

146
Q

What is spongiosis

A

Intercellular edema

147
Q

What is hyperkeratosis

A

Increase in S. Corneum/ keratin

148
Q

What is parakeratosis

A

Nuclei in S.corneum

149
Q

What is Acanthosis

A

Increase in S.spinosum

150
Q

What is acantholysis

A

Decreased cohesion’s between keratinocytes

151
Q

What is lentigenous

A

Linear pattern of melanocytes proliferation with epidermal nasal cell layer (reactive or neoplastic)

152
Q

Salmon pink rash then oval macular in Christmas tree distribution. Had flu recently.

Management

A

Herald patch originally

Remits spontaneously

153
Q

Intraepidermal bulla
Intercellular IgG deposits
Acatholysis

A

Pemphigus

Superficial

154
Q

Suprapubic pain, fever, dysuria, increased frequency of urinating

Treatment

A

Trimethoprim
Or
Nitrofurantoin

155
Q

Cystitis complications

A

Ascending infections causing pyelonephritis

156
Q

Cyclophosphamide associated with Supra pubic pain, dysuria, low grade fever

A

Haemorrhagic cystitis

157
Q

Painless haematuria, frequency, urgency

A

Bladder cancer

158
Q

Types of bladder cancer

A

TCC (most common) - smoking, aromatic amines
SCC - schistosomiasis
Adenocarcinoma - rare

159
Q

TCC bladder diagnosis

Complications

A

Cystoscopy and biopsy

Pyelonephritis or hydronephrosis if ureteral orifice involved

160
Q

60yo man dysuria, nocturia, overflow dribbling

Cause
Treatment

A

BPH - dihydrotestosterone medicated hyperplasia of prostrate forming large nodules

TURP
5-alpha reductase inhibitors (tamsulosin)

161
Q

Prostate cancer type

Spread

A

Adenocarcinoma in men over 50

Local to bladder and haematogenous to bone

162
Q

Prostate cancer diagnosis

A

Hi, Exam, PSA >4ng/ml is suggestive

163
Q

Risk factors for testicular cancer

Main type

A

Undescended testes
Low birth weight/SGA

Germ cell (95%)
- includes seminoma, yolk sac tumour, choriocarcinoma, teratoma
Vs
Sex cord - Stromal (5%)

164
Q

Seminoma

Histology

A

Most common type of germinal tumour
Peak age: 30s
Radiosensitive

Clear cells with prominent lymphoid infiltrate

165
Q

Teratoma testicular

Histology

A

Malignant when post-pubertal
Chemosensitive

Tumour trying to produce keratin

166
Q

Lace like growth pattern - testicular biopsy

A

Yolk cell tumour

167
Q

High grade, prominent nuclei

Necrotic testicular biopsy

A

Embronal carcinoma

168
Q

Choriocarcinoma

Histology

A

Subtype of germ cell cancer

Need both to diagnose:

1) cytotrophoblast cells - clear
2) Cynsitial trophoblastic cells - nucleated

169
Q

Prognosis of testicular germ cell cancers

A

5yr 95% prognosis

170
Q

Non germ cell testicular cancers

A

Lymohoma - older men, highly aggressive

Leydig cell - precocious puberty, usually benign

Sertoli cell - usually benign

171
Q

Nephrotic syndrome

A

Proteinuria (>3g/day)
Hypoalbuminaemia + hyperlipidaemia
Odoema

Swelling
Frothy urine

172
Q

Primary causes of nephrotic syndrome

A

1) Minimal change disease
2) Focal segmental glomerulosclerosis
3) Membranous glomerular disease
4) Diabetes
5) Amyloidosis

173
Q

Child with proteinuria, hypoalbuminaemia and oedema

What is this syndrome
What is it most likely caused by
Treatment

A

Nephrotic syndrome

Minimal change disease

90% respond to steroids

174
Q

Minimal change disease histology

A

Light micros: no changes

Electron micros: loss of podocyte foot processes

175
Q

Membranous glomerular disease histology

A

Light micros: diffuse glomerular basement membrane thickening

Electron micros: loss of podiatry foot processes, subepithelial deposits (spiked)

Immunofluorescence: Ig and complement granular deposits along GBM

176
Q

Ig and complement deposits along GBM - what is this?

