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MRCS > Pathology 1 > Flashcards

Pathology 1 Flashcards

1
Q

Define infective endocarditis

A

Inflammation of the endocardial surfaces of the heart including the heart valves

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2
Q

What is marantic endocarditis

A

Non bacterial thrombotic endocarditis
Tends to occurs in the setting of malignancy

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3
Q

Why are patients with rheumatic heart disease/ replaced heart valves more at risk of IE

A

More susceptible to IE as they are damaged or artificial which allows for increased chance of bacterial colonisation

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4
Q

What is the pathology of rheumatic heart disease

A

Host immune response to Group A streptococcal antigens
Antibodies/ CD4/ T cells directed against streptococcal M proteins can recognise cardiac self antigens which results in damage to the heart tissues leading to inflammation, progressive fibrosis and narrowing of the valve leaflets - causing them to fuse and to retract

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5
Q

What are the gross findings in acute IE

A

Valvular vegetations - found along lines of closure, with minimal effect on function

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6
Q

What are the gross findings in chronic IE

A

Commisural fibrosis
Valve thickening and calcification
Shortened and fused chordae tendinae

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7
Q

What are the microscopic findings of IE

A

Aschoff bodies
Plasma cells
Anitschkow cells (activated macrophages)

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8
Q

What are Aschoff bodies

A

granulomatous inflammation with central zone of degenerating ECM infiltrated with lymphocytes

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9
Q

What are the 5 types of necrosis

A

Coagulative
Liquefactive
Caseous
Fibrinoid
Fat

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10
Q

What would you assess for on ECHO in the context of IE

A

Valvular regurgitation
Leaflet change
Annular dilatation
chordal elongation/rupture
Increased echogenecity of subvalvular apparatus
pericardial effusion
Ventricular dilation and dysfunction

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11
Q

What organisms commonly cause IE

A

Staph aureus
Staph epidermis
Strep viridians
Coagulase negative staph
Enterococci
HACEK group

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12
Q

What organisms are part of the HACEK group

A

Haemophilus species
Aggregatibacter species
Cardiobacterium hominis
Eikenella
Kingella species

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13
Q

What organism causes IE in early valve replacement patients

A

Staph epidermis

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14
Q

What organism causes IE in IVDU patients

A

Staph aureus

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15
Q

What scoring on the Dukes criteria gives a diagnosis of IE

A

2 major + 0 minor criteria
1 major + 3 minor criteria
0 major + 5 minor criteria

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16
Q

What are the major criteria in the Dukes criteria

A

Typical IE organism in 2 cultures
1 culture for Cox Burnetti
Persistently positive cultures
Positive ECHO
Abnormal prosthetic valve activity on CT

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17
Q

What are the minor criteria in the Dukes criteria

A

Predisposing risk factors - known heart disease, IVDU
Fever > 38 degrees
Vascular sequelae
Immunological sequelae
Positive blood cultures
ECHO findings

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18
Q

What are the vascular sequelae in IE

A

Arterial emboli
Janeway lesions
Conjunctival haemorrhage

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19
Q

What are the immunological sequelae in IE

A

Glomerulonephritis
Roths spots
Osler nodes

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20
Q

Which patients develop right sided IE

A

IVDU patients

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21
Q

Which lesions are painful - janeaway lesions or Osler nodes

A

Osler nodes

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22
Q

Risk factors for IE

A

Structural heart disease
Prev IE
Valve replacement
Acquired heart disease w stenosis and regurgitation
HOCM
Cardiac device
IVDU
DM
Malignancy

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23
Q

What infectious organism is associated with colorectal cancer

A

Strep bovis

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24
Q

What are the cardiac complications of IE

A

Acute MI
Pericarditis
Arrythmia
Valvular insufficiency
Congestive cardiac failure
Anuerysm of aortic sinus
Intracardial abscess
Arterial emboli

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25
Q

What are the non cardiac complications of IE

A

Endocarditis associated glomerulonephritis
AKI
Stroke
Mesenteric/Splenic abscess/infarct

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26
Q

What are the clinical features of IE

A

Fever
Roths spots
Osler nodes
Murmur
Janeway lesions
Anaemia
Splinter haemorrhage
Emboli

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27
Q

What is the treatment of native valve IE

A

Amoxicillin
Flucloxacillin
Gentamicin

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28
Q

What is the treatment of prosthetic valve IE

A

Vancomycin
Gentamicin

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29
Q

What are the challenges with ABx therapy in IE

A

Valves do not have a specific blood supply
Bacteria hide within vegetations
Bacteria form a biofilm and can therefore be shielded from ABx

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30
Q

What is a biofilm

A

Glycocalyx covering

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31
Q

What it the management of IE refractory to treatment

A

Valve replacement
Heart transplant

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32
Q

What happens if HLA antigen matching is not done in valve replacement

A

Type I hypersensitivity and graft rejection

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33
Q

What causes aortic stenosis

A

Post inflammatory scarring eg. rheumatic heart disease
Senile calcific aortic stenosis
Calcification of congenitally deformed valve

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34
Q

What is the pathophysiology of stenosis

A

Lipid accumulation
Inflammation
Calcification - leads to valve thickening and stenosis

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35
Q

What is the sequelae of aortic stenosis

A

As aortic valve progresses from sclerosis to stenosis the left ventricle encounters chronic resistance to systolic ejection
Results in increased afterload
After time this results in left ventricular hypertrophy

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36
Q

What are the consequences of high left ventricular after load

A

Decreased left ventricle myocardial elasticity and coronary blood flow
Results in increased myocardial workload and oxygen consumption

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37
Q

What are the late manifestations of LVH

A

Small ventricular chamber
Insufficient stroke volume, cardiac output and ejective fraction
Increased pulmonary pressures

