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Arjun's Copy- Owen's Path > Histopathology > Flashcards

Histopathology Flashcards

1
Q

What are the layers of the epidermis
(superficial to deep)

A

Stratum corneum
Stratum lucidum
Stratum granulosum
Stratum spinosum
Stratum basale
Basement membrane

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2
Q

What cells make up the epidermis

A

Keratinocytes

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3
Q

What is contained within the dermis

A

Collagen
Elastin
Glands
Vascular supply

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4
Q

What does hyperkeratosis mean

A

Increase in size of stratum corneum
Increased keratin

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5
Q

What does parakeratosis mean

A

Increased nuclei in the stratum corneum
They get retained there

any keratosis is s. corneum

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6
Q

What does acanthosis mean

A

Increase in the stratum spinosum

acanthoSis (Spinosum)

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7
Q

What does acantholysis mean

A

Reduced cohesions between keratinocytes

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8
Q

What is spongiosis

A

Intercellular oedema

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9
Q

What does actinic mean

A

Damaged by the sun

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10
Q

What is a benign derm neoplasm

A

Seborrheic Keratosis

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11
Q

What do seborrheic keratoses appear like

A

Rough pigmented plaques
Waxy and stuck on
Coin shaped

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12
Q

Who do seborrheic keratoses appear in

A

Middle age and elderly

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13
Q

What is the histology of seborrheic keratoses

A

Horn cysts
Orderly hyper-proliferation of epidermis

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14
Q

What are horn cysts seen in

A

Seborrheic keratosis

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15
Q

What are the premalignant derm neoplasms

A

Actinic keratosis
Keratoacanthoma
Bowens disease

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16
Q

How do actinic keratoses appear

A

Papule or plaque
Skin is red
White or yellow scaly crusts

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17
Q

What skin pathology is described as sandpaper like texture

A

Actinic keratosis

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18
Q

Histology of actinic keratosis

A

SPAIN (it’s sunny in spain!)
Solar elastosis (an accumulation of abnormal elastin in the dermis of the skin, as a result of the cumulative effects of sun exposure- ‘photo-ageing’)
Parakeratosis
Atypia/dysplasia
Inflammation
Not full thickness

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19
Q

How does a keratoacanthoma appear

A

Dome shaped nodule with necrotic crusted centre

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20
Q

Histology of squamous cell carcinoma

A

Full thickness atypia/dysplasia throughout the epidermis spreading through basement membrane into dermis
Nuclear crowding

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21
Q

Histology difference between bowens disease and squamous cell carcinoma

A

SCC is bowens but it spreads through the basement membrane

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22
Q

How does bowens disease appear

A

Intra-epidermal squamous cell carcinoma
Flat
Red
Scaly patches
Stand alone

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23
Q

What are 2 precursors to SCC

A

Bowens disease
Actinic keratosis

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24
Q

Difference between actinic keratosis and bowens disease

A

Bowens disease is full thickness

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25
Q

How do basal cell carcinomas appear

A

Pearly surface
Telengiectasia
Rolled over edges

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26
Q

What is rodent ulcer

A

Basal cell carcinoma

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27
Q

Histology of BCC

A

Mass of basal cells pushing down into dermis
Palisading (alignment of nuclei in outermost layer)

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28
Q

Pathophysiology of amyloidosis

A

Excess proteins clumpb together to form beta sheets which make up fibrils
These then deposit in the EC space of tissues and cause damage

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29
Q

Why is AL amyloidosis called AL

A

Amyloid ‘light’- as excess light chains

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30
Q

What is a dyscrasia

A

Non specific term for disorder of blood

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31
Q

What is pathophysiology of AA amyloidosis

A

In chronic systemic inflammatory responses to infections, cancers and autoimmue conditions there is an excess of serum amyloid A which forms amyloid deposits in tissues

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32
Q

What is amyloid protein in AA amyloid

A

Serum amyloid A

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33
Q

What conditions cause AA amyloidosis

A

Infections- TB, osteomyelitis, IVDU skin infections, familial mediterranean fever
Autoimmine- IBD, RA, Ank spond
Cancer- Hodgkins lymphoma, Renal cell carcinoma

infections, inflammation, cancer again!

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34
Q

What is the most common form of familial amyloidosis

A

Familial mediterranean fever

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35
Q

Where is the amyloid deposition predominant in famial mediterranean fever

A

Kidney

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36
Q

Who does haemodialysis associated amyloidosis occur in

A

Chronic renal failure patients who are on especially peritoneal dialysis

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37
Q

What is the protein deposited in haemodialysis associated amyloidosis

A

Beta-2-microglobulin

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38
Q

What is most common presentation of amyloidosis

A

Nephrotic syndrome

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39
Q

Clinical features of amyloidosis

A

Carpal tunnel syndrome
Macroglossia
Hepatosplenomegaly
Restrictive cardiomyopathy
Nephrotic syndrome

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40
Q

Stain done for amyloidosis

A

Congo red stain under polarised light

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41
Q

Positive amyloid finding on congo red stain

A

Apple green birefringence- caused by beta pleated sheet configuration

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42
Q

What is negative congo red stain colour

A

Pink/red

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43
Q

When are neutrophils involved

A

Acute inflammation

esp bacterial

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44
Q

When are macrophages involved

A

Late acute inflammation (to clear debris)
Chronic inflammation like in granulomas

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45
Q

When are lymphocytes involved

A

Chronic inflammation
Lymphomas

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46
Q

When are plasma cells involved

A

Chronic inflammation
Myeloma

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47
Q

When are eosinophils involved

A

Allergic reactions
Parasitic infections
Hodgkins disease (reactive eosinophilia?)

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48
Q

When are mast cells involved

A

Allergic reactions

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49
Q

How do mast cells appear on histology

A

Lots of granules

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50
Q

Typical histological features of squamous cell carcinomas (not skin)

A

Keratin production
Intercellular bridges
Do not form glands

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51
Q

How do adenocarcinomas appear histologically

A

Form glandular epithelium
Form glands that can secrete substances

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52
Q

How do transitional cell carcinomas appear

A

Stretchy epithelium

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53
Q

Where do you get stretchy epithelium

A

Transitional cell carcinomas

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54
Q

What is the definition of histochemical stain

A

Result from the chemical reaction between stain and the tissue

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55
Q

What is the definition of immunohisto stain

A

Involves the antibodies against a specific antigen

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56
Q

What is lichenification

A

When skin becomes leathery and thick

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57
Q

What happens to skin if chronic atopic dermatitis

A

Lichenification

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58
Q

Acute histology of dermatitis

A

Spongiosis
Inflammatory infiltrate in the dermis (neutophils)
Dilated dermal capillaries

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59
Q

Chronic dermatitis histology

A

Acanthosis
Crusting
Hyperparakeratosis
T cells and eosinophil infiltrate

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60
Q

What is pathophysiology of seborrheic dermatitis

A

Inflammatory reaction to yeast infection- malassezia

cradle cap

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61
Q

What type of hypersentivity reaction is stevens johnsons syndrome

A

IV

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62
Q

What is the pathophysiology of SJS

A

Hypersensitivity reaction against the epidermis and mucosa which leads to necrosis of skin which can be wiped off

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63
Q

What determines if SJS or toxic epidermal necrolysis

A

<10% in SJS
>30% in TEN

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64
Q

What can cause SJS

A

Drugs- sulfonamides, lamotrigine/carbamezapine
Infection- CMV, mycoplasma

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65
Q

How does chronic plaque psoriasis appear

A

Salmon pink well demarcated red plaques with silver scales

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66
Q

Where does chronic plaque psoriasis appear

A

Extensors of knees, elbows and scalp

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67
Q

What is auspitz sign

A

Rubbing plaque leads to pinpoint bleeding

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68
Q

What is the koebner phenomenam

A

Lesions form at site of trauma- seen in psoriasis

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69
Q

Histopathology of psoriasis

A

Parakeratosis
Loss of granular layer
Clubbing of rete ridges giving test tubes in rack appearance
Munros abscesses
Dilated blood vessels

