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
Collection of histiocytes, macrophages +/- multi-nucleate giant cells
Granuloma
26
What is extrinsic allergic alveolitis
Immune mediateevlung disorders caused by prolonged exposure to inhaled organic antigen —> widespread alveolar inflammation
27
Histology of extrinsic allergic alveolitis
Polyploid plugs of loose connective tissue within alveoli/bronchioles - granuloma formation and organising pneumonia
28
Male smoker Proximal bronchi cavitating lesion seen in lungs. Pt has hypercalcaemia, haemoptysis and weight loss What type of tumour Histology
SCC (30-50%) Histology: keratinisation, intercellular prickles (desmosomes)
29
Female non smoker. Hx of weight loss, dyspnoea and hemoptysis Peripheral lesions seen on CXR and possible Mets. Type of lung cancer Histology
Adenocarcinima (20-30%) Histology: glandular differentiation Cytology: cells containing mucin vacuoles Molecular: EGFR mutations
30
Smoker. Cushingoid. Proximal weakness. Lack of co-ordination. Type of lung cancer Associated conditions Where does it arise from Mutations
Small cell lung cancer (20-25%) - strong relationship to smoking Ectopic ACTH Lamberton-Eaton Cerebellar degeneration Arises from neuroendocrine cells P53 and RB1 mutations
31
P53/ RB1 mutations Lung cancer? Prognosis and why
Small cell carcinoma Poor prognosis as - early Mets to adrenal, liver and brain Despite chemo sensitive
32
4 weeks after MI | Persistent ST elevation
Aneurysm
33
flushing, diarrhoeah, bronchoconsriction
carcinoid syndrome serotonin neoplastic syndrome - lung, ovary, testes, bowel tumours
34
EGFR mutation lung cancer
adenocarcinoma | TK inhibitor therapy
35
What does a Kras mutation in lung cancer tell you
Adeno/squamous carcinoma Poor prognosis No response to TK inhibitor
36
What does a ERCC1 mutation in lung cancer tell you
Non small cell lung cancer | Poorer response to cisplatin
37
Lung cancer staging
T(T1-4) N(0-2) M(0-1)
38
What is mesothelioma
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
39
Large pulmonary thrombo-embolism that straddles the main pulmonary arterial trunk at its bifurcation - Name - What does it lead to?
Saddle embolus Acute cor pulmonale Cardiogenic shock Death If >60% of pulmonary bed occluded
40
What is a wedge infarct
``` Pulmonary infarction (commonly after PE) Repeated infarctions can cause pulmonar HTN ```
41
Non thrombotic emboli examples
BM, amniotic fluid, tumour, air, foreign body
42
PE cause
95% caused by DVT
43
Risk factors for PE/DVT
``` Female Immobility Cardiac disease cancer Primary and secondary hypercoaguable states (Virchow's triad) ```
44
Define pulmonary HTN
Mean pulmonary arterial pressure of >25mmHg at rest
45
Pulmonary HTN classification
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
46
Complications of Pulmonary HTN
RHF Nutmeg liver Peripheral oedema
47
What is nutmeg liver
Venous congestion of organs | Due to pulmonary HTN
48
Intra alveolar fluid, iron laden macrophages
Pulmonary oedema | - Cause is Left heart failure
49
Lung expanded, firm, plum-coloured , airless Cause Clinical presentation
Diffuse alveolar damage ARDS adults - infection, aspiration, trauma HMD (hyaline membrane disease) neonates - insufficient surfactant production in prems
50
Normal oesophagus histology
Proximal 2/3 squamous Squamo-columnar junction/z-line Distal 1/3 columnar
51
GORD histopath
Reflux of gastric acid content ``` Consequences Ulceration (muscularis proposal) - haemorrhage, perforation Granulation tissue - fibrosis, structures Barretts oesophagus ```
52
Barrett oesophagus histopath Stages
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
53
Adenocarcinoma oesophagus histopath
Invading basement membrane unlike dysplasia Associated with Barrett Risk factors: smoking, obesity
54