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38
Q

What is the concern with aortic stenosis in the perioperative period

A

Patient has a fixed cardiac output and a limited coronary blood supply
They cannot respond to decreased after load which can occur with both anaesthesia and blood loss

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39
Q

How is coronary perfusion pressure calculated

A

Systemic diastolic pressure - LVED pressure

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40
Q

If on microscopy you visualised branching hyphae what type of organism is responsible and give examples

A

Fungal infection
Examples - candida, aspergillum, microsporum, triophyton, epidermophyton

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41
Q

What is the definition of a thrombus

A

Solid material formed from the constituents of blood

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42
Q

What factors does warfarin inhibit

A

Factors 2, 7, 9, 10

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43
Q

What are the clinical symptoms of aortic stenosis

A

Syncope
Anginal pain
Dysponea
Paroxysmal nocturnal dyspnoea
Orthopnea

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44
Q

What are the clinical signs of aortic stenosis

A

Pulsus arterans
Narrow pulse pressure
Ejection systolic murmur
Paradoxical splitting of S2

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45
Q

What is pulsus arterans

A

Pulse with alternating strong and then weak pulses

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46
Q

What is paradoxical splitting of S2

A

Occurs due to the closure of the aortic valves and pulmonary valve not being synchronous

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47
Q

What is severe aortic stenosis in terms of valve surface area and transvalvular pressure gradient

A

<1.0cm3
Confers to a transvalvular gradient of >40mmHg

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48
Q

What is giant cell arteritis

A

Inflammation of the large and medium sized blood vessels, predominantly affecting the temporal arteries

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49
Q

What is the pathology of giant cell arteritis

A

Medial granulomatous inflammation
Centred on the internal elastic lamina - producing elastic lamina fragmentation
Infiltrates of T cells and macrophages

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50
Q

What is meant by focal lesions in GCA

A

There are focal points of disease distribution along vessel with long segments of relatively normal artery

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51
Q

What are the clinical features of GCA

A

New onset headache in the temporal region
Scalp tenderness
Intermittent jaw claudication
Weight loss
Fever
Temporal artery thickening and modulatory
Visual field changes

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52
Q

What is the gold standard investigation for GCA

A

Temporal artery biopsy

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53
Q

What would a positive temporal artery biopsy show

A

Mononuclear cell infiltrates
Granulomatous inflammation with multinucleate giant cells

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54
Q

What is the management of GCA

A

Steroids
If eye involvement - IV Methylpred

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55
Q

When considering patients with steroids what should you think about

A

Immunosuppression
Bone quality

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56
Q

How should an addisonian crisis be avoided perioperatively

A

Double dose the patient steroids before theatre
Convert PO to IV hydrocortisone

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57
Q

What is osteoporosis characterised by

A

Low bone mass
Microarchitectural deterioration of bone tissue
Increased bone fragility
Loss of bone matrix

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58
Q

What are the pathological changes in osteoporosis

A

Histologically normal bone is decreased in quantity
Trabecullar plates become perforated, thin, and loser their interconnection - this leads to progressive micro fractures and eventually bone collapse

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59
Q

What is the mechanism of post menopausal osteoporosis

A

Increased osteoclast activity

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60
Q

What are the 3 main mechanisms of osteoporosis

A

Inadequate peak bone mass
Excessive bone reabsorption
Inadequate formation of new bone during bone turnover

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61
Q

What are the primary causes of osteoporosis

A

Idiopathic
Post menopausal

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62
Q

What are the secondary causes of osteoporosis

A

Addisons disease
TIDM
Hyper/hypothyroidism
Multiple myeloma
Hepatic insufficiency
Vitamin D/C deficiency
Malabsorption
Anaemia
Osteogenesis imperfecta

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63
Q

What is the mechanism of steroids on bone

A

Direct inhibition of osteoblast function
Direct stimulation of bone resorption
Inhibition of GIT calcium reabsorption
Stimulation of real calcium losses
Inhibition of sex steroids

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64
Q

What can cause pathological fracture

A

Multiple myeloma
Skeletal metastases
Pagets disease
Osteogenesis imperfecta
Radiotherapy
Osteomalacia
Rickets

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65
Q

What is multiple myeloma

A

Plasma cell neoplasm

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66
Q

What is multiple myeloma commonly associated with

A

Lytic bone lesions
Hypercalcaemia
Renal failure
Acquired immune deficiencies

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67
Q

What immunoglobulin is most commonly produced in multiple myeloma

A

IgG - 55%
IgA - 25%

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68
Q

What are the clinical features of multiple myeloma

A

M spike on protein electrophoresis
Ig light chains in urine - Bence Jone Protein
Hypercalcaemia
Anaemia
Bone lesions - lytic lesions, osteoporosis w compression #

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69
Q

What are Bence Jones proteins

A

Monoclonal globulin proteins/immunoglobulin light chains found in the urine
Produced by neoplastic plasma cells

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70
Q

What are the causes of fat embolism

A

Closed long bone fractures
Decompression sickness
Cardiopulmonary bypass grafting
Orthopaedic surgery - IM nailing, joint arthroplasty
Acute pancreatitis
DM

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71
Q

Define gangrenous necrosis

A

Necrosis of tissue with superadded putefraction

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72
Q

Define necrosis

A

Accidental and unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis

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73
Q

What are the types of cell deaths

A

Apoptosis
Necrosis

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74
Q

Describe the pathogenesis of necrosis

A

Severe/prolonged ischemia results in severe swelling of the mitochondria, calcium influx into the mitochondria and into the cell with rupture of lysosomes and plasma membrane
Cytochrome is released from the mitochondria

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75
Q

What is the physiology of apoptosis

A

Programmed cell death/ cell death following DNA damage
Cell shrinkage, and fragmentation into nucleosome sized fragments, with intact plasma membranes
Released as small apoptotic bodies