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70
Q

Clubbing of rete ridges giving test tubes in rack

A

Psoriasis

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71
Q

What is pathophysiology of psoriasis

A

Type IV hypersensitivity reaction

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72
Q

When does guttate psoriasis present

A

Childhood

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73
Q

What triggers guttate psoriasis

A

Post strep throat 2 weeks ago
Typically in children

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74
Q

How does guttate psoriasis appear

A

Small spots
Rain drop plaque distribution
Over trunk and limbs

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75
Q

What is erythodermic psoriasis

A

Widespread disease with systemic symptoms

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76
Q

Where does pustular psoriasis affect

A

Hands and feet

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77
Q

How does pustular psoriasis appear

A

Red skin with white elevations of pus

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78
Q

What are the nail changes seen in psoriasis

A

Pitting
Onycholysis
Subungal hyperkeratosis

POSH

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79
Q

Who does flexural psoriasis occur in

A

Elderly

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80
Q

Where does flexural psoriasis occur

A

Creases in the skin
Groin
Submammary
Natal cleft

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81
Q

Histopathology of sarcoidosis

A

Non-caseating granulomas
Schaumann and asteroid bodies
CD4+

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82
Q

What are schaumann and asteroid bodies

A

Inclusions of protein and calcium

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83
Q

Blood findings of sarcoid

A

Hypercalcaemia
High ACE
High ESR
Anaemia
Leukopaenia

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84
Q

Skin findings in sarcoid

A

Erythema nodosum
Lupus pernio
Skin nodules

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85
Q

Eye manifestations of sarcoid

A

Anterior Uveitis
Posterior uveitis
Uveoparotid fever (heerfordt’s syndrome)
Keratojunctivitis
Lacrimal gland enlargement

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86
Q

What happens in uveoparotid fever (heerfordt syndrome)

A

Bilateral uveitis
Parotid enlargement
Potentially facial nerve palsy

sarcoid!

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87
Q

Joint manifestation of sarcoid

A

Arthritis
Bone cysts

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88
Q

Heart presentation of sarcoid

A

Cardiomyopathy
Conduction problems
Valvular disease
Pericarditis

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89
Q

What is the pathophysiology of bullous pemphigoid

A

IgG abs bind to hemidesmosomes which anchor epidermis to basement membrane
Leads to detachment of epidermis and formation of SUBdermal bullae

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90
Q

What is the pathophysiology of pemhigus vulgaris

A

IgG binds to desmoglein 1&3 which connect keratinocyes and between mucous membranes
Leads to breaking between layers of epidermis causing INTRAdermal bullae

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91
Q

What is difference in bullae between pemphigus vulgaris and bullous pemphigoid

A

Bullae in bullous pemphigoid are tense on erythematous base- DO NOT rupture
Bullae in pemphigus vulagris are easily ruptured which leads to a raw red surface
Nikolsky positive in pemphigus vulgaris

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92
Q

Histopathology of bullous pemphigoid

A

Subepidermal bulla with eosinophils
Linear deposition of IgG along basement membrane

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93
Q

Histopathology of pemphigus vulgaris

A

Acantholysis
Intradermal bulla
Netlike pattern of IgG
Complement deposition

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94
Q

What is the pathophysiology of dermatitis herpetiformis

A

IgA binds to basement membrane forming subepidermal bulla

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95
Q

What is dermatitis herpetiformis associated with

A

Coeliac

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96
Q

How does dermatitis herpetiformis appear

A

Itchy vesicles on extensors of elbows
Buttocks

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97
Q

Histology of dermatitis herpetiformis

A

Microabscesses which coalesce to form subepidermal bullae
Neutrophil and IgA deposits at tips of dermal papillae

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98
Q

How do lichen planus plaques appear

A

Hyperpigmented
Itchy
Polygonal
Papules
Plaques
Fine white network on the surface called wickams striae

Ps

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99
Q

Where is lichen planus normally found

A

Inner surface of wrists
Oral mucous membranes with lacy appearance

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100
Q

Histopathology of lichen planus

A

Hyperkeratosis
Saw toothing of rete ridges
Basal cell degeneration

civette bodies too

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101
Q

What are wickhams striae

A

White network on top of plaques seen in lichen planus

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102
Q

What are annular target lesions seen in

A

Erythema multiforme

and lyme disease (erythema migrans-EM again)

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103
Q

Where are erythema multiforme lesions seen

A

Extensor surfaces of hands and feet

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104
Q

How do erythema multiforme lesions develop

A

Can become pleomorophic so are anything from macules, papules, petechiae and bullae

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105
Q

Causes of erythema multiforme

A

Infections- HSV, mycoplasma
Drugs- SNAPP (sulphonamides, NSAIDs, allopurinol, penicillin, phenytoin)

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106
Q

SNAPP causes of erythema multiforme

A

Sulphonamides
NSAIDS
Allopurinol
Penicillin
Phenytoin

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107
Q

What causes pityriasis rosea

A

Appears after viral illness

HHV6,HHV7

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108
Q

Development of pityriasis rosea

A

Salmon pink rash apppears first called herald patch
Oval macules in xmas tree distribution then appear

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109
Q

What is a herald patch

A

Erythematous patch with white centre seen in pityriasis rosea

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110
Q

What is the scientific word for moles

A

Melanocytic naevi

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111
Q

Histology of melanomas

A

Atypical melanocytes
Initially radial growth phase then vertical phase
Buckshot appearance in vertical phase

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112
Q

Steps of atherogenesis

A

Endothelial injury
LDL enters subintimal space and gets trapped
LDL oxidised
Oxidised LDL gets taken up by macrophages via scavenger receptors becoming foam cells
Foam cells apoptose which causes cholesterol core
Increase in adhesion molecules on endothelium results in more macrophages and t cells
Vascular smooth cells form fibrous cap

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113
Q

What receptors take up oxidised LDL into macrophages

A

Scavenger

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114
Q

Why is abdo aorta more affected by atherosclerosis

A

Around the origins of major branches there is turbulent blood flow which has a low oscillatory shear stress

around the ostia

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115
Q

What are ostia

A

Origins of major arteries

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116
Q

Which blood flow is anti-atherogenic

A

Laminar
Turbulent is atherogenic

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117
Q

How long of severe iscahemia causes myocyte death

A

20-40 mins

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118
Q

Complications of an MI

A

DARTH VADER
D-death
A- arrythmia
R- rupture
T- tamponade
H- HF
V- valve disease
A- aneurysm of ventricle
D- dresslers syndrome
E- embolism
R- recurrence

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119
Q

What can rupture most after MIs

A

Due to necrosis:
- Septum causing left to right shift or VSD
- Papillary muscle causing MR
- Ventricular wall causing haemopericardium

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120
Q

What valve disease is common post MI

A

Mitral regurgitation from papillary muscle rupture or necrosis

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121
Q

What causes persistent ST elevation post MI

A

Ventricular aneurysm which can develop for over a month after

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122
Q

Difference between pericardial effusion and tamponade

A

Tamponade is when the fluid obstructs the contractility of the heart

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123
Q

What causes fibrinous pericarditis post MI

A

If MI extends to the epicardium

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124
Q

Pericardial complications of MI

A

Fibrinous pericarditis
Dresslers
Effusion/tamponade
Early infarct associated pericarditis

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125
Q

What is a mural thrombus

A

Clot that sticks to wall of heart

blood clot that forms within the heart’s chambers or on the walls of blood vessels supplying the heart muscle.

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126
Q

When are mural thrombi common

A

Ventricular aneurysm

as allows a pouch of stagnant blood to form?

