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Phase 2a > ICS - Pathology 2 > Flashcards

ICS - Pathology 2 Flashcards

1
Q

Define inflammation

A

A local physiological response to tissue injury

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2
Q

Give an advantage of inflammation

A

Can destroy invading micro-organisms and can prevent the spread of infection

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3
Q

Give a disadvantage of inflammation

A

Can produce disease and lead to distorted tissues with permanently altered function

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4
Q

Define acute inflammation

A

Initial and often transient series of tissue reactions to injury

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5
Q

What are the main cells involved in acute inflammation?

A

Neutrophils and monocytes

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6
Q

What are the main steps of acute inflammation?

A
  • Initial reaction of tissue to injury- Vascular component (vessels dilate)- Exudative component (vascular leakage of protein-rich fluid)- Neutrophil polymorph (phagocytose)
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7
Q

Define exudate

A

A protein-rich fluid that leaks out of vessel walls due to increased vascular permeability

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8
Q

What are examples of acute inflammation?

A
  • Acute appendicitis- Frostbite - Streptococcal sore throat
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9
Q

What vascular changes occur in acute inflammation?

A
  • Increased blood flow through capillaries- Increased vascular permeability (exudation)
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10
Q

What is the role of tissue macrophages in acute inflammation?

A

Secrete chemical mediators that attract neutrophil polymorphs

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11
Q

What is the role of the lymphatic system in acute inflammation?

A

Lymphatic channels dilate and drain away oedematous fluid (reduces swelling). Antigens are also carried to lymph nodes for recognition by lymphocytes

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12
Q

What are the main steps of neutrophil polymorph migration?

A
  1. Margination 2. Adhesion/Pavementing3. Emigration4. Diapedesis
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13
Q

Describe margination (neutrophil polymorph migration)

A

Neutrophils migrate to the peripheral part of blood vessels near the endothelium due to increased plasma viscosity

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14
Q

Describe adhesion/pavementing (neutrophil polymorph migration)

A

Neutrophils adhere to vascular endothelium in venules. Results from interactions between paired adhesion molecules (on leucocyte and endothelial surfaces)

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15
Q

Describe emigration (neutrophil polymorph migration)

A

Neutrophils pass through endothelial cells and through the basal lamina into the adventitia

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16
Q

Describe diapedesis (neutrophil polymorph migration)

A

A passive process that depends on hydrostatic pressure. RBCs sometimes escape from vessels which indicates severe vascular injury (e.g. tear in vessel wall)

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17
Q

What is released from injured tissues that causes the acute inflammation response to spread?

A

Chemical mediators e.g. histamine and thrombin

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18
Q

Give 3 endogenous chemical mediators of acute inflammation

A
  1. Bradykinin2. Histamine3. Nitric oxide
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19
Q

What is the main source (and other sources) of histamine?

A

Mast cells (stored in granules in their cytoplasm)Also basophils, eosinophils and platelets

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20
Q

What do chemical mediators such as histamine cause?

A
  • Vasodilation- Emigration of neutrophils- Chemotaxis- Increased vascular permeability- Itching and pain
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21
Q

Give 6 causes of inflammation

A
  1. Microbial infections (bacteria, viruses)2. Hypersensitivity reactions (parasites, TB)3. Physical agents (trauma, burns, frost bite)4. Chemicals (corrosives, acids, alkalis)5. Bacteria toxins6. Tissue necrosis (ischaemia, infarction)
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22
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication

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23
Q

What does bacterial infection result in?

A

The release of exotoxins (involved in the initiation of inflammation) or endotoxins

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24
Q

What are the 5 cardinal signs of inflammation?

A
  1. Rubor (redness)2. Calor (heat)3. Tumor (swelling)4. Dolor (pain)5. Loss of function
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25
Q

What are the 4 outcomes of inflammation?

A
  1. Resolution2. Suppuration3. Organisation4. Progression
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26
Q

Describe resolution in inflammation

A
  • Complete restoration of tissues to normal- Minimal cell death and tissue damage- Rapid destruction of causal agent- Most common in organs capable of regeneration (e.g. liver)- E.g. acute lobar pneumonia
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27
Q

Describe suppuration in inflammation

A
  • Formation of pus- Pus accumulates and becomes surrounded by pyogenic membrane- Leads to granulation tissue and scarring- E.g. staphylococcus aureus
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28
Q

Describe organisation in inflammation

A
  • Replacement by granulation tissue (scar tissue formation)- Occurs when substantial volumes of tissue become necrotic or is not easily digested- Fibrosis occurs- E.g. pleural space following acute lobar pneumonia
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29
Q

Describe progression in inflammation

A
  • Causative agent is not removed - Progresses to chronic inflammation
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30
Q

How can acute inflammation be diagnosed histologically?

