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Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Describe acute inflammation

A

Sudden onset
Usually resolves by itself
Neutrophils are normally the main cells on site
Can progress to chronic inflammation

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2
Q

Describe chronic inflammation

A

Slow onset or following acute inflammation
Long duration
Might never resolve
Usually involves lymphocytes and macrophages as well as neutrophils

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3
Q

Describe the progression of acute inflammation

A

Injury/infection
Neutrophils arrive - phagocytosis and enzyme release
Macrophages arrive - phagocytosis
Resolution OR progression to chronic inflammation

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4
Q

Describe the progression of chronic inflammation

A

Macrophage or lymphocyte mediated inflammation or progression from acute inflammation
No/few neutrophils
Macrophages, lymphocytes present
Fibroblasts present
Resolution if no tissue damage OR repair/scar tissue formation if tissue is damaged

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5
Q

What is inflammation?

A

The body’s response to injury or infection, involving different types of cells

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6
Q

What are the causes of inflammation?

A

Injury
Infection
Autoimmunity
Over-reaction to a stimulus

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7
Q

What are the signs of inflammation?

A

Rubor - redness
Calor - heat
Dolor - pain
Tumour - swelling
Loss of function (as a result of these)

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8
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes
When macrophages cluster together to kill something but are ineffective. They get surrounded by lymphocytes

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9
Q

Describe granuloma formation in TB

A

The mycobacteria infect alveolar macrophages
Infected macrophages are surrounded by foamy macrophages, other macrophages, lymphocytes and fibrin
TB lies in dormancy and doesn’t spread
As CD4 and TNFa depletion, granuloma becomes unstable and fail
TB spreads around the body

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10
Q

What is fibrosis?

A

The accumulation of fibrous connective tissue in inflamed or damaged tissue

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11
Q

What do fibroblasts produce?

A

Collagen

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12
Q

Describe healing by 1st intention

A

A weak fibrin joint first (red)
Gradually replaced by a strong collagen joint (white)
Happens when the edges of the wound fit together well

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13
Q

Describe healing by 2nd intention

A

A large fibrin mesh forms which fills the wound
Granulation tissue forms
Bright dots of capillaries and fibroblasts grow in

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14
Q

Define atherosclerosis

A

The accumulation of fibrolipid plaques in systemic arteries (not pulmonary arteries)

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15
Q

Describe the pathophysiology of atherosclerosis

A

Endothelial damage theory:
ECs are damaged - hyperlipidaemia, shearing forces, free radicals from cigarette smoking, glycosylation products from poorly controlled Diabetes Mellitus
LDLs enter the endothelium and are oxidised
Macrophages engulf lipoproteins forming a foam cell
Foam cells form a fatty streak
Continued damage, macrophage recruitment, and lipid accumulation, forming a lipid core -> atheroma
Fibrotic tissue forms on the lesion an calcifies -> fibroatheroma

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16
Q

What is a thrombosis?

A

A solid mass of constituents formed within intact vascular system during life

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17
Q

Describe the pathophysiology of thrombosis

A

Endothelial cell damage
Platelets stick to the collagen underneath
Platelet aggregation
This causes turbulent flow in the vessel
RBCs get trapped
Formation of blood clot -> thrombus
Deposition of fibrin helps trap the RBCs, solidifying the thrombus

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18
Q

Why does thrombosis happen in veins more than arteries?

A

Arteries have laminar flow so cells rarely touch the sides
In veins, cells scrape along the sides causing EC damage

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19
Q

What is Virchow’s triad and what are the components?

A

The 3 factors increasing likelihood of thrombosis
- Change in vessel wall
- Change in blood flow
- Change in blood constituents

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20
Q

Define embolism

A

The process of a solid mass in the blood vessels being carried through the circulation to the place where it gets stuck and blocks the vessel
E.g. thrombus, air, cholesterol crystals, amniotic fluid, tumour

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21
Q

Where could a venous embolus go?

A

Through vena cava to pulmonary arteries

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22
Q

Where could an arterial embolus go?

A

Anywhere downstream of its entry point

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23
Q

Define ischaemia

A

A reduction in blood flow

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24
Q

Define infarction

A

A reduction in blood flow causing a subsequent death of cells

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25
Q

What is apoptosis?

