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MRCS > Pathology 2 > Flashcards

Pathology 2 Flashcards

1
Q

What is the epithelium of the oesophagus

A

Non keratinised stratified squamous epithelium

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2
Q

What are risk factors for squamous cell carcinoma of the oesophagus

A

ETOHXS
Smoking
Low vitamin A
Chronic achalasia

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3
Q

What are the risk factors for adenocarcinoma of the oesophagus

A

Barrett’s oesophagus
GORD
Obesity
High fat diet

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4
Q

Describe simply the pathology of squamous cell carcinoma of the oesophagus

A

Hyperplasia, leading to dysplasia then carcinoma sequence

Found in the middle/upper third of the oesophagus

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5
Q

Describe simply the pathology of adenocarcinoma of the oesophagus

A

Metaplasia, dyplasia and then carcinoma

Found in the lower third of the oesophagus

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6
Q

GORD is related to the development of what malignancy

A

Adenocarcinoma of the oesophagus

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7
Q

What happens to the oesophageal epithelium in Barrett’s oesophagus

A

Change in the normal epitheliumm of the oesophagus to specialised intestinal metaplasia

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8
Q

What stain is used in immunohistochemistry

A

Cytokeratin

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9
Q

In what T stage is oesophageal carcinoma invasive to surrounding structures

A

T4

T4a - invades resectable structures - pleura, pericardium, diaphragm
T4b - invades unresectable structures - aorta, trachea, vertebral body

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10
Q

What is the difference with nodal stage 1-3 in oesophageal cancer

A

N1 - 1-2 positive LN
N2 - 3-6 positive LN
N3 - >7

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11
Q

At what T stage is oesophageal carcinoma invasive to the muscle, and what stage is it invasive to the adventitia

A

T2 - invasion to the muscularis propriety
T3 - invasion to the adventitia

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12
Q

What are the histological grades of oesophageal cancer

A

G1 - well differentiated
G2 - moderately differentiated
G3 - Poorly differentiated
G4 - undifferentiated

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13
Q

What could cause a pleural effusion in a patient with gastric cancer

A

Spread of lung cancer cells to pleura
Lung metastasis
Obstruction to the thoracic duct

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14
Q

What is Lights Criteria for and what is it composed of

A

Lights criteria for assessment of exudation

Effusion: Serum protein >0.5
Effusion: Serum LDH >0.6
Effusion LDH - upper 2/3 of reference range

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15
Q

What are the palliative options in managing pleural effusions

A

Thoracocentesis
Indwelling pleural catheters
Pleuradesis
Pleuroperitoneal shunting

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16
Q

FNAC of a malignant LN in a patient with oesophageal cancer would show what

A

Metastatic adenocarcinoma with tumour cells having hyper chromatic eccentric nuclei and intralytoplastmic vaculations

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17
Q

Describe the following histopathology report in layman’s terms - max 4 sentences

Signet ring carcinoma
Positive LN
Margin positive
Spleen involved

A

Cancer of the stomach which has spread to the lymph nodes and the spleen
Incomplete resection
High possibility of recurrence
Patient will require further resection/chemo

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18
Q

Describe in brief the pathogenesis of gastric cancer

A

Normal mucosa
Chronic gastritis
Intestinal metaplasia
Dysplasia
Intramucosal carcinoma
Invasive gastric carcinoma

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19
Q

What is the most common type of gastric cancer

A

Adenocarcinoma

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20
Q

What types are included in the WHO classification of gastric adenocarcinoma

A

Signet cell carcinoma
Tubular carcinoma
Papillary adenocarcinoma
Mucinous adenocarcinoma
Mixed carcinoma

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21
Q

What is the Lauren Classification of Adenocarcinoma

A

Classification of gastric adenocarcinomas

Intestinal - tumours are well differentiated, grow slowly and tend to form glands
Men > women, older patients

Diffuse - tumour cells are poorly differentiated, behave aggressively and tend to scatter through the stomach
Younger patients

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22
Q

What is the Barmann classification for gastric cancer

A

Classifies the macroscopic appearances of the lesion

Polypoid growth
Fungating growth
Ulcerating growth
Diffusely infiltrating growth

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23
Q

Linitis plasticus is an example of what type of growth

A

Diffusely infiltrating growth

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24
Q

What paraneoplastic syndromes are associated with gastric cancer

A

Acanthosis nigricans
Dermatomyositis

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25
Q

What are the specific complications of a total gastrectomy ? Divide these into early and late complications.