A

Looking for the presence of neutrophil polymorphs

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31
Q

Give 4 systemic effects of acute inflammation

A
  1. Fever2. Feeling unwell3. Weight loss4. Reactive hyperplasia of the reticuloendothelial system
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32
Q

Define chronic inflammation

A

Subsequent prolonged response to tissue injury

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33
Q

What are the main cells involved in chronic inflammation?

A

Lymphocytes, macrophages and plasma cells

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34
Q

Give 4 causes of chronic inflammation

A
  • Primary chronic inflammation- Transplant rejection- Recurrent acute inflammation- Progression from acute inflammation
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35
Q

Give 5 examples of primary chronic inflammation

A
  1. Resistance of infective agent (e.g. TB, leprosy)2. Endogenous materials (e.g. necrotic tissue, uric acid crystals)3. Exogenous materials (e.g. silica, asbestos)4. Autoimmune conditions (e.g. rheumatoid arthritis, chronic gastritis)5. Primary granulomatous diseases (e.g. Crohn’s, sarcoidosis)
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36
Q

Give 4 macroscopic appearances of chronic inflamamtion

A
  • Chronic ulcer- Chronic abscess cavity- Granulomatous inflammation- Fibrosis
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37
Q

Give 4 microscopic appearances of chronic inflammation

A
  1. Lymphocytes, plasma cells and macrophages2. Exudation not common3. Evidence of continuing destruction4. Possible tissue necrosis
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38
Q

Define granulation tissue

A

Tissue composed of small blood vessels in a connective tissue matrix with myofibroblasts (important in healing and repair)

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39
Q

Define granuloma

A

Aggregate of epithelioid histocytes

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40
Q

Give examples of granulomatous diseases

A
  • TB- Leprosy- Crohn’s disease- Sarcoidosis
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41
Q

Explain the difference between resolution and repair

A

Resolution - initiating factor is removed and tissue is able to regenerateRepair - initiating factor is still present and tissue is unable to regenerate

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42
Q

Name 5 cells capable of regeneration

A
  1. Hepatocytes2. Osteocytes3. Pneumocytes4. Blood cells5. Gut and skin epithelial cells
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43
Q

Name 2 cells incapable of regeneration

A
  1. Myocardial cells2. Neuronal cells
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44
Q

What cells produce collagen in fibrous scarring?

A

Fibroblasts

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45
Q

Give an example of a chronic inflammatory process from the start

A

Infectious mononucleosis

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46
Q

Define laminar flow

A

Streamline movement of blood - cells travel in the centre of arterial vessels and don’t touch the sides

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47
Q

Define thrombosis

A

Solidification of blood contents that forms within vascular system during life

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48
Q

Give 2 reasons why thrombosis is uncommon

A
  1. Laminar flow2. Non sticky endothelial cells
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49
Q

What do platelets contain?

A
  1. Alpha granules (involved in platelet adhesion e.g. fibrinogen)2. Dense granules (involved in platelet aggregation e.g. ADP)
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50
Q

What is Virchow’s traid?

A

3 factors that can lead to thrombus formation:1. Reduced blood flow2. Blood vessel injury3. Increased coaguability

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51
Q

What are the 4 outcomes of thrombosis?

A
  1. Resolution (body dissolves and clears it)2. Organisation (becomes a scar and slightly narrows vessel lumen)3. Recanalisation (intimal cells may proliferate and capillaries may grow into thrombus and fuse)4. Embolus (fragments break off into circulation)
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52
Q

Describe an arterial thrombus

A
  • Commonly caused by atheroma- High pressure- Mainly made of platelets- Can lead to myocardial infarction/stroke- Treated by anti-platelets e.g. aspirin
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53
Q

Describe a venous thrombus

A
  • Commonly caused by stasis- Low pressure- Mainly made of RBCs- Can lead to deep vein thrombosis/pulmonary embolism- Treated by anti-coagulants e.g. warfarin, apixaban
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54
Q

Define embolus

A

Mass of material (usually a thrombus) in the vascular system able to lodge in a vessel and block its lumen

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55
Q

Give 6 causes of embolisms

A
  1. Thrombus2. Air (e.g. pressurised systems of IV fluids)3. Cholesterol crystals (from atheromatous plaques)4. Tumour5. Amniotic fluid6. Fat (severe trauma with multiple fractures)
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56
Q

Describe arterial embolisms

A
  • Systemic embolism- Can travel anywhere downstream of entry point- Cholesterol crystals from atheromatous plaques in the descending aorta can go to any lower limb or renal artery
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57
Q

What are mural thrombi?