SCC of oesophagus Associations Where in oesophagus
Etoh and smoking Afro carribean Middle and lower oesophagus Poor prognosis -early spread
55
Oesophageal varices define Cause Histology Management
Engorged dilated veins Cirrhosis/portal htn Thrombosed variceal focus Emergency endoscopy - sclerotherapy/banding
56
Acute gastrits causes
Aspirin/NSAIDs Corrosives Alcohol Acute H pylori
57
Chronic gastritis causes
H pylori (Antral usually) AI - pernicious anaemia Smoking, etoh
58
Gastric ulcer Symptoms Risk factors Complications
Breach through muscularis mucosa into submucosa Worse with food (unlike duodenal H.pylori Smoking NSAID Elderly Anaemia Perforation (erect CX) Malignancy
59
Investigating gastric ulcer
Biopsy for H.pylori status
60
Tumors of the stomach
95% adenocarcinoma ``` Rest MALT Neuroendocrine SCC GIST ```
61
H Pylori eradication
Triple therapy PPI Clarithromycin Amox or metro
62
Gastric lymphoma
Chronic antigen stimulation - chronic inflammation by H.pylori - B cell (marginal zone) lymphoma H pylori eradication if limited to stomach - will go away
63
Duodenitis, duodenal ulcer and H.pylori Risk factors
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)
64
Duodenal disease
``` Ulcer Immunosuppressive - CMV - cryptosporidisis Giardia lamblia Whippes disease Coeliac - MALT (Tcell) ``` Paeds - atresia - Stenosis - Hirschsprung
65
Coeliac histopath
Vilous atrophy Crypt hyperplasia Lymphocyte infiltration 10% get lymphoma
66
Cause of ischaemic colitis
arterial or venous occlusion Small vessel disease Low flow states Obsruction
67
Typical areas of ischamic colitis
Splenic flexure: SMA to IMA transition | Rectosigmoid IMA to internal ileac
68
Which type of IBD does smoking worsen?
Chron's
69
MZ twin conordance in IBD
Chron's 50% | UC 15%
70
Histopath chron's
``` Mouth to anus Skip lesions - cobblestone appearance First lesion - aphthous ulcer - deep rosethorn ulcer Non caseating granluomas Transmural inflammation Fistula/fissure common ```
71
UC histopath
Extends proximally from rectum continuously Small bowel not affected unless 'backwash ileitis' Mucosa only No granulomas/fistulas/fissures/strictures Can get pseudopolyps
72
IBD presentation
Chron's: Intermittent diarrhoea, pain and fever | UC: More bloody diarrhoea, mucus. Crampy abdo pain relieved by defecation.
73
IBD extra-GI manifestations
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
74
Chron's complications
Fissures/fistula Strictures (requiring resection) Abscess Perforation
75
UC complications
Severe haemorrhage Toxic megacolon 30% require colectomy within 3 years Adenocarcinoma (20-30X risk)
76
Chron's management
Mild: Pred Severe attack: IV hydrocortisone, metronidazole Additional: Azathioprine, methotrexate, infliximab
77
UC management
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)
78
Carcinoid syndrome manifestations Treatment
Bronchoconstriction Flushing Diarrhoea Octreotride (somatostatin analogue)
79
Types of non-neoplastic polyps
``` Hamartamous polyp (juvenile, peutz jegher) Hyperplastic - folds of mucosa grown to much - benign - seen at 50-60yo Inflammatory - psuedopolyps in UC ```
80
Multiple polyps, hyperpigmentation, freckles around mouth, palms and soles Condition Management
Peutz-Jegher syndrome (AD) Increased risk of intussusception and malignancy - regular GI, pevlis and gonadal surveillance
81
Risk factors for colon/rectum cancer
Size >4cm Proportion of villous component Degree of dysplastic change
82
Colon adenoma Symtoms
Benign dysplastic lesions - precursors to most adenocarcinomas (most remain benign) - takes 10 years Usually asymptomatic Bleed/anaemia
83
1000 adenomatous polyps. Condition Prognosis Genetics
Familial adenomatous polyposis >100polyps is diagnostic 100% develop cancer in 10-15yrs APC tumour suppressor gene - Chr 5q21 in 70%