A

Early
Anastamotic leak, pancreatitis, cholecystitis, hameorrhage, infection

Late
Vitamin B12 deficiency, metabolic bone disease, recurrence of malignancy, Dumping syndrome

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26
Q

What is dumping syndrome

A

Loss of the reservoir function of the stomach (eg. following gastrectomy) results in the rapid transit of highly osmotically active substances into the duodenum following meals

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27
Q

What are the symptoms of dumping syndrome

A

Early - 30-60 minutes following a meal - results in bloating, abdominal pain, diarrhoea and vasomotor symptoms

Late 1-3 hours following a meal - sudden absorption of high levels of glucose results in compensatory hyperinsulinaemia - results in subsequent hypo

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28
Q

What is the difference between Duke Stage 2 and 3

A

2 has no LN involvement and 3 does.

A and B refer to the same in both stage, a - no invasion through muscularis whereas b has invasion through muscularis

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29
Q

What are haemorrhoids

A

Swollen/Inflammed anal cushions

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30
Q

Why do haemorrhoids form

A

When the submucosal fibrous ligament which suspend the anal cushions become fragment (as a production of prolonged and repeated downward stress related to straining during defecation) the anal cushions are no longer restrained and can become engorged with blood

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31
Q

How does a thrombus haemorrhoid occur

A

Acute thrombosis results from sudden raised pressure causing rupture of the vascular plexus leading to blood clot at the anal verge

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32
Q

Define melanosis coli

A

Disorder of the pigmentation of the wall of the colon
Benign and may have no significant correlation with disease

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33
Q

What are the risk factors for atherosclerosis

A

Non modifiable - genetic, family history, male, age
Modifiable - Type IIDM, HTN, smoking, hyperlipidemia

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34
Q

Describe briefly the formation of a fibrofatty plaque from a normal artery

A

Insult to arterial wall from one of the aetiological factors, results in increased leucocyte adhesion molecules, exposure of endothelium to LDLs/AGEs. Leucocytes enter and scavenge LDLs/Lipids - development of foam cells and release of proinflammatory marker/molecules.
SMC proliferate and migration of leucocytes to the intima. Fixed atherosclerotic plaque in one of the coronary vessels, results in narrowing/blockage of the lumen

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35
Q

Describe the formation of a thrombus in an atherosclerotic vessel

A

Atheromatous plaque is acutely disrupted
Exposes sub endothelial collagen and necrotic plaques to the bloods.
Platelets adhere, aggregate and activate. Thromboxane A2 and ADP are released, causes further platelet aggregation and vasospasm
Activation of coagulation by exposure of tissue factor and other mechanisms add to a growth thrombus

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36
Q

What are the complications of atherosclerosis

A

Aneurysm and rupture - mural thrombus, embolisation and wall weakening
Occlusion of thrombus - plaque rupture, plaque erosion, plaque haemorrhage, mural thrombosis, embolisation
Crtical stenosis - from progressive plaque growth

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37
Q

What is the pathogenesis of an MI

A

Vascular obstruction, aerobic glycolysis ceases quickly leading to a drop in adenosine triphosphate (ATP) and accumulation of potentially noxious metabolites (lactic acid) in cardiac myocytes
Functional consequence is a rapid loss of contractility which occurs within minute or so of onset of ischaemia. Myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling follow

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38
Q

Define malignant melanoma

A

Malignant neoplasm of melanocytes, mainly arising in skin

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39
Q

What skin conditions are associated with malignant melanoma

A

Xeroderma pigmentosa
Albinism
Giant congenital pigmented naevus
Fitzpatrick type I skin
Dysplastic naevus
Multiple naevi

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40
Q

What are risk factors for malignant melanoma

A

Hutchinson’s melanotic freckles
Immunocompromised patients
PMH of melanoma
Red hair
Skin exposure

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41
Q

What is included in a pathology report for a malignant melanoma

A

Size
Breslow thickness
Depth of invasion
Ulceration, mitosis, lymphovascular involvement
Immunohistochemistry staining

