Pathology 2 Flashcards

(184 cards)

1
Q

What is the epithelium of the oesophagus

A

Non keratinised stratified squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are risk factors for squamous cell carcinoma of the oesophagus

A

ETOHXS
Smoking
Low vitamin A
Chronic achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for adenocarcinoma of the oesophagus

A

Barrett’s oesophagus
GORD
Obesity
High fat diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GORD is related to the development of what malignancy

A

Adenocarcinoma of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What stain is used in immunohistochemistry

A

Cytokeratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the histological grades of oesophageal cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the palliative options in managing pleural effusions

A

Thoracocentesis
Indwelling pleural catheters
Pleuradesis
Pleuroperitoneal shunting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe in brief the pathogenesis of gastric cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most common type of gastric cancer

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Linitis plasticus is an example of what type of growth

A

Diffusely infiltrating growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What paraneoplastic syndromes are associated with gastric cancer

A

Acanthosis nigricans
Dermatomyositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the specific complications of a total gastrectomy ? Divide these into early and late complications.
Early Anastamotic leak, pancreatitis, cholecystitis, hameorrhage, infection Late Vitamin B12 deficiency, metabolic bone disease, recurrence of malignancy, Dumping syndrome
26
What is dumping syndrome
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
27
What are the symptoms of dumping syndrome
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
28
What is the difference between Duke Stage 2 and 3
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
29
What are haemorrhoids
Swollen/Inflammed anal cushions
30
Why do haemorrhoids form
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
31
How does a thrombus haemorrhoid occur
Acute thrombosis results from sudden raised pressure causing rupture of the vascular plexus leading to blood clot at the anal verge
32
Define melanosis coli
Disorder of the pigmentation of the wall of the colon Benign and may have no significant correlation with disease
33
What are the risk factors for atherosclerosis
Non modifiable - genetic, family history, male, age Modifiable - Type IIDM, HTN, smoking, hyperlipidemia
34
Describe briefly the formation of a fibrofatty plaque from a normal artery
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
35
Describe the formation of a thrombus in an atherosclerotic vessel
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
36
What are the complications of atherosclerosis
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
37
What is the pathogenesis of an MI
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
38
Define malignant melanoma
Malignant neoplasm of melanocytes, mainly arising in skin
39
What skin conditions are associated with malignant melanoma
Xeroderma pigmentosa Albinism Giant congenital pigmented naevus Fitzpatrick type I skin Dysplastic naevus Multiple naevi
40
What are risk factors for malignant melanoma
Hutchinson's melanotic freckles Immunocompromised patients PMH of melanoma Red hair Skin exposure
41
What is included in a pathology report for a malignant melanoma
Size Breslow thickness Depth of invasion Ulceration, mitosis, lymphovascular involvement Immunohistochemistry staining
42
What is Breslows thickness
The depth of a malignant melanoma From the top of the stratum granulosum to the deepest part of the tumour
43
What is Clarks Level
The depth of invasion of a malignant melanom a
44
What features about a mole would make you concerned
Asymmetry Irregular borders Multicoloured
45
Describe the appearance of a BCC
Shiny pearly papule/nodule
46
Describe the appearance of a SCC
Hyperkeratotic lesion with crusting and ulceration
47
What are the poor prognostic features in a melanoma
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
48
What gene mutations are found in familial malignant melanoma
CDKN2 CDK4 MCIR BRCA2
49
What does Breslows thickness implicate in turns of excisions
<0.76 mm thickness - 1cm margin 0.76-1mm thickness - 2 cm margin >1mm thickness - 3 cm margin
50
How do you ensure adequate margins in excision of malignant melanoma
Frozen section Mohs micro surgery
51
How would an axillary arm thrombosis present
Swelling of the arm
52
When would you consider catheter directed thrombolysis of a DVT
If the clot is <14 days old
53
What monitoring blood test is required in a patient undergoing catheter directed
Monitor Fibrinogen - levels need to be <100mg/dL
54
What are the indications for an SVC filter
Failure of antiocoagulation Complete contraindication to anticoagulation Presurgical prophylaxis in the presence of substantial RF