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76
Q

What type of gangrene follow arterial occlusion

A

Dry

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77
Q

Where does dry gangrene commonly occur

A

Limbs

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78
Q

In which type of gangrene is there a clear line of demarcation

A

Dry

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79
Q

In what type of gangrene is the prognosis worse and why

A

Wet gangrene
Due to the profound toxaemia which accompanies it

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80
Q

What is the macroscopy in dry gangrene compared to wet gangrene

A

Dry - organ is dry, shrunken and black
Wet - parts moist, soft, swollen, rotten and dark

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81
Q

Describe coagulative necrosis

A

Loss of the nucleus with the cellular outline being preserved
commonly associated with ischaemia

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82
Q

What is the most common type of necrosis

A

Coagulative necrosis

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83
Q

Describe liquefactive necrosis

A

Enzymatic destruction of cells, with abscess formation following
Seen in the pancreas and the brain

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84
Q

Describe caseous necrosis

A

A combination of coagulative and liquefactive necrosis
Cheese like appearance of the necrotic material

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85
Q

What is caseous necrosis characteristic of

A

TB

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86
Q

Other than TB in what infections is caseous necrosis seen

A

Syphilis
Histoplasmosis
Coccidodomyosis

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87
Q

Describe fat necrosis

A

Results from the action of lipase on fatty tissue
Seen in breast, omentum and pancreatitis

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88
Q

Describe fibrinoid necrosis

A

Complexes of antigens and antibodies are deposited in the vessel walls with leakage of fibrinogen out of the vessels

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89
Q

Summarise atherosclerosis

A

Pathological process of the vasculature in which an artery wall thickens as a result of an accumulation of fatty materials, such as cholesterol

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90
Q

What are the risk factors for atherosclerosis

A

DM
FH
HTN
Smoking
Increased LDL

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91
Q

What is a pleural plaque a common manifestation of and how would you describe their appearance

A

Most common manifestation of asbestos exposure
Well circumscribed plaques of dense collegen, often calcified

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92
Q

What are the significance of pleural plaques

A

Increased risk of mesothelioma and lung adenocarcinoma

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93
Q

What are the two broad classifications of lung cancer

A

Small cell lung cancer
Non small call lung cancer

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94
Q

What are the different types of non small cell lung cancer

A

Adenocarcinoma
Squamous cell lung cancer
Large cell carcinoma

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95
Q

What is the most common lung cancer in non smokers

A

Adenocarcinoma

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96
Q

Which type of lung cancer is associated with paraneoplastic syndromes and why

A

Small cell lung cancers
They are cells of neuroendocrine differentiation so are able to release hormones

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97
Q

Where in the lung do squamous cell lung cancers arise

A

Centrally

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98
Q

How do you distinguish the epithelial origin of tumours

A

Immunihistochemistry

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99
Q

What can be used to treat epidermal growth factor positive tumours

A

Tyrosine kinase inhibitors - Imatinib

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100
Q

Imatinib is what kind of drug

A

Tyrosine kinase inhibitor

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101
Q

What are the systemic features of TB

A

Weight loss
Night sweats
Cervical lymphadenopathy

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102
Q

In younger patients with Hodgkin’s lymphoma where do they often experience lymphadenopathy

A

Anterior triangle

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103
Q

What are the investigations for TB

A

Culture
Ziehl neelson stain
Mantoux test
PCR
Quantiferon (interferon gamma assays)

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104
Q

If sending sputum cultures to the lab how should they be labelled and in what bag should they be sent

A

Labelled - Category B UN3373
Sent in a biohazard bag

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105
Q

What is BATEC/MIGT

A

Liquid media in which to culture TB
Mycobacterium growth indicator tube

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106
Q

What solid media is used to culture TB

A

Lowenstein Jensen media
Middlebrook media

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107
Q

What would FNAC in TB show

A

Necrotic tissues
Histocytes
Giant cells

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108
Q

Langherhan’s giant cells and Reed Sternberg cells are examples of what

A

Giant cells - multinucleate cells comprised of macrophages

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109
Q

What are some common causes of granulomas

A

TB
Sarcoidosis
Leprosy
Schistosomiasis
Crohn’s
RA

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110
Q

What needs to be done from a public health perspective in TB

A

Notify communicable disease control
Avoid working in food factory
Contact tracing
Direct observation of anti TB therapy

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111
Q

What ABx are commonly used in the treatment of TB

A

Isoniazid
Rifampicin
Pyrazanmide
Ethambutol

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112
Q

What are the different types of breast cancer

A

Ductal carcinoma
Lobular carcinoma
Medullary carcinoma

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113
Q

What is the most common type of breast cancer

A

Ductal carcinoma

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114
Q

What are the risk factors for breast cancer

A

Unopposed oestrogen (early menarche, OCP, HRT, nulliparous/ pregnancy >30, late menopause)
Obesity
Increasing age
FH - BRCA 1/2

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115
Q

What lead to unopposed oestrogen

A

Early menarche
OCP use
HRT use
Nulliparous
Pregnancy > 30

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116
Q

What are the clinical features of Paget’s disease

A

Itchy, red, flaking of the skin around the nipple

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117
Q

What imaging is used in suspected breast cancer and why does it differ

A

Differs depending on age
US < 35
Mammorgam >35

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118
Q

What findings on mammogram would make you suspicious of breast cancer

A

Speculated mass
Calcifications

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119
Q

What do pathology reports following WLE in breast cancer contain

A

Type of breast cancer
Number of positive LN
Margin status
HER2 receptor status
ER/PR receptor status
Ki67 proliferation status

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120
Q

What should be checked prior to any elective surgery

A

MRSA status

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121
Q

What is HER2 and where is it found

A

Human epidermal growth factor receptor 2
Found embedded in the cell membrane, it communicates molecular signals from outside the cell to inside the cell

