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Year 5 Pathology > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Definition of closed fracture

A

Clean break with intact soft tissue

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2
Q

Definition of comminuted fracture

A

Splintered bone with intact soft tissue

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3
Q

Definition of compound fracture

A

Fracture site communicates with skin surface

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4
Q

Stages of fracture repair

A
  1. Organisation of haematoma at # site (pro-callus)
  2. Formation of fibrocartilaginous callus
  3. Mineralisation of fibrocartilaginous callus
  4. Remodelling of bone along weightbearing lines
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5
Q

Common sites for osteomyelitis in adults

A

Jaw
Vertebrae
Toe

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6
Q

Features of osteomyeltis

A

General: Fever, Malaise, Leucocytosis, Chills
Local: Pain, Swelling, Redness
60% positive blood cultures

X-ray: mixed picture eventually lytic.

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7
Q

Stages of Lyme Disease

A

Stage 1 - Early localised characterised by rash (90%) usually within 7-10 days and between 1 & 50cm diameter.
Often thigh, groin, axilla (earlobe in children)

Stage 2 - Early Disseminated affects many organs, musculoskeletal, heart, nervous system.

Stage 3- Late, persistent dominated by arthritis.

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8
Q

Clinical features of rheumatoid arthritis

A 
Mild anaemia 
Raised ESR 
RF+ve 
\+/- rheumaoid nodules 
extra-articular features
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9
Q

Skin manifestations of rheumatoid arthritis

A

Pyoderma gangrenosum
Nodules
Ulcers (vasculitic)

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10
Q

Components of Felty’s syndrome

A

RA
Neutropenia
Splenomegaly

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11
Q

Eye manifestations of rheumatoid arthritis

A

Keratoconjunctivitis
Scleritis
Scleromalacia
Episcleritis

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12
Q

Lung manifestations of rheumatoid arthritis

A

Fibrosing alveolitis
Obliterative bronchiolitis
Pleural effusion
Lung nodules

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13
Q

Extra-articualr manifestations of RA

A 
Skin manifestations: ulcers, pyoderma gangrenosum, nodules
Lung manifestations e.g. fibrosis
Eye inflammation and scleromalacia 
Sjogren syndrome 
Carpal tunnel and peripheral neuropathy 
Raynauds 
Osteoporosis 
Vasculitis 
Felty's 
Splenomegaly 
Amyloidosis 
Lymphadenopathy 
Systemic symptoms/signs: fever, malaise, fatigue, weight loss
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14
Q

Rheumatoid arthritis affects small joints of the hands sparing the…

A

DIPJ

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15
Q

Deformities seen in rheumatoid arthritis

A 
Radial deviation of wrist 
Ulnar deviation of fingers
Swan neck deformity of fingers 
Boutonniere deformity of fingers
Z shaped thumb 
Swollen MP and PIP joints 
Dorsal subluxation of MP joints 
Atrophy of small hand muscles (Valleys)
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16
Q

Stages (histological) in development of rheumatoid arthritis

A
  1. Unknown antigen reaches synovial membrane
  2. T cell proliferation associated with increased B cells and angiogenesis
  3. Chronic inflammation and inflammatory cytokines
  4. Pannus formation
  5. Cartilage and bone destruction
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17
Q

Predominant inflammatory cell in the synovial space (in rheumatoid arthritis)

A

Neutrophil

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18
Q

Joint most commonly affected by gout

A

Great toe

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19
Q

When gout affects the big toe it is called

A

Podagra

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20
Q

Causes (conditions) of pseudogout

A 
Idiopathic
Primary hyperparathyroidism 
Diabetes mellitus
Hypothyroidism 
Wilsons disease
Hereditary
Low Mg
Low phosphate
Haemochromatosis
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21
Q

Crystals found in pseudogout

A

Calcium pyrophosphate

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22
Q

Birefringence: Gout is… Pseudogout is…

A

Gout: Negatively birefringent crystals
Pseudogout: Positively birefringent crystals

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23
Q

First line treatment for acute gout

A

Potent NSAID e.g. 500mg BD naproxen

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24
Q

Prophylaxis of pseudogout

A

Low dose colchicine (BD)

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25
Q

Treatment of pseudogout

A

Acute attack:
1 or 2 joints: Joint aspiration and intra-articular glucocorticoid (triamcinolone) injection
More than 2 joints: NSAIDs (first line) or colchicine

Prophylaxis: Colchicine

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26
Q

Prevention of gout

A

Acute attack: Potent NSAIDS e.g. naproxen (first line) or colchicine

Long term: allopurinol

Conservative: Reduced ETOH, and purine intake e.g. sardines, liver

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27
Q

Pseudogout crystal shape

A

Rhomboid

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28
Q

Medication used for pseudogout prophylaxis

A

Colchicine

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29
Q

A Brodie abscess is…

A

A subacute osteomyelitis that has been contained to a localised area and walled off by fibrous and granulation tissue.This is termed as Brodie’s abscess.

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30
Q

Most common causative organism in osteomyelitis

A

Staph. aureus

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31
Q

Oesophagus layers

A

Epithelium: stratified squamous epithelium except the bottom part
Submucosa
Muscularis propria

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32
Q

Epithelial cell type in (most) of the oesophagus

A

Stratified squamous

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33
Q

What is the Z-line (oesophagus)

A

Columnar epithelium in the stomach, stratified squamous in the oesophagus. The transition between the 2 types is visible as a zig-zag line known as the Z-line. It is at the bottom of the oesophagus

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34
Q

Definition of ulceration in the GI tract

A

Erosion of the surface going beyond the muscularis mucosae.

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35
Q

What is Barrett’s Oesophagus

A

AKA columnar lined oesophagus

Transformation of epithelial cells in the oesophagus from from stratified squamous epithelium to columnar epithelium

The columnar epithelium can be gastric type or intestinal type. Gastric type does not contain goblet cells. Intestinal type does.

Lose the sharp Z-line dividing white stratified squamous epithelium and red columnar epithelium.

In America for Barrett’s to be diagnosed the columnar epithelium must be intestinal type. In the UK this distinction is not made.

Barrett’s increased risk of cancer.

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36
Q

Squamous cell carcinomas produce…

A

Keratin

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37
Q

Adenocarcinomas produce…

A

Mucus

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38
Q

How does H.pylori cause lymphoma

A

H. pylori induces production of MALT (Mucosal Associated Lymphoid Tissue) in the stomach. A location where MALT is not normally found. If the drive on the proliferation of this lymphoid tissue continues for too long it can cause lymphoma in the stomach.

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39
Q

H pylori causes adenoma of the stomach due to

A

Inflammation which leads to metaplasia, which becomes dysplasia, which becomes adenocarcinoma

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40
Q

Which type of H.pylori is associated with more chronic infection?
Why?

A

cag-A-positive H. pylori

It has a needle like appendage that injects toxin into intracellular junctions separating the cells. It allows the bacteria to attach and colonise more easily and potentiates damage to the epithelium. It causes more inflammation.