55
What are the components of Virchows Triad
Hypercoagulable state Venous stasis Endothelial injury
56
What is the management of a suspected PE
CTPA SC LMWH In massive embolism - Thromolysis, embolectomy
57
What are the differential diagnosis for inguinal lymphadenopathy
Cellulitis of the lower extremities Venereal infections - syphilis, chancroid, herpes, lymphgranuloma venereum Lymphoma Metastatic melanoma
58
What are the different types of melanoma
Lentigo maligna Superficial/spreading flat melanoma Desmoplastic melanoma Acral melanoma Nodular melanoma
59
Where are acral melanomas found
Palms of hands, soles of feet, nail beds
60
What is a satellite lesion in malignant melanoma
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
61
KIT mutations are common in what type of malignant melanoma
Melanoma that develop from mucus membranes/melanomas on the hands/feet, melanomas in chronically sun damaged areas such as lentigo malgna melanoma
62
What should be examined when you are concerned about melanoma
Full body examination, including nail beds and soles
63
What is the treatment for a patient with metastatic melanoma
Excision of the primary lesion with safe margins Block LN dissection Radiotherapy
64
What are examples of gram negative diplococci
Neiserria sp. Moraxella catarrhelis Actintobacter Haemophilus Brucellia
65
What are examples of gram positive diplococci
Streptococcus Enterococcus
66
What is the diagnostic criteria of SIRS
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
67
What occurs in acute respiratory distress syndrome
Diffuse alveolar damage and lung capillary endothelial injury
68
Describe a basal cell carcinoma
Pearly papule with a central ulcer, with granulation tissue on a base with rolled in edges Surrounding telangiectasia
69
Define telangiectasia
Dilated sub epidermal blood vessels
70
What is the natural pathology of BCC
Indolent with slow progression Locally destructive with limited potential to metastasise
71
What are the treatment options for BCC
Surgical: Cutterage and electrodissection Excision and primary closure Cryotherapy Mohs microsurgery
72
What is the negative to managing BCC with cryotherapy
Cannot obtain a tissue sample
73
What is the advantage to managing BCC with Mohs micrographic surgery
Serial tangential horizontal sections are taken and examined histologically
74
What are topical management options for BCC
Topical photodynamic therapy - delta aminoevulomic acid applied Topical fluorouracil 5% Topical imiquinol 5%
75
What management of BCC best prevents recurrence
Mohs microscopic surgery
76
What is a common cause of skin graft failure
Wound infection Usually by staph aureus
77
What is the treatment for an active MRSA infection
OP - Clindamycin, Amox + Tetracycline/ Linezolid IP - Vancomycin, Linezolid, Daptomycin, Telovancin
78
What is the treatment for MRSA decolonisation
Nasal mupirocin Chlorohexadine body wash
79
Reed Sternberg cells are found in what condition
Hodgkins lymphoma
80
What is the mechanism of lymphatic spread in malignant cells
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
What is Sickle Cell Disease
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
What is the pathogenesis of sickle cell disease
Substitution mutation of valine for glutamic acid at the 6th amino acid residue of beta-globin
83
What are the complications of sickle cell disease
Vaso-occlusive criss Sequestrian crisis Aplastic crisis Chronic tissue hypoxia Increased susceptibility to infection with encapsulated organisms
84
What is the pathogenesis of vast-occlusive crisis
Triggered by infection, dehydration and acidosis Results in hand foot syndrome, acute chest syndrome, stroke and retinopathy, autosplenectomy
85
What is a sequestrian criss
Massive entrapment of sickle cells in the spleen which will lead to rapid splenic enlargement and hypovolaemic shock
86
What virus causes an aplastic crisis
Parovirus
87
What is the mechanism of autosplenectomy in sickle cell
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
What surgical conditions are associated with sickle cell disease
Gallstones Autosplenectomy Avascular bone necrosis Osteomyelitis Pulmonary HTN HF
89
Why are sickle cell patients immunocompromised
Autosplenectomy leads to an increased risk of infection with encapsulated organisms
90
What are the common organisms that sickle cell patients are at risk of
Streptococcus pneumoniae Haemophilus influenza Neisseria meningitides
91
What are the high grade brain tumours
Gliomas Glioblastoma multiforme Medullablastoma
92
What are the visual field defect associated with pituitary tumours
Superior hemianopia
93
What are the visual field defects associated with craniopharyngiomas
Inferior hemianopia
94
What are the clinical features of brain tumours
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
What is the mode of inheritance of PKD and what genes are implicated
AD PKD 1 and PKD 2
96
Describe the pathogenesis of cyst formation in PKD
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
