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Phase 2A > Pathology > Flashcards

Pathology Flashcards

1
Q

What is inflammation?

A

The local physiological response to tissue injury.

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2
Q

What is acute inflammation?

A

The initial and often transient series of tissue reactions to injury.

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3
Q

What is chronic inflammation?

A

The subsequent and often prolonged tissue reactions following the initial response.

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4
Q

Steps of acute inflammation

A
  1. Vascular component - blood vessels dilate
  2. Exudative component - protein-rich fluid leaks from vessels (oedema)
  3. Cellular component - neutrophil polymorphs attracted to site of injury by chemotaxins and begin phagocytosis of pathogens
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5
Q

Outcomes of acute inflammation

A
  • Complete resolution - total repair and destruction of the pathogen
  • Suppuration - pus discharge leading formation of an abscess
  • Organisation - growth of new capillaries and fibroblasts into damaged tissue –> fibrosis and scar formation
  • Chronic inflammation - from a persisting injury
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6
Q

Causes of acute inflammation

A
  • microbial infections (bacteria, viruses) - tissue damage as a result of cell death, endotoxins, hypersensitivity reactions
  • hypersensitivity reactions (parasites, bacteria) - excessive immune reaction damages tissue
  • physical agents (trauma, ionising radiation, temperature related)
  • chemicals (corrosives, acids) - gross tissue damage, chemical irritants
  • bacterial toxins
  • tissue necrosis (ischaemic infarction) - death of tissues from lack of oxygen
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7
Q

What are the 5 cardinal signs for acute inflammation?

A

Rubor - redness of skin due to blood vessel dilation in damaged area
Calor - increase in temperature of peripheral body parts due to increased blood flow (hyperaemia)
Tumor - swelling due to oedema and also from the migration of inflammatory cells to the area
Dolor - pain due to distortion of tissues from oedema and pus under pressure in abscess cavity, chemical mediators can also induce pain
Loss of function - movement inhibited by pain, severe swelling may immobilise tissues

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8
Q

What is the role of histamine and thrombin in the inflammatory response?

A

To cause up-regulation of adhesion molecules on the surface of endothelial cells which results in firm neutrophil adhesion to the endothelial surface.

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9
Q

Stages of neutrophil polymorph emigration

A
  1. Margination - migrate to edge of blood vessels
  2. Adhesion - selectins bind neutrophil; cause “rolling” along blood vessels margin
  3. Emigration + Diapedesis - movement out of blood vessels, through or in between endothelium, other inflammatory cells follow
  4. Chemotaxis - neutrophils travel to the site of inflammation
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10
Q

Action of neutrophils at the site of inflammation

A
  1. Phagocytosis
  2. Phagolysosome + bacteria killing
  3. Macrophages clear debris
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11
Q

Systemic effects of inflammation

A
  • pyrexia (fever)
  • constitutional symptoms (anorexia, weight loss, night sweats, headache, pain)
  • reactive hyperplasia (overgrowth of cells)
  • haematological changes
  • amyloidosis (build of amyloid in tissues - can lead to organ failure)
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12
Q

What cells are involved in inflammation?

A
  • neutrophil polymorphs (cytoplasmic granules full of enzymes that kill bacteria)
  • macrophages (phagocytic, remove debris, antigen-presenting)
  • lymphocytes (produce chemicals which attract other inflammatory cells, immunological memory)
  • endothelial cells (allow adherence of inflammatory cells, become porous to enable emigration of inflammatory cells, grow into damaged tissue to form new capillaries)
  • fibroblasts (form collagen in areas of chronic inflammation and repair)
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13
Q

What are granulomas?

A

Small area of chronic inflammation caused by an aggregation of epitheloid histocytes (specialised macrophages).
- Caseating = central region of necrosis, usually in lungs, response to infection
- Non-caseating - no central region of necrosis, response to contact with foreign material, sarcoidosis, vasculitis, crohn’s

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14
Q

Sequence of Chronic Inflammation

A
  • Either progresses from acute inflammation or starts as ‘chronic’ inflammation such as infectious mononucleosis
  • no or very few neutrophils
  • macrophages and lymphocytes, then usually fibroblasts
  • can resolve if no tissue damage but often ends up with repair and formation of scar tissue
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15
Q

What are resolution and repair?

A

Resolution = initiating factor removed, tissue undamaged or able to regenerate

Repair = initiating factor still present, tissue damaged and unable to regenerate, damaged tissue is replaced by fibrous tissue

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16
Q

Which cells regenerate?

A
  • hepatocytes
  • pneumocytes
  • all bloods cells
  • gut epithelium
  • skin epithelium
  • osteocytes
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17
Q

Which cells don’t regenerate?