Response to steroids

A

Membranous glomerular disease

Poor

177
Q

Focal segmental glomerular sclerosis histology

A

Light micros: focal and segmental glomerular consolidation and scarring, hyalinosis

Electron micros: loss of podocyte foot processes

Immunofluorescence: Ig and complement in scarred areas

178
Q

Prognosis of glomerular membrane disease

Prognosis of focal segmental glomerulosclerosis

A

40% ESRF after 2-20 yrs

50% ESRF in 10yrs

179
Q

Histology I’m diabetic nephrotic syndrome

A

Diffuse glomerular basement membrane thickening

Kimmelstiel Wilson nodules
Aka mesangial matrix nodules

180
Q

Amyloid nephrotic syndrome histology

A

Apple green birefringence with Congo red stain

181
Q

Nephritic syndrome clinical picture

What is nephritic syndrome

A 
Proteinuria
Haematuria
Azootemia
Red cell casts
Oliguria
HTN

Manifestation of glomerular infiltration

182
Q

Causes of nephritic syndrome

A

1) acute post infectious GN
2) IgA nephropathy
3) Rapidly progressive (crescentic) GN
4) Hereditary nephritis (Alport’s syndrome)
5) Thin basement membrane disease (benign familial haematuria)

183
Q

Composition of bone

A

Inorganic: 65%
- Contains 99% Calcium, 85% Ph, 65% Na and Mg of body’s total amounts

Organic: 35%
- Bone cells and protein matrix

184
Q

Bone structure

A

Outside lined by periosteum, then cortex, then medulla.

Long bones comprised of diaphysis and then epiphysis (distal)
Metaphysis is in between where growth plates fuse

185
Q

Types of bone and % of skeleton

A

Cortical - 80%

Cancellous - 20%

186
Q

What type of bone is long bone

A

Cortical: 80% of skeleton

  • Appendicular
  • Mainly mechanical and protective
  • Long bones
  • 80-90% calciufied
187
Q

What type of bone is pelvis and vertebrae

A

Cancellous: 20% of skeleton

  • Axial
  • 15-25% calcified
  • Mainly metabolic
  • Large surface
188
Q

Microanatomy of cortical bone

A

Micro column: has a central canal around which is
Concentric lamellae
- Between units is interstitial lamellae

Surrounding whole entity is circumferential lamellae
Deeper inside is trabecular lamellae

189
Q

Types of bone cells and function

A

Osteoblasts: build bone by laying down osteoid
Osteoclasts: multinuclueate macrophage cells - reabsorb/chew bone
Osteocytes: Osteoblast like cells which sit in lacunae

190
Q

Types of bone cells - histology

A

Osteoblast: Middle size, single nucleus
Osteoclast: Biggest bone cell - mostly pick with multiple purple nuclei
Osteocyte: Just a v small nuclei

191
Q

What is Paget’s disease
What is primarily affected

What are the phases

A

Disorder of bone turnover
Skull and vertebrae aka axial

1) Osteolytic
2) Osteolytic-osteosclerotic
3) Quiescent osteosclerotic

192
Q

Huge osteoclasts + Mosaic lines characteristic histology of

A

Paget’s disease

193
Q

Many multinucleate giant cells on histology is characteristic of what

A

Brown’s tumour

In hyperparathyroidism

194
Q

Fracture repair stages

A

1) Haematoma
2) Fibrocartilaginous callus
3) Mineralisation of fibrocatrilaginous callu
4) Remodelling of bone along weight-bearing lines

195
Q

Causative organisms of osteomyelitis and bones affected

Adults vs children

A

Adults: S. aureus.
- Vertebrae, jaw and toe (secondary to diabetic ulcers)

Children: H.influenza, Group B strep
- long bones

196
Q

X-ray changes of osteomyelitis

A

10 days post onset usually
- Mottled rarefaction (reduced density) and lifting of perisosteum

> 1 week: irregular sub periostal new bone formation called involucrum

10-14days: Irregular lytic estruction

3-6weeks: Areas of necrotic cortex may become detached - called sequestra

197
Q

Histology shows large cell with nuclei arranged in a horseshoe-shaped pattern in the cell periphery

  • What is this called
  • In which conditions
A

Langhans-type giant cell

Granulomatous conditions e.g. TB bone

198
Q

Target rash cause

Other symptoms common early and late

A 
Borrelia burgdorefi (lyme disease)
Central sparing = chronicum migrans

Early: Muskoskeletal, heart, nervous system
Late: Arthritis

199
Q

Nodes on DIPJ and PIPJ names and condition

A

DIPJ: Heberdens
PIPJ: Bouchards

Osteoarthritis

200
Q

What is osteoarthritis?

