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Phase 2a NEW > Pathology > Flashcards

Pathology Flashcards

1
Q

Causes of fluctuating cognitive function

A 
subdural haematoma
cerebral abscess
meningioma
acute aortic regurgiation 
hypertensive encephalopathy
alcohol intoxication
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2
Q

2 types of autopsy

A 
hospital autopsy (less than 10%)
medico-legal autopsy (over 90%)
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3
Q

autopsy requirements

A

consent needed

death certificate needed

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4
Q

Deaths referred to coroner

A 
presumed natural (cause of death not known/not seen by doctor in last illness)
presumed iatrogenic (clinical care - post-operative, anaesthetic, therapeutic complications)
presumed unnatural (accident, suicide, industrial (asbestos), unlawful killing, custody death)
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5
Q

Who makes referrals?

A

Doctors
Registrar of BDM (Births, Deaths, Marriages)
Police
Relatives

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6
Q

Who performs autopsies?

A

Doctors
Histopathologist (hospital and coronial)
Forensic pathologists (coronial)

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7
Q

Role of coroner (questions that they need to answer)

A

Who was deceased?
when and where death occurred?
How did they come about their death?

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8
Q

What is an autopsy?

A

1) History/scene
2) External exam
3) Evisceration
4) Internal exam
5) Reconstruction

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9
Q

Samples taken during autopsy

A 
Microbiology
Toxicology
XRAY
Histology
Genetics
Photographs
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10
Q

External exam

A

Identification - Gender, age, jewellery, clothing, body mod

Injuries

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11
Q

Evisceration

A 
Y-shaped incision
Open all body cavities
Examine all organs in situ
Remove thoracic and abdo organs
Remove brain
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12
Q

Internal exam

A

Internal organs, nodes, vessels, tracts and central NS

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13
Q

What is inflammation?

A

A reaction to injury or infection involving cells such as neutrophils and macrophages

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14
Q

When is inflammation bad?

A

Autoimmune

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15
Q

Inflammation classification

A

Acute (neutrophils) - sudden, short-duration, resolves usually
Chronic (lymphocytes and macrophages) - Slow onset, long-duration, may never resolve

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16
Q

Neutrophil polymorphs

A

Short lived cells, first line
First to act during acute inflammation
Use enzymes to kill bacteria, end up dying during the process resulting in puss

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17
Q

Macrophages

A 
Long-lived cells
Phagocytic 
Ingest bacteria
Carry debris away
Present antigen to lymphocytes
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18
Q

Lymphocytes

A

Longest lived cells
Produce chemicals which attract other inflammatory cells
Immunological memory

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19
Q

Endothelial cells

A

Become sticky in areas of inflammation so inflammatory cells adhere to them
Become porous to allow inflammatory cells into tissues

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20
Q

Fibroblasts

A

Long lived

Form collagen in areas of chronic inflammation and repair

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21
Q

Acute inflammation examples

A

Acute appendicitis

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22
Q

Acute inflammation outcomes

A

Resolution
Discharge of pus
Chronic inflammation

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23
Q

Chronic inflammation example

A

TB

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24
Q

Granulomas

A

Group of macrophages

Chronic inflammation

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25
Q

Treating inflammation

A

Inhibit prostaglandin synthetase (prostaglandins are chemical mediators of inflammation)
NSAIDs - Aspirin, Ibuprofen etc
Corticosteroids - bind to DNA and upregulate inhibitors of inflammation and downregulate chemical mediators of inflammation

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26
Q

LECTURE CATCHUP*

A

LC*

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27
Q

Carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic mutations
Apples to malignant neoplasms only

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28
Q

Oncogenesis

A

Benign and malignant tumors

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29
Q

Crcinogens

A

Agents known or suspected to cause tumours

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30
Q

Carcinogenic

A

Cancer causing

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31
Q

Oncogenic

A

Tumour causing

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32
Q

Muatgenic

A

Act on DNA

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33
Q

Risk of cancer - Environmental

A

85%

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34
Q

Hepatocellular carcinoma

A

Uncommon in UK/USA

Common in areas with increased Hep B/C and mycotoxins

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35
Q

Oesophageal carcinoma

A

High incidence in Japan, China, Turkey and Iran

- Dietary factors (Linhsien chickens and hot tea respectively)