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127
Q

What is nutmeg liver

A

The appearance of the liver due to chronic hepatic vein congestion

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128
Q

Long term what does nutmeg liver become

A

Cirrhosis aka cardiac cirrhosis

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129
Q

What are haemosedirin laden macrophages

A

Macrophages which have taken onto red blood cells in lungs after alveolar have burst
AKA heart failure cells

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130
Q

Histology post MI
- under 6 hours
- 6-24 hours
- 1-4 days
- 5-10 days
- 1-2wks
- weeks-months

A
  • Normal by histology, CK also normal
  • Loss of nuclei, necrotic cell death, homogenous cytoplasm
  • Infiltration of polymorphs then macrophages
  • removal of debris
  • granulation tissue, new blood vessels, collagen synthesis, myofibroblasts
  • decullarising scar tissue
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131
Q

Histology of heart in HF

A

Dilated heart with thin walls
Haemosiderin macrophages in lungs
Scarring
Fibrosis and replaced myocardium

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132
Q

Pathophysiology of rheumatic fever

A

Cell mediated immunity and antibodies to strep antigens cross react with myocardial antigens

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133
Q

Histology of rheumatic fever

A

Beady fibrous vegetations
Aschkoff bodies
Anitschow myocytes

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134
Q

Treatment for rheumatic fever

A

Benzylpenicillin

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135
Q

Diagnosis of rheumatic fever

A

Jones criteria
Group A strep infection and 2 major criteria
Group A strep infection and 1 major+ 2 minor

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136
Q

Major jones criteria

A

Carditis
Arthritis
Sydenhams chorea
Erythema marginatum
Subcut nodules

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137
Q

Minor jones criteria

A

Fever
Raised ESR or CRP
Migratory arthralgia
Malaise
Tachycardia
Prolonged PR interval
History of rheum fever

FRAPP/PEACE

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138
Q

How does rheum fever affect the following
- heart
- joints
- CNS
- skin

A
  • endocarditis, pericarditis, mycocarditis
  • arthritis, synovitis
  • subcut nodules, erythema marginatum
  • encephalopathy, sydenhams chorea
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139
Q

What is most common form of prostate cancer in over 50s

A

Adenocarcinoma

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140
Q

What is normal precursor of prostate cancers

A

Prostatic intraepithelial neoplasia
PIN

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141
Q

How is prostate cancer graded

A

Gleason

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142
Q

Rfs for RCC

A

Smoking
HTN
Obesity
Long term dialysis
Unopposed oestrogen
Heavy metals

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143
Q

3 types of malignant renal cancer

A

Renal cell carcinoma
Nephroblastoma
Transitional cell carcinoma

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144
Q

What group of people are nephroblastomas seen in

A

Childhood- is second most common childhood malignancy

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145
Q

Where do transitional cell carcinomas develop

A

Anywhere in urothelial tract- can be from renal pelvis to urethra
Most commonly in bladder

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146
Q

What are the types of renal cell carcinoma

A

Clear cell 70%
Papillary 15%
Chromophobe 5%

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147
Q

Difference in macroscopic appearance of renal cell carcinomas

A

Clear cell- golden yellow with haemorrhagic areas
Papillary- friable brown
Chromophobe- solid brown

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148
Q

Microscopic appearance of clear cell RCC

A

Nests of epithelium with clear cytoplasm

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149
Q

Microscopic appearance of papillary RCC

A

Papillary tubopapillary growth patter over 5mm

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150
Q

Microscopic appearance of chromophobe RCC

A

Sheets of large cells with distinct cell borders

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151
Q

Where do RCC appear from

A

Typically epithelial cells in the cortex of kidney

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152
Q

Microscopic appearance of nephroblastoma

A

Small round blue cells

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153
Q

Types of renal transitional cell carcinomas

A

Non-invasive papillary
Infiltrating/invasive urothelial carcinoma
Flat urothelial carcinoma in situ

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154
Q

How do non-invasive papillary urothelial carcinomas appear macroscopically

A

Frond like growths projecting from the walls
Often multifocal

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155
Q

How do non-invasive papillary urothelial carcinomas appear microscopically

A

The fronds which project are lined with urothelium

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156
Q

How do invasive urothelial carcinomas appear

A

Solid tumours stuck to pelvis

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157
Q

What are the 3 bladder tumours

A

Transitional cell 90%
Squamous cell carcinoma
Adenocarcinoma

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158
Q

What causes bladder squamous cell carcinomas

A

Schistomiasis

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159
Q

What causes bladder adenocarcinomas

A

Arise from intestinal metaplasia or urachal remnants

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160
Q

Location of the lung cancers

A

Proximal bronchi- small cell and squamous
Distal- adenocarcinoma

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161
Q

Histology of squamous cell lung cancer

A

Keratinisation
Intercellular prickles

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162
Q

Which lung cancer is associated with hypercalcaemia

A

Squamous cell carcinoma
PTHrp secretion

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163
Q

Histology of adenocarcinomas lung

A

G;andular differentiation- gland formation and mucin production

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164
Q

Which paraneoplastic syndromes are small cell carcinoma are associated with

A

SIADH
Cushing from ACTH
Lambert eaton

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165
Q

What cells does small cell lung cacner arise from

A

Neuroendocrine

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166
Q

Which lung cancers have high relationship to smoking

A

The S’s

Sqcc and SCLC

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167
Q

Histology of small cell carcinoma

A

Small
Poorly differentiated
Oat cells

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168
Q

Histology of large cell carcinoma

A

Poorly differentiated
Large cells
Large nuclei
Prominent nucleoli
No glandular or squamous differentiation

pleomorphic giant cells like DC of breast

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169
Q

How are tumours staged

A

TNM
Tumour- invasion
Nodes- lymph nodes involved
Mets

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170
Q

What are the 3 benign renal tumours

A

Papillary adenoma
Oncocytoma
Angiomyolipoma

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171
Q

Where are the renal papillae

A

Where collecting ducts enters the ureters

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172
Q

What are papillary adenoma

A

Renal epithelial tumours with a papillary structure
Less than 5mm

<15mm?

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173
Q

What is an oncocytoma

A

Benign renal epithelial tumour characterised by presence of oncocytes- eosinophillic cytoplasm

mahogany brown + central scar

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174
Q

What are angiomyolipomas made up of

A

Mesenchymal tumour
Fat
Blood vessels
Muscle

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175
Q

What renal cell carcinoma is common in dialysis associated cystic disease

A

Papillary carcinoma

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176
Q

Management of nephroblastoma

A

Nephrectomy with pre or post op chemo

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177
Q

What is myocyte disarray seen in

A

HCM

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178
Q

Where does hypertrophy occur in HOCM

A

Interventricular septum

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179
Q

What is most common gene affected in HOCM

A

Beta myosin heavy chain
BMHC

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180
Q

Most common cause of restrictive CM

A

Amyloidosis

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181
Q

What is libmen sacks endocarditis

A

Cardiac complication of SLE and APL where get vegetations on endocardium

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182
Q

Characteristics of libmen sacks endocarditis vegetations

A

Warty vegetations that are sterile and platelet rich

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183
Q

Organisms which cause acute endocarditis

A

Staph aureus
Strep pyogenes

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184
Q

Organisms which cause sub-acute endocarditis

A

Strep viridans
Staph epidermis
HACEK
Coxiella
Mycoplasma
Candida

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185
Q

What organisms are in HACEK

A

Haemophilus
Aggregatibacter
Cardiobacterum
Eikenella
Kingella

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186
Q

Most common valvular problems in IE

A

Mitral and aortic regurg

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187
Q

Immune phenomena in IE

A

Roth spots- in eyes
Osler nodes- red painful nodes on hnads or feet
Haematuria from glomerulonephritis

rememebr fROm jane c
as immune complex deposition
Immune phenomena result from the body’s immune response to the infection, leading to the formation of immune complexes and subsequent deposition in various tissues.

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188
Q

Thromboembolic complications of IE

A

Janeway lesions
Septic abscesses
Microemboli
Splinter haemorrhages
Splenomegaly

Embolic phenomena occur when fragments of infected material (vegetations) from the heart valves break off and travel through the bloodstream, lodging in distant organs and causing ischemia, infarction, or abscesses.

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189
Q

How is IE diagnosed

A

Dukes criteria
- 2 major
- 1 major and 3 minor
- 5 minor

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190
Q

Major dukes criteria

A

Positive blood culture growing typical IE organism
Vegetations on echo/new regurg murmur

BE TIMER

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191
Q

Minor dukes criteria

A

Risk factor
Fever
Thromboembolic phenomena
Immune phenomena
Positive blood cultures that dont meet major criteria

BE TIMER
(BE is major)
(timer = Temp, immune phenomena, microbiological (cultures not meeeting major), embolic, RFs)

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192
Q

Tx for IE

A

Start broad spectrum abx then treat according to sensitivities

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193
Q

Abx for subacute IE

A

Benzylpenicillin and gentamycin
OR
Vancomycin

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194
Q

Abx for acute IE

A

Flucloxacillin for MSSA
Rifampicin, vancomycin and gentamicin for MRSA

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195
Q

What are 5 benign neoplastic breast conditions

A

Fibroadenoma- most common
Intraductal papilloma
Radial scar
Phyllodes tumour
Fibrocystic disease

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196
Q

What are fibroadenomas

A

Benign neoplasms of fibrous tissue and glandular tissue

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197
Q

What causes fibroadenomas to increase in size

A

Pregnancy as hormone responsive

oestrogen so size changes in menstrual cycle too

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198
Q

Cytology of fibroadenoma

A

Branching sheets of epithelium in antler horn or honeycomb sheets
Bare nuclei and stroma