X ray features

A

Degenerative joint disease mainly affecting vertebrae, hips and knees

Loss of joint spaces
Osteophytes (bone outgrowth)
Subchondral sclerosis
Subchondral cysts

201
Q

Rheumatoid arthritis association with HLA

A

DR4 AND DR1

202
Q

Rheumatoid arthritis characteristic deformities

A

Radial deviation of wrist, ulnar of fingers
Swan neck and Boutonniere deformity of the fingers
Z shaped thumb

Symmetrical, small joints of hand and feet (sparing DIPJ), wrists, elbows, ankles and knees

203
Q

Histology rheumatoid arthritis

A

Proliferating synovitis with

1) Thickening of synovial mebranes
2) Hyperplasia of surface synoviocytes
3) Intense inflammatory cell infiltrate
4) Fibrin deposition and necrosis

Pannus formation

204
Q

Adolescent x ray shows metaphyseal lytic, permeative, elevated periosteum.

Condition
Name of elevated periosteum

A

Osteosarcoma
Codman’s triangle

Malignant mesenchymal cells - bone, cartilage and stroma
ALP+ve
Adolescents
Knee (60%)

205
Q

50yo x ray shows lytic bone with fluffy calcification
Condition
Bones affected

A

Chondrosarcoma

Axial, pelvis, proximal femur, proximal tibia

206
Q

Histology of chondrosarcoma

Prognosis

A

Malignant chondrocytes

Cartilage-producing tumours in axial skeleton

  • Age >40
  • X-ray shows lytic lesions with fluffy calcification
  • Ring and arc mineralisation
  • Malignant chondrocytes - purple/blue - found in matrix

70% 5 yr survival

207
Q

X ray shows onion skinning of periosteum
Condition
Age group affected
Location affected

A

Ewing’s sarcoma
Under 20s
Diaphysis/metaphysis of long bones, pelvis

208
Q

Histology of Ewing’s sarcoma

Chromosome translocations

A

Sheets and sheets of small round cells
CD99+

t(11;22)

  • Age <20y
  • Joints of long bones but not in knees
  • Onion skinning of periosteum
  • Lytic lesions
  • Sheets of small round blue cells
  • CD99 +ve, MIC2 +ve, ALP -ve
209
Q

Femus affected - histology showing chinese letters (misshapen bone trabeculae)

Condition
X-ray findings

A

Fibrous dysplasia - bening - 1st 3 decades of life

Soap bubble osteolyis
Shepherd’s crook deformity (of femoral head)
Multiple often affected

210
Q

Fibrous dysplasia associated with

A

Albright syndrome: cafe au lait spots, precocious puberty, polyostitic dysplasia

211
Q

Cartilage capped bony outgrowth histology
Condition
Age group affected
Site affected

A

Osetochondroma: benign
Adolescent
Metaphysis of long bones near tendon attachment sites

212
Q

Osteochondroma what is it?

Features

A

Cartilage capped bony outgrowth - benign
Mushroom on bone

Most common benign bone tumour

Diaphyseal acelasis/hereditary multiple exostoses = multiple extososes + short stature + bone deformities

213
Q

Endochondroma
Age affected
Site affected

A

Benign tumours of cartilage
Middle age

HANDS

214
Q

X ray showing lytic lesion , Cotton wool calcification - expansile o ring sign

A

Endochondroma - benign tumour of cartilage
Middle aged
Hand affected

215
Q

Knee epiphysis - lytic/lucent lesions right up to articular surface on x-ray
Condition
Age/gender affected

A

Giant cell (borderline malignancy)
Females more
20-40yrs

216
Q

What is giant cell malignancy
Histology

Site affected

A

Borderline malignany

Osteoclast-type multinucleate giant cells on background of spindle/ovoid cells

knee/end of long bones

217
Q

Immune cells involved in acute inflammation

A

Neutrophils

218
Q

Cells associated with chronic inflammation

A

Lymphocytes

219
Q

Bilobed nucelus and granular cell

A

Eosinophils

220
Q

Eosinophil associated conditions

A

Allergy
Parasites
Tumours (Hodkins)

221
Q

Keratin producing carcinoma with intercellular bridges

A

SCC

222
Q

Mucin producing carcinoma from glands

A

Adenocarcinoma

223
Q

Breast pathology shows: Dilation in one or more of the large lactiferous ducts
Name condition
Epidemiology
Cytology