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41
Q

Helicobacter infection increases the risk of gastric cancer …fold

A

8-fold

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42
Q

H. pylori is gram…

A

Negative

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43
Q

Causes of gastritis

A 
H. pylori 
Drugs e.g. NSAIDs
CMV
Strongyloides (parasite) 
IBD: Crohn's disease
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44
Q

Gastric cancer incidence high in which regions?

A

High incidence in Japan, Chile, Italy, China, Portugal, Russia

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45
Q

Gastric cancer

More common in men or women?

A

Men

1.8:1 ratio

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46
Q

Most gastric cancers are which type?

A

Adenocarcinomas

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47
Q

Describe the 2 types of gastric adenocarcinoma

A

Intestinal type: well differentiated. More closely linked wit intestinal metaplasia. Large glands containing goblet cells producing mucus.

Diffuse types: poorly differentiated, single cells (signet ring cells) containing mucus, not forming glands. Linitis plastica refers to the appearance of the stomach, resembling an old leather water bottle.

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48
Q

Types of gastric cancer

A 
Adenocarcinoma (95%)
Squamous cell carcinoma 
Lymphoma (MALToma) 
Gastrointestinal stromal tumours (GIST): sarcoma. Mostly benign. Common enough that a significant number are malignant. 
Neuroendocrine tumours
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49
Q

Gastric MALToma/ lymphoma usually originates from which cells?

A

B cells in the marginal zone of the MALT

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50
Q

Pathogens causing duodenal ulceration

A 
H. pylori 
CMV
Cryptosporidiosis 
Giardia lamblia 
Whipples disease: caused by tropheryma whippelii
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51
Q

Giardia common in which country

A

Russia

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52
Q

Antibodies found in coeliac disease

A

Endomysial antibodies

transglutaminase antibodies

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53
Q

MALToma associated with coeliac disease originates from which cells?

A

T cells

(enteropathy associated T cell lymphoma

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54
Q

Coeliac disease produces which histological changes?

A

Flattening/atrophy of duodenal villi
Hyperplasia of duodenal crypts
Increased lymphocytes

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55
Q

Hirschprungs disease

A

Congenital disorder.
Absences of ganglionic cells in myenteric plexus
Distal colon fails to dilate
Causes constipation, abdominal distension, vomiting, ‘overflow’ diarrhoea

Loss of function in RET proto-oncogene Cr10 and others…

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56
Q

…% of people with Hirschprung’s are male

A

80%

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57
Q

Gene associated with Hirschprung’s

A

RET proto-oncogene

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58
Q

Treatment of Hirschprung’s disease

A

Resection of affected part of colon (Distal)

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59
Q

Volvulus

A

Complete twisting of a loop of bowel at mesenteric base, around vascular pedicle

Leads to intestinal obstruction/infarction

In infants occurs in small bowel

Occurs in sigmoid colon in adults (common in elderly)

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60
Q

…% of diverticulae occur in the left colon

A

90%

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61
Q

Pathogenesis of pseudomembranous colitis

A

Proliferation of C.diff bacteria e.g. due to antibiotic use
Production of A and B toxins by the c.diff bacteria
Inflammatory response and formation of pseudomembrane composed of inflammatory debris and white cells

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62
Q

Distinctive clinical features of C.diff colitis

A 
Significant diarrhoea 
Fever 
Abdominal pain 
Recent antibiotic exposure 
Foul smelling stool (distinctive smell)
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63
Q

Treatment of C.diff colitis

A

Metronidazole or vancomycin

VANCOMYCIN MUST BE ORAL

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64
Q

Common sites for ischaemic bowel

A 
Splenuc flexure (SMA transition to IMA) 
Rectosigmoid (IMA transition to internal iliac)
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65
Q

Clinical features of IBD

A 
Diarrhoea +/- blood
Fever
Abdominal pain
Acute abdomen
Anaemia
Weight loss
Extra-intestinal manifestations
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66
Q

Peak age of Crohn’s onset

A

Peak onset on teens/twenties

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67
Q

Histological features of Crohn’s disease

A 
Whole of GI tract can be affected (mouth to anus) – commonly found in the terminal ileum and the large bowel
‘Skip lesions’
Transmural inflammation – entire thickness of wall inflammed 
Non-caseating granulomas (collections of macrophages)
Sinus/fistula formation 
Fat wrapping’
Thick ‘rubber-hose’ like wall
Narrow lumen
‘cobblestone mucosa’
Linear ulcers
Fissures
abscesses
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68
Q

Extra-intestinal manifestations of Crohn’s disease

A 
Arthritis
Uveitis
Stomatitis/cheilitis
Skin lesions
Pyoderma gangrenosum
Erythema multiforme
Erythema nodosum
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69
Q

Peak age of onset of ulcerative colitis

A

20-25 years

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70
Q

Key histological features of ulcerative colitis

A

Involves rectum and colon in contiguous fashion.
May see mild ‘backwash ileitis’ and appendiceal involvement but small bowel and proximal GI tract not affected.
Inflammation confined to mucosa
Bowel wall normal thickness
Shallow ulcers

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71
Q

Complications of ulcerative colitis

A

Severe haemorrhage
Toxic megacolon
Adenocarcinoma (20-30 x risk)

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72
Q

Extra-intestinal manifestations of ulcerative colitis

A 
Arthritis 
Myositis
Uveitis/iritis
Erythema nodosum, pyoderma gangrenosum
Primary Sclerosing Cholangitis (5.5% in pancolitis)
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73
Q

1st line drug for Crohn’s maintenance treatment

A

Mesalazine (or other 5-ASA)

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74
Q

1st line drug for ulcerative colitis maintenance treatment

A

Mesalazine (or other 5-ASA)

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75
Q

Two types of lower GI adenomas

A

Tubular
Villous

(can be a mixture of the two)

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76
Q

Histological features of (GI) tubular adenomas

A

Irregular, pseudo stratified, high nuclear to cytoplasmic ratio because they are dysplastic

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77
Q

Hamartomatous are seen in…

A

Peutz Jeghers

Juvenile polyposis

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78
Q

Juvenile polyps are…

A

Focal malformations of the mucosa and lamina propria
Usually seen in children under 5 years
Can cause bleeding

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79
Q

Features of Peutz Jeghers

A 
Multiple polyps (hamartomatous) 
Mucocutaneous pigmentation 
Freckles around mouth 
Increased risk of intussusception
Increased risk of malignancy: GI (including pancreas), gonad, breast
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80
Q

Gene affected in familial adenomatous polyposis (FAP)

A

Chromosome 5q21, APC tumour suppressor gene

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81
Q

Familial adenomatous polyposis (FAP) average:
Age of onset
Number of polyps

A

25

1000

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82
Q

Familial adenomatous polyposis (FAP):
Minimum number of polyps
Mode of inheritance

A

100

Autosomal dominant

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83
Q

Gardner syndrome is…

A

A variant of FAP with extra intestinal features such as:
multiple osteomas of skull & mandible
epidermoid cysts
desmoid tumors
dental caries, unerrupted supernumery teeth
post-surgical mesenteric fibromatoses