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42
Q

What is Breslows thickness

A

The depth of a malignant melanoma
From the top of the stratum granulosum to the deepest part of the tumour

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43
Q

What is Clarks Level

A

The depth of invasion of a malignant melanom a

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44
Q

What features about a mole would make you concerned

A

Asymmetry
Irregular borders
Multicoloured

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45
Q

Describe the appearance of a BCC

A

Shiny pearly papule/nodule

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46
Q

Describe the appearance of a SCC

A

Hyperkeratotic lesion with crusting and ulceration

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47
Q

What are the poor prognostic features in a melanoma

A

Increased Breslow thickness
Increased depth of invasion
Nodular or amelanotic
Presence of ulceration
Presence of lymphatic/perineural invasion
Present of regional/distant mets
Male
Old age

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48
Q

What gene mutations are found in familial malignant melanoma

A

CDKN2
CDK4
MCIR
BRCA2

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49
Q

What does Breslows thickness implicate in turns of excisions

A

<0.76 mm thickness - 1cm margin
0.76-1mm thickness - 2 cm margin
>1mm thickness - 3 cm margin

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50
Q

How do you ensure adequate margins in excision of malignant melanoma

A

Frozen section
Mohs micro surgery

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51
Q

How would an axillary arm thrombosis present

A

Swelling of the arm

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52
Q

When would you consider catheter directed thrombolysis of a DVT

A

If the clot is <14 days old

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53
Q

What monitoring blood test is required in a patient undergoing catheter directed

A

Monitor Fibrinogen - levels need to be <100mg/dL

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54
Q

What are the indications for an SVC filter

A

Failure of antiocoagulation
Complete contraindication to anticoagulation
Presurgical prophylaxis in the presence of substantial RF

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55
Q

What are the components of Virchows Triad

A

Hypercoagulable state
Venous stasis
Endothelial injury

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56
Q

What is the management of a suspected PE

A

CTPA
SC LMWH
In massive embolism - Thromolysis, embolectomy

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57
Q

What are the differential diagnosis for inguinal lymphadenopathy

A

Cellulitis of the lower extremities
Venereal infections - syphilis, chancroid, herpes, lymphgranuloma venereum
Lymphoma
Metastatic melanoma

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58
Q

What are the different types of melanoma

A

Lentigo maligna
Superficial/spreading flat melanoma
Desmoplastic melanoma
Acral melanoma
Nodular melanoma

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59
Q

Where are acral melanomas found

A

Palms of hands, soles of feet, nail beds

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60
Q

What is a satellite lesion in malignant melanoma

A

A form of local spreading malignant melanoma by contiguity and continuity leading to spreading to the surrounding area
They are found within the zone of the primary lesion

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61
Q

KIT mutations are common in what type of malignant melanoma

A

Melanoma that develop from mucus membranes/melanomas on the hands/feet, melanomas in chronically sun damaged areas such as lentigo malgna melanoma

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62
Q

What should be examined when you are concerned about melanoma

A

Full body examination, including nail beds and soles

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63
Q

What is the treatment for a patient with metastatic melanoma

A

Excision of the primary lesion with safe margins
Block LN dissection
Radiotherapy

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64
Q

What are examples of gram negative diplococci

A

Neiserria sp.
Moraxella catarrhelis
Actintobacter
Haemophilus
Brucellia

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65
Q

What are examples of gram positive diplococci

A

Streptococcus
Enterococcus

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66
Q

What is the diagnostic criteria of SIRS

A

At least 2 or more of the following
Body temp < 36 degrees >38
HR >90
RR >20 or PaCO2 of <4.3
WCC <4 >10
Hyperglycaemia in the absence of DM
Altered mental state

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67
Q

What occurs in acute respiratory distress syndrome

A

Diffuse alveolar damage and lung capillary endothelial injury

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68
Q

Describe a basal cell carcinoma

A

Pearly papule with a central ulcer, with granulation tissue on a base with rolled in edges
Surrounding telangiectasia

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69
Q

Define telangiectasia

A

Dilated sub epidermal blood vessels

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70
Q

What is the natural pathology of BCC

A

Indolent with slow progression
Locally destructive with limited potential to metastasise

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71
Q

What are the treatment options for BCC

A

Surgical:
Cutterage and electrodissection
Excision and primary closure
Cryotherapy
Mohs microsurgery