A

Duct ectasia - inflammatory

Multiparous, 40-60yo women. Smokers

Nipple discharge cytology:Proteinaceous material, inflammat ory cells

224
Q

Thick white nipple secretions
Name condition
Other symptoms

A

Duct ectasia - no increased risk of malignancy

Mass, nipple retraction due to fibrosis

225
Q

Lactating woman with painful red breast and fever
Name condition

Associated with

A

Acute mastitis - inflammation of breast - no risk of cancer
- due to cracked skin and stasis of milk

Complicates duct ectasia
Staph infection

226
Q

Treatment of acute mastitis

A

Painful red breast and fever in lacting woman

tx: Antibiotics + treatment of duct ectasia (drainage)

227
Q

Painless breast lump after trauma, surgery, radiotherapu, nodular panniculitis

Epidemiology

Histology

A

Fat necrosis - inflammatory reaction to damaged adipose tissue (typically obese middle aged)
- Onset can be 10yrs after trauma

benign but can mimic cancer

Fat cells surrounded by inflammatory cells e.g. foamy macrophages, giant cells, lymphocytes and plasma cells
- Later: fibrosis and calcification

228
Q

What is fibrocystic disease of breast

Risk of subsequent breast cancer

A

Group of alterations in breast which reflect normal but exaggerated response to hormones - benign

  • Cystic change - often calcified
  • Fibrosis secondaru to cyst rupture
  • Adenosis - increased number of acinar per lobule (normal in pregnancy

Benign - no risk

229
Q

Breast mouse
Name condition
Age of presentation

Management

A

Fibroadenoma - spherical, freely mobile, variable size and rubbery - benign. Fibrous epithelial tumour. Compressed slit like ducts

Any reproductive age, usually 20-30yrs

Shelling out is curative

230
Q

Fibroadenoma histology

A

Stromal and fibrous cells

231
Q

What is Phyllodes tumour

A

Arise from interlobular stroma (like fibroadenomas - can arise within existing or de novo), with increased cellularity and mitoses

In >50yo presents as a palpable mass
Low grade or high grade. Most benign but can be aggressive

232
Q

Phyllodes tumoru cytology

A

Overlapping cells

Leaf like frongs on histology

233
Q

Bloody discharge form nipple

A

Ductal papilloma - benign papillary tumour arising within duct system of breast

NO LUMP, not seen on mammogram.
3D clusters on cytology

Central = from large lactiferrous ducts. May bleed
Peripheral = from terminal ducts
234
Q

Ductal papilloma histology

A

3D clusters on cytology

235
Q

What is radial scar

Management

A

Benign sclerosing lesion in breast - central scarring surrounded by proliferating glandular tissue in stellate pattern

Offer excision because of v small chance of malignancy in surrounding breast

236
Q

Eczema around nipple and darkening of areola
Name of this

Condition associated

A

Paget’s disease of the nipple

Breast cancer - 10% of ductal carcinomas in situ have this

237
Q

Ductal carcinoma in situ detection

Prognosis
Classification

A

Appear as areas of microcalcification on mammography

Much increased risk of progressing to invasive breast Ca
Low, intermediate, high grade

238
Q

Breast biopsy - punched out spaces that are regular and round, overlapping cells, calcified

Management

A

Ductal carcinoma in situ

Complete surgical excision with clear margins = curative
Higher grace DCIS - more likely to occur.

239
Q

What is invasive breast carcinoma

A

Malignant tumours epithelial, which infiltrate teh breast and
Tumour gone out of BM and invaded the stroma

240
Q

Mutation associated with breast cancer

A

BRCA 1 and BRCA 2

241
Q

Breast histology (suspected cancer): Cells aligned in single file chains/strands

A

Invasive lobular cancer

242
Q

Breast histology (suspected cancer): well formed tubules with low-grade nuclei. Rarely palpable as <1cm

A

Tubular carcinoma

243
Q

Breast histology (suspected cancer): Sheets of atypical cells with lymphocytic infiltrate

A

Basal like carcinoma
Stain positive for CK5/6/14
Often associated with BRCA mutations

Cam spread to vascular invasion and distant metastatic spread

244
Q

How are breast cancers graded

A 
Core needle biopsy to assess nuclear pleomorphism, tubule formation and mitotic activity
Scored 3 for each
3-5: grade 1
6-7: grade 2
8-9: grade 3
245
Q

Receptor status of breast carcinomas

A

Low grade tumours: ER/PR +ve and HER2 -ve
High grade tumours: HER2 +ve, ER/PR -ve
Basal like carcinoma: Triple negative

246
Q

Prognostic factors breast cancer

A

Most important: axillary lymph nodes

But also: tumour type, histological type and grade

247
Q

Age of breast cancer screening

A

50 to their 71st birthday every 3 years.