84
Condition similar to FAP Differences
Gardner's syndrome Extra intestinal manifestations too - Osteomas of skull and mandible - Epidermoid cysts - desmoid cysts - Dental caries
85
Young (<50yo) bowel cancer proximal t splenic flexure Condition
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
86
Colorectal carcinoma Type of cancer Age Location in bowel
Adenocarcinoma in 98% 60-79 45% in rectum
87
Colorectal carcinoma risk factors
Diet, lack of exercise, obesity, familial syndromes, IBD NSAIDs protective (COX-2 overexpressed in 90%)
88
Investigation bowel cancer
Proctoscopy, sigmoidoscopy, colonoscopy, barium enema, bloods CT/MRI CEA (monitor disease)
89
Staging colorectal carcinoma
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%)
90
Right hemicolectomy for cancer located where
Caecum, ascending colon and proximal transverse
91
Extended right hemicolectomy for cancer located where
Transverse colon
92
Left hemicolectomy for cancer located where
Descending colon and distal transverse
93
Sigmoid colectomy for cancer located where
Sigmoid
94
Anterior resection for cancer located where
>1-2cm above anal sphincter | - allows preservation of anal sphincter
95
Adomino-perinal resection for cancer located where
<1-2cm above anal sphincter | - associated with permanent colostomy
96
Pancreatic carcinoma types Location Risk factors
``` Ductal adenocarcinoma (85%) Also can have acinar cell cancers ``` Head of pancreas Smoking, diet, FAP, HNPCC, diabetes, chronic pancreatitis
97
Painless jaundice, weight loss, steatorrhoea
Pancreatic carcinoma | - Jaundice if obstructing common bile duct
98
Prognosis of pancreatic ductal carcinoma
5 year survival ~ 5%
99
Ca 19-9
Pancreatic tumour marker
100
Severe epigastric pain radiating to back Relieved by sitting forward Vomiting
Acute pancreatitis
101
Histology it acute pancreatitis
Coagulative necrosis
102
Complications of acute pancreatitis
Pseudo cyst, abscess | Shock, hypoglycaemia, hypocalcaemia
103
Chronic pancreatitis causes
80% alcohol Haemochromatosis Duct obstruction: gall stones, CF, tumours Autoimmune (IgG4) - gG4-POSITIVE PLASMA CELLS-->Tx with steroids
104
Epigastric pain radiating to back, weight loss, steatorrhoea, DM
Chronic pancreatitis
105
Histology chronic pancreatitis
Fibrosis and loss of exocrine tissue (atrophy of acinar cells) - not of duct cells Duct dilation, secretions, calcification
106
Complications of chronic pancreatitis
Pseudocyst Diabetes Pancreatic cancer Malabsorption
107
Structural unit of the liver
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
108
Significance of liver zones
1) near portal tract (periportal hepatocytes) have rich blood supply 2) hepatocytes grow up 3) centrilobular hepatocytes bear terminal hepatic vein - more metabolically active
109
Portal tract with no bile duct
Indicates bile duct disease going on
110
Liver functions
``` Metabolism Hormone metabolism Bile synthesis Protein synthesis Storage Immune function ```
111
Metabolic function of the liver
Involved in glycolysis, glycogen storage, glucoses synthesis , amino acid synthesis, fatty acid synthesis makes, drug metabolism
112
Hormone metabolism by the liver
Activation of vit D Conjugation and secretion of steroid hormones Peptide hormone metabolism (GH, PTH, insulin)
113
Bile synthesis by liver
600-1000ml daily
114
Protein synthesis by liver
All proteins except gamma globulins | - Notable albumin, fibrinogen and coagulation factors
115
Storage function of liver
Large amounts: Glycogen, vitA, D, B12 | Small amounts: Vit K, folate, iron and copper
116
Immune function of the liver
Antigens from gut arrive via portal circulation | Phagocytosed by Kupffer cells
117
Liver cirrhosis definition
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
118
Extrahepatic shunting of blood through?