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72
Q

What is the negative to managing BCC with cryotherapy

A

Cannot obtain a tissue sample

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73
Q

What is the advantage to managing BCC with Mohs micrographic surgery

A

Serial tangential horizontal sections are taken and examined histologically

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74
Q

What are topical management options for BCC

A

Topical photodynamic therapy - delta aminoevulomic acid applied
Topical fluorouracil 5%
Topical imiquinol 5%

75
Q

What management of BCC best prevents recurrence

A

Mohs microscopic surgery

76
Q

What is a common cause of skin graft failure

A

Wound infection
Usually by staph aureus

77
Q

What is the treatment for an active MRSA infection

A

OP - Clindamycin, Amox + Tetracycline/ Linezolid
IP - Vancomycin, Linezolid, Daptomycin, Telovancin

78
Q

What is the treatment for MRSA decolonisation

A

Nasal mupirocin
Chlorohexadine body wash

79
Q

Reed Sternberg cells are found in what condition

A

Hodgkins lymphoma

80
Q

What is the mechanism of lymphatic spread in malignant cells

A

Malignant cells release growth factors, such as VEGF-C to induced lymphatic vessel expansion (lymph angiogenesis) in primary tumours, drains to the sentinel LN causing LN mets

81
Q

What is Sickle Cell Disease

A

Mutation in the beta globin which promotes the polymerisation of deoxygenated haemoglobin
Leads to red cell distortion, haemolytic anaemia, microvascular obstruction and ischaemic damage

82
Q

What is the pathogenesis of sickle cell disease

A

Substitution mutation of valine for glutamic acid at the 6th amino acid residue of beta-globin

83
Q

What are the complications of sickle cell disease

A

Vaso-occlusive criss
Sequestrian crisis
Aplastic crisis
Chronic tissue hypoxia
Increased susceptibility to infection with encapsulated organisms

84
Q

What is the pathogenesis of vast-occlusive crisis

A

Triggered by infection, dehydration and acidosis
Results in hand foot syndrome, acute chest syndrome, stroke and retinopathy, autosplenectomy

85
Q

What is a sequestrian criss

A

Massive entrapment of sickle cells in the spleen which will lead to rapid splenic enlargement and hypovolaemic shock

86
Q

What virus causes an aplastic crisis

A

Parovirus

87
Q

What is the mechanism of autosplenectomy in sickle cell

A

In early childhood the spleen is enlarged by up to 500g by red pulp congestion which is caused by trapping of sickled cells in the cords and sinuses
With time chronic erythrostatsis leads to splenic infarction, fibrosis and progressive shrinkage so that by early adulthood only a small amount of fibrous splenic tissue is left

88
Q

What surgical conditions are associated with sickle cell disease

A

Gallstones
Autosplenectomy
Avascular bone necrosis
Osteomyelitis
Pulmonary HTN
HF

89
Q

Why are sickle cell patients immunocompromised

A

Autosplenectomy leads to an increased risk of infection with encapsulated organisms

90
Q

What are the common organisms that sickle cell patients are at risk of

A

Streptococcus pneumoniae
Haemophilus influenza
Neisseria meningitides

91
Q

What are the high grade brain tumours

A

Gliomas
Glioblastoma multiforme
Medullablastoma

92
Q

What are the visual field defect associated with pituitary tumours

A

Superior hemianopia

93
Q

What are the visual field defects associated with craniopharyngiomas

A

Inferior hemianopia

94
Q

What are the clinical features of brain tumours

A

Headache - worse in the morning
N+V
Seizures
Progressive focal neurological defects
Cognitive/behavioural symptoms
Symptoms relating to the position of the mass - frontal lobe lesion assoc w personality changes, parietal lobe lesion assoc w dysarthria
Papilloedema

95
Q

What is the mode of inheritance of PKD and what genes are implicated

A

AD
PKD 1 and PKD 2

96
Q

Describe the pathogenesis of cyst formation in PKD

A

The cells of the renal tubules divide repeatedly until causing outouching of the tubular wall with the formation of saccular cysts that fills with fluids derived from glomerular filtrate that enters from the afferent tubule segment
Progressive expansion eventually causes most of the emerging cysts to separate form the parent tubule leaving an isolated sac that fills with fluid by transepithelial secretion
The isolated cyst expands relentlessly as a result of continued proliferation with secreation of fluids