A

Programmed cell death (affects an individual cell)

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26
Q

Give an example of pathology relating to apoptosis

A

Cancer - lack of apoptosis
HIV - causes apoptosis of CD4 cells

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27
Q

Define necrosis

A

Traumatic cell death (whole sheets of cells)

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28
Q

Give an example of a pathology relating to necrosis

A

Frostbite
Cerebral infarction (stroke)
Pancreatitis

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29
Q

Define Atrophy

A

A decrease in the size of a tissue caused by a decrease in the number of constituent cells or the size of constituent cells, or both

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30
Q

Give an example of a pathology relating to atrophy

A

Cerebral atrophy in Dementia
Muscular atrophy
Optic atrophy

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31
Q

Define hypertrophy

A

An increase in the size of a tissue caused by an increase in the size of constituent cells

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32
Q

Give an example of a pathology relating to hypertrophy

A

Myofibril or sarcophagi can hypertrophy in muscles
Left ventricular hypertrophy in heart

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33
Q

Define hyperplasia

A

An increase in the size of a tissue caused by an increase in the number of constituent cells

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34
Q

Give an example of a pathology relating to hyperplasia

A

Benign prostatic hyperplasia
Endometrial hyperplasia

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35
Q

Define metaplasia

A

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

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36
Q

Give an example of a pathology relating to metaplasia

A

Bronchi changing from ciliated columnar epithelium to squamous due to smoking
Barret’s Oesophagus - epithelium changes from squamous to columnar due to GORD

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37
Q

Define dysplasia

A

The morphological changes seen in cells in the progression to becoming cancer

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38
Q

Define a tumour

A

Any abnormal swelling

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39
Q

Define neoplasm

A

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

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40
Q

What spectrums are neoplasms measured on?

A

Benign to malignant
Subclinical to fatal

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41
Q

What is angiogenesis?

A

The growth or new blood vessels
Essential to tumour growth beyond around 2mm

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42
Q

What are methods of tumour classification?

A

Behavioural and histogenic

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43
Q

What is tumour behavioural classification divided into?

A

Benign, borderline and malignant

44
Q

Describe benign tumours

A

Non-invasive
Localised
Close resemblance to normal tissue
Low mitotic activity
Circumscribed
Often normal nuclear morphometry
Necrosis, ulceration is rare
Mucosal surface growth is usually exophytic

45
Q

Describe malignant tumours

A

Invasive
Metastasises
Rapid growth rate/increased mitotic activity
Variable resemblance to normal tissue
Poorly defined
Hyperchromatic and pleomorphic nuclei
Necrosis and ulceration is common
Mucosal surface growth is usually endophytic

46
Q

What is the histogenesis of a neoplasm?

A

The specific cell type of origin of the neoplasm

47
Q

What is a carcinoma?

A

Malignant epithelial neoplasm

48
Q

What is a papilloma?

A

Benign, non-glandular/non-secretory, epithelial neoplasm

49
Q

What is an adenoma?

A

Benign, glandular/secretory, epithelial neoplasm

50
Q

What is a lipoma?

A

Benign connective tissue neoplasm of adipocytes

51
Q

What is a chondroma?

A

Benign connective tissue neoplasm of cartilage

52
Q

What is an osteoma?

A

Benign connective tissue neoplasm of bone

53
Q

What is an angioma?

A

Benign connective tissue neoplasm of vascular tissue

54
Q

What is a rhabdomyoma?

A

Benign connective tissue neoplasm of striated muscle

55
Q

What is a leiomyoma?

A

Benign connective tissue neoplasm of smooth muscle
In the uterus, this is called a fibroid

56
Q

What is a neuroma?

A

Benign connective tissue neoplasm of nerve cells

57
Q

What is a Liposarcoma?

A

Malignant connective tissue neoplasm of adipose tissue

58
Q

What is a chondrosarcoma?

A

Malignant connective tissue neoplasm of cartilage

59
Q

What is an osteosarcoma?

A

Malignant connective tissue neoplasm of bone

60
Q

What is an angiosarcoma?

A

Malignant connective tissue neoplasm of vascular tissue

61
Q

What is a rhabdomyosarcoma?

A

Malignant connective tissue neoplasm of striated muscle

62
Q

What is a leiomyosarcoma?

A

Malignant connective tissue neoplasm of smooth muscle

63
Q

Which cells does Burkitt’s Lymphoma affect and what causes it?

A

B cells
Caused by Epstein Barr Virus

64
Q

Which cells does Ewing sarcoma affect?

A

Long bones

65
Q

Which cells does Grawitz tumour affect?

A

Renal cell (carcinoma)

66
Q

Which cells does Kaposi’s sarcoma affect and what causes it?

A

The skin or mucosal membranes of GI tract from the mouth to the anus
Human Herpes 8 Virus

67
Q

What is a melanoma?

A

A malignant neoplasm of melanocytes

68
Q

What is a mesothelioma?

A

A malignant neoplasm of mesothelial cells

69
Q

What is a lymphoma?

A

A malignant neoplasm of lymphoid cells

70
Q

What is a myeloma?

A

A malignant neoplasm of myeloid cells

71
Q

How are malignant tumours graded?

A

By how closely they resemble the tissue of origin
High grade = poor resemblance = poorly differentiated

72
Q

What does it mean if a neoplasm is anaplastic?

A

The cell type of origin can’t be determined

73
Q

What is tumour staging?

A

How much a tumour has spread

74
Q

What are the three categories in tumour staging?