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199
Q

How do intraductal papillomas present

A

Bloody discharge or clear
Lump
Can be pain

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200
Q

Histology of intraductal papilloma

A

Papillary mass with a dilated duct lined by epithelia

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201
Q

What is a radial scar

A

A benign sclerosing lesion often found on histology
Called scar as what appears like under the microscope histologically

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202
Q

Histology of radial scar

A

Central fibrous stellate area

called radial scar as this is how it appears on histology

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203
Q

What are radial scars over 1 cm called

A

Complex sclerosing lesions

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204
Q

How does radial scar appear on mammography

A

Stellate area which can be confused for carcinoma

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205
Q

How do phyolldes tumours present

A

Palpable masses in over 50s

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206
Q

How does fibrocystic breast disease present

A

Lumpiness in breasts which changes according to cycle

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207
Q

Histology of fibrocystic breast disease

A

Fibrous tissue containing cysts with flattened and cuboidal epithelium

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208
Q

What are the breast proliferative conditions

A

A group of intraductal epithelial proliferations which are asymptomatic but can develop into a breast carcinoma
Usual epithelial hyperplasia
Flat epithelial atypia
In situ lobular neoplasia

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209
Q

What is the difference between the 3 breast proliferative conditions with regards to their histology

A

Usual type- growth of epithelial and glandular tissue protruding into lumen in fronds
Flat atypia- multiple layers forming a smaller but regular circular lumen
Intralobular neoplasia- solid proliferation of aplastic cells where can just see the lumen

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210
Q

What cancers does BRCA increase the risk of

A

Breast
Ovarian
Pancreatic
Prostate

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211
Q

Wht does pregnancy reduce the risk of breast cancer

A

There is differentiation of milk producing luminal cells which removes them from pool of potential cancer cells

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212
Q

What is pagets disease of the breast

A

underlying ca, get nipple (P disease of the NIPPLE) then areola

opposite way round in eczema

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213
Q

What is the screening programme for breast cancer

A

47-73 year olds invited every 3 years for mammography

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214
Q

What is looked for on mammography in breast cancer screening

A

Microcalcifications (DC) or a mass

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215
Q

What is difference in detection of lobular and ductal carcinoma in situ

A

Lobular- always on biopsy as no microcalcification
Ductal- appear as areas of microcalcifications on mammogram. Typically on screening unless get pagets

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216
Q

What do lobular breast carcinomas lack

A

Protein E-cadherin

so little cohesion betw cancer cells hence less mass forming, more diffuse pattern

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217
Q

Which breast cancer does pagets develop from

A

Ductal

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218
Q

Histology of ductal carcinoma in situ

A

Ducts filled with atypical epithelial cells

219
Q

How are invasive breast carcinomas classified

A

Ductal
Lobular
Tubular
Mucinous

220
Q

Histology of invasvie ductal carcinoma

A

Carcinoma which isnt classified into another group
Big pleiomorphic cells which invade into the stroma(ie beyond duct)

221
Q

Histology of invasive lobular carcinoma

A

Well formed tubules with low grade nuclei

chains/strands/single file of cells

222
Q

Histology of breast mucinous carcinoma cells

A

Produce abundant amounts of extracellular mucin which dissect surrounding tissue

223
Q

How are breast cancers investigated

A

Triple assessment
Exam, Mammogram/US (<35 as denser breast tissue), FNA and cytology (or biopsy and histology)

1 stop clinic?

224
Q

What receptors are tested for in breast cancer and which has best prognosis

A

HER2-poor prognosis but herceptin
ER/PR- very good prognosis as will respond to tamoxifen

225
Q

Which drug is used to treat ER/PR positive cancer

A

Tamoxifen

226
Q

Which drug is used to treat HER 2 positive cancer

A

Herceptin/trastuzumab- monoclonal Ig to Her2

227
Q

What is problem of herceptin therapy

A

Direct toxic affect on myocardium
Must monitor LVEF

228
Q

What is most significant prognostic factor in breast cancer

A

Axillary lymph node involvement

229
Q

Histology of basal like carcinoma

A

Sheets of markedly atypical cells with lymphocyte involvement

+ve for cytokeratin 5/6
usually triple negative

230
Q

What gene associated with male breast cancer

A

BRCA2- in familial cases at higher risk and not BRCA1

231
Q

What are 2 benign liver lesions

A

Hepatic adenoma
Haemangioma- most common

232
Q

What is main cause of hepatic adenoma

A

OCP

233
Q

How do hepatic adenomas present

A

Abdo pain and intraperitoneal bleeding

234
Q

What is the most common liver malignancy

A

Secondary metastases from GI tract, breast or lung

235
Q

What are the 5 liver malignancies

A

Hepatocellular carcinoma
Cholangiocarcinoma
Hepatoblastoma
Secondary tumours
Haemangiosarcoma

236
Q

What are cholangiocarincomas

A

Adenocarcinomas which arise from bile ducts

237
Q

Causes of cholangiocarcinoma

A

PSC
Parasitic liver disease
Chronic liver disease
Congenital liver abnormalities
Lynch syndrome 2

238
Q

Who do hepatoblastomas occur in

A

Children- they present with an abdo mass

239
Q

What is most common site of pancreactic adenocarcinoma

A

Head of the pancreas

240
Q

Risk factors for pancreactic adenocarcinoma

A

Smoking
Diet
HNPCC
FAP
BRCA

241
Q

What is trousseaus syndrome

A

Superficial thrombophlebitis

migratory thrombophlebitis

242
Q

Presentation of insulinoma

A

Hypoglycaemic attacks

whipple’s triad

243
Q

Presentation of gastrinoma

A

Zollinger Ellison syndrome- high acid output so get recurrent ulceration of the stomach

244
Q

Presentation of a vipoma

A

Diarrorhoea as VIP- vasoactive intestinal peptide

245
Q

Presentation of glucagonoma

A

Necrolytic migratory erythema

246
Q

How are neuroendocrine tumours classified

A

Function- symptoms of hormone excess
Non-function

247
Q

Histology of pancreatic endocrine tumour

A

Cells arranged in nests or trabeculae with grannular cytoplasm

248
Q

Epithelial anamtomy of oesophagus

A

Proximal 2/3 squamous epithelium (white)
Distal 1/3 columnar epithelium (pink)
Joined by the squamous columnar junction- Zline

249
Q

GORD pathophysiology and what can lead to

A

Acid from stomach is refluxed up into oesophagus which causes oesophagitis and maybe- malaena, haemorrhage, haematemesis, stricture, barretts oesophagus

250
Q

What is barrets oesophagus

A

After chronic GORD can get metaplasia in the oesophagus from squamous epithelia to columnar which have goblet cells
Get upwards movement of the SCJ

251
Q

What are 2 oesophageal cancers

A

Adenocarcinoma
Squamous cell carcinoma

252
Q

What is main risk factor for oesophageal adenocarcinoma

A

Barretts oesophagus
Can also be smoking, obesity and radiation exposure

253
Q

Where do you get adenocarcinomas in the oesophagus

A

Distal 1/3 as associated with barrets oesophagus

254
Q

Risk factors for squamous cell carcinoma of oesophagus

A

Smoking
Alcohol

255
Q

Where are squamous cell carcinomas normally found in the oesophagus

A

Middle third

256
Q

What antibiotics cause C.diff

A

3 C’s
Ciprofloxacin
Ceph
Clindamycin

257
Q

What is diagnostic test for c diff

A

Stool assay for the toxin- PCR

258
Q

Treatment for C diff

A

Oral vancomycin

259
Q

What is diverticular disease

A

Low fibre diets cause high intraluminal pressure which causes outpouchings at weak points in the bowel walls

260
Q

Complications of diverticular disease

A

Diverticulitis- can get peritonism, perofration, fistula, obstruction from fibrosis

261
Q

Where do most outpouchings in diverticular disease occur

A

Sigmoid

262
Q

What are carcinoid tumours cancers of

A

Enterochromaffin cells most commonly found in the bowel

type of neuroendocrine cell

263
Q

Where can carcinoid tumours develop from

A

Most commonly the bowel
Lungs (SCLCs!), ovaries and testes

264
Q

What is carcinoid syndrome

A

Triad of;
Bronchoconstriction
Flushing
Diarrhoea
Caused by excess of serotonin (5-hydroxytryptamine)