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84
Q

Hereditary non-polyposis colorectal cancer features

A

Autosomal dominant mutation in DNA mismatch repair genes
Causes cancers in right colon (High frequency of carcinomas proximal to splenic flexure)
Causes few polyps
Fast progression to malignancy
Onset of colorectal cancer at an early age (under 50)
Poorly differentiated and mucinous carcinoma more frequent
Multiple synchronous cancers
Also associated with cancers of endometrium, ovary, small bowel, urinary system (including kidney)

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85
Q

Turcot syndrome is

A

Variant of Hereditary non-polyposis colorectal cancer (or FAP) also associated with brain cancers

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86
Q

Dukes staging of colon cancers

A 
A = confined to wall of bowel
B = through wall of bowel (through muscularis propryia)
C = lymph node metastases
D = distant metastases
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87
Q

Causes of acute pancreatitis

A 
Idiopathic
Gallstones
Ethanol
Trauma
Scorpion bite
Mumps/malignancy
Autoimmune
Steroids 
Hypercalciamia/hyperlipidaemia/hyperparathyroidism
ERCP
Drugs (e.g. azathioprine, tetracycline, valproic acid, thiazide, co-trimoxazole) 
Can be divided into 6 categories:
Obstruction of ducts 
Metabolic/toxic
Poor blood supply (Shock and hypothermia) 
Infection/inflammation 
Autoimmine
Idiopathic
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88
Q

Effect of chronic pancreatitis on calcium

A

Causes hypocalcaemia

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89
Q

First pancreatic pro-enzyme activated in pancreatitis pathophysiology

A

Trypsinogen to trypsin

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90
Q

Pancreatic enzymes released from which cells

A

Acinar cells

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91
Q

How does gallstones cause pancreatitis

A

Stone lodged distal to merging of pancreatic and common bile ducts
Reflux of bile up pancreatic duct
Activation of trypsinogen to trypsin and then activation of ther pancreatic enzymes

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92
Q

How does alcohol (ethanol) cause pancreatitis

A

Alcohol leads to spasm/oedema of Sphincter of Oddi and the formation of a protein rich pancreatic fluid which can produce plugs which obstruct the smaller pancreatic ducts

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93
Q

Damage caused by release of lipases in pancreatitis

A

Fat necrosis: Fatty acids and glycerides bind with calcium and magnesium forming soaps seen as yellow/white foci.

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94
Q

Damage caused by release of elastases in pancreatitis

A

Damage to blood vessels and possible haemorrhagic pancreatitis

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95
Q

Damage caused by release of proteases in pancreatitis

A

Parenchymal destruction

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96
Q

Complications of acute pancreatitis

A

Pancreatic : pseudocyst, abscess
Gastrointestinal: UGI erosions, ileus, peritonitis
Systemic: shock, hypoglycaemia, hypocalcaemia

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97
Q

Pattern of injury in pancreatitis

A

Chronic inflammation with parenchymal fibrosis and loss of parenchyma
Duct strictures with intrapancreatic, calcified stones with secondary dilatations

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98
Q

Complications of chronic pancreatitis

A

Malabsorption

Diabetes mellitus (it is the acini cells that are damaged not the islets of langerhans. Therefore a lot of pancreatitis is required to result in diabetes)

Pseudocyts

Carcinoma of the pancreas (?)

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99
Q

Pacreatic pseudocysts are lined by…

A

Fibrous tissue, granulation tissue, inflammatory cells

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100
Q

Most pancreatic carcinomas are…

A

Ductal

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101
Q

Types of cystic neoplasms

A

Serous
Mucinous
Intraductal Papillary Mucinous Neoplasm (IPMN)

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102
Q

Risk factors for pancreatic carcinoma

A

Smoking - doubles the risk (25% of cases)
BMI and dietary factors e.g. meat and fat
Chronic pancreatitis
Diabetes – doubles the risk (80% of cases)
Genetic e.g. Peutz-Jeghers syndrome (polyp with pigmentation around the buccal cavity and other areas)
Age (increases with age)

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103
Q

Components of the metabolic syndrome

A 
Fasting hyperglycaemia 
Hypertension
Central obesity 
Dyslipidaemia 
Microalbuminaemia
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104
Q

Clinical features of acute pancreatitis

A

Severe epigastric pain radiating to back relieved by sitting forward.
Vomiting
Raised amylase
Raised lipase

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105
Q

Pancreatic intraductal neoplasia can lead to…

Mutation in which gene is commonly found in these lesions?

A

Ductal carcinoma

K-ras (95% of cases)

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106
Q

Macroscopic appearance of ductal carcinoma (pancreas)

A

Gritty and grey
Invades adjacent structures
Tumours in the head present earlier and, therefore, tend to be smaller

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107
Q

Microscopic appearance of ductal carcinoma

A

Moderately differentiated
Glandular (adenocarcinoma)
Secretes mucin
Set in fibrous stroma

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108
Q

Most pancreatic ductal carcinomas are in the…

A

Head of the pancreas

followed by, diffuse, then body, then tail

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109
Q

How and where does ductal pancreatic carcinoma spread

A

Direct: Bile ducts, duodenum
Lymphatic: Regional lymph nodes
Blood: Liver
Serosa: Peritoneum

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110
Q

2 main complications of ductal pancreatic cancer

A

Venous thrombosis: (they secrete mucin and once in the blood stream it activates the clotting cascade and forms thrombi in various parts of the body)

Chronic pancreatitis

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111
Q

Features of cystic pancreatic tumours

A

Usually multilocular
Contain serous or mucin secreting epithelium (cf. ovarian tumours)
Usually benign, mucinous tumours may be malignant

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112
Q

Appearance of neuroendocrine tumours (islet cell)

A

Circumscribed
Uniform cells
Cells arranged in nests/trabeculae with granular cytoplas,

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113
Q

Clinical features of ductal carcinoma of the pancreas

A 
Older 
Male
Weight loss (cachexia and anorexia) 
Upper abdominal and back pain (chronic, persistent and severe) 
Painless jaundice 
Pruritus 
Steatorrhoea 
DM 
Recurrent thrombophlebitis
Ascites 
Abdominal mass
Virchow's node 
Courvoursiers sign

Bloods: low Hb, raised Bili, raised Ca, positive CA19.9

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114
Q

What is courvoiser’s sign

A

Courvoisier’s law (or Courvoisier syndrome, or Courvoisier’s sign or Courvoisier-Terrier’s sign) states that in the presence of a palpably enlarged gallbladder which is nontender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones.

Usually, the term is used to describe the physical examination finding of the right-upper quadrant of the abdomen. This sign implicates possible malignancy of the gall bladder or pancreas and the swelling is unlikely due to gallstones

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115
Q

Pancreatic cancer tumour marker

A

CA19.9

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116
Q

Chemotherapy pancreatic cancer

A

5-FU

Palliative

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117
Q

Pancreatic neuroendocrine are usually secretory or non-secretory?