A

Thrombi that attach to the wall of blood vessels and cardiac chambers. Mural thrombi in the left ventricle can go anywhere in the systemic circulation

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58
Q

Describe venous embolisms

A
  • Pulmonary embolism- Emboli travel to the vena cava and lodge in the pulmonary arteries- The lungs acts as a filter for venous emboli (blood vessels split down to capillary size)
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59
Q

Define ischaemia

A

Reduction in blood flow

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60
Q

Define infarction

A

Necrosis of part of an organ that occurs when the artery supplying it becomes obstructed

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61
Q

Give 3 examples of organs with a dual arterial supply

A
  • Liver (hepatic arteries and portal veins)- Lungs (bronchial arteries and pulmonary veins)- Some areas of the brain around the circle of willis
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62
Q

Why are tissues with an end arterial supply more susceptible to infarction?

A

Only have a single arterial supply

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63
Q

What is a reperfusion injury?

A

Damage to tissue during reoxygenation due to the release of waste products

64
Q

Give a drug that is used to prevent thrombosis

A

Aspirin (inhibits platelet aggregation)

65
Q

What are the main steps of coagulation?

A
  • Vascular spasm- Primary platelet plug (adhesion, activation, aggregation)- Secondary stable plug
66
Q

Define atherosclerosis

A

Disease characterised by the formation of atherosclerotic plaques in the intima of vessel walls

67
Q

Where is atherosclerosis more common and why?

A

Systemic circulation as it is a higher pressure system

68
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids2. Fibrous tissue3. Lymphocytes
69
Q

Briefly describe the formation of an atheromatous plaque

A
  • Damage to endothelial cells - secrete chemoattractants- LDL in the blood will accumulate in the arterial wall- Macrophages attracted to site and take up lipids to form foam cells- Foam cells accumulate in the intima to form a fatty streak- Foam cells rupture to release lipids, cytokines and growth factors- Smooth muscle cells proliferate and migrate from the media to the intima- Dense fibrous cap (collagen) forms around the lipid core
70
Q

Give 7 risk factors for atherosclerosis

A
  1. Hypercholesterolaemia2. Smoking3. Hypertension4. Hyperlipidaemia5. Uncontrolled diabetes mellitus6. Male sex7. Increasing age
71
Q

Give 5 preventative measures for atherosclerosis

A
  • Smoking cessation- Blood pressure control- Weight reduction- Taking low dose aspirin regularly- Statins
72
Q

How does smoking increase the risk of atherosclerosis?

A

Cigarette smoke releases free radicals, nicotine and carbon monoxide into the body which all damage endothelial cells

73
Q

How does hypertension increase the risk of atherosclerosis?

A

Greater force exerted on endothelial cells and so more likely to cause damage

74
Q

Define apoptosis

A

Programmed cell death of a single cell without harm to surrounding cells

75
Q

Why is apoptosis good?

A
  • Removal of cells during development- Removal of cells during normal turnover (e.g. cells in intestinal villi at tips replaced by cells from below)
76
Q

What is the role of the p53 protein?

A

Looks for DNA damage and if detected, triggers apoptosis

77
Q

Give 4 inhibitors of apoptosis

A
  • Growth factors- Extracellular cell matrix- Sex steroids- Some viral proteins
78
Q

Give 8 inducers of apoptosis

A
  1. Growth factor withdrawal2. Loss of matrix attachment3. Glucocorticoids4. Some viruses5. Free radicals6. Ionising radiation7. DNA damage8. Ligand binding at ‘death receptors’
79
Q

Apoptosis can be turned on by a family of protease enzymes called …

A

Caspases

80
Q

Caspases can be activated by the activation of …

A

FAS receptor

81
Q

Describe the intrinsic pathway of apoptosis

A
  • Uses pro- and anti-apoptotic members of the Bcl-2 family (Bax and Bcl-2)- Ratio determines cell’s susceptibility to apoptotic stimuli
82
Q

What do Bcl-2 and Bax do?