248
Q

Breast histology male breast in gynaecomastia

A

Epithelial hyperplasia, finger like projections into ducts

249
Q

SLE symptoms and signs

A

S: serositis
O: oral ulcers
A: arthritis
P: photosensitivity

B: blood disorders (AIHA, ITP, pancytopenia)
R: renal involvement
A: ANA+
I: Immune phenomena (dsDNA, anti-smith, anti-histone - drug related, anti-SM, antiphospholid)
N: Neuro symptoms

M: Malar rash
D: discoid rash

250
Q

Skin histopathology in SLE

A

Lymphoycte infiltration of upper dermis, extravasation of RBC in upper dermis, vacules in basal dermis

Immunofluorescence: Immune complex deposition between dermis and epidermis

251
Q

Renal histopathology in SLE

A

Thickening of capillary walls in glomerulus (thick pink wall) - wire loop
- because immune complex deposition in basement membrane

252
Q

Cardiac histopathology in SLE

A

Non-infective endocarditis - vegetations on valves called Libman sacks

253
Q

What is the definition of scleroderma

A

Fibrosis and excess collagen. (localised form is called morphea in the skin)

2 types:
Limited (CREST) - anticentromere ab
Diffuse - anti topoisomerase ab (aka scl70)

254
Q

Anti-centromere antibody +

Name condition + features

A

Limited scleroderma
Skin changes limited to face and distal to elbows and knees

Calcinosis
Raynauds
Eosophageal dysmotility
Sclerodayctyl
Telangectasia

Pulmonary HTN

255
Q

Anti-topoisomerase ab +

Name condition + features

A

Diffuse systemic scleroderma

Skin changes anywhere + CREST + Widespread organ involvement

Pulmonary fibrosis

256
Q

HLA DR5 and DRw8 associated with

A

Both types of systemic scleroderma

257
Q

Histology in scleroderma of skin

A

Excess collagen.

Onion skin thinning of arterioles - obliteration of lumen

258
Q

What is mixed connective tissue disorder

A

Overlap of SLE, scleroderma, Polymyositis, Dermatomyositis

259
Q

SLE HLA association

A

DR3 or DR 2

260
Q

Nucleolar pattern of ANA staining

A

Scleroderma

261
Q

Speckled pattern of ANA testing

A

Mixed connective tissue disorder

262
Q

Tender inflammed muscles, proximal muscle weakness
+
Erythematous rash over knucles name
Erythematous rash over eyes

A

Dermatomyositis

Gottron’s paupules
Heliotrope rash

263
Q

Lymphadenopathy, arthritis, erythema nodosum, bilateral hilar lymphadenopathy

Condition and other organs that may be affected

A

Sarcoidosis - non-caseating granulomas

Skin - lupus pernio (nose), skin nodules
Kidneys, eyes, Liver, heart, neuro

264
Q

Asthma, eosinophilia and vasculitis

Diagnosis
Test to do

A

Eosinophilic granulomatosis with polyangitis (small vessel vasculitis)

pANCA (anti-MPO)

265
Q

ENT, Lung, kidney involvement

Diagnosis
Test to do

A

granulomatosis with polyangitis

cANCA

266
Q

What is sarcoid

A

Multisystem disease of non-caseating granulomas

  • skin
  • lung
  • joints
  • lymph nodess
267
Q

Most common thyroid cancer

Histology

A

Papillary - non-functioning, may get cervical lymphadenopathy mets

May be Psommoma bodies
Optically lear nuclei
Intranuclear inclusions

Prognosis good

268
Q

Follicular carcinoma of thyroid metastasize to where

A

lung, bone, liver

269
Q

Medullary carcinoma of thyroid histopathology

A

80% sporadic in 40-50yo, 20% MEN in younger

Derive from parafollicular C cells - produce calcitonin
This calcitonin broken down and deposited as amyloid - STAIN

270
Q

Define cerebral oedema
Causes
Result

How is cerebral oedema reduced?