A

Non-secretory

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118
Q

Types of secretory pancreatic endocrine tumour

A

Insulinoma
Gastrinoma: Zollinger-Ellison syndrome
VIPoma: secrete vasoactive intestinal peptide and cause diarrhoea (chronic watery with expected effects) RARE
Glucagonoma: causes necrolytic migrating erythema

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119
Q

Tumours in MEN 2A

A

Parathyroid
Thyroid
Phaeochromacytoma

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120
Q

Tumours in MEN 2B

A

Medullary thyroid
Phaeochromacytoma
Neuroma

(also marfanoid phenotype)

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121
Q

Commonest type of pancreatic endocrine secretory tumour

Prognosis?

A

Insulinoma

Not likely to metastasise

122
Q

What are Rokitansky-Aschoff sinuses?

A

Pseudodiverticulae in the gallbladder wall.

Not abnormal but associated with cholecystitis

123
Q

Types pancreatic malformations

A

Ectopic pancreas: more common in stomach and small intestine

Pancreas divisum: failure of fusion of dorsal and ventral buds leading to increased risk of pancreatitis

Annular pancreas: second part of the duodenum is surrounded by a ring of pancreatic tissue continuous with the head of the pancreas. This portion of the pancreas can constrict the duodenum and block or impair the flow of food to the rest of the intestines. It can present with duodenal obstruction at approximately 1 year. However many cases will be asymptomatic.

124
Q

Causes of increased epithelial lymphocytes in gut

A 
Coeliac disease
Cows milk protein sensitivity
Drugs (NSAIDs)
IgA deficiency
Tropical sprue
Post infective malabsorption
Dermatitis herpetiformis
(lymphoma)
125
Q

Causes of villous atrophy

A 
Coeliac disease
Giardiasis (very rarely)
Tropical sprue
Crohn’s disease
Radiation/chemotherapy
Bacterial overgrowth
Nutritional deficiencies (b12 and folate, secondary to ability to synthesis new DNA)
Graft versus host disease
Microvillous inclusion disease (in children)
Common variable immunodeficiency
126
Q

Complications of coeliac disease

A 
Malabsorption
Osteomalacia and osteoporosis
Neurological disease
Epilepsy
Cerebral calcification
Lymphoma
Hyposplenism
127
Q

Autoimmune and other conditions associated with coeliacs disease

A

Dermatitis herpetiformis (prevalence = 100%)
Type 1 diabetes mellitus (prevalence = 7%)
Autoimmune thyroid disease
Down’s syndrome

128
Q

Neurosurgery:

What is a Stereotactic biopsy?

A

I biopsy of an inoperable tumour.
Stereotactic neurosurgery involves mapping the brain in a three dimensional coordinate system. With the help of MRI and CT scans and 3D computer workstations, neurosurgeons are able to accurately target any area of the brain in stereotactic space (3D coordinate system). Stereotactic brain biopsy is a minimally invasive procedure that uses this technology to obtain samples of brain tissue for diagnostic purposes.

129
Q

Neurosurgery:

What is an open biopsy?

A

A biopsy of an inoperable but approachable tumour.

130
Q

How to name a CNS tumour

A

Names derive from putative cell of origin

Differentiation

Descriptive

131
Q

Grading of CNS tumours is based on…

A

Outcome: survival time

132
Q

Grades of CNS tumour (and brief description of each)

A

Long-term survival / cured – Grade I
Cause death in more than 5 yrs – Grade II
Cause death within 5 yrs – Grade III
Cause death within 6 mo-1yr – Grade IV

133
Q

WHO grading system for CNS tumours is only reliable for…

A

Diffuse astrocytomas and meningiomas

134
Q

Most common type of primary CNS tumour in adults

A

Gliomas

135
Q

Types of gliomas

A

Diffuse infiltration
Fibrillary, gemistocytic astrocytoma (all grades)
Oligodendroglioma (all grades)
Mixed oligo-astrocytoma

Compressive margins
Pilocytic astrocytoma
Pleomorphic xantoastrocytoma
Subependymal astrocytoma
-------------------------------------
Ganglioglioma
Ependymoma
136
Q

Infiltrative gliomas: possible grades

A

2-4

137
Q

Most aggressive form of glioma

A

Glioblastoma (GBM)

138
Q

Types of glial cells

A 
Glial cells are non neuronal cells. They include: 
Oligodendrocytes
astrocytes
ependymal cells 
Microglia,

In the peripheral nervous system glial cells include: Schwann cells and satellite cells.

139
Q

80% of gliomas are which specific type?

A

Diffuse astrocytomas

140
Q

Mutation of… is present in 80% of cases of diffuse astrocytomas

A

IDH1

141
Q

Features of diffuse astrocytomas

A

Infiltrative
Most commonly in cerebral hemispheres but can be found elsewhere e.g. cewrebellum (10%) and brainstem (more common in children/young adults)
WHO grade 2, progressing in 5-7 years to grade 4 GBM
Most common in ages 30-40
Low vascularity but endothelial and capillary proliferation
No necrosis at core
IDH1 mutation in 80%

142
Q

About …% of glioblastomas develop from a lower grade astrocytoma

A

10%

143
Q

Features of an oligodendroglioma

A

5% of all primary brain tumours
Almost exclusively in cerebral hemispheres – frontal lobe in 50-60% of cases
WHO grade II – Anaplastic WHO grade III – difficult grading
Presents with long history of neurological signs – seizure is more frequent
Extends to grey matter
Chemosensitive

Better prognosis than astrocytomas – resection is important

80% mutation of IDH1; 75% codeletion 1p19q; usually normal p53

144
Q

Features of pilocytic astrocytoma

A

WHO grade I
Usually 1st and 2nd decade - 20% of CNS tumours below 14 years and 15% between 14-18 years
Often cerebellar, optic-hypothalamic, brain stem
Often cystic. Always contrast enhancement
They can disseminate in the subarachnoid space (es: follow nerve roots)
Compressive margins (never diffuse infiltration)
Always show marked nuclear atypia and vascular/endothelial proliferation
Very often Rosenthal fibres (eosinophilic/pink staining) and granular bodies
Hallmark: Piloid “hairy” cell

145
Q

WHO definition of a medulloblastoma

A

A malignant, invasive embryonal tumour of the cerebellum with preferential manifestation in children, predominantly neuronal differentiation, and an inherent tendency to metastasize via CSF pathway

146
Q

Features of a medulloblastoma

A

Rare (0.5 per 100,000 year, in children)
75% arise in the vermis in children and hemispheric in adults
Present with cerebellar signs, cranial hypertension
WHO grade IV

147
Q

Medulloblastomas present with…

A

Cerebellar signs, cranial hypertension

148
Q

Features of meningiomas

A 
24-30% primary intracranial tumours
Incidental in up to 10% of post-mortem
Usually adults – rare in patients younger than 40 (more aggressive)
Focal symptoms (seizure, compression)
Any site of craniospinal axis
149
Q

Grading of meningiomas based on histology (and projected outcome)

A 
Grade I – benign
Grade II (atypical) – 20% of meningiomas; 40% recurrence
Grade III (anaplastic) – 1% of meningiomas; often lethal in 1 year
150
Q

What is the virchow robin space?