265
Q

What is diagnostic test for carcinoid syndrome

A

24hr urine 5-HIAA
5-hydroxyindoleacetic acid

266
Q

Treatment for carcinoid syndrome

A

Octreotide- somatostatin analogue

so stops release of hormones in carcinoid

267
Q

What do you get in a carcinoid crisis

A

Life threatening vasodilation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia

268
Q

How to tell if sputum sample actually contains cells from the alveoli

A

Will contain macrophages

269
Q

What is the stain for melanin

A

Fontana-Mason stain

270
Q

What stain is used for haemochromatosis

A

Prussian blue

271
Q

What is cytokeratin a marker of

A

Epithelial- if not positive then not a carcinoma

272
Q

Describe the structure of hepatic lobule

A

In the shape of hexagon with each corner a portal triad. In the centre is a branch of the hepatic vein. Running from the portal triad to the central hepatic vein is a sinusoid

273
Q

What is the structural unit of the liver

A

Hepatic lobule

274
Q

In what direction does blood and bile run in a hepatic lobule

A

Blood runs towards the centrilobular vein
Bile runs towards to portal triad

275
Q

How are liver endothelium different

A

Are spaces in between endothelium which allow for movement of molecules to hepatocytes across the space of disse

discontinuous endothelium?

276
Q

How are liver cells divided in the hepatic lobule

A

Zone 1- these are closest to the portal triad (periportal triad)
Zone 2- mid zone
Zone 3- perivenular hepatocytes

277
Q

What are features of perivenular hepatocytes

A

Most mature and metabolically active

278
Q

Which liver zone is most susceptible to iscahemia

A

Zone 3 nearest the hepatic vein as least oxygenated

279
Q

Which liver zone is first affected by toxic substances and viral hepatitis

A

Zone 1

280
Q

What is the immune function of the liver

A

Antigens from gut reach the liver and are phagocytosed by Kupffer cells

281
Q

What is only protein the liver doesnt produce

A

Gamma globulins

282
Q

First investigation if suspect pre hepatic jaundice

A

FBC and blood film

283
Q

Which test determines the proportion of conj vs not bilirubin

A

Van der bergh
Direct reaction- measures conjugated
Indirect - measures unconjugated

284
Q

What is inheritance of gilberts

A

recessive

285
Q

What can confirm gilberts

A

fasting bilirubin

286
Q

What is pathophysiology of gilberts

A

UDP glucuronyl transferase deficiency

287
Q

Transmission of hep A

A

Farco oral

288
Q

Can you get Hep A again

A

No

289
Q

What are soider naevi, duputyrens contracture, palmar erythema etc all signs of

A

Chronic stable liver disease

290
Q

What are the signs of portal hypertension

A

Distended veins- but gut caput
Ascites
Splenomegaly

291
Q

Sites of porto-systemic anastamoses

A

Oesophageal varices
Rectal varices
Umbilical vein
Splen-renal shunt

butt gut caput

292
Q

What causes itching in liver disease

A

Urobilinogen and stercobilingoen

ie bile salts

293
Q

Which liver disease causes itching

A

Post hepatic

294
Q

What is histopathology of acute hepatitis

A

Spotty necrosis concentrated around the portal triad

i.e. zone 1 (as think - this is first zone acutr viral heps hit!)

295
Q

Where are stellate cells found in the liver

A

Space of disse

stellAte so normally just store vit A - when activated then fibroblasts

296
Q

Which hepatitis infections can not cause chronic hepatitis

A

A and E

297
Q

How is chronic hepatits staged and graded

A

Stage= fibrosis
Grade= inflammation

298
Q

Histopathology of chronic hepatitis

A

Portal inflammation
Lobular inflammation
Interface hepatitis (piecemeal necrosis)
Bridging from portal vein to central vein

299
Q

What is peacemeal necrosis/ interface hepatitis

A

Where can’t see border between portal tract and parenchyma due to inflammation

300
Q

What is critical stage in hepatitis to cirrhosis interface

A

Bridging from portal vein to central vein

301
Q

Histopathology of a cirrhotic liver

A

Hepatocyte necrosis
Fibrosis
Nodules of regenerating hepatocytes
Disturbance of vascular architecture

302
Q

How can liver cirrhosis be classified

A

Based on the size of the regenerating nodules
- micronodular <3mm
- macronodular >3mm

303
Q

What causes macronodular cirrhosis

A

Viral
Wilsons
Alpha 1 antitrpsin

304
Q

What causes micronodular cirrhosis

A

Alcoholic hepatitis
Bilary tract disease

305
Q

What is extrahepatic shunting

A

When blood backlogs into sites of portosystemic anastamoses

306
Q

What is intrahepatic shunting

A

When blood goes through the liver but does not contact hepatocytes/not filtered

307
Q

What is gene involved in haemochromatosis

A

HFE Chr 6

308
Q

What is gene involved in wilsons

A

ATP7B chromosome 13

309
Q

What is used to predict prognosis in liver cirrhosis

A

Child pughs score

310
Q

Proper term for fatty liver

A

Hepatic steatosis

311
Q

Histology of hepatic steatosis

A

Fat droplets in hepatocytes

312
Q

Histology of alcohol hepatitis

A

Hepatocyte ballooning and necrosis
Mallory denk bodies
Pericellular fibrosis
Megamitochondria
Mainly seen in zone 3

313
Q

What are mallory denk bodies

A

Filaments of collagen

314
Q

What colour do mallory bodies stain

A

pink/Blue- trichome

315
Q

What is the most common cause of chronic liver disease in the west

A

NAFLD

316
Q

Histology of NASH

A

Similar to alcohol hepatitis
Mallor denk bodies
Hepatocyte ballooning

317
Q

What is steatosis versus hepatitis

A

Steatosis is fat accumulation whereas hepatitis is with inflammation

318
Q

What is included in NAFLD

A

Simple steatosis
NASH

319
Q

What are the antibodies in type 1 and type 2 autoimmune hepatitis

A

Type 1- anti-SMA, ANA
Type 2- Anti- LKM (liver kidney microsomal)

320
Q

Blood findings of PBC

A

Raised ALP
Raised cholesterol
Raised anti-mitochondrial antibodies

key is cholesterol - get xanthelasma and xanthoma

321
Q

What is US finding of PBC

A

No bile duct dilatation

322
Q

Histology of PBC

A

Bile duct loss with granulomas

323
Q

What is PSC

A

Inflammation and obliterative fibrosis of both intrahepatic and extrahepatic bile ducts

PBC is intrahepatic only - hence dont get signs on US (like BD dilation) or ERCP signs (like beading) as you do in PSC

324
Q

What is main association of PSC

A

UC

325
Q

Blood findings of PSC

A

High ALP
High p-ANCA

326
Q

US finding of PSC

A

Bile duct dilation
Dont see this in PBC

327
Q

ERCP finding PSC

A

Beading of bile ducts

328
Q

Histology of PSC

A

Onion skinning fibrosis- ocncentric fibrosis

329
Q

What is PSC a main risk factor for

A

Cholangiocarcinoma

330
Q

What is typical disease course when patients are infected with TB

A

Infection usually asymptomatic becomes latent in a Gohn focus then gets reactivated in times of immunosuppression to give post primary TB
Primary TB is when get symptoms on initial presentation

331
Q

What is a ghon focus

A

Primary TB lesion in the pleura

332
Q

Histology of TB

A

Caseating granulomas

333
Q

Typical presentation of TB

A

Lung symptoms
Nights sweats etc

FLAWS + pulmonary sxs

334
Q

What are some less common presentations of TB

A

Mainly seen in immunocompromised patients
Potts disease
Miliary disease
Subacute meningitis
Tuberculoma

335
Q

Main difference between male and female teratomas

A

Male are normally malignant

336
Q

Where else can teratomas be found

A

Pineal gland
Base of skull
Mediastinum
Wherever germ cells have originated from

337
Q

What is the main stain for NE tumours

A

Chromogranin
Can also do synaptophysin, CD56

Then can do individual hormones

338
Q

Where are NE tumours normally found

A

Gut
Lung
THymus
Skin

339
Q

How are NET graded

A

Ki-67 index

340
Q

Where are Zollinger Ellison tumours normally found

A

Pancreas or duodenum
Secrete gastrin which drives acid production

341
Q

Most common cancer in children

A

ALL

342
Q

How are brain tumours classified

A

Primary vs secondary
Intra-axial versus extra axial

343
Q

Supratentorial tumour presentatoion

A

Focal neurology
Seizures
Personality changes

344
Q

Infratentorial tumour presentation

A

Cerebellar ataxia
Long tract signs
Cranial nerve palsy

345
Q

Where are diffuse gliomas found

A

Supra-tentorial

346
Q

What brain tumour is found in childhood and is indolent

A

Pilocytic astrocytoma

347
Q

How do pilocytic astrocytomas appear on MRI

A

Well circumcised
Cystic
Enhancing lesion
IN CEREBELLUM

348
Q

Histology of pilocytic astrocytoma

A

Piloid hairy cells
Rosenthal fibres

349
Q

Mutations seen in astrocytoma and oligodendromas (ie diffuse gliomas)

A

Point mtation in IDH1/2

remember diffuse gliomas seen in adults (hence supra-tentorial)
circumscribed gliomas in children so infra

350
Q

Histology of astrocytoma

A

Low mitosis
No vascular necrosis or proliferation
IDH1 detected on immunohistochemistry

351
Q

What are gliobastoma mutliforme

A

Most aggressive and frequent glioma Grade 4

352
Q

MRI findings of glioblastoma multiforme

A

Heterogenous appearance

353
Q

Where are secondary brain tumours normally seen

A

Grey/white matter junction

as vessels thin here so get stuck

354
Q

Where do medulloblastomas originate from

A

Neuroepithelial cells
Neuronal precurors of cerebellum

355
Q

Most common brain tumour in children

A

Pilocytic astrocytoma
2nd- medulloblastoma

356
Q

Difference in communicating vs non communicating hydrocephalus

A

Non- obstruction in passage of fluid
Communicating -can’t reabsorb or overproduction

357
Q

Common site of obstructing CSF flow

A

Cerebral aqueduct

358
Q

Most common site of brain intra-parenchymal haemorrhage

A

Basal ganglia

359
Q

Cause of intra parenchymal haemorrhage

A

HTN in over 50% of cases

360
Q

What are lacunar infarcts

A

Bleeds which occur in the brain

occlusion (blockage) of small, penetrating arteries that supply blood to deep structures of the brain, such as the basal ganglia, thalamus, internal capsule, and brainstem

361
Q

What is a cavernous angioma

A

Well defined lesion composed of packed vessel with no parenchyma interposed between vascular spaces
Presents with low pressure bleeds- headahce, focal deficits, seizures

362
Q

What is diangosis when target sign on imaging in brain

A

CAVERNOUS angioma

popcorn/berry sign

363
Q

What causes SAH

A

Berry aneurysm in circle of willis

364
Q

Most common site of berry aneurysm

A

Internal carotid artery bifurcation

365
Q

What is global cerebral ischaemia

A

Systemic circulation failure

366
Q

Causes of ischaemia in brain

A

Extracerebral thrombosis
Embolism from heart or carotid- most often seen in MCA

367
Q

Histology of cerebral infarct

A

Tissue necrosis
Rarely haemorrhagic
Permenant damage in affeced area
No recovery

368
Q

Histology of cerebral haemorrage

A

Bleeding
Dissection of parenchyma
Fewer macrophages
Limited tissue damage
Chance of recovery

369
Q

What are common signs of brain fracture on examination

A

Straw coloured otorrhoea and rhinorhhoea

370
Q

What is battles sign

A

Bleeding behind ear showing skull base fracture

371
Q

What are contusions

A

Brain in collision with skull and get surface bruising

372
Q

What is diffuse axonal injury

A

The long connecting fibers in the brain called axons are sheared as the brain rapidly accelerates and decelerates inside the hard bone of the skull
Usually causes a coma

373
Q

What is chronic traumatic encephalopathy

A

Effects on brain of repeated trauma to head

374
Q

Neuropathology of Alzheimers

A

Extracellular plaques of beta amyloid
Neurofibrillatory tangles of Tau
Cerebral beta amyloid angiopathy
Cerebral atrophy

375
Q

Long term imaging finding of AD

A

Cortical atorphy
Widening of ventricles
Narrowed gyri
Widened sulci

376
Q

How is staining for Tau done

A

Immunohistochemistry

377
Q

Staging done for alzheimers

A

Braak

378
Q

Pathophysiology of parkinsons

A

Reduced stimulation of cortex by basal ganglia due to dopaminergic loss in substantia nigra

379
Q

Histology of lewy body dementia

A

Alpha synuclein
Ubiquitin
Lewy bodies

380
Q

How does mutiple system atrophy differ to parksinsons

A

Alpha synuclein in the glial cells not neurones histologically

381
Q

Histology of picks disease

A

Fronto-temporal atrophy
Marked gliosis and neuronal loss
Ballon neurones
Tau positive pick bodies

382
Q

What is stained positively in frontotmeporal dementia linked to chr 17

A

Tau

383
Q

Pathophysiology of frontotmeporal dementia linked to chr 17

A

Defect in tau generation
Only see atrophy unilaterally

hyperphosphorylated tau = pick bodies

384
Q

What are 2 types of barretts oesophagus

A

Gastric metaplasia- without goblet cells
Intestinal type metaplasia- with goblet cells

??

385
Q

Most common oesophageal cancer in developed world

A

Adenocarcinoma

386
Q

Most common oesophageal cancer in developing world

A

SCC

387
Q

What are 2 types of gastritis

A

Acute
Chronic

388
Q

Acute gastritis causes

A

Aspirin
NSAIDS
Alcohol
Corrosives
Hpylori
Crohns

389
Q

Chronic gastritis causes

A

Autoimmune- pernicious anemia
Bacteria- h pylori in antrum
Chemical- NSAIDS, bile reflux in antrum

abc

390
Q

Complications of H.pylori

A

Lymphoma
Metaplasia->adenocarcinoma pathway
Ulcers

391
Q

Which Hpylori virulence factor is most associated with chronic inflammation and ultimately cancer

A

Cag A

392
Q

Nicher pathogenic causes of gastritis

A

CMV, strongyloides (threadworm)

393
Q

Difference between gastritis and ulcer

A

Ulcers breach through muscularis mucosa into submucosa

otherwise it’s an erosion

394
Q

Complications of ulcers in stomach

A

Bleeding- anamemia, shock
Perforation

395
Q

Histology of gastric epithelial dysplasia

A

Cytological and histological features of malignancy but doesnt invade through BM

396
Q

Most common cancer in stomach

A

Adenocarcinoma

397
Q

How are gastric adenocarcinomas classifed

A

Intestinal- well differentiated - associated with h pylori - goblet cells
Diffuse- poorly differentiated - associated with worse prognosis

398
Q

What are signet ring cells seen in

A

Diffuse gastric adenocarcinomas

399
Q

Most common cause of gastric ulcer

A

Hpylori

400
Q

What makes duodenum more vulnerable to H pylori

A

Increased acid production leaks into duodenum causing gastric metaplasia

401
Q

Pathogens other than H pylori causing duodenal ulcer

A

CMV
Giardia lamblia- most important
Tropheryma whippeli

402
Q

What causes whipples diseases

A

Tropheryma whippelii- causes duodenal ulcers and gastritis

403
Q

Main cause of villous atrophy

A

Coeliac
Only if on gluten though, if not willbe normal

404
Q

Diagnosing coeliac

A

Tisse transglutaminase ABs
Endomysial
Biopsy but patient must be on gluten

405
Q

Biopsies of coeliac

A

Villous atrophy
Crypt hyperplasia
See flattened villi
Increased intraepithelial lymphocytes- normal range less than 20 lymphocytes/100 enterocytes

406
Q

What else can present with villous atropy

A

Tropical sprue

407
Q

Causes of chronic hepatitis

A

Viral
Drugs
Autoimmune

408
Q

What is haemosiderosis

A

Accumulation of iron in macrophages from blood transfusions

409
Q

Pathophysiology of alpha-1-antitrypsin

A

Failure to secrete it
Intra cytoplasmic inclusions due to misfolded protein
Causes hepatitis and pneumonitis

410
Q

Causes of hepatic granulomas

A

PBC
Drugs
TB
Sarcoid

411
Q

How is calcium stored in the bone

A

As calcium hydroxapatite

412
Q

What are the types of bone

A

Cortical and cancellous

413
Q

What is difference in distribution and function of cancellous versis cortical bone