A
  • Bcl-2 inhibits apoptosis- Bax enhances apoptosis
83
Q

Describe the extrinsic pathway of apoptosis

A
  • Ligand-binding at death receptors on the cell surface- This promotes clustering on the cell surface and initiates cascade- Caspases are activated and apoptosis is triggered
84
Q

Give an example of a disease where there is a lack of apoptosis

A

Cancer. Mutations in p53 gene so p53 protein cannot detect DNA damage. Results in increasing tumour size and accumulation of genetic mutations

85
Q

Give an example of a disease where there is too much apoptosis

A

HIV. Apoptosis induced in CD4 helper cells which reduces their numbers and produces an immunodeficient state

86
Q

Define necrosis

A

Traumatic cell death of a large number of cells

87
Q

Give 3 examples of events that can lead to necrosis

A
  • Frost bite- Avascular necrosis- Infarction
88
Q

Name the 4 types of necrosis

A
  1. Coagulative (caused by ischaemia)2. Liquefactive (lack of substantial supporting stroma in brain)3. Caseous (‘cheese’ pattern)4. Gangrene (necrosis with rotting of tissue)
89
Q

Define hypertrophy

A

Increase in the size of a tissue due to an increase in the size of its constituent cells

90
Q

Define hyperplasia

A

Increase in the size of a tissue due to an increase in the number of its constituent cells

91
Q

Define atrophy

A

Decrease in the size of a tissue due to a decrease in the size or number of its constituent cells

92
Q

Define metaplasia

A

Change in cell differentiation from one fully-differentiated cell type to another fully-differentiated cell type

93
Q

Give an example of a disease that demonstrates metaplasia

A

Barrett’s oesophagus - continued acid reflux causes the cells at the lower end of the oesophagus to change from stratified squamous cells to columnar

94
Q

Describe metaplasia in smoking

A

Bronchial epithelium changes from ciliated columnar to squamous when exposed to cigarette smoke continuously

95
Q

Define dysplasia

A

Morphological changes that may be seen in cells in the progression to becoming cancer

96
Q

Define neoplasia

A

Uncontrolled, abnormal growth of cells or tissues (cancer)

97
Q

What is a neoplasm composed of?

A

Neoplastic cells and stroma

98
Q

Define carcinogenesis

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

99
Q

Define carcinogenic, oncogenic and mutagenic

A

Carcinogenic - cancer causing (malignant only)Oncogenic - neoplasm causing (both benign and malignant)Mutagenic - acts on DNA

100
Q

What percentage of cancer risk is environmental?

A

85% environmental and 15% genetic

101
Q

Give 5 host factors that can affect cancer risk

A
  1. Ethnicity2. Diet/lifestyle (diet/exercise/sexual behaviour)3. Constitutional factors (age/gender/inherited predisposition)4. Premalignant conditions5. Transplacental exposure
102
Q

Give an example of transplacental exposure causing an increased cancer risk

A

Diethylstilbestrol associated with increased risk of vaginal cancer

103
Q

Give the 5 classes of carcinogens

A
  1. Chemical2. Viral3. Ionising and non-ionising radiation4. Hormones, parasites and mycotoxins5. Miscellaneous
104
Q

Define carcinogen

A

Environmental agents known or suspected to cause neoplasms

105
Q

Describe chemical carcinogens

A

Most require metabolic conversion from pro-carcinogens to ultimate carcinogens

106
Q

Give 4 examples of chemical carcinogens

A
  • Polycyclic aromatic hydrocarbons cause lung/skin cancer (cigarettes/mineral oils)- Aromatic amines cause bladder cancer (rubber/dyes)- Nitrosamines cause gut cancer- Alkylating agents cause leukaemia - small risk in humans (found in chemotherapeutic agents)
107
Q

What causes skin cancer?

A

Exposure to UV light

108
Q

Give 2 examples of miscellaneous carcinogens

A

Asbestos and metals

109
Q

How are neoplasms classified?

A

Behavioural and histogenetic classifications

110
Q

Describe the behavioural classification of neoplasms

A

Can be classified as benign, malignant or borderline

111
Q

Describe the histogenetic classification of neoplasms

A

Classified based on the specific cell of origin of the tumour (if origin is unknown, it is anaplastic)

112
Q

Give 7 features of benign neoplasms

A
  1. Non-invasive2. Localised3. Exophytic (grows outwards)4. Low mitotic activity5. Necrosis and ulceration are rare6. Normal nuclei7. Close resemblance to normal tissue
113
Q

Give 7 features of malignant neoplasms

A
  1. Invasive2. Metastases3. Endophytic (grows inwards)4. High mitotic activity5. Necrosis and ulceration are common6. Poorly defined border7. Poor resemblance to normal tissue
114
Q

Give 4 consequences of benign neoplasms

A
  1. Pressure on adjacent structures2. Obstruction to flow3. Transformation into malignant neoplasms4. Anxiety
115
Q

Give 4 consequences of malignant neoplasms

A
  1. Destroy surrounding tissue2. Blood loss due to ulceration3. Pain4. Anxiety
116
Q

What is a papilloma?