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36
Q

Behavioral risks

A

Lung cancer - smoking

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37
Q

Occupational risks

A

Bladder cancer - Dye and rubber industry

Scrotal cancer - Chimney sweeps

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38
Q

Classes of carcinogens

A 
Chemical
Viral
Ionising and non-ionising radiation 
Hormones, parasites and mycotoxins 
Misc
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39
Q

Chemical carcinogens

A

Tend to require conversion from pro-carcinogen to ultimate carcinogen
Enzyme required may be confined to certain organs
Some act directly

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40
Q

Chemical carcinogens

A

Polycyclic aromatic hydrocarbons - Lung and skin cancer - Smoking
Aromatic amines - Bladder cancer - Rubber/dye industry
Nitrosamines - Gut cancer
Alkylating agents - Leukaemia

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41
Q

Radiant energy

A

UV light - Melanoma
Xeroderma pigmentosum condition has increased risk
Ionising radiation for long term increases skin cancer in radiographers
Lung cancer in uranium miners
Thyroid cancer in Ukranian children

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42
Q

Biological agents

A

Hormones - Oestrogen - Breast/endometrial cancer
Anabolic steroids - HCC
Mycotoxins - Aflatoxin B1 - HCC
Parasites - cHLOARCHIS SINESIS - Cholangiocarcinoma
Schistosomiasis - Bladder cancer

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43
Q

Misc

A

Asbestos

Metals

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44
Q

Host factors

A

Race - Increased Oral cancer in SE asia (reverse smoking, betal chewing), Decreased skin cancer in blacks (melanin)
Diet
Age - Increases
Gender - Breast cancer
Premalignant lesions - Colonic polyps, UC.
Transplacental exposure - Diethylstiboestrol - Increased vaginal cancer

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45
Q

Cancer

A

Latent interval between exposure and cancer development

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46
Q

Tumour

A

Any abnormal swelling - Neoplasm (tends to be), inflamamtion, hypertrophy, hyperplasia

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47
Q

Neoplasia

A

A lesion which is autonomous, abnormal, persistent and is a new growth. It persists after the initiating stimulus has been removed

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48
Q

Neoplasia

A

25% of pop

20% of all deaths

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49
Q

Deaths from cancer

A

Prostate cancer is most common in men, but lung cancer is most common killer
Breast cancer is most common in women though

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50
Q

Structure of neplasms

A

Neoplasm, neoplastic cells, derived from nucleated cells usually monoclonal, growth pattern and synthetic activity related to the parent cell,

Neoplasm, stroma, connective tissue framework, mechanical support, nutrition.

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51
Q

Tumour angiogenesis

A

1) Avascular tumour nodule
2) Vascularised tumour
3) Vascularised tumour with central necrosis

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52
Q

Neoplasm structure

A

Tumour cells + stroma

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53
Q

Classifying neoplasms

A

Behavioral: Benign/borderline/malignant
Histogenetic: Cell of origin

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54
Q

Benign neoplasms

A 
Localised
Non-invasive
Slow growth rate
Low mitotic activity 
Close resemblance to normal tissue 
Circumscribed or encapsulated 
Necrosis rare
Ulceration rare
Growth on mucosal surfaces often exophytic
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55
Q

Benign neoplasms concerns

A 
Pressure on adjacent structures
Obstruct flow
Produce hormones
Transform to malignant neoplasm
Anxiety
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56
Q

Malignant neoplasms

A 
Invasive
Metastases
Rapid growth rate 
Variable resemblance to normal tissue 
Poorly defined/irregular border 
Hyperchromatic nuclei
Increased mitotic activity 
Necrosis and ulceration common
Growth on mucosal surfaces and skin often endophytic
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57
Q

Malignant neoplasms concerns

A 
Destruction of adjacent tissue 
Mets
Blood loss from ulcers
Obstruction of flow
Hormone production 
Paraneoplastic effects 
Anxiety and pain
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58
Q