122
Q

In what percentage of breast cancer cases is HER2 over expressed

A

15%

123
Q

What does immunohistochemsistry measure

A

The amount of a certain protein in cells (eg. the amount of HER2 protein in cells)

124
Q

What does fluorescent in situ hybridisation measure

A

The number of copies of a gene in a cell (eg. HER2 in breast cancer cells)

125
Q

What is Herceptin and what is it used for

A

Monoclonal antibody which interferes with HER2 and causes AB mediated destruction of cells overproducing HER2

126
Q

What is Trastuzumab also known as

A

Herceptin

127
Q

What is the normal mechanism of HER2

A

HER protein binds to EGF and stimulates cell proliferation, leading to the inhibition of MAPC + P13K AKt

128
Q

When would a mastectomy be more appropriate that a wide local excision

A

In multifocal disease
When there is high tumour: breast tissue
If the patient would prefer this

129
Q

What additional therapy is used in breast cancer if the tumour is found to be ER positive

A

Tamoxifen - If they are pre menopausal
Anastrazole - if they are post menopausal

130
Q

What is the MOA of anastrozole

A

Aromatase inhibitor which prevents peripheral conversion to oestrogen

131
Q

What is included in the Nottingham prognostic index

A

Maximum invasive carcinoma size
Lymph node stage
Histological grade

132
Q

Which conditions characterise MEN 1

A

Pituitary adenoma
Parathyroid hyperplasia
Pancreatic tumours

133
Q

Which conditions characterise MEN 2a

A

Parathyroid hyperplasia
Medullary thyroid cancer
Phaeochromocytoma

134
Q

Which conditions characterise MEN 2b

A

Marfanoid body habitus
Mucosal neuromas
Medullary thyroid cancer
Phaeochromocytoma

135
Q

The MENIN gene on chromosome 11 is associated with which condition

A

MEN 1

136
Q

The RET oncogene on chromosome 10 is associated with which conditions

A

MEN 2a and MEN 2b

137
Q

What is the common clinical presentation in a patient with MEN 1 syndrome

A

Hypercalcaemia

138
Q

Define hyperplasia

A

Increase in the number of cells in a tissue or organ as a response to a stimulus

139
Q

What is the microscopic appearance of parathyroid hyperplasia

A

Commonly chief cell hyperplasia
Can be in a diffuse or nodular pattern
Islands of oxyphil, poorly developed, delicate fibrous strands may envelope the nodules

140
Q

What are the clinical features of an insulinoma

A

Stupor
Confusion
Hypoglycaemia
Symptoms often precipitated by fasting or exercise

141
Q

What would be the biochemical findings in a patient with an insulinoma

A

High circulating levels of insulin
High insulin :glucose ratio

142
Q

What are the causes of unresponsive hypoglycaemia

A

Abnormal insulin sensitivity
Diffuse liver disease
Inherited glycogenosis
Ectopic production of insulin

143
Q

What is the 2 hit hypothesis in genetics

A

Gene mutations can occur through two routes - sporadic or familial
For more tumour suppressor genes the mutations are recessive in nature and therefore both genes would need to be mutated before this becomes apparent
Therefore for them to be deactivated they would need to be mutated twice (eg. one familial one sporadic)

144
Q

What is a telomere and what is its function

A

A region of repetitive nucleotide sequence at the end of a chromosome
It protects the end of a chromosome from deterioration/from fusion with neighbouring chromosomes

145
Q

What is the single best test for a diagnosis of a thyroid nodule

A

Fine needle aspiration and cytology

146
Q

What is the microscopy findings from FNAC of a medullary thyroid cancer

A

Malignant cell features (lack of differentiation, BM invasion)
Amyloid deposits
Immunohistochemistry stains positive for calcitonin, negative for thyroxine

147
Q

What is the cell source in medullary thyroid cancer

A

Parafollicular C cells

148
Q

How does immunohistochemistry work

A

It is a method which localises specific antigen/cells based on AB recognition. Compliment fixation
Ab are linked to an enzyme/ fluorescent dye (antigen) which allows them to be visualised under microscopy

149
Q

What is the management of medullary thyroid cancer

A

Total thyroidectomy with block neck dissection

150
Q

At what T level is thyroid cancer extending beyond the capsule of the thyroid

A

T4

T1 < 1cm
T2 >1 cm <4cm
T3 >4cm
T4 - extending beyond the thyroid capsule

151
Q

Below what age does staging of thyroid medullary cancer differ

A

< 45 y/o

152
Q

What are the clinical features of a phaeochromocytoma

A

Headache
Tachycardia
Sweating

Intermittent nature of the symptoms

153
Q

What investigations are needed for a diagnosis of phaeochromocytoma

A

Blood - plasma metanephrines, plasma catecholamines, catecholamine simulation test
Urine - fractionated metanephrines, total metanephrines, catecholamines, VMA
Imaging - US, CT, MRI, MIBG scintagraphy

154
Q

What are the appearances of phaeochromocytoma on CT compared to MRI

A

CT scan - shows high enhancement
MRI scan - low fat content

155
Q

Define pleomorphic

A

Remarkable histological diversity

156
Q

What is the most common benign parotid swelling

A

Pleomorphic adenoma

157
Q

What are the miscroscopic appearances of a pleomorphic adenoma

A

Consists of a mixture of ductal (epithelial) and myoepithelial cells

158
Q

What clinical signs would make you suspicious of a parotid malignancy rather than a benign swelling

A

Facial nerve affected
Rapidly increasing in size
Fixity to the underlying structures
Invasion of the overlying skin

159
Q

What are the benign parotid tumours

A

Pleomorphic adenoma
Warthin’s tumour
Oncocytoma
Other adenomas (basal cell)
Ductal papillomas