A

Cortical
- long bones
- 80-90% calcified and mainly protective and mechanical

Cancellous
- vertebrae and pelvis
- 15-25% calcified
- mainly metabolic

414
Q

What is metabolic bone disease

A

Disordered bone turnover due to imblalance of chemicals and hormones
Leads to osteopenia (loss of bone mass)

415
Q

Whre is gold standard site for bone histology

A

Iliac crest

416
Q

What is renal osteodystophy

A

Encompasses all of the bone changes seen in CKD
- osteomalacia
- osteosclerosis
- osteoporosis
- osteitis fibrosa cystica

417
Q

Which viruses have been implicated in pagets disease

A

Parvomyxovirus

418
Q

When are langhans giant cells seen

A

Granulomas

419
Q

When does lyme disease affect bones

A

Very late
Get inflammatory arthropathy

420
Q

What is tophus seen in

A

Gout

421
Q

What are gout crystals

A

Negative birefringent needle shaped monosodium urate crystals

422
Q

What are crystals in pseudogout

A

calcium pyrophosphate in knees
calcium phosphate in knees and shoulders
Rhomboid shaped and positively birefringent

423
Q

Aetiology of pseudogout

A

Idiopathic
Metabolic- haemochromatosis, primary HPT
Hereditary
Traumatic

424
Q

What are dermoid cysts

A

Mature cystic teratomas which contain teeth, hair etc from any lineage
Normally found on neck and head

425
Q

Where and in who are primary bone tumours found

A

Around the knee
In young people and children

426
Q

How can bone tumours present

A

Pain
Swelling
Deformity
Fractures easily

427
Q

How to diagnose bone tumours

A

First investigation an XRAY
Desired diagnosis technique a needle biopsy with a jamshidi needle

428
Q

Who does fibrous dysplasia occur in

A

Females more than men
First 3 decades

429
Q

Where does fibroud dysplasia occur and what is x ray finding

A

Ribs and proximal femur
Soap bubble osteolysis and shepherds crook deformity if in proximal femur

430
Q

What is fibrous dysplaia associated with

A

McUne albright syndrome (if polyostotic)- cafe au lait spots and endocrine problems

431
Q

What is soap bubble osteolysis seen in

A

Fibrous dysplasia

and giant cell tumour

432
Q

Histology of fibrous dysplasia

A

Chinese letters
(misshapen bone trabeculae)

433
Q

What do you see shephards crook deformity of femur in

A

Fibrous dysplasia

434
Q

What is most common benign bone tumour

A

Osteochondroma

435
Q

How do osteochondromas appear histologically and on x ray

A

Bony protuberance capped in cartilage- histology
Mushroom cap on bone- x-ray
Osteo (bone) chond (cartilage) roma

436
Q

Where do you see osteochondromas

A

End of long bones

437
Q

How do endchondromas appear histologically

A

Normal cartilage

438
Q

What appears with cotton wool or popcorn calcifcation

A

Endochondromas

439
Q

Where do endchondromas appear

A

“Ends”
Hands for example

440
Q

Sheets of multi-nucleate giant cells on background of spindle cells taken from bone

A

Giant cell tumours (borderline malignancy)

441
Q

What is most common malignant bone tumour

A

Metases however not at below elbow and knee

442
Q

What are the 3 malignant bone tumours

A

Osteosarcoma
Chondrosarcoma
Ewings sarcoma (primitive peripheral neuroectodermal tumour)

443
Q

Who and where do osteosarcomas occur

A

Adolescent
Normally around the knee

444
Q

What is codmans traingle or elevated perisosteum seen in

A

Osteosarcoma

445
Q

What are malignant mesenchymal cells seen in

A

Osteosarcoma

446
Q

X ray finding of osteosarcoma

A

Elevated periosteum (Codmans triangle)
Sunburst appearnace

447
Q

MOst common primay bnoe sarcoma

A

Osteosarcoma

448
Q

Who are chondrosarcoma seen in and where are they

A

Middle age
Axial bones

chondro and central

449
Q

Histology of chondrosarcoma

A

Malignant chondrocytes

450
Q

What is fluffy calcification seen in

A

Chondrosarcoma

451
Q

Who are ewings sarcoma seen in and where

A

Long bones and pelvis
Adolescents

452
Q

Histology of ewings sarcoma

A

Sheets of small round cells
CD99+VE (MIC 2)

453
Q

What is onion skinning of perisoteum seen in

A

Ewings sarcoma

454
Q

Which bone tumour can be diagnosed genetically

A

Ewings sarcoma
T11:22 translocation

455
Q

Difference in ALP staining between malignant bone tumours

A

Osteosarcoma- postive
Ewings sarcoma- negative

456
Q

What is Radiolucent nidus with sclerotic
rim ‘Bull’s-eye’ seen in

A

Osteoid osteoma

457
Q

Where are simple bone cysts appear and how do they appear

A

Humerus and femur
Lytic well defined small fluid fille dlesions

458
Q

Skin findings of SLE

A

Malar rash
Photosensitive rash
Discoid rash with atrophic centre

459
Q

What is a titre with regards to ANA

A

The titre is the highest dilution factor at which they are present within their serum

460
Q

What are the autonatibodies in SLE

A

Anti-DsDNA
Anti-Smith (ribonucleoproteins)
Anti-histone

461
Q

What is signifcance of anti-histone autoantibodies in SLE

A

That it is drug induced lupus from hydralazine etc

462
Q

Most specific antibodie for SLE

A

Anti-smith (ribonucleoproteins)

463
Q

Main histological finding with refgards to SLE

A

Immune complex deposition

464
Q

SLE criteria

A

4 out of 11
SOAP BRAIN MD
Serositis
Oral ulcers
Arthritis
Photosenstivity
Blood disorders
Renal
ANA+ve
Immune phenomena (autoantibodies)
Neurological signs
Malar rash
Discoid rash

465
Q

Pathophysiology of systemic scelrosis

A

Fibrosis and excess collagen deposition

466
Q

Types of systemic sclerosis

A

Diffuse
Limited
Morphoea- if localised to 1 area

467
Q

What is presentation of limited systemic scleorderma

A

CREST
Calcinosis
Raynauds
Esophageal dysmobility
Scleodactyly
Telengiectasia

468
Q

What is histology of limited systemic scelrosis

A

Increased collagen deposition
Fibrosis
Arteriole onion skinning appearnace

469
Q

Antibody difference between diffuse and limited systemic scelrosis

A

Diffuse- anti-scl-70 (anti-topoisomerase)
Limited- anticentromere
REMEMBER AS LACA

470
Q

What is speckled immunofluorescence associated with in ANA testing

A

Mixed connective tissue disease

471
Q

Differences between limited and diffuse systemic sclerosis

A

Limited- confined to face and distal aspects of limbs (distal to knee and elbow)- typically CREST
Diffuse- widespread including renal, cardio symptoms
Complication of limited is pulomanry htn (key primary pulm HTN) whereas is pulm fibrosis in diffuse (key 2ndary pulm HTN in diffuse, 2ndary to fibrosis)

472
Q

What is pathophysiology of myositis’

A

Typically an underlying malignancy
Autoimmune condition agaisnt the muscle

473
Q

Skin findings in dermatomyositis

A

Gottrons papules- callouses on knuckles
Heliotrope rash- reddening around eyes and face

474
Q

CNS presentation of sarcoid

A

Meningitis
Cranial nerve palsy

475
Q

What is the classfifcation of vasculitidies

A

Large vessel
- takayasu
- GCA

Medium vessel
- polyarteritis nodosa
- kawasakis
- thromboangiitis obliterans

Small vessel
- microscopic polyangiitis
- granluomatosis with polyangiitis
- IgA nephropathy
- eosinophillic granluomatosis with polyangiitis