Histogenetic classifiation

A

Histogenesis - specific cell of origin of a tumour

histopathlogyical examination

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59
Q

nomenclature of neoplasia

A

neoplasms may arise from epithelial cells, connective tissue, lymphoid tissue

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60
Q

nomenclature of neoplasms

A

all neoplasms have suffix -oma

prefeix depending on behavioural classificaiton and cell type

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61
Q

Benign epithelial noeplasms

A

Papilloma - benign tumour of non-glandular, non-secretory epithelium
prefix with cell type of origin e.g. squamous cell papiloma

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62
Q

benign epithelial neoplasms

A

adenoma - benign tumour of glandular or secretory epithelium

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63
Q

malignant epithlial neoplasms

A

carcinoma - malignant tumour of epithelial cells
prefixed by name of epithelial cell type e.g. trnaslational cell carcinoma
Carcinomas of glandular epithelium - adenocarcinomas

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64
Q

Benign connective tissue neoplasms

A 
Lipoma - adipocytes 
Chondroma - cartilage 
Osteoma - bone
Angioma - vascular 
Angiolipoma - blood and fat cells neoplastic
Rhabdomyoma - sriated muscle 
Leiomyoma - smooth muscle
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65
Q

Maligantn connective tissue neoplasms

A

Liposarcoma - adipose tissue
Rhabdomyosarcoma - striated muscle
Osteosarcoma - bone
etc

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66
Q

Carcinomas and sarcomas classified further

A

Degree of differentiation

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67
Q

Anaplastic

A

Where cell type of origin is unknown

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68
Q

Some exceptions

A

Not all -omas are neoplasms: granuloma, tuberculoma, mycetoma
Not all malignant tumours are carcinoma or saroma: melanoma, mesothelioma, lymphoma

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69
Q

cancer summary

A

Behaviour: benign or malignant

histogenesis: cell of origin
suffix: -oma denotes neoplasm
prefix: benign or malignant, and cell type

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70
Q

Carcinoma in situ

A

Not invaded anywhere

71
Q

Invasive carcinoma

A

Invaded basement membrane

Can be micro-invasive

72
Q

Cancer growth

A

Invasion of basement membrane - proteases (matrix metalloproteinases in liver cancer)
Invade bm - cancer cells moving through bm
Invasion of extracellular matrix using proteases, then cell motility again to invade through again.
Move into and travel through lymphatic or blood vessel
Stick to side of vessel wall
Out into extracelllular matrix
Regrowth and create own blood supply (angiogenesis) at metastatic site

73
Q

Inhibitors of angiogenesis

A

Avastin (standard treatment for macular degeneration)

74
Q

Routes for mets

A

Blood vessels

75
Q

Common organ for mets to occur

A

Any common cancers, sarcomas, often mets to lung

76
Q

Colorectal/colon cancer tends to spread to

A

Liver

Also anything which drains to portal venous system mets to liver

77
Q

tumours that mets to bone

A 
prostate 
breast
lung
kidney 
thyroid
78
Q

lung cancers

A

non-smoker - adenocarcinoma

smoker - squamous cells carcinoma

79
Q

Chemotherapy

A

Vinblastine (antimicrotubule agent)
Etoposide
Ifosamide (binds to dna directly and cross links it to prevent replication)
cisplatin does same as ifosamide

80
Q

Chemotherpay

A

Uusally hits normal cells which are dividing - myelosuppression, hair loss, diarrhoea
Good for fast dividing tumours (lymphomas, acute leukaemias), not for slower dividing ones

81
Q

Increase in tumour size

A

Cell division

Lack of apoptosis

82
Q

Targeted chemo

A

more effective

less se

83
Q

How to find differences between normal and cancerous tissue

A

gene arrays
proteomics
tissue microarrays

84
Q

How to exploit differences

A

make a monoclonal ab against growth factor receptors to prevent growth factors binding so no activation signals and no proliferation
Small molecular inhibitor of growth factor receptor, same effects but harder to make

85
Q

Cetuximab

A

mab on end means monoclonal ab
Chimeric so that body does not identify as foreign
EGFR blocker

86
Q

Herceptin

A

Chimeric mab against EGFR 2 (Her-2)
Her-2 has a TKI switch
2 Her-2 molecules binding together activates signals for proliferations
Hereceptin mab causes Her-2 protein to be endocytosed and destroyed, this reduces her-2 numbers and so reduces its activity
Lymphocytes then are triggered and join
Her-2 gene is amplified in breast cancer, so Herceptin is used for adjuvant chemo in her2-positive breast cancer