A

Excess accumulation of fluid in the brain parenchyma

1) vasogenic - disruption of blood brain barrier
2) cytotoxic - secondary to cellular injury aka hypoxia/ischaemia

Raised ICP

Brain reduces oedema itself by

  • tightening tight junctions
  • astrocytes actively effluxing water
  • water going into ventricles

Steroids can also reduce oedema

271
Q

Nephron filtration through various parts

A

1) PCT: Active reabsorption Na, also glucose, AA Phosphate, K

2) LOH
- D/thin limb: Only permeable to water
- Asc limb: Active reabsorption of Sodium and chloride

3) PCT:
- pH balance - active transport H+/HCO3-
- Na, K regulation - active transport (aldosterone)
- Calcium regulation (PTH, 1,25 vit D)

4) CD
- water reabsorption (ADH)
- pH regulation (proton excretion)

272
Q

Polycystic kidney disease presentation
Genes

Associated conditions

A

HTN, haematuria, flank pain
PKD1, PKDS2

Liver cysts
Berry aneurysm

273
Q

Asymptomatic haematuria causes

A

1) Thin basement membrane disease (benign familial haematuria) - hereditary defect in type IV collagen. Benign in most, may lead to scarring in few

2) IgA nephropathy (Berger disease)
- Commonest glomerulonephritis WW. IgA predominant deposition in glomeurli. Often macroscopic/microscopic haematuria. MAY cause proteinuria, AKI.
- Aetiology not well understood.
- Can be seen with HSP

Alport syndrome

274
Q

Causes of acute renal failure

A

Pre-renal
- Failure of perfusion

Rena;

  • Acute tubular injury (most common cause)
  • Acute glomerulonephritis
  • Thrombotic microangiopathy

Post-renal
- Obstruction to urine flow

275
Q

Causes of ATN

Histopathology

A

Hypovolaemia
Nephrotoxins: aminoglycosides, NSAIDs, contrast, Hb, myoglobin, ethylene glycol

Necrosis of short segments of tubules

276
Q

Benign renal tumours

A
  1. Papillary adenoma
    - Formed of papillary cells ± tubules
    - <15mm by definition
    - Trisomy 7, loss of chromosome Y
  2. Renal oncocytoma
    - PINK oncocytic cells
    - Naked eye - mahogany brown with central scar
  3. Renal angiomyolipoma
    - Made of blood vessels, smooth muscle and fat
    - Can be seen in tuberous sclerosis
    - Remove if >4cm
277
Q

Malignant renal tumours

A
  1. Clear cell renal carcinoma
    - Most common type - linked to vhl
    - Clear cells = small round blue cells in capillary network
    - LEIBOVICH RISK MODEL (risk progression index)
    - Loss of Chr 3p
  2. Renal papillary carcinoma
    - Papillary cells FRIABLE FRAGILE BROWN
    - >15mm by definition
    - Loss of chromosome Y, trisomy 7
  3. Chromophobe renal cell carcinoma
    - Different coloured cells
    - Distinct cell borders and thick vascular walls
  4. Nephroblastoma
    - Made of 3 layers of tissue: stromal, epithelial and blastoma
    - Children
    - Good prognosis
278
Q

Bladder cancers

A

Transitional cell carcinomas

  • Most common bladder cancer
  • Associated with smoking and aromatic amines
  • Painless haematuria
  • 3 subtypes: Clear cell transitional carcinoma, Infiltrations transitional carcinoma and flat epithelial carcinoma in situ

SCC
- Associated with Schistosomiasis

Adenocarcinoma
- Rare

279
Q

Prostate pathology

A

Benign Prostate Hyperplasia

  • Increase in the numbers of cells in the prostate
  • Very common, aetiology unknown
  • Presents with LUTS
  • Mx - alpha-blockers (tamsulosin), 5a=reductase inhibitors (finasteride), TURP

Prostate cancer

  • Develops from prostate intraepithelial neoplasia
  • Risk factors = smoking, FHx, red meat consumption
  • Prognosis - GLEASON SCORE
280
Q

What are the two layers of epithelium in breast tissue?

A
  • Outer layer = myoepithelium

- Inner layer = luminal cells

281
Q

What’s the terminal duct lobular unit?