Oesophageal varices Caput medusae Retroperitoneal space
119
Causes of liver cirrhosis
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)
120
Genetic causes of liver cirrhosis
``` Haemochromatosis (HFE gene, Chr6) Wilson disease (ATP7B gene Chr 13) Alpha-1 antitrypsin deficiency (A1AT) Galactosaemia Glycogen storage disease ```
121
Cirrhosis classification
Micronodular (<3mm) - caused by alcohol, biliary tracy disease Macronodular (>3mm) - caused by viral, Wilson, alpha-1 antitrypsin deficiency)
122
Causes of portal hypertension >10-12mmHg leading to venous system dilation and collateral vessel formation
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
123
Budd chiari syndrome
Abdominal pain Ascites Liver enlargement
124
Treatment of the collateral vessels formed by portal HTN
Thrombolytic Treat underlying cause TIPS (transjugular intrahepatic portosystemic shunt)
125
Alcoholic liver disease patterns and order
1) Fatty liver 2) Alcoholic hepatitis 3) Alcoholic Cirrhosis
126
What is fatty liver Macroscopic features Microscopic features
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
What is alcoholic hepatitis Macroscopic features Microscopic features
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
Alcoholic cirrhosis Macroscopic features Microscopic features
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
What is non alcoholic fatty liver disease Categories
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
Autoimmune hepatitis associated conditions Genetic association Epidemiology
Coelia, RA, SLA, thyroiditis, Sjogrens, UC HLA-DR3 Females, young and postmenopausal
131
Types of autoimmune hepatitis Treatment Prognosis
1) ANA, anti-SMA, anti-actin 2) Anti-LKM Immunosuppression until transplant - but disease returns in 40%
132
What is PBC Male or female predominant
Autoimmune destruction of intrahepatic bile ducts - granulomas = loss of bile ducts - -> cholestasis - -> slow development of cirrhosis Female Ursodeoxycholic acid treatment in early disease
133
Steatorrhoea, pruritus, fatigue, xanthelasma, arthropathy High ALP, high cholesterol, hyperbillirubinaemia. Anti-mitochondrial antibody +ve What is the condition Histology Treatment
PBC No bile duct dilation Intrahepatic bile duct loss with granulomas Ursodeoxycholic acid tx in early disease - 25% remission
134
What is PSC Male or female predominant
Inflammation and fibrosis of extrahepatic and intrahepatic bile ducts - -> multifocal strictures - -> dilation of preserved sements Male
135
45yo male, UC High ALP, high p-ANCA Diagnosis What will be shown on US + ECRCP At risk of
PSC Bile duct dilation Beading of bile ducts Cholangiocarcinoma
136
Causes of hepatic granulomas
PBC + Drugs Non specific: TB and sarcoid
137
Most common benign liver tumour Others
Haemangioma Liver cell adenoma Bile duct adenoma
138
Rhodanine stain
Liver biopsy for dx of Wilson disease
139
Most common malignant liver tumour
METS From Bowel, Breast, bronchus
140
Hepatic adenoma presentation Management
Benign Abdo pain/intraperitoneal bleeding Resection if: Symptomatic >5cm No shrinkage when stopping OCP
141
What is a cholangiocarcinoma | Prognosis
Adenocarcinoma arising from bile ducts - intra or extra hepatic Poor prognosis
142
Cholagiocarcinoma causes
``` PSC Chronic liver disease Parasites Congenital liver abnormalities Lyn snydrome type 2 ```
143
HCC causes Investigations
``` Hep B/C Alcoholic cirrhosis NAFLD Aflatoxin Androgenic steroids ``` Alpha feoprotein US
144
What is alpha-fetoprotein
liver tumour marker (HCC)
145
Skin pathology | - layers
Epidermis - renews every 15-30days Dermis: vascular and nerves Subcutaneous: fatty tissue
146
What is spongiosis
Intercellular edema
147
What is hyperkeratosis
Increase in S. Corneum/ keratin
148
What is parakeratosis
Nuclei in S.corneum
149
What is Acanthosis
Increase in S.spinosum
150
What is acantholysis
Decreased cohesion’s between keratinocytes
151
What is lentigenous
Linear pattern of melanocytes proliferation with epidermal nasal cell layer (reactive or neoplastic)
152
Salmon pink rash then oval macular in Christmas tree distribution. Had flu recently. Management
Herald patch originally Remits spontaneously
153
Intraepidermal bulla Intercellular IgG deposits Acatholysis
Pemphigus Superficial
154
Suprapubic pain, fever, dysuria, increased frequency of urinating Treatment
Trimethoprim Or Nitrofurantoin
155
Cystitis complications
Ascending infections causing pyelonephritis
156
Cyclophosphamide associated with Supra pubic pain, dysuria, low grade fever
Haemorrhagic cystitis
157
Painless haematuria, frequency, urgency
Bladder cancer
158
Types of bladder cancer
TCC (most common) - smoking, aromatic amines SCC - schistosomiasis Adenocarcinoma - rare
159
TCC bladder diagnosis Complications
Cystoscopy and biopsy Pyelonephritis or hydronephrosis if ureteral orifice involved
160
60yo man dysuria, nocturia, overflow dribbling Cause Treatment
BPH - dihydrotestosterone medicated hyperplasia of prostrate forming large nodules TURP 5-alpha reductase inhibitors (tamsulosin)
161
Prostate cancer type Spread
Adenocarcinoma in men over 50 Local to bladder and haematogenous to bone
162
Prostate cancer diagnosis
Hi, Exam, PSA >4ng/ml is suggestive
163
Risk factors for testicular cancer Main type
Undescended testes Low birth weight/SGA Germ cell (95%) - includes seminoma, yolk sac tumour, choriocarcinoma, teratoma Vs Sex cord - Stromal (5%)
164
Seminoma Histology
Most common type of germinal tumour Peak age: 30s Radiosensitive Clear cells with prominent lymphoid infiltrate
165
Teratoma testicular Histology
Malignant when post-pubertal Chemosensitive Tumour trying to produce keratin
166
Lace like growth pattern - testicular biopsy
Yolk cell tumour
167
High grade, prominent nuclei | Necrotic testicular biopsy
Embronal carcinoma
168
Choriocarcinoma Histology
Subtype of germ cell cancer Need both to diagnose: 1) cytotrophoblast cells - clear 2) Cynsitial trophoblastic cells - nucleated