Why is important in CNS tumours?

A

It is the immunological space between an artery and vein and the pia mater. It can be expanded by leucocytes.

Psueudoinvasion of meningiomas can occur along the space.

151
Q

Commonest type of CNS tumour

A

Metastases/secondary

152
Q

Tumours that most commonly metastasise to the CNS

A

Lung ca, melanoma, breast ca, renal ca and colon ca.

153
Q

ICP is measured in mmHg and at rest, is normally…

mmHg for a supine adult

A

7–15

154
Q

CSF is produced by…

A

Choroid plexus: 70-80%
Ependyma and subarachnoid vessels
Parenchymal capillaries

155
Q

Normal CSF volume is…

A

90-150ml

156
Q

Types of hydrocephalus

A

Non-obstructive/communicating: reduced reabsorption

Obstructive/non-communicating: Actual obstruction to flow of CSF

157
Q

70-80% of strokes are which type?

A

Ischaemic

158
Q

Embolic occlusion leading to stroke usually occurs in which vessels

A

Middle cerebral artery branches

159
Q

Non-traumatic intraparenchymal haemorrhage most commonly occurs in…

A

Most common in basal ganglia

160
Q

Risk factors for non-traumatic intraparenchymal haemorrhage

A

HTN (over 50% of bleeds)
Atherosclerosis
clotting disorders, neoplasms, amyloid, vasculitis, vascular malformations

161
Q

Signs/symptoms of intraparenchymal haemorrhage

A

Raised intracranial pressure; severe headache, vomiting, rapid loss of consciousness; focal neurology

162
Q

Cerebral AVMs present with… they become symtomatic between ages of…

A

Haemorrhage, seizures, headache, focal neurological deficits
20-50

(the risk if bleeding is around 1% annually but rises if bleed occurs. The risk of re-bleed is around 6% annually)

163
Q

What is a cavernous angioma?

A

Well-defined malformative lesion composed of closely packed vessels with no parenchyma interposed between vascular spaces

(so basically a cavernous space filled with vessels)

164
Q

Features of a cavernous angioma

A

Presents after 50
Has a few feeding vessels
Bleeds at low pressure
Present with headache, seizures, focal deficits, haemorrhage (similar to an AVM)
Angiography is usually NEGATIVE unlike AVM
Treatment is surgical

165
Q

Types of brain herniation

A

Transtentorial (uncal gyral, mesial temporal) – medial temporal lobe compressed against the free margin of the tentorium cerebelli

Subfalcine (cingulate gyrus) – cingulate gyrus displaced under the falx cerebri

Tonsillar – cerebellar tonsils through the foramen magnum, this causes brain stem compression

166
Q

Cause of most sub-arachnoid haemorrhages

A

Berry aneurism.

(In most of the 1% of people who have them they cause no problems.
Berry aneurisms tend to occur in the circle of willis at the junctions of the large vessels: most of them occur (80%) at the internal carotid artery bifurcation. The other 20% occur in the posterior circulation (vertibrobasilar circulation))

167
Q

Common locations of berry aneurisms

A

Berry aneurisms tend to occur in the circle of willis at the junctions of the large vessels: most of them occur (80%) at the internal carotid artery bifurcation. The other 20% occur in the posterior circulation (vertibrobasilar circulation)

168
Q

…% of people with berry aneurisms have multiple ones.

A

30%

169
Q

Risk factors for berry aneurisms

A

Autosomal dominant polycystic kidney disease

(ADPKD)Ehlers-Danlos syndrome (type IV)
Marfan syndrome (controversial 3) 
coarctation of aorta 
bicuspid aortic valve
neurofibromatosis type 1 (NF1) 
hereditary haemorrhagic telangiectasia
alpha 1 antitrypsin deficiency 
cerebral arteriovenous malformation: a flow related aneurysm
fibromuscular dysplasia
170
Q

% of people who die within days of a berry aneurism bleed

A

50% die within a few days, “Warning Bleed”

Prognisis worse if rupture after a warning bleed

171
Q

Components of GCS (just the responses tested)

A 
eye response	(max 4)
verbal response (max 5)
motor response (max 6)
172
Q

Subdural bleeds are due to bleeding from which type of vessel?

A

Veins.

173
Q

Most extradural bleeds originate from which vessels

A

Meningeal arteries,

174
Q

Unique feature of prion diseases

A

Proteinaceous infection only. No DNA or RNA involved.

175
Q

List prion diseases found in humans

A

Creutzfeldt-Jakob disease
Gerstmann-Straüssler-Sheinker syndrome
Kuru
Fatal familial insomnia

176
Q

Features of new varian CJD

A

Sporadic neuropsychiatric disorder

Patients

177
Q

What is Gerstmann-Straüssler-Sheinker syndrome?

A

A familial version of CJD

178
Q

Neuropathology of Alzheimer’s disease

A 
Extracellular plaques (protein deposition)
Neurofibrillary tangles (within neurons) 
Cerebral amyloid angiopathy (CAA)
Neuronal loss (cerebral atrophy)
179
Q

Key proteins in Alzheimer’s disease

A

A-beta peptide.

Tau

180
Q

A-Beta peptide is part of which protein

A

Amyloid precursor protein

Notes: Role of APP unclear but is is physiological. The processing of the precursor protein can be amyloidogenic, in which case inact ABeta protein is released and can begin forming plaques.

181
Q

Which form of tau is pathological

A

Hyperphosphororylated tau is the pathological form.

182
Q

How is amyloid plaque formed in Alzheimer’s disease

A

Amyloid precursor protein is processed. The processing of the precursor protein can be amyloidogenic, in which case inact ABeta protein is released. If a cell produces too much A beta it releases it, the A beta can then begin forming plaques.

183
Q

Alzheimer’s disease usually starts in which lobe?

A

Temporal (amnesia)

Then progresses to parietal (difficulty dressing)
Then frontal (personality changes)
The occipital (difficulty recognising people)
184
Q

What is Braack staging used for?

A

Staging of alzheimer’s disease according to progression of tau pathology.

Stages 1 to 6. Disease starts in anterior hippocampus, spreads to posterior hippocampus, then temporal cortex, then occipital cortex.

Staging of Parkinson’s using alpha synuclein. Stages 1-6.