A

Duct + acinar tissue

All breast cancers arise from here

282
Q

Inflammatory breast disease

A

DUCT ECTASIA

  • Inflammation and dilation of breast duct
  • Smoking = biggest risk factor
  • Lump with thick white nipple secretions
  • There can be slit-like nipple retraction
  • Cytology of nipple discharge = proteinaceous material, inflammatory cells

ACUTE MASTITIS

  • Inflammation of breast tissue
  • Associated with lactation(Staphyloccal infection)
  • If not lacating - keratinising squamous metaplasia
  • Painful tender breast
  • Neutrophils
  • Incision & drainage + Abx

FAT NECROSIS

  • Inflammatory reaction to adipose injury e.g. radiotherapy
  • PAINLESS breast lump
  • Giant multinucleate cells
283
Q

Benign breast disease

A

Fibrocystic breast disease

  • Fibrous and cystic changes to breast tissue
  • Changes with cycle
  • Calcification may be seen

Fibroadenoma

  • Fibrosis of stroma and glandular tissue
  • Mouse
  • Generally self-resolving

Phyllodes tumour

  • Leaf-like
  • Malignant potential
  • Pink = benign, purple = malignant

Duct papilloma

  • NO LUMP!!!
  • Central papillomas - arise from large lactiferous ducts
  • Perpheral papillomas - arise from small terminal ductules
  • Central papillomas can give bloody discharge

Radial scar

  • Central scarring surrounded by proliferating glandular mesenchyme
  • Excise, because there can be malignancy at the edges
284
Q

Proliferative breast disease

A

Usual epithelial hyperplasia

  • Proliferation of the epithelial cells - 4-5cells thick into lumen
  • No direct increase risk in malignancy (yes it is?)
  • Serrated lumen

Atypical ductal hyperplasia

  • Epithelial proliferation - multiple layers of cells
  • Rounded lumen
  • 4 x risk of cancer so remove

Atypical lobular hyperplasia

  • Proliferation into the acinar space
  • May not be able to see lumen
  • 7-12x risk of cancer
285
Q

Breast cancer - carcinoma in situ

A

30% of breast cancer
- Can be DUCTAL (DCIS) or LOBULAR (LCIS)

Lobular CIS
- Loss of E-adherin

Ductal CIS

  • Areas of calcification
  • Intraductal epithelial proliferation along the length of the duct
  • Low-grade - cribriform appearance
  • High-grade - larger cells, can’t see lumen well, only one central lumen, containing necrotic material
286
Q

Invasive breast cancer

A
  • Invasion through the BM and INTO STROMAL TISSUE
  • Associated with high lifetime oestrogen exposure and BRCA mutation

Types of invasive breast cancer

  • Ductal - large pleomorphic cells, abnormal chromatin, invading into stroma
  • Tubular - elongated tubules of cells
  • Lobular - linear arrangement of cells in Indian file pattern
  • Mucinous - lots of mucin production
  • Basal like carcinoma - sheets of markedly atypical cells
287
Q

Breast basal-like carcinoma

A

Sheets of atypical cells with predominantly lymphocytic infiltration

  • Associated with BRCA mutations
  • Positive staining for CK5/6, CK14
  • Usually triple-negative

Propensity to invade vasculature and spread disstantly

288
Q

Breast cancer screening

A
  • All women aged 47-73, every 3 years
  • Looks for masses and abnormal calcification
  • If mammogram is abnormal, may need to be recalled for further investigation
  • Triple assessment = examination + USS + FNA/core biopsy
289
Q

Benign bone tumour

A

Osteochondroma

  • Age 10-20, M>F
  • Cartilagenous surface overlying the normal bone
  • Affects knees and elbows

Endochondroma

  • Cartilganeous proliferation within the bone
  • Hands and feet
  • X-ray - POPCORN CALCIFICATION

Giant cell tumour

  • Borderline malignancy
  • Malignant stromal cells
  • Occurs in the epiphyses and can burst through the bone into surrounding tissue
  • X-ray - lytic lesions
  • Histology - osteoclasts, on a background of spindle cells
290
Q

Malignant bone tumours

A
  • Osteocarcoma :(
  • Chondrosarcoma :)
  • Ewing’s sarcoma :/
291
Q

Patterns of injury in acute pancreatitis

A
  • Periductal injury - most common, usually secondary to obstruction
  • Perlobular injury - necrosis at edges of lobules
  • Panlobular injury - develops from periductal or perilobular injury
292
Q

Pancreatic neoplasms

A

CARCINOMA

  • 85% of all pancreatic cancers are ductal carcinomas
  • Acinar carcinoma

CYSTIC NEOPLASMS - usually benign

  • Seroud cystadenoma
  • Mucinous cystadenoma
293
Q

Pancreatic ductal carcinomas

A

Usually at head of pancreas
- K-RAS MUTATION!!