A
  • myocardial cells
  • neurones
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18
Q

Healing by 1st intention

A

Healing of a wound in which the edges are closely re-approximated so there is minimal granulation and scar formation.

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19
Q

Healing by 2nd intention

A

Healing of a wound where the wound is left open and left to heal by itself, filling in and closing up naturally.

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20
Q

What is thrombosis

A

The formation of a solid mass from blood constituents in an intact vessel in a living person.

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21
Q

What is an embolism

A

When a solid mass in the blood (embolus) is carried through the circulation to a place where it gets stuck and blocks the vessel.

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22
Q

Why are clots rare?

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
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23
Q

How is a thrombus formed?

A
  1. Damage to endothelial cells in the vessel causes cells to lift from vessel wall, exposing collagen
  2. Platelets then begin to stick to this exposed collagen, and release the chemicals which cause platelet aggregation. Platelet aggregation also starts off the cascade of clotting proteins in the blood.
  3. Red blood cells then get trapped within the aggregating platelets.
  4. Clotting factors join the red blood cells and platelets, and the clotting cascade forms a large protein molecule fibrin, which then gets deposited and forms the clot.
  5. Positive feedback loop –> can end up causing a thrombus, blocking the artery
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24
Q

What is granulation tissue?

A

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

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25
Q

Give an example of a granulomatous disease

A

TB. leprosy, Crohn’s disease, sarcoidosis

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26
Q

Which enzyme in the blood can act as a marker for granulomatous disease when active?

A

Angiotensin converting enzyme (ACE)

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27
Q

What 3 factors can lead to thrombosis formation?

A
  1. Change in vessel wall
  2. Change in blood constituents.
  3. Change in blood flow.
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28
Q

Define ischaemia

A

Decreased blood flow

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29
Q

Define infarction

A

Decreased blood flow with subsequent cell death.

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30
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.

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31
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 wilis)
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32
Q

What can happen if ischaemia is rectified?

A

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

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33
Q

What are the consequences of an arterial embolus?

A

Stroke, MI, gangrene etc.

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34
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.

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35
Q

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

A

venous system

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36
Q

What drug can be used to prevent thrombosis?

A

Aspirin

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37
Q

Define atherosclerosis

A

Thickening or hardening of arteries as a result of plaque build up in the inner lining of an artery

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38
Q

What are 5 risk factors for atherosclerosis?

A
  • Hypertension
  • Smoking
  • Obesity
  • High cholesterol
  • Type 1 Diabetes
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39
Q

Is atherosclerosis more common in the systemic or pulmonary circulation?

A

More common in the systemic circulation because the pressure is higher

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40
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids
  2. Fibrous tissue
  3. Lymphocytes
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41
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage

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42
Q

How does aspirin prevent thrombosis?

A

It prevents the coagulation of platelets.

43
Q

What are the 4 stages of atherosclerosis?

A
  1. Endothelial dysfunction
  2. Formation of lipid layer or fatty streak within the intima
  3. Migration of leukocytes and smooth muscle cells into the vessel wall
  4. Foam cell formation and degradation of the extracellular matrix
44
Q

What is a foam cell?

A

Cholesterol-containing cells which form atheromatous plaque.

45
Q

Define apoptosis

A

Programmed cell death of a single cell.

46
Q

What is the role of p53 protein?

A

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

47
Q

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

A

p53 protein

48
Q

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

A

Caspases

49
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor

50
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.

51
Q

Give an example of disease where there is too much apoptosis

A

HIV

52
Q

Define necrosis

A

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

53
Q

Give 3 examples of events that can lead to necrosis

A
  1. Frost bite
  2. Avascular necrosis
  3. Infarction
54
Q

Give 3 difference 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.
55
Q

What is the intrinsic pathway of apoptosis?

A

The pro-apoptotic factors BAX and BAK are active and stimulate the release of cytochrome C from pores in the mitochondrial membrane.
This activates caspases which cause apoptosis.

56
Q

What happens if Bcl-2 and Bcl-xl are overactivated?

A

They inhibit release of cytochrome C resulting in inappropriate cell survival.

57
Q

What is the extrinsic pathway of apoptosis?

A

The binding of Fas-L to Fas receptors or TNF-a to TNF-R receptors on the CSM causes the activation of initiator caspases. This activates caspases which cause apoptosis.

58
Q

What is the cytotoxic pathway of apoptosis?

A

Cytotoxic T cells bind to a membrane and activates granzyme-B which breaks through the membrane causing the release of perforin. Perforin activates caspases resulting in apoptosis.

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 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. (e.g. Barrett’s oesophagus SSE to CE)

63
Q

Define dysplasia

A

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

64
Q

What is a tumour?