160
Q

What are the malignant parotid tumours

A

Mucoepidermoid cyst
Adenocarcinoma
Acinic cell carcinoma
Adenoid cystic carcinoma
Malignant mixed cell tumour
Squamous cell carcinoma
Other carcinoma

161
Q

What is the difference between cytology and histology

A

Cytology - study of cellular function and structure
Histology - study of tissue under a microscope

162
Q

Describe the generic features of malignant cells

A

Invasive
Increased mitotic rate
Lack of differentiation - this can extend to complete anaplasia

163
Q

In regard to malignancy what does presence of anaplastic cells

A

Tends to indicate a very aggressive malignancy

164
Q

List the features of anaplastic cells

A

Loss of normal tissue architecture
Pleomorphism - nuclei often very large and show prominent nucleoli
Hyperchromatic nuclei (stain darker)
High nuclear: cytoplasmic ratio

165
Q

If you visualised epitheloid cells with brown cytoplasm under microscope following FNAC what would you be concerned about

A

Malignant melanoma

166
Q

Lymphoid cells with pleomorphism is found in what conditon

A

Lymphoma

167
Q

What is meant by a high sensitivity test

A

The ability to correctly identify a disease
True positive rate

168
Q

What is meant by a high specificity test

A

The ability to correctly identify those without disease
True negative rate

169
Q

What are the units of radiotherapy

A

Coulomb/kg
Gray (Gy)
Sievert
Becquerel

170
Q

What is a Coulomb

A

The unit to express exposure in radiotherapy

171
Q

What is a Gray

A

The unit to express dose in radiotherapy
The absorption of one joule of radiation energy per kg of matter

172
Q

What is a sievert

A

The unit to express dose equivalent in radiotherapy
It takes into account the relative biological effectiveness of ionising radiation

173
Q

What is a becquerel

A

The unit to express activity in radiotherapy
relates to the activity of a quantity of radioactive material in which one nucleus decays per second

174
Q

What is one sievert equivalent to

A

The amount of radiation roughly equivalent in biological effectiveness to one gray

175
Q

What are the risk factors for nasopharyngeal carcinoma

A

Male > Female
Ethnicity (China, Hong Kong, Singapore, Malaysia, Philippines)
Diet (consumption of salted fish containing carcinogenic volatile nitrosamines)
EBV/HPV infection
FH
Tobacco use

176
Q

What are the main risk factors of oral candida

A

Immunosuppression - steroids, chemotherapy, biologics, ABx
Diabetes

177
Q

What are the common clinical features of nasopharyngeal carcinoma

A

Headache
Sore throat
Neck swelling
Struggling with hearing/speaking
Airway obstruction
Recurrent ear infections

178
Q

Why would first presentation of neck swelling in the context of nasopharyngeal carcinoma possibly indicate poor prognosis

A

Neck swelling often representative of metastatic spread to the lymph nodes

179
Q

Why should recurrent ear infections in an adult be taken seriously

A

If adults are presenting with an ear infection out of the context of LRTI then it may represent nasopharyngeal carcinoma

180
Q

What is Trotter’s syndrome

A

A cluster of symptoms associated with advanced nasopharyngeal carcinoma

181
Q

What are the symptoms of Trotter’s syndrome

A

Unilateral conductive deafness due to middle ear effusion
Trigeminal neuralgia
Soft palate immobility
Difficulty opening mouth

182
Q

What causes pain in Trotter’s syndrome

A

Neuralgic pain from the mandibular branch of the trigeminal nerve in foramen vale through which the tumour enters the calvarium

183
Q

If nasopharyngeal carcinoma was to locally spread where could it spread to

A

Sphenoid and cavernous sinus
Nasal cavity
Orbital invasion
Oropharynx (Tonsillar pillars)
C1 vertebrae
Lateral parapharyngeal space
Middle ear cavity
Base of skull
Chivus

184
Q

What are the common causes of LN tumours

A

Lymphoma (Hodgkins and Non-hodgkins)
Leukaemia
Metastatic

185
Q

Define an abscess

A

A focal collection of pus that may be caused by a seeding of pyogenic organisms into tissues or be secondary infections of necrotic foci

186
Q

Describe the structure of an abscess

A

Central, largely necrotic region
Rimmed by a layer of preserved neutrophils
Surrounding zone of dilated vessels and fibroblasts

187
Q

Describe neutrophil activation and migration

A

Neutrophils activated by chemokine - resulting in margination and rolling along the vessel wall
Firm adhesion to the endothelium which is facilitated by increased activity of integrins
Stable adhesion
Migration between endothelial cells and into interstitial tissues towards a chemo attractant stimulus

188
Q

What are carcinoid tumours

A

Slow growing neuroendocrine tumours

189
Q

What cells do carcinoid tumours arise from

A

Enterochromaffin cells (Kulchistky cells) in the crypts of Lieberkilin

190
Q

Where are carcinoid tumours most commonly found

A

Small intestine
Terminal 1/3 of the appendix
Rectum
Lung
Stomach

191
Q

What hormones are released from carcinoid tumours

A

Serotonin
Bradykinins
Prostaglandins
Histamines
Substance P
Tachykinins

192
Q

What are the common clinical features of a carcinoid tumour

A

Periodic abdominal pain
Periodic diarrhoea/constipation
Carcinoid syndrome

193
Q

What are the features of carcinoid syndrome

A

Cutaneous flushing
Diarrhoea and malabsorption
Cardiac manifestations (Valvular heart lesions, fibrosis of the endocardium)
Wheeze/asthma like symptoms - due to bronchial constriction

194
Q

Why do symptoms of carcinoid tumours only tend to present following metastasis to the liver

A

The hormones produced by primary carcinoid tumours cannot get into systemic circulation because of first pass metabolism
However following metastasis to the liver - the hormones produced bypass first metabolism and so are released into systemic circulation