A

Benign tumour of non-glandular epithelium

117
Q

What is an adenoma?

A

Benign tumour of glandular epithelium

118
Q

What is a carcinoma?

A

Malignant epithelial tumour

119
Q

What is an adenocarcinoma?

A

Malignant tumour of glandular epithelium

120
Q

What is a lipoma?

A

Benign tumour of adipocytes

121
Q

What is a rhabdomyoma?

A

Benign tumour of striated muscle

122
Q

What is a leiomyoma?

A

Benign tumour of smooth muscle

123
Q

What is a chondroma?

A

Benign tumour of cartilage

124
Q

What is an osteoma?

A

Benign tumour of bone

125
Q

What is a sarcoma?

A

Malignant tumour of connective tissue

126
Q

What is a liposarcoma?

A

Malignant tumour of adipocytes

127
Q

What is a neuroma?

A

Benign tumour of nerves

128
Q

What is a rhabomyosarcoma?

A

Malignant tumour of striated muscle

129
Q

What is a leiomyosarcoma?

A

Malignant tumour of smooth muscle

130
Q

What is a chondrosarcoma?

A

Malignant tumour of cartilage

131
Q

What is an osteosarcoma?

A

Malignant tumour of bone

132
Q

What is a melanoma?

A

Malignant tumour of melanocytes

133
Q

What is a lymphoma?

A

Malignant tumour of lymphoid cells

134
Q

What is a mesothelioma?

A

Malignant tumour of mesothelial cells (pleura)

135
Q

Define metastasis

A

The process whereby malignant tumours spread from their site of origin to form other tumours at distant sites

136
Q

What never metastasises?

A

Basal cell carcinomas

137
Q

What are the 7 steps of metastasis?

A
  1. Detachment2. Invasion3. Intravasation4. Evasion5. Adherence6. Extravasation7. Proliferation
138
Q

What is required for invasion (tumour metastasis)?

A

Proteases and cell motility

139
Q

What is required for intravasation (tumour metastasis)?

A

Collagenases and cell motility

140
Q

What is required for extravasation (tumour metastasis)?

A

Adhesion receptors, collagenases and cell motility

141
Q

Give 3 tumour evasion methods

A
  1. Aggregation with platelets2. Shedding of surface antigens3. Adhesion to other tumour cells
142
Q

Which 5 carcinomas most commonly spread to bone?

A

PB KTL1. Prostate2. Breast3. Kidneys 4. Thyroid5. Lungs

143
Q

Carcinomas that commonly spread to the axillary lymph nodes are …

A

Breast carcinomas

144
Q

Which route of metastasis do carcinomas prefer?

A

Lymphatic spread

145
Q

Which route of metastasis do sarcomas prefer?

A

Haematogenous spread (often spread to lung via vena cava –> heart –> pulmonary arteries)

146
Q

Which tumours commonly metastasise to the liver?

A
  • Colon- Stomach- Pancreas- Carcinoid(via portal vein)
147
Q

Describe tumour staging

A

T - primary tumour (size)N - lymph node status (degree of lymph node involvement)M - metastatic status (extent of distant metastases)

148
Q

How would you cure a basal cell carcinoma and why?

A

Complete local excision as they do not metastasise

149
Q

How would you treat leukaemia and why?

A

Chemotherapy as it is systemic and so circulates all around the body

150
Q

Why is adjuvant therapy often used?

A

Micrometastases may form

151
Q

Give an advantage of chemotherapy

A

Works well against fast dividing tumours e.g. lymphomas

152
Q

Give a disadvantage of chemotherapy

A

Non selective for tumour cells, normal cells are affected

153
Q

What is targeted chemotherapy most effective against?

A

Slower dividing tumours e.g. lung, colon and breast

154
Q

What is targeted chemotherapy?

A

Cancer cells and normal cells can be differentiated

155
Q

What kind of drugs can be used in targeted chemotherapy?

A

Monoclonal antibodies and small molecular inhibitors

Phase 2a (29 decks)

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