169
Prognosis of testicular germ cell cancers
5yr 95% prognosis
170
Non germ cell testicular cancers
Lymohoma - older men, highly aggressive Leydig cell - precocious puberty, usually benign Sertoli cell - usually benign
171
Nephrotic syndrome
Proteinuria (>3g/day) Hypoalbuminaemia + hyperlipidaemia Odoema Swelling Frothy urine
172
Primary causes of nephrotic syndrome
1) Minimal change disease 2) Focal segmental glomerulosclerosis 3) Membranous glomerular disease 4) Diabetes 5) Amyloidosis
173
Child with proteinuria, hypoalbuminaemia and oedema What is this syndrome What is it most likely caused by Treatment
Nephrotic syndrome Minimal change disease 90% respond to steroids
174
Minimal change disease histology
Light micros: no changes | Electron micros: loss of podocyte foot processes
175
Membranous glomerular disease histology
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
Ig and complement deposits along GBM - what is this? Response to steroids
Membranous glomerular disease Poor
177
Focal segmental glomerular sclerosis histology
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
Prognosis of glomerular membrane disease Prognosis of focal segmental glomerulosclerosis
40% ESRF after 2-20 yrs 50% ESRF in 10yrs
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Histology I’m diabetic nephrotic syndrome
Diffuse glomerular basement membrane thickening Kimmelstiel Wilson nodules Aka mesangial matrix nodules
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Amyloid nephrotic syndrome histology
Apple green birefringence with Congo red stain
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Nephritic syndrome clinical picture What is nephritic syndrome
``` Proteinuria Haematuria Azootemia Red cell casts Oliguria HTN ``` Manifestation of glomerular infiltration
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Causes of nephritic syndrome
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)
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Composition of bone
Inorganic: 65% - Contains 99% Calcium, 85% Ph, 65% Na and Mg of body's total amounts Organic: 35% - Bone cells and protein matrix
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Bone structure
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
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Types of bone and % of skeleton
Cortical - 80% | Cancellous - 20%
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What type of bone is long bone
Cortical: 80% of skeleton - Appendicular - Mainly mechanical and protective - Long bones - 80-90% calciufied
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What type of bone is pelvis and vertebrae
Cancellous: 20% of skeleton - Axial - 15-25% calcified - Mainly metabolic - Large surface
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Microanatomy of cortical bone
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
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Types of bone cells and function
Osteoblasts: build bone by laying down osteoid Osteoclasts: multinuclueate macrophage cells - reabsorb/chew bone Osteocytes: Osteoblast like cells which sit in lacunae
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Types of bone cells - histology
Osteoblast: Middle size, single nucleus Osteoclast: Biggest bone cell - mostly pick with multiple purple nuclei Osteocyte: Just a v small nuclei
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What is Paget's disease What is primarily affected What are the phases
Disorder of bone turnover Skull and vertebrae aka axial 1) Osteolytic 2) Osteolytic-osteosclerotic 3) Quiescent osteosclerotic
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Huge osteoclasts + Mosaic lines characteristic histology of
Paget's disease
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Many multinucleate giant cells on histology is characteristic of what
Brown's tumour | In hyperparathyroidism
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Fracture repair stages
1) Haematoma 2) Fibrocartilaginous callus 3) Mineralisation of fibrocatrilaginous callu 4) Remodelling of bone along weight-bearing lines
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Causative organisms of osteomyelitis and bones affected | Adults vs children
Adults: S. aureus. - Vertebrae, jaw and toe (secondary to diabetic ulcers) Children: H.influenza, Group B strep - long bones
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X-ray changes of osteomyelitis
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
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Histology shows large cell with nuclei arranged in a horseshoe-shaped pattern in the cell periphery - What is this called - In which conditions
Langhans-type giant cell Granulomatous conditions e.g. TB bone
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Target rash cause Other symptoms common early and late
``` Borrelia burgdorefi (lyme disease) Central sparing = chronicum migrans ``` Early: Muskoskeletal, heart, nervous system Late: Arthritis
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Nodes on DIPJ and PIPJ names and condition
DIPJ: Heberdens PIPJ: Bouchards Osteoarthritis
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What is osteoarthritis? X ray features
Degenerative joint disease mainly affecting vertebrae, hips and knees Loss of joint spaces Osteophytes (bone outgrowth) Subchondral sclerosis Subchondral cysts
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Rheumatoid arthritis association with HLA
DR4 AND DR1
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Rheumatoid arthritis characteristic deformities
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
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Histology rheumatoid arthritis
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
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Adolescent x ray shows metaphyseal lytic, permeative, elevated periosteum. Condition Name of elevated periosteum
Osteosarcoma Codman's triangle Malignant mesenchymal cells - bone, cartilage and stroma ALP+ve Adolescents Knee (60%)
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50yo x ray shows lytic bone with fluffy calcification Condition Bones affected
Chondrosarcoma Axial, pelvis, proximal femur, proximal tibia
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Histology of chondrosarcoma | Prognosis
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
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X ray shows onion skinning of periosteum Condition Age group affected Location affected
Ewing's sarcoma Under 20s Diaphysis/metaphysis of long bones, pelvis
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Histology of Ewing's sarcoma Chromosome translocations
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
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Femus affected - histology showing chinese letters (misshapen bone trabeculae) Condition X-ray findings
Fibrous dysplasia - bening - 1st 3 decades of life Soap bubble osteolyis Shepherd's crook deformity (of femoral head) Multiple often affected
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Fibrous dysplasia associated with
Albright syndrome: cafe au lait spots, precocious puberty, polyostitic dysplasia
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Cartilage capped bony outgrowth histology Condition Age group affected Site affected
Osetochondroma: benign Adolescent Metaphysis of long bones near tendon attachment sites
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Osteochondroma what is it? | Features
Cartilage capped bony outgrowth - benign Mushroom on bone Most common benign bone tumour Diaphyseal acelasis/hereditary multiple exostoses = multiple extososes + short stature + bone deformities
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Endochondroma Age affected Site affected
Benign tumours of cartilage Middle age HANDS
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X ray showing lytic lesion , Cotton wool calcification - expansile o ring sign
Endochondroma - benign tumour of cartilage Middle aged Hand affected
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Knee epiphysis - lytic/lucent lesions right up to articular surface on x-ray Condition Age/gender affected
Giant cell (borderline malignancy) Females more 20-40yrs
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What is giant cell malignancy Histology Site affected
Borderline malignany Osteoclast-type multinucleate giant cells on background of spindle/ovoid cells knee/end of long bones
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Immune cells involved in acute inflammation
Neutrophils
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Cells associated with chronic inflammation
Lymphocytes
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Bilobed nucelus and granular cell
Eosinophils
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Eosinophil associated conditions
Allergy Parasites Tumours (Hodkins)
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Keratin producing carcinoma with intercellular bridges
SCC
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Mucin producing carcinoma from glands
Adenocarcinoma
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Breast pathology shows: Dilation in one or more of the large lactiferous ducts Name condition Epidemiology Cytology
Duct ectasia - inflammatory Multiparous, 40-60yo women. Smokers Nipple discharge cytology:Proteinaceous material, inflammat ory cells
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Thick white nipple secretions Name condition Other symptoms
Duct ectasia - no increased risk of malignancy | Mass, nipple retraction due to fibrosis
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Lactating woman with painful red breast and fever Name condition Associated with
Acute mastitis - inflammation of breast - no risk of cancer - due to cracked skin and stasis of milk Complicates duct ectasia Staph infection
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Treatment of acute mastitis
Painful red breast and fever in lacting woman | tx: Antibiotics + treatment of duct ectasia (drainage)
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Painless breast lump after trauma, surgery, radiotherapu, nodular panniculitis Epidemiology Histology
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
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What is fibrocystic disease of breast Risk of subsequent breast cancer
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
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Breast mouse Name condition Age of presentation Management
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
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Fibroadenoma histology
Stromal and fibrous cells
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What is Phyllodes tumour
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
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Phyllodes tumoru cytology
Overlapping cells | Leaf like frongs on histology
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Bloody discharge form nipple
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 ```
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Ductal papilloma histology
3D clusters on cytology
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What is radial scar Management
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
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Eczema around nipple and darkening of areola Name of this Condition associated
Paget's disease of the nipple Breast cancer - 10% of ductal carcinomas in situ have this
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Ductal carcinoma in situ detection Prognosis Classification
Appear as areas of microcalcification on mammography Much increased risk of progressing to invasive breast Ca Low, intermediate, high grade