Ductal carcinoma arises from dysplastic ductal lesions in one of 2 pathways:

  1. Pancreatic Intraductal Neoplasm (PanIN)
  2. Intraductal Mucinous Papillary Neoplasm (IMP)
294
Q

Chronic cholecystitis

A
  1. Thickened GB wall
  2. Rokitansky Acschoff sinuses
    - Diverticula in the gallbladder
    - Seen in chronic cholecystitis
    - Occur with gallstones
295
Q

Gastric cancer

A
  • Intestinal - well differentiated
  • Diffuse - poorly differentiated (linitis plastica, signet ring cell)

Signet ring cell - contains mucin which pushes nucleus to cell periphery
- Can metastasise to ovaries =Krukenburg tumour

296
Q

Types of haemorrhage and bleed

A

Extra dural = middle meningeal artery. Trauma + lucid interval
Subdural = Communicating veins. Trauma

297
Q

Endometrial cancer types

A

Endometrioid - perimenopausal, oestrogen sensitive, good prognosis
Non endometrioid - clear cell, older, bad, hobnail

298
Q

Ovarian cancers

A

Ovarian sex cord tumours most common in post menopausal women

  • Granulosa-theca cells (& therefore tumours) convert androgens to oestrogen
  • Sertoli-Leydig - androgen
  • Ovarian fibroma - Meig’s syndrome (ascites + pleural effusion)

Germ cell: teratoma, dysgerminoma, choriocarcinoma (secrete hCG)

Epithelial - most ovarian tumours

  • Serous - most common, psammoma bodies
  • Mucinous - mucin secreting cells
  • Endometrioid - tubular glands
  • Clear cell - hobnail
299
Q

Alzheimer’s

A

Cortical atrophy
Neurofibrilary tangles of tau
a B amyloid plaques

300
Q

Rheumatic fever

A

Strep pyogenes. Mitral valve - antigenic mimicry
Histology: beady fibrous vegetations (veruccae)
- Aschoff bodies (small giant cell granulomas)
- Anitschov myocytes (regenerating myocytes)

2 major or 1 major + 2 minor
Cardititis
Arthritis
Sydenhams chorea
Erthema marginatum
Subcutaneous nodules

Minor: Fever, ESR/CRP, micgratory arthralgia, previous rheumatic fever, malaise, tachy

Vegetations are small and warty

TREATMENT = BEN PEN (Erythryomycin if allergic)

301
Q

Cardiomyopathy

A

Restrictive

  • Caused by sarcoid, amyloid, radiation
  • HF due to diastolic dysfunction
  • Pericardial constriction

Hypertrophic

  • Caused by genetic, storage diseases
  • HTN, AS
  • HF due to diastolic dysfunction

Dilated

  • Caused by: alcohol, genetic, myocarditis, haemochromatosis,
  • HF due to systolic dysfunction
  • IHD, valvular HD, HTN, congenital HD
302
Q

Saddle shaped ST wave

A

Pericarditis

Chest pain relieved on sitting forward. Pericardial rub

303
Q

Genetic defect in myofilament formation leading to huge mytoses

A

Hypertrophic cardiomyopathy

  • often go on to develop dilated cardiomyopathy
  • AD inheritance

HOCM is obstruction of outflow tract!! = sudden death

304
Q

Who should do the MCCD

Reasons for referral to coroner

A

Last doctor to attend to the patient

Cause unknown
Not seen by a doctor during illness/last 14 days
During or within 12 months of pregnancy
Death in custody, while detained under Mental Health Act
Death due to suicide
Accident, trauma, industrial
Medical/surgical treatment
Abortion, anaesthetic care, lack of medical care, murder, self neglect

305
Q

HTN in upper extremities

A

co-arctation of the aorta

306
Q

Disease that affects the external caratid

A

GIANT CELL ARTERITIS

307
Q

ground glass appearance of lungs in adult

A

Diffuse alveolar damage
Due to infection, aspiration, trauma, inhaled irritants, blood transfusion, DIC, drug overdose, pancreatitus, idiopathic

Exudative phase –> hyaline membranes –> organising phase (granulation sitting in alveolar spaces)

40% die
Some resolve, some have residual fibrous scarring

Path (6 decks)

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