195
Q

What investigations are used in the diagnosis of carcinoid syndrome

A

Chromogranin A
Urinary 5 hydroxyindoleactic acid (5 HIAA)
Histolopathology - immunohistochemistry of samples positive for Chromogranin A

196
Q

Define Type I DM

A

Absolute insulin deficiency of insulin secretion caused by pancreatic beta cell destruction

197
Q

Define Type II DM

A

Combination of peripheral resistance to insulin action and an inadequate compensatory response of insulin secretion by the pancreatic beta cells (relative insulin deficiency)

198
Q

What are the effects of insulin on adipose tissue

A

Increased glucose uptake
Increased lipogenesis
Decreased lipolysis

199
Q

What are the effects of insulin on striated muscle

A

Increased glucose uptake
Increased glycogen synthesis
Increased protein synthesis

200
Q

What are the effects of insulin on the liver

A

Decreased gluconeogenesis
Increased glycogen synthesis
Increased lipogenesis

201
Q

Which hormones increased blood glucose levels

A

Glucagon
Catecholamines
Glucocorticoids
Somatrophin

202
Q

When should a VRII be used in the pre operative period

A

When a patient is undergoing a major procedure or in patients with poor glycaemic control

Major procedure- surgery requiring fasting period >1 missed meal

203
Q

When should a VRII be stopped

A

Should be stopped when the patient can be safely converted back to SC insulin, when E+D, once this has occurred should be stopped 30-60 minutes following the first meal

204
Q

In the pre operative period what would be considered good glycemic control

A

HbA1C < 69mmol or 8.5%

205
Q

What background fluids should be used alongside a VRII

A

KCl, Glucose, NaCl

206
Q

Which anti diabetic drugs should be stopped if insulin is started

A

Acarbose
Meglitinides
Sulfonylureas
Pioglitazone
Gliptins
SGLT2 inhibitors

Can be restarted when the patient is E+D normally

207
Q

Why should SGLT2 inhibitors be stopped in the perioperative period

A

When taken in periods of stress (dehydration, acute illness) they can be associated with DKA

208
Q

Why should sulfonylureas be stopped in the preoperative period

A

They are associated with hypoglycaemia when taken in the fasted state

209
Q

When should metformin be stopped

A

In the perioperative period if a patient is going to miss more than one meal, or if they are at risk of developing an AKI

210
Q

What are the immediate and late complications in a surgical patient with DM

A

Early - Hypo/hyperglycaemia, dehydration +/- electrolyte imbalances, HHS, DKA

Later - infection, impaired wound healing

211
Q

What is the presumed aetiology of ulcerative colitis

A

Genetic susceptibility with abnormal host response to colonic flora
Genetic polymorphism in TLR, loss of homeostasis between host mucosal immunity and microflora
Disrupted balance between regulatory and effector T cells

212
Q

What does ulcerative colitis look like when visualised on colonoscopy

A

Hyperaemic/haemorrhagic colonic mucosa
Pseudopolyps
Inflammation confined to the mucosa - makes it friable and oedematous

213
Q

What is the histology of of ulcerative colitis

A

Crypt abscesses
White cell infiltrate into the lamina propia
Mucin depletion

214
Q

What is the difference between distal colitis and extensive colitis

A

Distal colitis - inflammation extends to the splenic flexure
Extensive colitis - extends to the hepatic flexure

215
Q

What are the extra-intestinal manifestations of ulcerative colitis

A

Clubbing
Apthous ulcers
Erythema nodusum
Pyoderma gangrenosum
Iritis/uveitis/episcleritis
Primary sclerosis cholangitis

216
Q

What are the intestinal symptoms of ulcerative colitis

A

Episodic/chronic diarrhoea +/- blood and mucus
Crampy abdominal pain
Tenesmus
Systemic - fever, malaise, anorexia, weight loss

217
Q

What is the Timeline and Witts criteria used for

A

Severity scoring in ulcerative colitis

218
Q

What are the potential complications of ulcerative colitis

A

Obstruction
Toxic megacolon
fistula formation
abscess
malabsorption
malignancy
gallstones

219
Q

What medication can be used in ulcerative colitis but has no place in the management of Crohn’s

A

5 ASA - Mesalazine, sulfasalazine

220
Q

What are the endoscopic findings in a patient with Crohn’s disease

A

Transmural granulomatous inflammation which is uncontinous
Skip lesions between areas of active disease
Bowel is thickened with a narrowed cobblestone appearance due to deep ulcers and fissures

221
Q

What are the intestinal symptoms of Crohn’s disease

A

Bowel ulceration
Abdominal tenderness +/- RIF mass
Perianal fistula /abscess
Skin tags
Anal strictures
Dysphagia
Apthous ulcers

222
Q

The terminal ileum is affected in 70% of patients with which disease

A

Crohn’s disease

223
Q

What is the Montreal classification used for

A

Severity scoring in Crohn’s disease

224
Q

A string sign on barium XR is seen in what disease

A

Crohn’s disease

225
Q

Methotrexate is used in the management of which inflammatory bowel disease

A

Crohn’s disease

226
Q

Why do patients with Crohn’s disease often develop vitamin A, D, E and K deficiency

A

Crohn’s disease most commonly affects the terminal ileum, which is where Vitamin A,D, E and K are absorbed.

227
Q

Describe the adenocarcinoma sequence

A

It is the stepwise accumulation of mutations of oncogenes and tumour suppressor genes
1. Loss of APC gene leads to hyperplasia
2. KRAS mutation leads to dysplasia
3. Loss of p53 results in adenocarcinoma

228
Q

APC and p53 are what type of genes

A

Tumour supressor genes

229
Q

KRAS gene mutation is known as what type of gene

A

Oncogene

230
Q

What are oncogenes

A

Mutated proto-oncogenes
They encode oncoprotein which have the ability to promote cell growth in the absence of normal growth promoting signals

231
Q

Why can oncogenes result in excessive cell proliferation

A

Cells expressing oncogenes are freed from normal checkpoints and controls that limit growth.

