Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A ICS, Microbiology, Public Health, GP and ILAs > ICS Pathology > Flashcards

ICS Pathology Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Define inflammation.

A

A local physiological response to tissue injury.

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

Give a benefit of inflammation.

A

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

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

Give a disadvantage of inflammation.

A

Inflammation can produce disease and can lead to distorted tissues with permanently altered function.

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

Define exudate.

A

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

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

What are the 4 outcomes of inflammation?

A
  1. Resolution.
  2. Suppuration.
  3. Organisation (scar tissue formation).
  4. Progression onto chronic inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give 6 causes of acute inflammation.

A
  1. Microbial infections (bacteria and viruses).
  2. Chemicals (corrosives, acids/alkalis).
  3. Physical agents (trauma, burns, frost bite).
  4. Hypersensitivity reactions (TB).
  5. Bacterial toxins.
  6. Tissue necrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication.

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

What does bacterial infection result in?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give 5 cardinal signs of inflammation.

A
  1. Redness (rubor).
  2. Swelling (tumor).
  3. Pain (dolor).
  4. Heat (calor).
  5. Loss of function.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can acute inflammation be diagnosed histologically?

A

By looking for the presence of neutrophil polymorphs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 3 endogenous chemical mediators of acute inflammation.

A
  1. Bradykinin.
  2. Histamine.
  3. Nitric Oxide.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 4 systemic effects of acute inflammation?

A
  1. Fever.
  2. Feeling unwell.
  3. Weight loss.
  4. Reactive hyperplasia of the reticuloendothelial system.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What cells are involved in chronic inflammation?

A

Macrophages and plasma cells (B and T lymphocytes).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What cell can form when several macrophages try to ingest the same particle?

A

Multinucleate giant cell.

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

Give 4 causes of chronic inflammation.

A
  1. Primary chronic inflammation.
  2. Transplant rejection.
  3. Recurrent acute inflammation.
  4. Progression from acute inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give examples of primary chronic inflammation.

A
  1. Infective substances having resistance to phagocytosis e.g. TB, leprosy.
  2. Endogenous materials e.g. uric acid crystals.
  3. Exogenous materials e.g. asbestos.
  4. Autoimmune diseases e.g. chronic gastritis, rheumatoid arthritis etc.
  5. Other chronic inflammatory diseases e.g. chronic inflammatory bowel disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In which type of inflammation would you see neutrophil polymorphs?

A

Acute inflammation.

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

What are some macroscopic features of chronic inflammation?

A
  1. Chronic ulcer.
  2. Chronic abscess cavity.
  3. Granulomatous inflammation.
  4. Fibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is granulation tissue?

A

Granulation tissue is composed of small blood vessels in a connective tissue matrix with myofibroblasts. It is important in healing and repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define granuloma.

A

An aggregate of epithelioid histocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give an example of a granulomatous disease.

A

TB, leprosy, Crohn’s disease and sarcoidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

A

Angiotensin converting enzyme.

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

What kind of disease is TB?

A

A granulomatous disease.

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

What is the difference between resolution and repair?

A

Resolution is when the initiating factor is removed and the tissue is able to regenerate. In repair, the initiating factor is still present and the tissue is unable to regenerate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name 5 types of cells capable of regeneration.

A
  1. Hepatocytes.
  2. Osteocytes.
  3. Pneumocytes.
  4. Blood cells.
  5. Gut and skin epithelial cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells.

2. Neuronal cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Define abscess.

A

Acute inflammation with a fibrotic wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Define thrombosis.

A

Formation of a solid mass from blood constituents in an intact vessel in the living.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give 2 reasons why thrombosis formation is uncommon.

A
  1. Laminar flow.

2. Non sticky endothelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 3 factors that can lead to thrombosis formation?

A
  1. Change in vessel wall.
  2. Change in blood constituents.
  3. Change in blood flow.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define embolus.

A

A mass of material (often a thrombus) in the vascular system that is able to become lodged in a vessel and block it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Define ischaemia.

A

Decreased blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Define infarction.

A

Decreased blood flow with subsequent cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A

They only have a single arterial supply and so if this vessel is interrupted infarction is likely.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give 3 examples of organs with a dual arterial supply.

A
  1. Lungs (bronchial arteries and pulmonary veins).
  2. Liver (hepatic arteries and portal veins).
  3. Some areas of the brain around the circle of willis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What can happen if ischaemia is rectified?