The mutations PKD 1 and PKD 2effect what type of proteins
Polycystin 1, 2 Fibrocystin Nephrocystin
98
In PKD which other organs may have cysts present
Liver Spleen Pancreas Ovaries
99
What are the complications of cystic kidneys
Renal failure Infection HTN
100
What extra-renal manifestations of PKD can occur
Liver cysts Pancreatic cysts Brain Aneurysm Mitral valve prolapse
101
What causes pain in PKD
Weight of the kidney dragging on its pedicle Stretching of the renal capsule by cysts
102
What are the clinical features of PKD
Pain Irregular abdominal pass Haematuria Infection Hypertension Uraemia
103
What are the differential diagnosis for renal cysts
Simple cysts Acquired cystic kidney disease VHL Medullary Sponge Kidney Tuberous Sclerosis
104
What matching is required prior to a renal transplant
ABO blood matching HLA matching
105
Which HLA matching are the most important
HLA - A HLA - B HLA - DR
106
Describe hyperacute graft rejection
Occurs within a few minutes of clamp release due to preformed Ab Immediate loss of graft occurs
107
Describe accelerated acute graft rejection
Occurs in the first few days following surgery Involves cellular and AB mediated injury Commonly causes by presensitisation of the donor
108
Describe acute graft rejection
Most common Seen days-weeks after surgery Predominately a cell mediated process - lymphocyte predominate Cellular infiltrates and apoptosis cellularly
109
Describe chronic graft rejection
Graft atrophy and atherosclerosis are seen. Fibrosis often occurs as a late event
110
What malignancies are associated with immunosuppression
SCC Cervical Ca BCC Lymphoma Kaposi's sarcoma
111
What would a pathology report of a testicular teratoma detail
Histopathology would show multiple different cell types - due to teratoma having 3 germ cell lines
112
Define cryptochidism
Complete/partial failure of the intra-abdominal tests to descend into the scrotal sac and is associated with testicular dysfunction
113
What are the risk factors for cyrptochidism
LBW infants FH Prematurity High abdominal pressure - eg. Gastroschisis Down's Syndrome
114
How much higher is the risk of testicular cancer with cryptorchidism
3-5x higher risk
115
What are the complications of cryptorchidism
Infertility Hernia Testicular torsion
116
What is the management of testicular teratoma
Orchiectomy Chemotherapy Orchiopexy on the contralateral testical
117
What are the types of seminomatous tumours
Seminomas Spermatocytic seminoma
118
What are the sex cord stromal tumours
Leydig cell tumours Sertoli cell tumours
119
Describe the spread of testicular teratoma
Initially to para-aortic lymph nodes Following this it is locoregional
120
What are the tumour markers measured in testicular cancer
AFP HCG LDH
121
Why are tumour markers helpful in testicular cancer
Evaluation of testicular masses Staging - if increased markers after orchidectomy then ?metastatic disease Assessing tumour burden Monitoring the response to treatment
122
How does haematoma resolution occur
Lysis of clot by macrophages - 1 week Growth of fibroblasts from into the haematoma - 2 weeks
123
Define metastasis
Survival and growth of cells at a site distant from their primary origin
124
Why are patients with malignancies at risk of PE
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
What is a choriocarcinoma
Highly malignant testicular tumour
126
What are the cell types in a choriocarcinoma
Synctiotrophoblasts Cytotrophoblasts
127
Which tumour markers are measure in choriocarcinoma
B HCG
128
Describe how a prostate biopsy is taken
TRUS guided from mid lobe parasagittal plane at the apex, the mid gland and the base bilaterally
129
Why are multiple biopsies required for a prostate biopsy
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
What immunohistochemistry is used to differentiate between rectal and prostate cells in a needle biopsy
alpha methyl coenzyme A racemase - in prostate ca CEA - rectal ca
131
What should happen to PSA level following a successful prostatectomy
Fall below detectable in 4-6 weeks
132
What causes PSA to rise
BPH Prostatitis Infarction of nodular hyperplasia Instrumentation of the prostate Ejaculation
133
What scoring system is used for Prostate Ca and describe its application
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
What type of bony mets are associated with prostate cancer
Sclerotic lesions Increased bone deposition due to increased osteoblastic activity
135
Describe androgen deprivation in prostate ca
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
Define an abscess
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
Describe the structure of an abscess
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
What organisms can cause abscesses
Bacterial Fungal Viral Parasitic
139
What pyrogens are associated with abscesses
TNF IL-1 IL-6
140
How is a fever produced
Pyrogens (TNF, IL-1, IL-6) stimulates prostaglandins synthesis in the vascular and perivascular cells of the hypothalamus
141
Define cellulitis
Spreading bacterial infection fo the skin which affects the dermis and subcutaneous fat. Characterised by redness, warmth, swelling and pain
142
When should ABx be used in treatment of abscess
Evidence of overlying cellulitis Abscess cavity not been left open to drain freely
143
Define giant cells
Multinucleate cells derived from the fusion of multiple activated macrophages
144
What is the macroscopy of LN in inflammation
Reactivate follicular hyperplasia
145
What are the causative organisms of osteomyelitis in adults
Staph aureus Enterobacter Streptococcus
146
Salmonella can cause osteomyelitis in which patient group
Sickle cell
147
How is osteomyelitis classified and describe the classification system
Cierny Classification Anatomic location Host type
148
In the Cierny Classification describe the different stages of anatomical location
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
In the Cierny classification describe the different host types
Type A - Normal Type B - Comrpomised (L - Localised, S - Systemic) Type C - Treatment worse than the infection
150
How does exogenous osteomyelitis occur
Acute - from open #/bone exposed at the time of surgery Chronic - from neglected wounds - Diabetic feet/Decubitus ulcers
151
How does Haematogenous osteomyelitis occur
Blood Bourne organism in sepsis - seeding of infection in bone
152
What is the most common type of osteomyelitis in adults compared to children
Adults - exogenous Children - haematogenous
153
What is the pathogenesis of osteomyelitis
Invasion and inflammation Suppuration Necrosis (sequestrian) New bone formation Resolution
154
What is sequestrian in regard to osteomyelitis
Dead bone that has become separated during the process of necrosis from normal bone
155
What complication are sinuses in osteomyelitis at risk of and why
Increased risk of SCC Chronic irritation of the skin leads to hyperplasia, dysplasia and then carcinoma
156
What are the differential diagnosis for a swollen knee
Haemarthrosis OA and overuse Septic arthritis Polyarthritis (RA, Reiters syndrome) Gout Pseduogout Trauma Tumours
157
What is the single best test for a swollen knee
Join aspiration Urgent gram stain, MCS and cytology
158
Why is removal of metalwork necessary in osteomyelitis
It is a septic focus
159
Negatively bifringent needle shaped crystals are associated with what
Gout
160
Positively bifringent rhomboid shaped crystals are associated with
Pseudogout
161
What are the XR findings in pseudogout
Chondrocalcinosis
162
Calcium pryophsophatedihydrate is associated with what condition
pseudo gout
163
Define a pathological fracture
A fracture which has occurred without adequate trauma is caused by a pre-existing pathological bone lesion
164
What are the neoplastic causes of a pathological fracture
Primary bone tumour - multiple myeloma Metastatic deposits
165
What are the non neoplastic causes of a pathological fracture
Osteoporosis Osteomyelitis Radiotherapy Osteomalacia Osteogenesis imperfecta Bone cyst Paget's disease
166
What are the malignancies that most common metastasise to bone
Breast Prostate Lung Thyroid Kidney
167
Why will medullary thyroid cancer not show up on the radioactive iodine scan
Medullary thyroid cancer cell type if parafollicular cells which do not uptake iodine
168
What are the complications of incorrect blood transfusion
Acute haemolytic reaction Febrile non haemolytic transfusion reaction Delayed haemolytic transfusion reaction Tranfusion realtid lung injury
169
Describe haemolysis
Rupture of RBC and release of cytoplasmic contents into the surrounding fluids
170
What is DIC
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
What are the clinical features of DIC
Widespread haemorrhage Thrombocytopenia Decreased fibrinogen
172
What is the function of platelets
Adhesive and cohesive function leads to the formation of a haemostatic plug They activate coagulation mechanisms
173
From which precursor cells do platelets form
Magakaryocytes
174
What are the late manifestations of Hep C infections
Cirrhosis HCC
175
Which coagulation test reflects in intrinsic pathway
APTT
176
Which coagulation test reflects the extrinsic and common pathway
PT
177
IgE is involved in which hypersensitivity reaction
Type I - Anaphylaxis
178
IgG is involved with which hypersensitivity reaction
Type II - Cytotoxic Type III - Immune complex
179
T cells are involved in which hypersensitivity reaction
Type IV - Delayed
180
What does Group cross matching do
Test donor cells against recipients to detect any potential incompatibility through which AB in recipients cause haemolysis
181
What are the stages of bone healing
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
What is PVL Staph Aureus
Panton Valteine Leukcoidin - a cytotoxin produced by staph aureus which causes leucocyte destruction and tissue necrosis Associated with increased virulence of staph aureus
183
What is the MOA of PVL staph aureus
Creates pores in the membranes of infected cells and cause of necrotic lesions involving skin or mucosa including necortic haemorrhage pneumonia.
184