A

any abnormal swelling (e.g. neoplasm, inflammation, hypertrophy, hyperplasia)

65
Q

Define neoplastic transformation

A

The accumulation of genetic alterations and epigenetic changes that generate cells which escape from normal regulatory growth mechanisms to form a tumour.

66
Q

Define malignant tumours

A

Tumours which are relatively fast-growing and invade and metastasise to other tissues

67
Q

Define cancer

A

a malignant neoplasm.

68
Q

How can the gross appearance of tumours be described?

A
  • sessile = sitting on the surface (usualy benign)
  • pendunculated/polyploid = lump on surface, stalked (usually benign)
  • papillary = finger-like growths (usually benign)
  • exophytic/fungating = has ulcerations (breaks in the skin) and necrosis (usually malignant)
  • ulcerated = shiny red lump, grows deeper and forms holes (usually malignant)
  • annular = “apple core” lesion with tubular structure, common in the large bowel
69
Q

What are the distinguishing histological features of tumours?

A
  • loss/reduction of differentiation
  • loss/reduction of cellular cohesion
  • nuclear enlargement, hyperchromasia (dark nucleus) and pleomorphism (variation in the size and shape of cells)
  • increased mitotic activity
70
Q

Define benign tumours

A

Non-invasive, localised tumours which grow slowly and remain localised

71
Q

How do benign tumours cause clinical problems?

A
  • pressure on adjacent tissues
  • obstruction to the flow of fluid
  • production of a hormone
  • transformation into a malignant neoplasm
  • anxiety
72
Q

How do malignant tumours affect the body?

A
  • pressure on and destruction of adjacent tissues
  • formation of secondary tumours (metastases)
  • blood loss from ulcerated surfaces
  • obstruction of flow
  • production of a hormone
  • other paraneoplastic effects causing weight loss and debility
  • anxiety and pain
73
Q

What is histogenetic classification?

A

The classification of tumours by tissue or cell of origin, determined by degree of histological resemblance to parent tissue which is graded, correlating to the associated clinical behaviour.

74
Q

How do metastases evade host immune defence?

A
  • aggregation with platelets
  • shedding of surface antigens
  • adhesion to other tumour cells
75
Q

What is a neoplasm?

A

A new lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed.

76
Q

What is the structure of neoplasms?

A

Neoplastic cells and stroma

77
Q

What is a carcinoma?

A

A malignant tumour of epithelial cells.

78
Q

Which tumours metastasise to bone?

A

Breast cancer
Lung cancer
Thyroid cancer
Kidney cancer
Prostatic cancer
(BLTKP)

79
Q

Define carcinogenesis

A

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

79
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic

80
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
81
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
82
Q

What types of cancer do polycyclic aromatic hydrocarbons cause?

A

Lung cancer and skin cancer

83
Q

What exposes people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils

84
Q

What type of cancer do aromatic amines cause?

A

Bladder cancer

85
Q

What types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

A

People working in the rubber/dye industry

86
Q

What type of cancer do nitrosamines cause?

A

Gut cancer

87
Q

What type of cancer do alkylating agents cause?

A

Leukaemia (small risk in humans)

88
Q

What is a papilloma

A

Non-glandular benign epithelial tumour

89
Q

What is an adenoma?

A

A benign tumour of glandular epithelium

90
Q

What is a leiomyoma?

A

A benign smooth muscle neoplasm

91
Q

What is a rhabdomyoma?

A

A benign striated muscle neoplasm

92
Q

What is a sarcoma?

A

Malignant connective tissue neoplasm

93
Q

What is a neuroma?

A

A benign neoplasm of nerves

94
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage

95
Q

What is a liposarcoma?

A

A malignant neoplasm of adipose tissue

96
Q

What is a melanoma?

A

A malignant neoplasm of melanocytes

97
Q

What does it mean if a sarcoma/carcinoma is well differentiated?

A

It has a close resemblance to normal tissue and so is low grade with a better prognosis.

98
Q

What is a chondroma?

A

A benign tumour of the cartilage

99
Q

What is an angiosarcoma?

A

A malignant neoplasm of a blood vessel

100
Q

What are the characteristics of neoplastic cells?

A
  • Autocrine growth stimulation
  • Evasion of apoptosis
  • Telomerase
  • Sustained angiogenesis + ability to invade BM
101
Q

What are the steps in the metastasis pathway?

A
  1. Detachment from primary neoplasm
  2. Invasion of other tissue
  3. Invasation of blood vessel
  4. Evasion of host defence, adherence to bv wall
  5. Extravasation to distant site
102
Q

What are the methods by which neoplasms metastasise?

A
  • Haematogenous - via blood -> bone, breast, lung, liver
  • Lymphatic - secondary formation in lymph nodes
  • Transcoelemic - via exudative fluid accumulation in body cavity, spread through pleural, pericardial, peritoneal effusions

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