A

Re-perfusion injury can occur due to the release of waste products.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the consequences of an arterial embolus?

A

An arterial embolus can go anywhere! The consequences could be stroke, MI, gangrene etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the consequences of a venous embolus?

A

An embolus in the venous system will go onto the vena cava and then through the pulmonary arteries and become lodged in the lungs causing a pulmonary embolism. This means there is decreased perfusion to the lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Through which blood system would an embolus have travelled if it resulted in a pulmonary embolism?

A

Venous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What drug can be used to prevent Thrombosis?

A

Aspirin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Define atherosclerosis.

A

Inflammatory process characterised by hardened plaques in the intima of a vessel wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Is atherosclerosis more common in the systemic or pulmonary circulation?

A

It is more common in the systemic circulation because this is a higher pressure system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids.
  2. Fibrous tissue.
  3. Lymphocytes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give 5 risk factors for atherosclerosis.

A
  1. Cigarette smoking.
  2. Hypertension.
  3. Hyperlipidaemia.
  4. Uncontrolled diabetes mellitus.
  5. Lower socioeconomic status.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What can be done to prevent atherosclerosis?

A

Reduce risk factors and taking low dose aspirin regularly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why can cigarette smoking lead to atherosclerosis?

A

Cigarette smoking releases free radicals, nicotine and CO into the body. These all damage endothelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why can hypertension lead to atherosclerosis?

A

A higher blood pressure means there is a greater force exerted onto the endothelial cells and this can lead to damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Define apoptosis.

A

Programmed cell death of a single cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the role of p53 protein?

A

p53 protein looks for DNA damage, if damage is present p53 switches on apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What protein can switch on apoptosis if DNA damage is present?

A

p53 protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Activation of which family of protease enzymes can turn on apoptosis?

A

Caspases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

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

A

Cancer; mutations in p53 mean cell damage isn’t detected.

55
Q

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

A

HIV.

56
Q

Define necrosis.

A

Unprogrammed death of a large number of cells due to an adverse event.

57
Q

Give 3 examples of events that can lead to necrosis.

A
  1. Frost bite.
  2. Avascular necrosis.
  3. Infarction.
58
Q

Give 3 differences between apoptosis and necrosis.

A
  1. Apoptosis is programmed cell death whereas necrosis is unprogrammed.
  2. Apoptosis tends to effect only a single cell whereas necrosis effects a large number of cells.
  3. Apoptosis is often in response to DNA damage. Necrosis is triggered by an adverse event e.g. frost bite.
59
Q

Define hypertrophy.

A

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

60
Q

Define hyperplasia.

A

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

61
Q

Define atrophy.

A

Decrease in the size of a tissue due to a decrease in the size of the constituent cells OR due to a decrease in the number of constituent cells.

62
Q

Define metaplasia.

A

A change in the differentiation of a cell from one fully differentiated cell type to another fully differentiated cell type.

63
Q

Give an example of a disease that demonstrates metaplasia.

A

Barrett’s oesophagus - the cells at the lower end of the oesophagus change from stratified squamous cells to columnar.

64
Q

Define dysplasia.

A

Morphological changes seen in cells in the progression to becoming cancer. The cells become more ‘jumbled up’.

65
Q

Define acute inflammation.

A

Initial and short lived tissue reactions to injury.

66
Q

Define chronic inflammation.

A

Subsequent and prolonged tissue reactions to injury.

67
Q

What happens to a cell when the telomere gets too short?

A

It can no longer divide.

68
Q

Give an example of:

a) a dividing tissue.
b) a non dividing tissue.

A

a) Gut or skin tissue can divide.

b) Brain tissue is non dividing.

69
Q

Why can excision be used as a cure for basal cell carcinoma?

A

Because BCC doesn’t metastasise.

70
Q

Suggest a treatment that could be used for leukemia?

A

Chemotherapy. Leukemia is systemic, it circulates all around the body, therefore excision can’t be used.

71
Q

Define carcinoma.

A

Malignant tumour of epithelial tissue.

72
Q

Give an example of 5 carcinoma’s that can spread to bone.

A
  1. Breast.
  2. Kidney.
  3. Lung.
  4. Prostate.
  5. Thyroid.
73
Q

Give an example of a carcinoma that can spread to the axillary lymph nodes.