87
Q

How to detect her-2 amplification

A

FISH - Fluorescent in situ hybridisation

Immunohistochemistry

88
Q

Anti-PD1

A

PD1 overexpression in tumours causes immunosuppression

89
Q

Small molecular inhibitors

A

Gleevec - Inhibits c-kit receptor

Gefitinib - EGFR TKI inhibitor

90
Q

Transfusion consists of

A

RBCs
Platelets
Volume (saline)

91
Q

MI treatment (atherosclerosis)

A

PCI
Stent
Anticoag

92
Q

How to avoid DVT in post surgery

A

gENERAL PROPHYLAXIS - ted STOCKINGS, HEPARINS

lONG TERM - IVC cage and anti coag

93
Q

Coroner

A

Interested in non-natural deaths

94
Q

Several chest infections may indicate

A

Lung cancer (asbestos, car fumes, soot, smoking)

95
Q

Tissue for diag (lung)

A

Sputum
bronchoscopy
Pleural biopsy

96
Q

Histology and cytology of lung cancer

A

Small cell cancer is worse than large cell

97
Q

TNM staging is applied to all tumours

A

T - Tumour size (larger the grade, larger tumour size)
N - Lymph nodes (Larger grade, further LN spread)
M - Mets (Distant is worse)

98
Q

Resolution vs repair

A

Resolution - Initiating factor removed, tissue undamaged or able to regenerate
Repair - Initiating factor still present. tissue damaged and unable to regenerate

99
Q

Cells that can regenerate

A 
Hepatocytes
Pneumocytes
All blood cells
Gut epithelium
Skin epithelium
Osteocytes
100
Q

Skin wounds - Healing by 1st intention

A

1) Incision
2) Exudation of fibrinogen
3) Weak fibrin join
4) Epidermal regrowth and collagen synthesis
5) Strong collagen join

101
Q

Skin wounds - Healing by 2nd intention

A

1) Tissue loss
2) Granulation tissue
3) Organisation
4) Eary fibrous scar
5) Scar contraction

102
Q

Repair

A

Replacement of damaged tissue by fibrous tissue

103
Q

Collagen is produced by

A

Fibroblasts

104
Q

Cells that can’t regenerate

A

Myocardial cells

Neurones

105
Q

Upper abdo pain

A

Refer for OGD (Oesophagogastroduodenoscopy)
Suspect gastritis
Check for any inflammation via biopsy
Infection by helicobacter indicated by raised urease levels
Gastrin overproduction - excess acid from body gland gastric cells
Gastritis increases risk of gastric/duodenal ulceration
Treat with antibiotics

106
Q

Types of inflammatory cells

A 
Macrophage 
Plasma cell
Neutrophil 
Lymphocyte 
Giant cell
107
Q

The inflammatory process also stimulates

A

Kinin system
Fibrinolytic system
Coagulation system
Complement cascade

108
Q

Scarring

A

Healing response which seals up the tissues

But contractures/adhesions alter anatomy and can get worse with time

109
Q

Lymphoma

A

Malignant neoplasm of lymphoid cells

110
Q

Chemo treatment

A

Damages fast dividing neoplastic cells but also hits - Hair, marrow and GI tract

111
Q

Thrombosis

A

1) Normal laminar flow
2) Endothelial cell injury
3) Platelet aggregation
4) Thrombus formation
5) Fibrin deposition

112
Q

Thrombosis

A

Solid mass of blood constituents formed within intact vascular system during life

113
Q

Thrombosis triad

A

Change in vessel wall - endo cell injury due to smoking which changes wall and also blood flow
Change in blood flow
Change in blood constituents

114
Q

Aspirin

A

Inhibits platelet aggregation

115
Q

Embolus

A

Solid mass in blood being carried through circulation to a place where it gets stuck and blocks the vessel
This solid mass tends to be a thrombus such as a DVT of the leg veins which breaks off and embolises through the large veins and right side of the heart to the lungs

116
Q

Ischaemia

A

Reduction in blood flow

117
Q

Infarction

A

Reduction in blood flow with subsequent death of cells

118
Q

Why blood clots don’t form all the time

A

Laminar flow - Cells travel in the centre of arterial vessels and don’t touch the sides
Endothelial cells which line vessels are not sticky when healthy