A

Tumour- the size and extent or depth of the tumour
Nodes - the extent of lymph node metastases
Metastases - the extent of metastases/spreading to the rest of the body

75
Q

What is carcinogenesis?

A

The transformation of normal cells to neoplasticism cells through permanent genetic mutations/alterations - only malignant tumours

76
Q

What is oncogenesis?

A

The transformation of normal cells to neoplasticism cells through permanent genetic mutations/alterations - benign and malignant tumours

77
Q

What is a carcinogen?

A

An agent known or suspected to cause tumours

78
Q

Define mutagenic

A

Capable of causing a mutation

79
Q

What are the host factors that increase the risk of cancer?

A

Ethnicity
Diet and lifestyle
Age
Gender
Underlying conditions
Transplacental exposure

80
Q

What are the classes of carcinogens?

A

Chemical
Biological
Radiant
Viral
Miscellaneous

81
Q

Give some examples of biological carcinogens

A

Hormones e.g. anabolic steroids, oestrogen
Mycoproteins produced by fungi
Parasites e.g. shistosoma

82
Q

Give some examples of radiant carcinogens

A

UVA, UVB, x-rays, gamma rays

83
Q

Give some examples of viral carcinogens

A

DNA viruses e.g. HH8V, EBV, HBV, HPV, MCV,
RNA viruses e.g. HTLV-1, HCV

84
Q

Give some examples of miscellaneous carcinogens

A

Asbestos
Some metals e.g. arsenic

85
Q

What is a carcinoma in situ?

A

A carcinoma that hasn’t breached the basement membrane

86
Q

What is a micro-invasive carcinoma?

A

A carcinoma that has only invaded the basement membrane a little bit so only has a small risk of spreading

87
Q

What is an invasive carcinoma?

A

A carcinoma that has invaded the basement membrane

88
Q

How do carcinomas invade through the basement membrane?

A
  1. Neoplastic cells produce proteases that break down collagen in the basement membrane
  2. they then use cell motility to move across the basement membrane and into the extracellular matrix
89
Q

Define metastasis

A

The development of secondary malignant growths at a distance from the primary site of cancer

90
Q

Describe the process of metastasis

A
  1. Invasion (of vessels like lymphatics and venules)
  2. Evasion of host immune response
  3. Extravasation (leaving the vessel)
  4. Invasion of the extracellular matrix
  5. Tumour growth
91
Q

Describe the ways that neoplastic cells can evade the host immune response

A
  1. Aggregation with platelets to disguise themselves
  2. Releasing antigens to ‘confuse’ lymphocytes
  3. Adhesion to other neoplastic cells to protect the ones at the centre
92
Q

What are the types of autopsy?

A

Hospital
Medico-legal (corneal and forensic)

93
Q

When are deaths referred to the coroner?

A
  1. If the cause of death is unknown (but presumed natural) and they haven’t seen a doctor within the past 14 days
  2. If the death is presumed iatrogenic
  3. If the death is presumed unnatural
94
Q

What is the purpose of an autopsy?

A

To identify the deceased
To find out when they died
To find out where they died
To find out how they died

95
Q

What is the clotting cascade?

A

A series of reactions in response to bleeding which ultimately produces a blood clot.
It stabilises the platelet plug.

96
Q

Describe platelet plug formation

A
  1. Endothelial injury
  2. Exposure of collagen and release of Von Willebrand factor
  3. Adhesion of GP1B surface proteins on platelets to Von Willebrand factor
  4. Activation of platelets
  5. Aggregation of platelets to fibrinogen
97
Q

Draw the clotting cascade

A
98
Q

What causes the intrinsic pathway of the clotting cascade

A

Collagen exposure

99
Q

What causes the extrinsic pathway of the clotting cascade

A

Damage to endothelial tissue releasing tissue factor

100
Q

What are the Vitamin K dependent clotting factors?

A

X, IX, VII, II
10, 9, 7, 2

101
Q

What is Prothrombin Time (PT)?

A

The time taken for fibrin to form via the extrinsic pathway of the clotting cascade

102
Q

What is the normal range for prothrombin time?

A

9-12 seconds

103
Q

Name some causes of prolonged prothrombin time?

A

Disseminated intravascular coagulation (DIC)
Vitamin K deficiency
Chronic Liver Disease

104
Q

What is International Normalised Ratio (INR)?

A

The patient’s prothrombin time compared to a normal PT

105
Q

What is Activated Partial Thromboplastin Time (APTT)?

A

The time taken for fibrin to form via the intrinsic pathway of the clotting cascade

106
Q

What is the normal range for the activated partial thromboplastin time?

A

23-28 seconds

107
Q

What are some causes of prolonged Activated Partial Thromboplastin Time?

A

Disseminated Intravascular Coagulation (DIC)
Clotting factor deficiencies
Von Willebrand’s Disease
Lupus anticoagulation

Phase 2a (9 decks)

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