97
Q

The mutations PKD 1 and PKD 2effect what type of proteins

A

Polycystin 1, 2
Fibrocystin
Nephrocystin

98
Q

In PKD which other organs may have cysts present

A

Liver
Spleen
Pancreas
Ovaries

99
Q

What are the complications of cystic kidneys

A

Renal failure
Infection
HTN

100
Q

What extra-renal manifestations of PKD can occur

A

Liver cysts
Pancreatic cysts
Brain Aneurysm
Mitral valve prolapse

101
Q

What causes pain in PKD

A

Weight of the kidney dragging on its pedicle
Stretching of the renal capsule by cysts

102
Q

What are the clinical features of PKD

A

Pain
Irregular abdominal pass
Haematuria
Infection
Hypertension
Uraemia

103
Q

What are the differential diagnosis for renal cysts

A

Simple cysts
Acquired cystic kidney disease
VHL
Medullary Sponge Kidney
Tuberous Sclerosis

104
Q

What matching is required prior to a renal transplant

A

ABO blood matching
HLA matching

105
Q

Which HLA matching are the most important

A

HLA - A
HLA - B
HLA - DR

106
Q

Describe hyperacute graft rejection

A

Occurs within a few minutes of clamp release due to preformed Ab
Immediate loss of graft occurs

107
Q

Describe accelerated acute graft rejection

A

Occurs in the first few days following surgery
Involves cellular and AB mediated injury
Commonly causes by presensitisation of the donor

108
Q

Describe acute graft rejection

A

Most common
Seen days-weeks after surgery
Predominately a cell mediated process - lymphocyte predominate
Cellular infiltrates and apoptosis cellularly

109
Q

Describe chronic graft rejection

A

Graft atrophy and atherosclerosis are seen. Fibrosis often occurs as a late event

110
Q

What malignancies are associated with immunosuppression

A

SCC
Cervical Ca
BCC
Lymphoma
Kaposi’s sarcoma

111
Q

What would a pathology report of a testicular teratoma detail

A

Histopathology would show multiple different cell types - due to teratoma having 3 germ cell lines

112
Q

Define cryptochidism

A

Complete/partial failure of the intra-abdominal tests to descend into the scrotal sac and is associated with testicular dysfunction

113
Q

What are the risk factors for cyrptochidism

A

LBW infants
FH
Prematurity
High abdominal pressure - eg. Gastroschisis
Down’s Syndrome

114
Q

How much higher is the risk of testicular cancer with cryptorchidism

A

3-5x higher risk

115
Q

What are the complications of cryptorchidism

A

Infertility
Hernia
Testicular torsion

116
Q

What is the management of testicular teratoma

A

Orchiectomy
Chemotherapy
Orchiopexy on the contralateral testical

117
Q

What are the types of seminomatous tumours

A

Seminomas
Spermatocytic seminoma

118
Q

What are the sex cord stromal tumours

A

Leydig cell tumours
Sertoli cell tumours

119
Q

Describe the spread of testicular teratoma

A

Initially to para-aortic lymph nodes
Following this it is locoregional

120
Q

What are the tumour markers measured in testicular cancer

A

AFP
HCG
LDH

121
Q

Why are tumour markers helpful in testicular cancer

A

Evaluation of testicular masses
Staging - if increased markers after orchidectomy then ?metastatic disease
Assessing tumour burden
Monitoring the response to treatment

122
Q

How does haematoma resolution occur

A

Lysis of clot by macrophages - 1 week
Growth of fibroblasts from into the haematoma - 2 weeks

123
Q

Define metastasis

A

Survival and growth of cells at a site distant from their primary origin

124
Q

Why are patients with malignancies at risk of PE

A

Hypercoagulable state - tumour cells produce and secrete pro-coagulant/fibrinolytic substances which activate the coagulation cascade
Venous stasis - compression of vessels by tumour burden/by increased LN

125
Q

What is a choriocarcinoma

A

Highly malignant testicular tumour

126
Q

What are the cell types in a choriocarcinoma

A

Synctiotrophoblasts
Cytotrophoblasts

127
Q

Which tumour markers are measure in choriocarcinoma

A

B HCG

128
Q

Describe how a prostate biopsy is taken

A

TRUS guided from mid lobe parasagittal plane at the apex, the mid gland and the base bilaterally