119
Q

Most common type of thrombosis

A

DVT - Deep Vein Thrombosis (hosital inpatients)

120
Q

Prevention of DVT for inpatients

A

Mobilisation
Low dose SC heparin
Venous stockings

121
Q

Less common causes of embolus

A

Air - pressurised systems of IV fluids/bloods
Cholesterol crystals from atheromatous plaques
Tumour
Amniotic fluid in pregnant women

122
Q

Embolism venous route

A

Embolus which enetrs the venous system will travel to the vena cava, through the right side of the heart and will lodge into the pulmonary arteries
From here it cannot get into the arterial circulation of the heart because the blood vessels in the lung split down to capillary size, so the lung acts as a filter for any venous emboli

123
Q

Ischaemia

A

Simply a reduction in blood flow to a tissue without any other implications

124
Q

Infarction

A

Reduction in blood flow to a tissue that is so reduced that it cannot even support mere maintenance of the cells in that tissue so they die
Infarction is usually macroscopic caaused by thrombosis of an artery - such as thrombus in the LAD coronary artery causing infarction of the anterior wall of the left ventricle

125
Q

Organs with dual arterial supply

A

Less suspectible to infarction
Liver - Portal venous and hepatic artery
Lung - Pulmonary venous and bronchial artery
Brain - COW

126
Q

Coronary artery infarctions

A

Right CA - Inferior infarct, can also include posterior septum
LAD - Anterior infarct (sudden death)
Circumflex artery - Lateral infarct

127
Q

Regional transmural myocardial infarction

A

Infarction that is transmural through all cardium layers (endocardium to epicardium layers)

128
Q

Subendocardial myocardial infarction

A

Infarct of the myocardium that is subendocardial

129
Q

Initial reaction of tissue to injury

A

Vascular - Dilation of vessels
Exudative - Vascular leakage of protein-rich fluid
Neutrophil polymorphs are charcteristic of cells recruited to the tissue

130
Q

Materials that resist digestion

A

Keratin
Necrotic bone
Cholesterol crystals
Sodium urate

131
Q

Stroke

A

Cerebral infarction

132
Q

Heart attack

A

Myocardial infarction

133
Q

Infarction and ischaemia

A

Infarction is always due to ischaemia but ischaemia does not always cause infarction

134
Q

Angina

A

Ischaemia may cause chest pain but no infarction

135
Q

Atheroma

A

AKA Atherosclerosis
Pathology of arteries involving deposition of lipids in the arterial wall with surrounding fibrosis and chronic inflammation
These plaques can enlarge to occlude the lumen of vessels
Predominant cause of MI and CI

136
Q

Atheroma - Risk factors

A 
Raised serum lipids (LDL/triglycerides cause direct damage to endothelial cells)
Hypertension (Shearing force on endothelial cells which are delicate in nature)
Diabetes mellitus (Superoxide anions
Smoking (CO, nicotine)
137
Q

Atheroma formation - 2 Processes

A 
Endothelial damage (due to lipids, raised BP, smoking)
Chronic inflammation (Macrophages and fibroblasts)
138
Q

Prevention/slowing progression of atheromas

A

Reducing lipids
Reducing BP
Smoking cessation
Low dose aspirin will reduce amount of platelet aggregation at site of endothelial damage

139
Q

Atherosclerosis

A

Common in high pressure systems such as aorta rather than low pressure systems such as pulmonary arteries

140
Q

Plaque composition

A

Fibrous tissue
Lipids - cholesterol
Lymphocytes

141
Q

Atherosclerosis - Complications

A

MI
Cerebral infarct (CI) due to carotid atheroma embolising and causing TIA or CI
Aortic aneurysms - Rupture causes sudden death
Gangrene

142
Q

Apoptosis

A

Programmed cell death of a single cell

143
Q

Necrosis

A

Unprogrammed death of a large number of cells due to an adverse event such as infarction, burns, frostbite, etc

144
Q

Apoptosis

A

Important in normal body function
In the gut, there is a steady turnover of cells with stem cells dividing to produce new cells which mature and differentiate and eventually die by apoptosis