A

Breast carcinomas.

74
Q

Why is adjuvant therapy often used in the treatment of carcinomas?

A

Micrometastes are possible even if a tumour is excised and so adjuvant therapy is given to suppress secondary tumour formation.

75
Q

Give an advantage and a disadvantage of conventional chemotherapy.

A
  • Advantage: works well for treatment against fast dividing tumours e.g. lymphomas.
  • Disadvantage: it is non selective for tumour cells, normal cells are hit too; this results in bad side effects such as diarrhoea and hair loss.
76
Q

What kind of carcinomas would targeted chemotherapy be most effective against?

A

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

77
Q

What is the theory behind targeted chemotherapy?

A

It exploits the differences between cancer cells and normal cells; this means it is more effective and has less side effects.

78
Q

What kind of drugs can be used in targeted chemotherapy?

A

Monoclonal antibodies (MAB) and small molecular inhibitors (SMI).

79
Q

What is required for a tumour to invade through a basement membrane?

A
  1. Proteases.

2. Cell motility.

80
Q

What is required for a tumour to enter the blood stream (intravasation)?

A
  1. Collagenases.

2. Cell motility.

81
Q

What is required for a tumour to exit the blood stream (extravasation)?

A
  1. Adhesion receptors.
  2. Collagenases.
  3. Cell motility.
82
Q

Give 2 promoters of tumour angiogenesis.

A
  1. Vascular endothelial growth factors.

2. Fibroblast growth factors.

83
Q

Give 3 inhibitors of tumour angiogenesis.

A
  1. Angiostatin.
  2. Endostatin.
  3. Vasculostatin.
84
Q

What 3 mechanisms do tumour cells use to evade host immune defence in the blood?

A
  1. Platelet aggregation.
  2. Adhesion to other tumour cells.
  3. They shed surface antigens so as to ‘distract’ lymphocytes.
85
Q

Give an example of a malignant tumour that often spreads to the lung.

A

Sarcoma (via venae cavae -> heart -> pulmonary arteries).

86
Q

Give an example of carcinomas that can spread to the liver.

A

Colon, stomach and pancreatic carcinomas can spread to the liver via the portal vein.

87
Q

What causes the pain associated with acute inflammation?

A
  1. Stretching and distortion of tissues due to oedema and pus under high pressure in an abscess cavity.
  2. Chemical mediators e.g. bradykinin and prostaglandins, are also known to induce pain.
88
Q

Describe the process of neutrophil polymorph migration into tissues as seen in acute inflammation.

A
  1. Margination of neutrophils.
  2. Pavementing of neutrophils.
  3. Neutrophils pass between endothelial cells.
  4. Neutrophils pass through basal lamina and migrate into adventitia.
89
Q

What is the main source of histamine?

A

Mast cells; histamine is stored in granules in their cytoplasm.

90
Q

What enzymatic cascade systems does plasma contain?

A
  1. The complement system.
  2. The kinin system.
  3. The coagulation system.
  4. The fibrinolytic system.
91
Q

What is the role of tissue macrophages in acute inflammation?

A

They secrete chemical mediators that attract neutrophil polymorphs.

92
Q

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

A

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

93
Q

What is the major role of neutrophil polymorphs in acute inflammation?

A

Phagocytosis!

94
Q

Define carcinogenesis.

A

A multistep process in which normal cells become neoplastic cells due to mutations.

95
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic.

96
Q

Give 5 host factors that can affect cancer risk.

A
  1. Race.
  2. Diet.
  3. Constitutional factors (gender, age).
  4. Premalignant conditions.
  5. Transplacental exposure.
97
Q

Give an example of a situation when transplacental exposure lead to an increase in cancer risk.

A

The daughters of mothers who had taken diethylstiboestrol for morning sickness had an increased risk of vaginal cancer.

98
Q

Name the 5 different categories of carcinogens.

A
  1. Viral.
  2. Chemical.
  3. Ionising and non-ionising radiation.
  4. Hormones, parasites and mycotoxins.
  5. Miscellaneous e.g. asbestos and metals.
99
Q

What causes skin cancer?

A

Exposure to UV light.

100
Q

Chemical carcinogens: what types of cancer do polycyclic aromatic hydrocarbons cause?

A

Lung cancer and skin cancer.

101
Q

Chemical carcinogens: what can expose people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils.

102
Q

Chemical carcinogens: what types of cancer do aromatic amines cause?