129
Q

Why are multiple biopsies required for a prostate biopsy

A

Often only a scant amount of tissue available for histological examination in needle biopsies
Malignant glands may be mixed in with benign gland + histological findings may be subtle

130
Q

What immunohistochemistry is used to differentiate between rectal and prostate cells in a needle biopsy

A

alpha methyl coenzyme A racemase - in prostate ca
CEA - rectal ca

131
Q

What should happen to PSA level following a successful prostatectomy

A

Fall below detectable in 4-6 weeks

132
Q

What causes PSA to rise

A

BPH
Prostatitis
Infarction of nodular hyperplasia
Instrumentation of the prostate
Ejaculation

133
Q

What scoring system is used for Prostate Ca and describe its application

A

Gleason score
Most common and second most common histology is graded and then the numbers are added together
Gleason score 1-5 and then added together - out of 10 in totally

134
Q

What type of bony mets are associated with prostate cancer

A

Sclerotic lesions
Increased bone deposition due to increased osteoblastic activity

135
Q

Describe androgen deprivation in prostate ca

A

The growth and survival of prostate cancer cells are dependent on androgens which bind to androgen receptors and induce the expression of progrowth and survival genes

136
Q

Define an abscess

A

A focal collection of pus that may be caused by seeding of pyogenic organism into a tissue or by secondary infection of necrotic foci

137
Q

Describe the structure of an abscess

A

Wall - granulation tissue
Centre - largely necrotic region rimmed by a layer of preserved neutrophils
Surrounding dialled vessels and fibroblast proliferation indication of attempted repair

138
Q

What organisms can cause abscesses

A

Bacterial
Fungal
Viral
Parasitic

139
Q

What pyrogens are associated with abscesses

A

TNF
IL-1
IL-6

140
Q

How is a fever produced

A

Pyrogens (TNF, IL-1, IL-6) stimulates prostaglandins synthesis in the vascular and perivascular cells of the hypothalamus

141
Q

Define cellulitis

A

Spreading bacterial infection fo the skin which affects the dermis and subcutaneous fat. Characterised by redness, warmth, swelling and pain

142
Q

When should ABx be used in treatment of abscess

A

Evidence of overlying cellulitis
Abscess cavity not been left open to drain freely

143
Q

Define giant cells

A

Multinucleate cells derived from the fusion of multiple activated macrophages

144
Q

What is the macroscopy of LN in inflammation

A

Reactivate follicular hyperplasia

145
Q

What are the causative organisms of osteomyelitis in adults

A

Staph aureus
Enterobacter
Streptococcus

146
Q

Salmonella can cause osteomyelitis in which patient group

A

Sickle cell

147
Q

How is osteomyelitis classified and describe the classification system

A

Cierny Classification

Anatomic location
Host type

148
Q

In the Cierny Classification describe the different stages of anatomical location

A

Stage I - medullary - limited to medullary canal
Stage II - superficial - limited to the external bone, doesn’t penetrate the cortex
Stage III - Localised, penetrates the cortex but stable
Stage IV - Diffuse throughout

149
Q

In the Cierny classification describe the different host types

A

Type A - Normal
Type B - Comrpomised (L - Localised, S - Systemic)
Type C - Treatment worse than the infection

150
Q

How does exogenous osteomyelitis occur

A

Acute - from open #/bone exposed at the time of surgery
Chronic - from neglected wounds - Diabetic feet/Decubitus ulcers

151
Q

How does Haematogenous osteomyelitis occur

A

Blood Bourne organism in sepsis - seeding of infection in bone

152
Q

What is the most common type of osteomyelitis in adults compared to children

A

Adults - exogenous
Children - haematogenous

153
Q

What is the pathogenesis of osteomyelitis

A

Invasion and inflammation
Suppuration
Necrosis (sequestrian)
New bone formation
Resolution

154
Q

What is sequestrian in regard to osteomyelitis

A

Dead bone that has become separated during the process of necrosis from normal bone

155
Q

What complication are sinuses in osteomyelitis at risk of and why

A

Increased risk of SCC
Chronic irritation of the skin leads to hyperplasia, dysplasia and then carcinoma

156
Q

What are the differential diagnosis for a swollen knee

A

Haemarthrosis
OA and overuse
Septic arthritis
Polyarthritis (RA, Reiters syndrome)
Gout
Pseduogout
Trauma
Tumours

157
Q

What is the single best test for a swollen knee

A

Join aspiration

Urgent gram stain, MCS and cytology

158
Q

Why is removal of metalwork necessary in osteomyelitis

A

It is a septic focus

159
Q

Negatively bifringent needle shaped crystals are associated with what

A

Gout

160
Q

Positively bifringent rhomboid shaped crystals are associated with

A

Pseudogout

161
Q

What are the XR findings in pseudogout

A

Chondrocalcinosis

162
Q

Calcium pryophsophatedihydrate is associated with what condition

A

pseudo gout

163
Q

Define a pathological fracture

A

A fracture which has occurred without adequate trauma is caused by a pre-existing pathological bone lesion

164
Q

What are the neoplastic causes of a pathological fracture

A

Primary bone tumour - multiple myeloma
Metastatic deposits

165
Q

What are the non neoplastic causes of a pathological fracture

A

Osteoporosis
Osteomyelitis
Radiotherapy
Osteomalacia
Osteogenesis imperfecta
Bone cyst
Paget’s disease

166
Q

What are the malignancies that most common metastasise to bone

A

Breast
Prostate
Lung
Thyroid
Kidney

167
Q

Why will medullary thyroid cancer not show up on the radioactive iodine scan

A

Medullary thyroid cancer cell type if parafollicular cells which do not uptake iodine

168
Q

What are the complications of incorrect blood transfusion

A

Acute haemolytic reaction
Febrile non haemolytic transfusion reaction
Delayed haemolytic transfusion reaction
Tranfusion realtid lung injury

169
Q

Describe haemolysis

A

Rupture of RBC and release of cytoplasmic contents into the surrounding fluids

170
Q

What is DIC

A

Disseminated intravascular coagulation
Pathological consumptive coagulopathy due to activation of the coagulation and fibrinolytic system

Activation of the thrombolytic pathway leads to the formation of micro thrombi with consumption of clotting factors and platelets

171
Q

What are the clinical features of DIC

A

Widespread haemorrhage
Thrombocytopenia
Decreased fibrinogen

172
Q

What is the function of platelets

A

Adhesive and cohesive function leads to the formation of a haemostatic plug
They activate coagulation mechanisms

173
Q

From which precursor cells do platelets form

A

Magakaryocytes

174
Q

What are the late manifestations of Hep C infections

A

Cirrhosis
HCC

175
Q

Which coagulation test reflects in intrinsic pathway

A

APTT

176
Q

Which coagulation test reflects the extrinsic and common pathway

A

PT

177
Q

IgE is involved in which hypersensitivity reaction

A

Type I - Anaphylaxis

178
Q

IgG is involved with which hypersensitivity reaction

A

Type II - Cytotoxic
Type III - Immune complex

179
Q

T cells are involved in which hypersensitivity reaction

A

Type IV - Delayed

180
Q

What does Group cross matching do

A

Test donor cells against recipients to detect any potential incompatibility through which AB in recipients cause haemolysis

181
Q

What are the stages of bone healing

A
  1. Haematoma formation at fracture site - tissue in fracture site swells, very painful with obvious
  2. Fibrocartilage develops over a 3-4 week period (capillary growth into haematoma, phagocytic cells invading and cleaning up debris in injury site. Fibroblasts and osteoblasts migrate to site and beginning bone reconstruction)
  3. Bony callus presents 3-4 weeks post injury and prominent 2-3 month following the injury.
    Continued migration and multiplying of osteoblasts and osteocytes
  4. Remodelling - compact bone laid down in order to reconstruct the shaft
182
Q

What is PVL Staph Aureus

A

Panton Valteine Leukcoidin - a cytotoxin produced by staph aureus which causes leucocyte destruction and tissue necrosis
Associated with increased virulence of staph aureus

183
Q

What is the MOA of PVL staph aureus

A

Creates pores in the membranes of infected cells and cause of necrotic lesions involving skin or mucosa including necortic haemorrhage pneumonia.

184
Q
A

MRCS (17 decks)

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