185
Q

Key protein in Parkinson’s disease

A

α-synuclein

Lewy bodies are immunopositive for this

186
Q

Causes of parkinsonism

A 
Idiopathic Parkinson’s disease
Drug-induced Parkinsonism
Multiple system atrophy 
Progressive supranuclear palsy
Corticobasal degeneration
Vascular pseudoparkinsonism 
Alzheimer’s changes
Fronto-temporal neurodegenerative disorders 
20 other disorders
187
Q

Features of Pick’s disease

A

Fronto-temporal atrophy (problems with decision making)
Marked gliosis and neuronal loss
Balloon neurons
Tau positive Pick bodies

188
Q

Neurodegenerative diseases where Tau is a major protein

A

Alzheimer’s
Pick’s disease

Progressive supranuclear palsy
Corticobasal degeneration

189
Q

Neurodegenerative diseases where alpha synuclein is a major protein

A

Parkinson’ disease

Multiple system atrophy (affects glial cells)

190
Q

The anterior pituitary secretes

A 
Prolactin 
ACTH 
TSH
GH
FSH
LH
191
Q

Pituitary adenomas are microadenomas if less than…

A

1cm

192
Q

Peak age of pituitary adenoma incidence

A

40-60 years

193
Q

Clinical features of growth hormone adenomas

A

Prepubertal children - gigantism
Adults - acromegaly
Diabetes mellitus, muscle weakness, hypertension, congestive cardiac failure

Bitemporal hemianopia

194
Q

What is Sheehan’s syndrome

A

Hypopituitarism caused by ischaemic necrosis following PPH (pituitary enlarges during pregnancy).

195
Q

Most cases of hypopituitarism caused by…

A

Nonsecretory pituitary adenomas – compress the other cells that do produce hormones

196
Q

Clinical manifestations of anterior pituitary hypofunction

A

Children - growth failure (pituitary dwarfism)
Gonadotrophin deficiency - amenorrhea and infertility in women. Decreased libido and impotence in men
TSH and ACTH deficiency - hypothyroidism and hypoadrenalism
Prolactin deficiency - failure of post-partum lactation

197
Q

The posterior pituitary releases…

A

antidiuretic hormone (ADH) and oxytocin

198
Q

Role of calcitonin

A

promotes absorption of calcium by the skeletal system

199
Q

Calcitonin is synthesised by…

A

Thyroid contains a population of parafollicular or ‘C’ cells that synthesize calcitonin

200
Q

Non-thyroid disease associated causes of thyrotoxicosis

A 
Struma ovarii (ovarian teratoma with ectopic thyroid)
Factitious thyrotoxicosis (exogenous thyroid intake)
201
Q

Most common cause of endogenous hyperthyroidism is…

A

Graves disease

202
Q

Grave’s disease triad

A

Thyrotoxicosis
Infiltrative ophthalmopathy with exophthalmos in up to 40%
Infiltrative dermopathy (pretibibial myxoedema) in a minority of cases

203
Q

Most cases of thyroid carcinoma are…

Anaplastic
Follicular
Medullary or
Papillary

A

Papillary (75-85%)
Follicular (10-20%)
Medullary (5%)
Anaplastic (

204
Q

Ionising radiation increases the risk of…. thyroid carcinomas

A

papillary

205
Q

Histological features of papillary carcinoma

A

May have papillary architecture (but not all)
BUT diagnosis is based on nuclear features
Optically clear nuclei
Intranuclear inclusions
May be psammoma bodies (calcification)

206
Q

Clinical features of papillary thyroid carcinomas

A 
Nonfunctional
Present as painless mass in neck
May present with metastasis in cervical lymph node
May present with swollen lymph nodes
10 year survival up to 90%
207
Q 
Peak age of thyroid carcinoma incidence:
Papillary
Follicular
Anaplastic 
Medullary
A

Any age
Middle age
Elderly patients
50-60

208
Q

Histological features of follicular thyroid carcinoma

A

Follicular morphology
May be well demarcated with minimal invasion or clearly infiltrative
(spreads early)

209
Q

Follicular thyroid carcinoma usually metastasises via bloodstream to..

A

Bone, liver, lungs

210
Q

Histological features of medullary thyroid carcinoma

A

Neuroendocrine neoplasm derived from parafollicular C cells

Calcitonin produced is broken down and deposited as amyloid. Congo red dye can be used to show amyloid

211
Q

Medullary thyroid cancer is associated with MEN….

A

2

212
Q

Which type of thyroid carcinoma usually causes death within a year?

A

Anaplastic

213
Q

Parathyroid hyperplasia is associated with MEN…

A

1

214
Q

Normal parathyroid gland is …% fat

A

50

215
Q

Clinical manifestations of hypoparathyroidism

A

Neuromuscular irritability - tingling, muscle spasms, tetany
Cardiac arrhythmias
Fits
Cataracts

216
Q

Adrenal cortex contains…. cells

Adrenal medulla contains… cells

A

Cortex – epithelial cells

Medulla – neural cells

217
Q

Zones of adrenal gland from outside to in

A

Zona glomerulosa
Zona fasciculata
Zona reticularis
Medulla

218
Q

The adrenal medulla secretes

A

Adrenaline and noradrenaline

219
Q

Zona glomerulosa (of adrenal gland) secretes

A

Aldosterone

220
Q

Zona fasciculata (of adrenal gland) secretes

A

Glucocorticoids

221
Q

Zona reticularis (of adrenal gland) secretes

A

Androgens and glucocorticoids

222
Q

Most cases of Cushing’s syndrome caused by

A

Most cases caused by administration of exogenous glucocorticoids

223
Q

Effect of iatrogenic (administration of exogenous glucocorticoids) Cushing’s syndrome on adrenals. Contrast with Cushing’s disease

A

PCS – adrenals become hyper plastic (also with paraneoplastic cushings)
ICS – adrenal atropy

224
Q

Most cases of primary hyperaldosteronism due to…

A

Bilateral adrenal hyperplasia

225
Q

What is Waterhouse-Friderichson syndrome?

A

Adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically the pathogen is the meningococcus Neisseria meningitidis

226
Q

3 Causes of acute adrenal insufficiency

A

Sudden withdrawal of corticosteroid therapy
Haemorrhage (neonates)
Sepsis with DIC (Waterhouse-Friderichson syndrome)

227
Q

Features of adrenocortical carcinomas

A

Carcinomas
Rare
Usually large
More commonly associated with virilizing syndrome than adenoma

228
Q

Phaeochromocytoma rule of 10s

A

10% arise in association with a familial syndrome inc. MEN 2A and 2B, von Hippel-Lindau disease and Sturge-Weber syndrome
10% are bilateral
10% are malignant
In addition 10% of catecholamine-secreting tumours arise outside the adrenal (paragangliomas)

229
Q

What is Von Hippel-Lindau (VHL) disease?

A

Von Hippel-Lindau (VHL) disease is an inherited disorder causing multiple tumours, both benign and malignant, in the central nervous system (CNS) and viscera. The most common tumours are retinal and CNS haemangioblastomas, renal cell carcinoma (RCC), renal cysts and phaeochromocytoma.

230
Q

Tumours associated with the MEN sydromes are more or less aggressive than sporadic tumours?

A

More aggressive

231
Q

Dose of ACTH in short synacthen test

Describe test

A

250mcg

Measure cortisol + ACTH at start of test

Administer 250 micrograms synthetic ACTH by IM injection.

Check cortisol at 30 and 60 minutes.

232
Q

Genes associated with polycystic kidney disease

A

PKD1

PKD2

233
Q

Renal failure due to PKD develops at what age?

A

Renal failure develops from 40-70 years

234
Q

How is acute renal failure classified (what are the categories, and examples)?

A

Pre-renal
Failure of perfusion

Renal
Acute tubular injury
Acute glomerulonephritis
Thrombotic microangiopathy

Post-renal
Obstruction to urine flow

235
Q

Why does acute renal tubular injury cause failure of glomerular filtration?

A

Blockage of tubules by casts
Leakage of fluid from tubules to interstitium reducing flow
Secondary haemodynamic changes

236
Q

Glomerulonephritis sufficiently severe to cause renal failure is almost always associated with…

A

Glomerular crescents

237
Q

Glomerulonephritis presents with…

A

Presents with oliguria with urine casts containing red and white blood cells

238
Q

Acute glomerulonephritis

A

Acute inflammation of glomeruli leading to reduction in glomerular filtration

239
Q

Crescentic glomerulonephritis is….

A

Rapidly progressing glomerulonephritis. It is characterised by a progressive rapidly deteriorating in kidney function

240
Q

Causes of crescentic glomerulonephritis

A

Immune complex: SLE, IgA nephropathy, post-infectious GN

Anti-GBM disease

Pauci-immune – associated with anti-neutrophil cytoplasm antibodies (ANCA)

241
Q

What is pauci-immune glomerulonephritis

A

A type of crescentic glomerulonephritis associated with ANCAs in which only scanty deposits of immunoglobulin and complement are present in glomeruli.

The ANCA anatibodies cause neutrophil activation which leads to glomerular necrosis. The condition also involves vasculitis in other organs e.g. lungs (haemorrhage).

It is associated with causes of vascular inflammation including Wegener granulomatosis and microscopic polyangitis

242
Q

Brief pathogenesis of renal thrombotic microangiopathy

A

Red blood cells may become damaged by fibrin leading to haemolysis – microangiopathic haemolytic anaemia

Diarrhoea associated
Caused by bacterial gut infection – usually E. coli
Releases toxin that targets the renal endothelium

Non-diarrhoea associated
Often associated with abnormalities of proteins that control activation of the complement pathway on endothelium
May be familial

243
Q

Nephrotic syndrome involves proteinuria above…

A

3.5g/24h

244
Q

Features of nephrotic syndrome

A

Breakdown of selectivity of the glomerular filtration barrier leading to massive protein leak

Key features:
Proteinuria > 3.5g/day
Hypoalbuminaemia
Oedema

Also Hyperlipidaemia

245
Q

Systemic causes of nephrotic syndrome

A

Diabetes mellitus
Amyloidosis
SLE

246
Q

Local (primary glomerular disease) causes of nephrotic syndrome

A

Minimal change disease
Focal and segmental glomerulosclerosis
Membranous glomerulonephritis

247
Q

How to test for amyloid deposits (histology)

A

Stains with Congo red stain and looks green under polarised light (apple green birefringence)

248
Q

Commonest amyloid proteins in kidney

A

AL (amyloid light chains) derived from Ig light chains

SAA: serum amyloid associated protein. Acute phase protein raised in certain chronic inflammatory conditions e.g. RA

249
Q

80% of patients with AL (amyloid light chains) will have…

A

Multiple myeloma

250
Q

Nephrotic syndrome: Histological changes of minimal change disease:
Electron microscopy
Light microscopy
immunofluorescence

A

Glomeruli look normal apart from loss of podocyte foot processes on electron microscopy

No changes on light microscopy

No immune deposits visible

251
Q

Commonest cause of nephrotic syndrome in children is….

A

Minimal change disease

252
Q

Which PRIMARY cause of nephrotic syndrome responds best to steroids…

A

Minimal change disease

253
Q

Which PRIMARY cause of nephrotic syndrome responds least to steroids…

A

Membranous glomerular disease

254
Q

Nephrotic syndrome: Histological changes of membranous glomerular disease

Electron microscopy
Light microscopy
Immunofluorescence

A

Light microscopy: Diffuse glomerular basement membrane thickening

Electron microscopy: Loss of podocyte foot processes and subepithelial deposits (spikey)

Immunofluorescence: Ig and complement in granular deposits along entire glomerular basement membrane

255
Q

Nephrotic syndrome: Histological changes of focal segmental glomerularsclerosis

Electron microscopy
Light microscopy
Immunofluorescence

A

Electron microscopy: Loss of podocyte foot processes

Light microscopy: Focal and segmental glomerular consolidation and scarring. Hyalinosis.

Immunofluorescence: Ig and complement in scarred areas

256
Q

Primary causes of membranous glomerulonephritis

A

Many associated with antibodies to phospholipase A2 receptor

257
Q

Secondary causes of membranous glomerulonephritis

A

SLE
Infection
Drugs
Malignancy

258
Q

Manifestations of thin basement membranes

A

Hereditary defect in type IV collagen

In most cases microscopic haematuria is the only consequence

259
Q

Commonest form of glomerulonephritis worldwide is…

A

IgA nephropathy

260
Q

Normal GFR is above…

A

90

261
Q 
Stages of chronic kidney disease. GFR in: 
Stage 1
Stage 2
Stage 3
Stage 4
Stage 5
A 
Stage 1: >90 (normal)
Stage 2: 60-89 (mild)
Stage 3: 30-59 (moderate)
Stage 4: 15-29 (severe)
Stage 5:
262
Q

Top 5 causes of chronic renal failure

A

Diabetes (19.5%)
Glomerulonephritis (15.3%)
Hypertension & Vascular disease (15%)
Reflux nephropathy (chronic pyelonephritis) (9.5%)
Polycystic kidney disease (9.4%)

263
Q

List 4 malignant bone tumours

A

Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma
Giant cell (borderline malignancy)

264
Q 
Features of osteosarcoma: 
Age peak 
Bone(s) commonly affected 
Histology features
X ray appearance
A

Adolescence

Knee (60%)

Malignant, mesenchymal cells, ALP positive

Elevated periosteum (Codman’s triangle), Sunburst appearance

265
Q 
Features of chondrosarcoma 
Age peak 
Bone(s) commonly affected 
Histology features
X ray appearance
A

> 40 years

Axial skeleton
Femur/ tibia/ pelvis

Malignant chondrocytes

Lytic lesion with fluffy calcification, axial skeleton

266
Q 
Features of Ewing's sarcoma 
Age peak 
Bone(s) commonly affected 
Histology features
X ray appearance
A
267
Q

Genetic mutation found in most cases of Ewing’s sarcoma

A

Translocation 11:22 (which fuses the EWS gene of chromosome 22 to the FLI1 gene of chromosome 11)

268
Q

Presentation of Ewing’s sarcoma

A

Localized pain, swelling, and sporadic bone pain with variable intensity

Signs and symptoms of systemic inflammatory illness such as fever, anaemia and leucocytosis.