232
Q

What is the function of tumour suppressor genes

A

Genes which inhibit cell proliferation or promote death of cells that have damaged DNA

233
Q

What is KRAS

A

GTPase - converts GTP to GDP

234
Q

What may result in more p53 protein

A

DNA damage and stress signals

235
Q

What does increased amount of p53 protein result in

A

Growth arrest - stops progression of cell cycle with damaged DNA
DNA repair - can be activated during growth arrest
Apoptosis - ‘last resort’ to avoid proliferation of cells containing abnormalities

236
Q

What does the loss/mutation of p53 result in

A

DNA damage no longer induces cell cycle arrest/repair therefore genetically damaged cells proliferate giving rise to malignant neoplasms

237
Q

What is the function of APC

A

It encodes a factor that negatively regulates the WNT pathway in colonic epithelium by promoting the formation of a complex that degrades beta-catenin

238
Q

What happens with a mutated APC

A

The factor which binds to beta catenin is not formed. Therefore excess beta catenin accumulates which can translocate to the nucleus where it binds to a transcription factor and activate cell proliferation - it does this irrespective of the WNT pathway

239
Q

What does TNF do in IBD

A

Causes epithelial tight junction permeability to increase causing a flux or luminal bacterial components which activate an innate and adaptive immune response

240
Q

What does FAP stand for and what is it also known as

A

Familial Adenomatous Polyposis, also known as Gardeners syndrome

241
Q

What is FAP

A

An autosomal dominant condition characterised by the lack of APC tumour suppressor gene on the long arm of chromosome 5
Leads to the development of hundreds of tubular adenomas, conferring a 100% risk of CRC by 40

242
Q

What chromosome is APC found on

A

Chromosome 5

243
Q

What is the findings of FAP on colonoscopy

A

Multipel polyps
Largest around 7mm

244
Q

What are the non neoplastic types of polyps

A

Harmatomatous
Metaplastic

245
Q

What are the neoplastic types of polyps

A

Villous
Tubulovillious
Tubular

246
Q

What are the extracolonic manifestations of FAP

A

Mandibular osteomas
Desmoid tumours
Sebaceous cysts

247
Q

What is the management of FAP

A

Prophylactic near total colectomy by the age 25

248
Q

If a patient with FAP had a child what would you recommend

A

Endoscopic surveillance from 12 y/o

249
Q

Define dysplasia

A

Disordered cellular development characterised by increased mitosis, pleomorphism without the ability to invade the basement membrane

250
Q

Define ulcer

A

A lesion in the mucous membrane or the skin resulting from the gradual disintegration of surface epithelial cells

251
Q

What are the risk factors for gallbladder cancer

A

Age >70 y/o
Female > male
FH
Gallstones
Chronic cholecystitis
Ethnicity - Mexican/ native american
Smoking
GB polyps >1cm
Obesity
Porcelain GB
Chronic typhoid infection
ABPJ
Choledochal cyst

252
Q

Where does GB cancer directly invade

A

Segments 4 or 5 of the liver

253
Q

Common sites of metastasis in GB cancer

A

Liver
Stomach
Duodenum
Porta hepatic LN
CBD

254
Q

what is the histolopathology of GB cancer

A

Adenocarcinoma

255
Q

What is the most common organism implicated in SSI

A

Staph aureus

256
Q

Surgical site infection in a POD3 patient, with yellowish granules is likely to be caused by what organism

A

Actinobacillus

257
Q

What causes yellow discharge in an actinobacillus infection

A

Sulphur granules

258
Q

What organisms cause necrotising fascitis

A

Group A streptococcus
Staph aureus
Clostridium perfinges
Bacteroides fragilis
MSRA

259
Q

What is the scoring system that can be used in necrotising fascitis patients

A

Laboratory risk indicator for necrotising fasciitis

Score >6 indicative

260
Q

What is the pathophysiology of necrotising fasciitis

A

Rapidly progressing
Extensive acute inflammatory reaction involving the subcutaneous fat which can go deep into skeletal muscles and further
Extensive suppuration and bacterial colonisation with associated intravascular thrombosis

261
Q

What ABx are used in the management of necrotising fasciitis

A

Clindamycin
Flucloxacillin
Gentamicin
Metronidazole
Penicillin

262
Q

What would be the differential diagnosis for post operative bloody diarrhoea

A

Pesudomembranous colitis
Bowel ischaemia
Curling’s ulcer
Infective gastroenteritis

263
Q

What is the pathophysiology of pseudomembranous colitis

A

Often triggered by ABx therapy which disrupts normal microbiota and allows C.Difficile to colonise and grow.
Release of C.Difficile toxin disrupts epithelial function
Subsequent inflammatory response
Neutrophil eruption form colonic crypts which spreads to form mucopurulent psuedomembranes

264
Q

What infetion is pseudomembranous colitis associated with

A

C. difficile

265
Q

What are the appearances of pseudomembranous colitis on colonoscopy

A

Yellowish plaques

266
Q

Describe the pathophysiology of diverticulosis

A

Colonic diverticula result from the unique structure of the colonic muscularis propria and the elevated intraluminal pressure in the sigmoid colon
Where nerves, arterial vasa recta and their connective tissue sheaths penetrate the inner circular muscular coat focal discontinuities are created - so when there is increased pressure are such points outpouching can occur

267
Q

Why does diverticulosis occur in the large bowel and not the small bowel

A

In the colon the wall is not reinforced by external longitudinal layer of muscular propria, as this is gathered as the Taenia coli