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Breast biopsy - punched out spaces that are regular and round, overlapping cells, calcified Management
Ductal carcinoma in situ Complete surgical excision with clear margins = curative Higher grace DCIS - more likely to occur.
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What is invasive breast carcinoma
Malignant tumours epithelial, which infiltrate teh breast and Tumour gone out of BM and invaded the stroma
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Mutation associated with breast cancer
BRCA 1 and BRCA 2
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Breast histology (suspected cancer): Cells aligned in single file chains/strands
Invasive lobular cancer
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Breast histology (suspected cancer): well formed tubules with low-grade nuclei. Rarely palpable as <1cm
Tubular carcinoma
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Breast histology (suspected cancer): Sheets of atypical cells with lymphocytic infiltrate
Basal like carcinoma Stain positive for CK5/6/14 Often associated with BRCA mutations Cam spread to vascular invasion and distant metastatic spread
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How are breast cancers graded
``` 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 ```
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Receptor status of breast carcinomas
Low grade tumours: ER/PR +ve and HER2 -ve High grade tumours: HER2 +ve, ER/PR -ve Basal like carcinoma: Triple negative
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Prognostic factors breast cancer
Most important: axillary lymph nodes But also: tumour type, histological type and grade
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Age of breast cancer screening
50 to their 71st birthday every 3 years.
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Breast histology male breast in gynaecomastia
Epithelial hyperplasia, finger like projections into ducts
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SLE symptoms and signs
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
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Skin histopathology in SLE
Lymphoycte infiltration of upper dermis, extravasation of RBC in upper dermis, vacules in basal dermis Immunofluorescence: Immune complex deposition between dermis and epidermis
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Renal histopathology in SLE
Thickening of capillary walls in glomerulus (thick pink wall) - wire loop - because immune complex deposition in basement membrane
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Cardiac histopathology in SLE
Non-infective endocarditis - vegetations on valves called Libman sacks
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What is the definition of scleroderma
Fibrosis and excess collagen. (localised form is called morphea in the skin) 2 types: Limited (CREST) - anticentromere ab Diffuse - anti topoisomerase ab (aka scl70)
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Anti-centromere antibody + | Name condition + features
Limited scleroderma Skin changes limited to face and distal to elbows and knees ``` Calcinosis Raynauds Eosophageal dysmotility Sclerodayctyl Telangectasia ``` Pulmonary HTN
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Anti-topoisomerase ab + | Name condition + features
Diffuse systemic scleroderma Skin changes anywhere + CREST + Widespread organ involvement Pulmonary fibrosis
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HLA DR5 and DRw8 associated with
Both types of systemic scleroderma
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Histology in scleroderma of skin
Excess collagen. | Onion skin thinning of arterioles - obliteration of lumen
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What is mixed connective tissue disorder
Overlap of SLE, scleroderma, Polymyositis, Dermatomyositis
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SLE HLA association
DR3 or DR 2
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Nucleolar pattern of ANA staining
Scleroderma
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Speckled pattern of ANA testing
Mixed connective tissue disorder
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Tender inflammed muscles, proximal muscle weakness + Erythematous rash over knucles name Erythematous rash over eyes
Dermatomyositis Gottron's paupules Heliotrope rash
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Lymphadenopathy, arthritis, erythema nodosum, bilateral hilar lymphadenopathy Condition and other organs that may be affected
Sarcoidosis - non-caseating granulomas Skin - lupus pernio (nose), skin nodules Kidneys, eyes, Liver, heart, neuro
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Asthma, eosinophilia and vasculitis Diagnosis Test to do
Eosinophilic granulomatosis with polyangitis (small vessel vasculitis) pANCA (anti-MPO)
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ENT, Lung, kidney involvement Diagnosis Test to do
granulomatosis with polyangitis cANCA
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What is sarcoid
Multisystem disease of non-caseating granulomas - skin - lung - joints - lymph nodess
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Most common thyroid cancer | Histology
Papillary - non-functioning, may get cervical lymphadenopathy mets May be Psommoma bodies Optically lear nuclei Intranuclear inclusions Prognosis good
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Follicular carcinoma of thyroid metastasize to where
lung, bone, liver
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Medullary carcinoma of thyroid histopathology
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
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Define cerebral oedema Causes Result How is cerebral oedema reduced?