269
Q

Presentation of osteosarcoma

A

Pain that may be worse at night
Pain in femur or immediately below the knee
Pathological fractures

270
Q

Signs/symptoms of chondrosarcoma

A

Back or thigh pain
Sciatica
Bladder Symptoms
Unilateral oedema

271
Q

Malignant bone tumours more common in middle age/older people

A

Chondrosarcoma

272
Q 
Features of Giant cell tumour of bone
Age peak 
Bone(s) commonly affected 
Histology features
X ray appearance
A

20-40 years (F>M)

Knee epiphysis

Osteoclast tyoe multinucleate giant cells on background of spindle/ovoid cells. Usually NOT malignant.

Lytic/lucent lesions right upto articular surface

273
Q

What is osteosarcoma?

A

An osteosarcoma is a cancerous tumor in a bone. Specifically, it is an aggressive malignant neoplasm that arises from primitive transformed cells of mesenchymal origin (and thus a sarcoma) and that exhibits osteoblastic differentiation and produces malignant osteoid

274
Q

What is chondrosarcoma?

A

Chondrosarcoma is a cancer composed of cells derived from transformed cells that produce cartilage. Resistant to chemotherapy and radiotherapy.

275
Q

What is Ewing’s sarcoma?

A

A malignant small, round, blue cell tumor. It is a rare disease in which cancer cells are found in the bone or in soft tissue. The most common areas in which it occurs are the pelvis, the femur, the humerus, the ribs and clavicle (collar bone)

276
Q 
Features of osteoid osteoma (adolescent)
Bone affected 
Special features 
Histology 
X ray
A

Tibia/femur

Small benign bone forming lesion, night pain releived by aspirin.

Normal bone

Radiolucent nidus with sclerotic rim

277
Q 
Features of osteoma (middle age) 
Bone affected 
Special features 
Histology 
X ray
A

Head and neck

Bony outgrowths attached to normal bone 
Gardners syndrome (a subtype of FAP): multiple osteomas, GI polyps, and epidermoid cysts

Normal bone

Radiolucent nidus with sclerotic rim

278
Q 
Features of osteochondroma 
Age affected
Bone affected 
Special features 
Histology 
X ray
A

Adolescent (develop during skeletal growth and cease when the growth plates fuse at puberty)

Long bones

Cartilage capped bony outgrowth
Hereditary multiple exostoses: multiple exostoses (bony spurs), short stature, and bone deformities.

Cartilage capped bony outgrowth

Well defined bony protuberance from bone.

279
Q

What is diaphyseal aclasis?

A

Hereditary multiple exostoses (HME or MHE), also known as diaphyseal aclasis, is a rare medical condition in which multiple bony spurs or lumps (also known as exostoses, or osteochondromas) develop on the bones of a child. HME is synonymous with multiple hereditary exostoses and multiple osteochondromatosis

280
Q 
Features of enchondroma 
Age affected
Bone affected 
Special features 
Histology 
X ray
A

Middle age

Hands

Benign tumours of cartilage.
Ollier’s syndrome: multiple enchondromas
Maffuci’s syndrome: multiple enchondromas and haemangiomas

Normal cartilage

Lytic lesion, cottom wool calcification, expansile, O ring sign.

281
Q

What is Ollier’s syndrome?

A

Multiple enchondromas

282
Q

What is Maffuci’s syndrome?

A

Multiple enchondromas and haemangiomas

283
Q 
Features of fibrous dysplasia 
Age affected
Bone affected 
Special features 
Histology 
X ray
A

Middle age (F>M)

Femur

A bit of bone is replaced by fibrous tissue.
Albright syndrome: polyostotic dysplasia, cafe au lait spots, precocious puberty.

Chines letters (misshapen bone trabeculae)

Soap bubble osteolysis
Shepherd’s crook deformity

284
Q

Features of sarcoidosis (by organ system)

A

Skin: Lupus pernio, erythema nodosum

CNS: Meningitis, cranial nerve lesions

Eyes: Uveitis, keratoconjunctivitis

Parotids: Bilateral enlargement

Lungs: BHL (bilateral hilar lymphadenopathy), fibrosis, lymphocytosis (CD4+ in BAL)

Liver: Hepatitis, cholestasis & cirrhosis

285
Q

3 key lab features of sarcoidosis

A

Hypergammaglobulinaemia
Raised ACE
Hypercalcaemia (due to Vit D hydroxylation by activated macrophages)

286
Q

Clinical features of Kawasaki’s disease

A 
Fever
Erythema of palms & soles, desquamation
Conjunctivitis
Lymphadenopathy
Coronary arteries may be affected (MI)
otherwise disease is self limiting
287
Q

Features of polyarteritis nodosa

A 
Necrotising arteritis
Polymorphs, lymphocytes, eosinophils
Arteritis is focal and sharply demarcated
Heals by fibrosis
More often renal and mesenteric arteries

Nodular appearance on angiography (small aneurysms

288
Q

Polyarteritis nodosa usually happens in which arteries?

A

renal and mesenteric arteries

289
Q

Cause of histological ‘Onion skin’appearance in scleroderma skin histology

A

Intimal thickening of small arteries

290
Q

What is dyskaryosis

A

Abnormal cytologic changes of squamous epithelial cells characterized by hyperchromatic nuclei and/or irregular nuclear chromatin. May be followed by the development of a malignant neoplasm.

291
Q

Cell type in the ectocervix

A

The ectocervix is covered with nonkeratinized stratified squamous epithelium

292
Q

Precancerous changes in the ectocervix squamous cells is known as

A

Cervical intraepithelial neoplasia, CIN

293
Q

Grades of cervical intraepithelial neoplasia

Importance

A

CIN1
CIN2
CIN3

The risk of developing cancer is related to the grade of CIN. Most cases of CIN1 will go back to normal without any treatment.
CIN2 and CIN3 may develop into cancer in some cases, if left untreated

294
Q

Cervical Glandular Intraepithelial Neoplasia is

A

Pre-cancerous change involving the inner glandular cells of the cervix.

295
Q

Women of what ages are invited for cervical screening

A

25-65

296
Q

Cervical screening is repeated every … years

A

3-5

297
Q

NHS cervical screening programme triage system

A

Low grade and borderline abnormalities have a HR-HPV test.
If HR-HPV positive – refer to colposcopy
If HR-HPV negative – routine recall
High grade abnormalities refer to colposcopy – no HR-HPV test

298
Q

90% of genital warts caused by which HPV subtypes?

A

6 and 11

299
Q

HPV subtype that cause most cervical cancers

A

16 and 18

Approx 70% of cervical cancers

300
Q

Effect of smoking on HPV

A

Smoking can make clearing HPV from the body less effective and can make clearance of minor smear abnormalities slower and less efficient

301
Q

General uses of fine needle aspirations (cytology)

A 
Immediate on site evaluation
Primary diagnosis
Rules out other diagnoses
Staging
Post adjuvant therapy staging
Differentiate a new primary from recurrence
302
Q

Advantages of cytology fine needle aspiration

A 
Accurate
Quick
Acceptable to patient
Rapid turnaround time
Organised into fast access clinics run by cytopathologists for aspiration of palpable swellings

Cheap
Triage material for ancillary tests
On-site diagnosis allows immediate patient management

Year 5 Pathology (7 decks)

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