268
Q

What is the cause of diverticulitis in diverticular disease

A

Obstruction of the diverticular leads to inflammatory changes producing diverticulitis and peridiverticulits. Because the wall of the diverticulum is only supported by the muscularis mucosa and a thin layer of subserosal adipose tissue, inflammation and increased pressure within an obstructed diverticulum can lead to perforation

269
Q

What is the Hinchey Classification

A

The classification for perforated diverticulitis

270
Q

Describe the different grades of the Hinchey Classification

A

I - Pericolic abscess
IIa - Distant abscess amenable to percutaneous drainage
IIb - Complex abscess with fistula that is not amenable to drainage
III - Generalised purulent peritonitis
IV - Faecal peritonitis

271
Q

Define diverticulosis

A

Presence of diverticula but asymptomatic

272
Q

Define diverticular disease

A

Diverticula and symptoms

273
Q

Define diverticulitis

A

Evidence of diverticular inflammation +/- localised symptoms and signs

274
Q

What is the link between endometriosis and ovarian cancer

A

Endometriosis increases the risk of ovarian cancer by 3.5x

275
Q

What are the different theories of the pathogenesis of Endometriosis

A

Regurgitation theory - retrograde mensturation, explains endometriosis within the endometrial cavity
Benign metastasis theory - spreads via the blood and lymphatic system
Metaplastic theory - directly arises from coelomic epithelium
Extrauterine stem cell/progenitor cell theory - differentiation into endometrium

276
Q

How would intrapertioneal endometriosis be described

A

Burn powder
Dark blue/black
Chocolate cysts

277
Q

What is the epithelium of the uterus

A

Simple columnar epithelium supported by thick vascular stroma
Endometrium - inner layer, along with mucus membrane

278
Q

What are the two layers of endometrium

A

Basal layer
Functional layer - thickens and then is sloughed during mensturation

279
Q

What is the cause of pain in endometriosis

A

Cyclical pain as tissue under hormonal control
Intrapelvic bleeding
Periuterine adhesions form

280
Q

What are the risk factors for peptic ulcer disease

A

H Pylori infection
NSAIDs
Smoking

281
Q

What is the CLO test

A

Campylobacter like organism test
Dependent on the presence of H. Pylori and urease produced by the bacteria (converts urea to ammonia which increases the pH)

282
Q

What enzymes does H Pylori produce

A

Ureases - catalyses the hydrolysis of urea to ammonia
Proteases
Phospolipases

283
Q

What is the action of the enzymes produced by H Pylori

A

Infects the stomach
Produces ureases, (allows pH to increase to allow survival), proteases, phospholipases
The production of ammonia, and the damage to gastric mucosa from other enzymes produced causes inflammation

284
Q

What is the pathophysiology of H Pylori colonisation

A

Flagella allows motility
Urease - generates ammonia from endogenous urea, thereby elevates local gastric pH around the organism and protecting the bacteria from the acidic pH of the stomach
Adhesins - enhance bacterial adherence to surface alveolar cells
Toxins - such as cytotoxin associated gene A (saga) may be involved

285
Q

What types of gastric cancer are associated with H Pylori

A

Adenocarcinoma
Mucosal associated lymphoid tissue tumour (MALT)

286
Q

Hashimotos thyroiditis is associated with what infection

A

H Pylori

287
Q

What is the MOA of PPI

A

Binds irreversibly to the H+/K+ ATPase on gastric parietal cells - stops the secretion of H+ and therefore HCl does not form

288
Q

What does H Pylori eradication therapy entail

A

7 days
Omeprazole 20mg BD
Clarithromycin 500mg BD
Amoxicillin 1g BD (Metro if pen allergic)

Confirmation of healing of gastric ulcers on endoscopy after 6-8 weeks

289
Q

What is the action of HCl

A

Activates pepsinogen to pepsin which helps in proteolysis
Antimicrobial

290
Q

Why can NSAID use precipitate PUD

A

Topical irritation of epithelium by NSAIDs - impairs the barrier properties of the mucosa
Suppression of gastric PG synthesis - due to inhibition of cycloxygenase
Reduction of gastric mucosal blood flow
Interference with superficial healing

291
Q

How is hypercalcaemia linked to PUD

A

Hypercalcaemia leads to increased gastrin release, which leads to increased HCl production

292
Q

What are the common causes of hypercalcaemia

A

Malignancy
Renal failure
Hyperparathyroidism

293
Q

How are parathyroid glands localised intraoperatively

A

Pathological lab procedure to perform rapid microscopic analysis of a specimen
Specimen fixed onto a metallic disc and then rapidly frozen to -20/30 degrees
Embedded into gel like medium, cut and then stained

294
Q

What is the normal epithelium of the gastric mucosa in the antrum of the stomach

A

Simple columnar with mucosal and goblet cells

295
Q

What is the histology of a parathyroid adenoma

A

Uniform polygonal chief cells with small centrally placed nuceli
A few nests of oxyphil cells are present
A rim of compressed, non neoplastic parathyroid tissues generally separated by a fibrous capsule

296
Q

If the parathyroid glands are not in their normal position where may they be found and why

A

Superior mediastinum

Thymus originates from the third branchial arch - so will occasionally drag the inferior parathyroid glands down into the mediastinum

297
Q

What are the clinical features of hypercalcaemia

A

Nephroliathis with resultant polyuria and polydipsia
Bone pain/#
Tired and depressed
Pancreatitis
PUD
Constipation
N+V

298
Q

What are the three types of hyperparathyroidism and the common causes of each

A

Primary - usually a solitary adenoma, parathyroid carcinoma
Secondary - Chronic renal failure
Tertiary - Autonomous ongoing parathyroid hyperplasia

299
Q

In which kind of hyperparathyroidism is the calcium normal or low

A

Secondary

300
Q

In which kind of hyperparathyroidism is phosphate increased

A

Secondary

301
Q
A

MRCS (17 decks)

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