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
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Nephron filtration through various parts
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)
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Polycystic kidney disease presentation Genes Associated conditions
HTN, haematuria, flank pain PKD1, PKDS2 Liver cysts Berry aneurysm
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Asymptomatic haematuria causes
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
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Causes of acute renal failure
Pre-renal - Failure of perfusion Rena; - Acute tubular injury (most common cause) - Acute glomerulonephritis - Thrombotic microangiopathy Post-renal - Obstruction to urine flow
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Causes of ATN Histopathology
Hypovolaemia Nephrotoxins: aminoglycosides, NSAIDs, contrast, Hb, myoglobin, ethylene glycol Necrosis of short segments of tubules
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Benign renal tumours
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
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Malignant renal tumours
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
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Bladder cancers
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
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Prostate pathology
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
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What are the two layers of epithelium in breast tissue?
- Outer layer = myoepithelium | - Inner layer = luminal cells
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What's the terminal duct lobular unit?
Duct + acinar tissue All breast cancers arise from here
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Inflammatory breast disease
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
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Benign breast disease
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
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Proliferative breast disease
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
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Breast cancer - carcinoma in situ
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
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Invasive breast cancer
- 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
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Breast basal-like carcinoma
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
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Breast cancer screening
- 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
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Benign bone tumour
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
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Malignant bone tumours
- Osteocarcoma :( - Chondrosarcoma :) - Ewing's sarcoma :/
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Patterns of injury in acute pancreatitis
- Periductal injury - most common, usually secondary to obstruction - Perlobular injury - necrosis at edges of lobules - Panlobular injury - develops from periductal or perilobular injury
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Pancreatic neoplasms
CARCINOMA - 85% of all pancreatic cancers are ductal carcinomas - Acinar carcinoma CYSTIC NEOPLASMS - usually benign - Seroud cystadenoma - Mucinous cystadenoma
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Pancreatic ductal carcinomas
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)
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Chronic cholecystitis
1. Thickened GB wall 2. Rokitansky Acschoff sinuses - Diverticula in the gallbladder - Seen in chronic cholecystitis - Occur with gallstones
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Gastric cancer
- 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
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Types of haemorrhage and bleed
Extra dural = middle meningeal artery. Trauma + lucid interval Subdural = Communicating veins. Trauma
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Endometrial cancer types
Endometrioid - perimenopausal, oestrogen sensitive, good prognosis Non endometrioid - clear cell, older, bad, hobnail
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Ovarian cancers
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
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Alzheimer's
Cortical atrophy Neurofibrilary tangles of tau a B amyloid plaques
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Rheumatic fever
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)
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Cardiomyopathy
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
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Saddle shaped ST wave
Pericarditis Chest pain relieved on sitting forward. Pericardial rub
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Genetic defect in myofilament formation leading to huge mytoses
Hypertrophic cardiomyopathy - often go on to develop dilated cardiomyopathy - AD inheritance HOCM is obstruction of outflow tract!! = sudden death
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Who should do the MCCD Reasons for referral to coroner
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
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HTN in upper extremities
co-arctation of the aorta
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Disease that affects the external caratid
GIANT CELL ARTERITIS
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ground glass appearance of lungs in adult
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