476
Q

Histology of GCA

A

Granulomatous transmural inflammation + giant cells +
skip lesions

477
Q

Presentation of GCA

A

Over 50
Preceding polymyalgia rheumatica
eadache over eye
Vision difficulty

478
Q

Presentation of takayasus arteritis

A

Japanese women
Cold hands
No pulse
Low BP
Claudication
Bruits

pulseless! as affects aortic arch

479
Q

What is presentation of thromboangiitis obliterans

A

Heavy smoker and a young man
Feet ulcers
Arterial limb disease

480
Q

Investigation for thromboangiitis obliterans and the findings

A

Angiogram
Shows corkscrew appearance from segmental occlusive lesions

481
Q

Which vessels does polyarteritis nodosa normally affect

A

Renal and mesenteric

482
Q

What condition is normally associated with polyarteritis nodosa

A

Hep B

483
Q

Angiogram finding of polyarteritis nodosa

A

Microaneurysms on angiography (“string of pearls / rosary
bead appearance

484
Q

Histology of polyarteritis nodosa

A

fibrinoid necrosis & neutrophil infiltration

485
Q

Hallmarks of polyangiitis with granulomatosis

A

ENT- saddle nose, sinusitis, episatxis
Lung- pulm heamorrhage, cavitation
Renal- glomerulonephritis

divide into URT, LRT and renal

486
Q

AB in polyangiitis with granulomatosis

A

Cytoplasmic ANCA against proteinase 3

487
Q

AB in eosinophilic polyangiitis with granulomatosis

A

Perinuclear- ANCA against myeloperoxidase

488
Q

Presentation of eosinophilic polyangiitis with granulomatosis

A

Asthma
Eosinophilia
Allergic rhinits
Vasculitis evidence

489
Q

Presentation of micropscopic polyangiitis

A

Renal and pulomary syndrome

490
Q

AB in microsopic polyangiitis

A

Perinuclear- ANCA against myeloperoxidase

491
Q

Main structure of breast and the 2 epithelial cells

A

Are large ducts with a termina ductal lobular unit
Luminal and myoepithelial cells

492
Q

2 Most common breast lesions that presents with discharge

A

Papilloma
2nd- duct ectasia

493
Q

How are aspirates of breast lumps coded

A

C1- inadequate
C2- benign
C3- atypia, probably benign
C4- suspicion of malignancy
C5- malignant

c for cytology

494
Q

Presentation of duct ectasia

A

Older women
Multiparous
Green/wihte discharge
Usually discharge sometimes with breast mass and nipple retracition so easily mistaken for cancer

495
Q

Cytology of duct ectasia discharge

A

Proteinaceous material and inflammatory cells

496
Q

Histology of duct ectasia

A

Dilated duct
Inspissated secretions
Periductal and interstitial inflammation – granulomatous

497
Q

Most common organism for acute mastitis

A

Staph

498
Q

Presentation of fat necrosis

A

Breast mass
Late stages may show calcification
Preceded by trauma, surgery, radiotherapy as is inflam response to damaged adipose tissue

499
Q

Histology of fat necrosis

A

Central focus of necrotic fat cells surrounded by lipid filled macrophages and neutrophilic infiltrates

  • Cytology – empty fat spaces , histiocytes and giant cells [BUZZWORDS]
500
Q

What is a galactocele

A

Cystic dilation of a duct during lactaction

501
Q

Presentation of galactocele

A

Multiple tender palpable nodules
Infection may convert these to acute mastitis or abscesss

502
Q

Histology of pagets breast disease

A

Cells with abundant pale clear cytoplasm which contains mucin
Large and prominent nuclei

503
Q

What is level of critical artery stenosis

A

70%

504
Q

What causes prinzmetal angina

A

Coronary artery spasms

505
Q

What is difference in name of tumour of large vs small nerve tumour

A

Small- neurofibroma
Larger (spinal cranial nerve)- schwannoma

506
Q

What are gliomas

A

Tumours of non neuronal cells
Includes astrocytoma, ependymoma, o
ligodendromas etc

507
Q

What is most common primary brain tumour in an adult

A

Mengioma- mainly occurs in elderly
GBM? i think most common aggressive

508
Q

What happens if pia mater torn when brain collides with the skull

A

Becomes a laceration not a contusion

509
Q

What is name of stain done for copper

A

Rhodanine

510
Q

Cases which promote coroner referral

A

o Unknown cause of death

o Sudden or unexpected death (inclusive of all deaths <24hours after admission to hospital)

o Deceased person not seen by a doctor within 28 days before death

o The death is considered suspicious/unnatural/violent

o The death may be due to an accident, self-neglect (i.e. drug-use death) or neglect on the behalf of others

o The death is/could be due to the deceased’s prior employment (including industrial disease)

o The death may be due to an abortion

o The death occurred during an operation or before recovery from anaesthetic

o The death occurred during or shortly after a period of police custody

o The death may be suicide (can only be confirmed by a coroner)

511
Q

How do death certificates work in terms of cause of death

A

Section 1 is the cause of death can can have 1a, 1b, 1c
1a is the immediate cause
1b caused A
1c caused B etc
The last 1 letter is cause of death

Section 2 includes what lead may have contributed to death ie DM, HTN etc

512
Q

Presentation of the connective tissue myositis’

A

Proximal muscle weakness
Can get SOB and arrythmias

513
Q

How does wilsons present

A

Liver cirrhosis- often in kids
Neuro- dementia, seizures and parkinsons

Also seen in eyes, kidneys and heart

514
Q

How can haemochromatosis present

A

Liver- cirrhosis
Heart- cardiomyopathy
Pancreas- DM
Gonads- atrophy and impotence

515
Q

Blood finding of wilsons

A

Low caeruplasmin

516
Q

What antibodies suggest that it is drug induced lupus

A

Anti-histone

517
Q

Which infection of genital tract is associated with spontaneous abortion and chorioamnionitis

A

Mycoplasma

518
Q

Pathogenesis of staph, strep, coliform bacteria and clostridium causing PID

A

Secondary to abortion
Start in lymphatics then spread by blood and lymph upwards

519
Q

What is dyskaryosis

A

Change in the appearance of cells

520
Q

How are HPV infections divided

A

Latent
- HPV resides in cells but does not produce infective virions
Productive
- DNA replication independant of cells own replication

521
Q

How does HPV transform cells

A

Produces 2 proteins- E6 and E7 which inactivate tumour suppressor genes
E6- p53
E7- Rb

522
Q

HPV vaccine schedule

A

Given between 12-13
2nd dose 6-24 months later

523
Q

What tumour suppressor gene mutation is associated with serous endometrial carcinoma in 90% of cases

A

p53

524
Q

What are the types of ovarian tumours

A

Epithelial
Sex chord stromal
Germ cell
Miscellaneous

525
Q

Histology of serous cystadenoma

A

Columnar epithelium
Psammoma bodies

526
Q

Histology of mucinous cystadenoma

A

Mucin producing cells

527
Q

Which tumours are associated with pseudomyxoma peritonei

A

Mucinous ovarian adenomas
Appendicular tumours

528
Q

Histology endometrioid ovarian tumours

A

Tubular glands mimicking the endometrium

529
Q

Histology of clear cells ovarian tuours

A

Clear cells with clear cytoplasm
Hobnail appearance

530
Q

What ovarian tumours are endometriosis associated with

A

Clear cell
Endometrioid

531
Q

Difference between immature and mature teratomas in ovaries

A

Mature
- cystic
- differentiation into mature tissues like skin teeth etc

Immature
- solid
- embryonal tissue
- secrete AFP

532
Q

Which ovarian tumours secrete AFP

A

Immature teratomas

also yolk sac

533
Q

What is most common malignant ovarian tumour in young women

A

Dysgerminoma (female counterpart to testicular seminoma)

534
Q

What are the ovarian germ cell tumours

A

Dysgerminoma
Teratoma
Choriocarcinoma

535
Q

What are the ovarian epithelial tumours

A

Serous
Mucinous
Endometrioid
Clear cell

536
Q

What ovarian tumour secretes HcG

A

Choriocarcinoma

537
Q

What are the sex chord tumours of ovaries

A

Granulosa-theca cells
Fibromas
Sertoli-Leydig

538
Q

What do granulosa theca cells produce

A

E2
Signs include oestrogenic effects- irregular menstrual cycles, breast enlargement, endometrial/breast hyperplasia

539
Q

What do sertoli leydig tumours produce

A

Androgens- look for signs of breast atrophy, clitoral enlargement, hirsutism, deep voice

540
Q

Histology of granulosa theca cell tumours

A

Cal-exner bodies

541
Q

Histology of krukenberg tumours

A

Mucin producing signet ring cells

542
Q

Test for coeliac if IgA deficient

A

Straight to biopsy

543
Q

What is stained for in parkinsons

A

Alpha synuclein

544
Q

What do germ cell tumours secrete

A

AFP
LDH
bHCG

Arjun's Copy- Owen's Path (8 decks)

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