145
Q

Apoptosis

A

Implemented by Caspases and Bcl2 protein

146
Q

Alternatives to apoptosis for cells

A

Autophagy
Closing down protein synthesis
Cell cycle arrest

147
Q

Apoptosis

A

If a cell has a lot of DNA damage then apoptosis will be preferred over the other options

148
Q

Apoptosis process

A

1) Bcl2 protein and activated Fas receptor signal Caspases

2) Caspases cause apoptosis

149
Q

Necrosis example

A 
Toxic spider venom
Frostbite 
Cerebral infarction 
Avascular necrosis of bone
Pancreatitis
150
Q

Necrosis types

A

Coagulative
Liquifactive
Caseous

151
Q

Sickle cell anaemia - Genetic cause

A

1) Point mutation in the beta-globin chain of haemaglobin
2) Causes the hydrophilic amino acid glutamic acid to be replaced with the hydrophobic amino acid valine at the 6th position
3) This is a very specific genetic abnormaility
4) This always produces an abnormal haemaglobin which causes RBCs to sickle (deform) when oxygen sats are low

152
Q

Sickle cell anaemia

A

Single gene disorder - abnormality of a single gene causes disease

153
Q

Polygenic diseases

A

Genetic diseases resulted from the interaction of several different genes usually on different chromosomes

154
Q

Breast cancer

A

Polygenic disorder

BRCA1 and BRCA2 along with many other genes

155
Q

Congenital disease

A

Born with it (genetic)

156
Q

Rhesus haemolytic disease

A

In newborns where maternal antibodies attack RBCs of baby in utero

157
Q

Fetal alcohol syndrome

A

Baby with facial characteristics - Small eye openings, smooth philtrum, thin upper lip

158
Q

Pituitary adenoma

A

Growth hormone excess

159
Q

Hypertrophy

A

Increased tissue size due to increased cell size

160
Q

Hyperplasia

A

Increased tissue size due to increased number of cells

161
Q

Hypertrophy examples

A

Physiological - Skeletal muscle cells

Pathological - Myocardium undergoes hypertrophy in patients with raised BP

162
Q

Hyperplasia examples

A

Physiological - During pregnancy and lactation, the breast epithelial cells respond to increased physiological demands by undergoing hyperplasia
Pathological - Prostate undergoes hyperplasia with age in response to a relative excess of oestrogen stimulation

163
Q

Atrophy

A

Decrease in size of an organ or tissue

164
Q

Atrophy examples

A

Physiological - Thymus in early adult life. Genitals, mandible, cerebrum and lymphoid tissue atrophy in later life
Pathological - Occurs as a result of a loss of blood supply, loss of innervation, pressure, lack of nutrition, lack of hormonal stimulation, or as a result of hormonal stimulation

165
Q

Metaplasia

A

Reversible transformation of a mature differentiated cell type into another fully differentiated cell type
It is an adaptive response to injurous stimuli

166
Q

Metaplasia examples

A

Transformation of the normal pseudostratified columnar ciliated epithelium ciliated epithelium of the bronchi into squamous epithelium following repeating smoking

167
Q

Dysplasia

A

Premalignant condition characterised by increased growth, cellular atypia and decreased differentiation
Caused by long exposure to chronic inflammation and carcinogenic substances

168
Q

Dysplasia examples

A

HPV infection in squamous epithelium of uterine cervix

169
Q

Ageing manifestations

A 
Cancer development
Neurodegeneration - Alzheimer's dementia and Parkinson's disease
Osteoarthritis 
Hearling loss
Vision loss
Reduced immunity
170
Q

Ageing manifestations - Cellular causes

A

Damage to mitohondrial DNA
Accumulation of toxic by-products of metabolism
Free-radical generation
Time-dependent activation of ageing and death genes

171
Q

Oestrogen and bone relationship

A

Lack of oestrogen = decreased bone formation and increased bone resorption

172
Q

Neurodegeneration during ageing - mechanisms

A

Cortical atrophy
Shrinkage of hippocampus
Enlarged ventricles

173
Q

Muscle degeneration

A

Decreased growth hormone
Decreased testosterone
Increased catabolic cytokines

174
Q

Deaffness - mechanism

A

Loss of hair cells in cochlear which are unable to regenerate

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