A

Bladder cancer.

103
Q

Chemical carcinogens: what types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

A

People who work in the rubber/dye industry.

104
Q

Chemical carcinogens: what type of cancer do nitrosamines cause?

A

Gut cancer.

105
Q

Chemical carcinogens: what type of cancer do alkylating agents cause?

A

Leukaemia; the risk is small in humans.

106
Q

Define neoplasm.

A

An autonomous, abnormal, persistent new growth.

107
Q

What is a neoplasm composed of?

A
  1. Neoplastic cells.

2. Stroma.

108
Q

Describe neoplastic cells.

A

Neoplastic cells are derived from nucleated cells. They’re usually monoclonal and their growth is related to the parent cell.

109
Q

Describe the stroma of a neoplasm.

A

Connective tissue composed of fibroblasts and collagen; it is very dense. There is a lot of mechanical support and blood vessels provide nutrition for the neoplastic cells.

110
Q

What is essential for neoplasm growth?

A

Angiogenesis.

111
Q

What does a neoplasm release in order to initiate angiogenesis?

A

Vascular endothelial growth factors.

112
Q

Why does necrosis often occur in the centre of a neoplasm?

A

The neoplasm grows quickly and outgrows its vascular supply.

113
Q

What are the advantages of classifying neoplasms?

A

It helps to determine the appropriate treatment and prognosis.

114
Q

What are the two ways in which neoplasms can be classified?

A
  1. Behavioural classification.

2. Histogenetic classification.

115
Q

What is the behavioural classification of neoplasms?

A

Neoplasms can be classified as benign, malignant or borderline. Borderline tumours (e.g. some ovarian lesions) defy precise classification.

116
Q

What is the histogenetic classification of neoplasms?

A

Histopathological tests specify tumour type by determining the cell of origin of a tumour. If the origin is unknown the tumour is said to be anaplastic.

117
Q

What are the 7 main features of benign neoplasms.

A
  1. Localised.
  2. Non-invasive.
  3. Slow growth, low mitotic activity.
  4. Close resemblance to normal tissue.
  5. Normal nuclei.
  6. Necrosis and ulceration are rare due to slow growth.
  7. Exophytic growth.
118
Q

What are the consequences of benign neoplasms?

A
  1. Pressure on adjacent structures.
  2. Obstruction to flow.
  3. Transformation into malignant neoplasms.
  4. Anxiety.
119
Q

What are the 7 main features of malignant neoplasms.

A
  1. INVASIVE!
  2. Metastases.
  3. Rapid growth, high mitotic activity.
  4. Resemblance to normal tissue.
  5. Poorly defined border due to invasive nature.
  6. Necrosis and ulceration are common.
  7. Endophytic growth.
120
Q

What are the consequences of malignant neoplasms?

A

Destroy surrounding tissue, blood loss due to ulceration, pain, anxiety.

121
Q

Define carcinoma.

A

MALIGNANT EPITHELIAL NEOPLASM!

122
Q

Define sarcoma.

A

Malignant connective tissue neoplasm.

123
Q

What is a rhabdomyoma?

A

Benign striated muscle neoplasm.

124
Q

What is an adenoma?

A

Benign tumour of glandular epithelium.

125
Q

What is a papilloma?

A

A non-glandular benign tumour.

126
Q

What is a leiomyoma?

A

A benign smooth muscle neoplasm.

127
Q

What is a neuroma?

A

A benign neoplasm of nerves.

128
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage.

129
Q

What is a liposarcoma?

A

A malignant neoplasm of adipose tissue.

130
Q

What is a melanoma?

A

A malignant neoplasm of melanocytes.

131
Q

What is a lymphoma?

A

A malignant neoplasm of lymphoid cells.

132
Q

What is a mesothelioma?

A

A malignant neoplasm of mesothelial cells.

133
Q

Carcinomas and sarcomas are further classified according to the degree of differentiation. Is a carcinoma/sarcoma with a close resemblance to normal tissue classified as well differentiated or poorly differentiated?

A

A carcinoma/sarcoma with a close resemblance to normal tissue is classified as well differentiated. These types of neoplasms are low grade and have a better prognosis.

134
Q

Define adenocarcinoma.

A

A malignant neoplasm of glandular epithelium.

Phase 2A ICS, Microbiology, Public Health, GP and ILAs (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions