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Phase 2A revision > PATHOLOGY COPY > Flashcards

PATHOLOGY COPY Flashcards

1
Q

Causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents  
Chemicals
Tissue necrosis
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2
Q

What makes up the cellular exudate for acute inflammation?

A

Neutrophil polymorphs
Macrophages
Lymphocytes

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3
Q

Causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progressing from acute inflammation
Recurrent episodes of acute inflammation

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4
Q

Causes of primary chronic inflammation

A

Exogenous materials
Endogenous materials
Resistance of infective agent to phagocytosis and intracellular killing – TB
Autoimmune diseases – rheumatoid arthritis
Primary granulomatous diseases – Crohn’s

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5
Q

What is the cellular exudate in chronic inflammation mainly made of?

A

Lymphocytes
Plasma cells
Macrophages
Fibroblasts

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6
Q

How does organisation occur?

A

Granulation tissue is formed and dead tissue is removed by phagocytosis
Granulation tissue contracts and accumulated collagen to form a scar

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7
Q

When does an arterial thrombosis normally occur?

A

When superimposed on atheroma

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8
Q

How does an arterial thrombus occur?

A

Vessel wall damage
Laminar flow disruption
Collagen exposed
Platelets stick to collagen and aggregate - positive feedback
Rbc’s can get trapped - thrombus formation and fibrin deposition (fibrinogen –> fibrin by platelet factors)
Fibrin mesh holds it all together
Thrombus can then build up and occlude artery

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9
Q

What are the outcomes of a thrombus?

A
  1. Lysis and resolution
  2. Organisation – into a scar
  3. Recanalisation – scar and residual thrombus
  4. Embolism – breaks off
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10
Q

What are the functions of histamine?

A 
Vasodilation
Emigration of neutrophils (chemotaxis) 
Increase vascular permeability
Pain 
Itching
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11
Q

Role of plasma factors

A

Complement system
Kinin system
Coagulation cascade (pro-clotting)
Fibrinolytic system (anti-clotting)

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12
Q

What is the microscopic appearance of chronic inflammation?

A

Chronic ulcer
Abscess cavity
Granulatomous inflammation
Fibrosis

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13
Q

What is a histiocytic giant cell?

A

Indeigestible foreign material causes macrophages to fuse together - multinucleate giant cells
Can collect and form granulomas

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14
Q

What is end arterial supply?

A

Single artery supplies organ - more susceptible to infarction

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15
Q

What are watershed territories?

A

Parts of the brain the have a dual blood supply, but low BP can cause ischaemia

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16
Q

Explain the pathogenesis of atherosclerosis

A
  1. Endothelial cell damage – see risk factors
  2. Repeated endothelial damage -> multiple thrombi -> aggregation -> atheroma formation
  3. Vascularised plaque can haemorrhage – propagates atheroma formation
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17
Q

What are the complications of atherosclerosis?

A

Cerebral/myocardial infarct
AAA –> weakens aorta and leads to aortic rupture
Peripheral vascular disease - gangrene

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18
Q

What types of DNA damage cause apoptosis to occur?

A

Single/double stand break
Base alteration
Cross linking

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19
Q

Explain mechanism of apoptosis

A
  1. P53 (gatekeeper of genome) detects DNA damage -> acts as switch for apoptosis
  2. Bcl2 and Fas ligand receptor signal for capsases -> apoptosis
  3. Membrane bound cell fragments engulfed by macrophages
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20
Q

Example of normal apoptosis

A

Removal of finger webbing during development

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21
Q

In what is excess apoptosis present?

A

HIV mediated T cell destruction

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22
Q

Give examples of necrosis

A

Myocardial/cerebral infarction
Avascular necrosis of bone - scaphoid or head of femur break
Caseous necrosis - pathological sign of TB

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23
Q

Define hypertrophy

A

Increase in size of a tissue caused by an increase in size of the constituent cells (eg skeletal muscle)

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24
Q

Define hyperplasia

A

Increase in size of a tissue caused by an increase in number of the constituent cells (eg. enlarged prostate)

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25
Q

What are other examples of developmental conditions?

A

Cleft lip/palate - cells fail to migrate and join

Ventricular septal defect (VSD)

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26
Q

What is congenital development?

A

Present at birth - can be inherited or acquired

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27
Q

Name 5 types of necrosis

A 
Caseous necrosis 
Coagulative necrosis 
Colliquative necrosis 
Fibrinoid necrosis 
Fat necrosis
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28
Q

What is coagulative necrosis?

A

Cells become firm and pale

Seen in most tissues

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29
Q

What is colliquative necrosis?

A

Dead area is liquefied

Seen in brain

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30
Q

What is fibrinoid necrosis a microscopic feature of?

A

Malignant hypertension - in arterioles

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31
Q

What can cause necrosis?

A

Ischaemia
Metabolic
Trauma

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32
Q

Name 5 cancers that commonly spread to bone

A
  1. Breast
  2. Thyroid
  3. Kidney
  4. Lung
  5. Prostate
33
Q

What does oncogenesis refer to?

A

Benign and malignant tumours

34
Q

Define carcinogen

A

Mutagenic (act on DNA) agents that cause (or are suspected to cause) tumours

35
Q

Name the carcinogen classes

A

Chemical
Radiation
Biological organisms
Miscellaneous

36
Q

Give an example of a mycotoxin carcinogen

A

Mycotoxin (Aflatoxin B1) –> hepatocellular cancer

37
Q

Name host factors for carcinogenesis

A

Race
Constitutional
Premalignant conditions
Transplacental exposure

38
Q

Define Neoplasm

A

A lesion resulting from the NEW AUTONOMOUS ABNORMAL growth of cells that PERSISTS after removal of initiating stimulus

39
Q

What is the structure of a neoplasm?

A

Neoplastic cells

Stroma - connettive tissue framework

40
Q

What does the stroma provide of the neoplasm?

A

Mechanical support
Nutrition
Intracellular signalling
Contains blood vessels which perfuse the tumour

41
Q

A tumour <2mm is known as a …?

A

Avascular nodule

42
Q

What neoplasms do epithelial cells form?

A

Carcinomas

43
Q

What neoplasms do connective tissues form?

A

Sarcomas

44
Q

What is a papilloma?

A

A benign non glandular epithelial neoplasm

45
Q

What is a carcinoma?

A

A malignant non glandular epithelial neoplasm

46
Q

What is a adenocarcinoma?

A

A malignant glandular epithelial neoplasm

47
Q

Name some benign connective tissue neoplasms

A 
Lipoma = adipocytes 
Chondroma = cartilage 
Osteoma = bone 
Angioma = vascular 
Rhabdomyoma = striated muscle
Leiomyoma = smooth muscle 
Neuroma = nerves
48
Q

Name some malignant connective tissue neoplasms

A 
Liposarcoma = adipose tissue 
Chondrosarcoma = cartilage 
Osteosarcoma = bone 
Angiosarcoma = vascular 
Rhabdomyosarcoma = striated muscle 
Leiomyosarcoma = smooth muscle
49
Q

What are the types of grade of malignancy?

A

Low grade – looks like parent tissue (well differentiated)
High grade – doesn’t look like parent tissue (poorly differentiated)
Anaplastic – unknown origin cell type

50
Q

What is a carcinoma in situ?

A

Carcinoma fills cavity but has not invaded any other tissue

51
Q

What are the 8 stages of metastasis?

A
  1. Detachment
  2. Invasion
  3. Intravasation
  4. Evasion
  5. Adherence
  6. Extravasation
  7. Growth
  8. Angiogenesis
52
Q

Explain invasion

A

Some cells go through the basement membrane into the extracellular matrix using enzymes (proteases, collagenase, cathepsin D, urokinase-like plasminogen activator)

53
Q

What is intravasation?

A

Tumour cells move from ECM to blood/lymph vessels

54
Q

What is evasion?

A

Aggregate with platelets, shed surface antigens and stick to other tumour cells

55
Q

Explain adherence

A

Adherence of ells to endothelium at a remote location

56
Q

Explain extravasation

A

Tumour cells move from vessels to new tissue area

57
Q

What is angiogenesis?

A

Formation of blood vessels

58
Q

Name 3 routes of metastasis

A

Haematogenous - by blood stream
Lymphatic
Transoelomic - in pleural, pericardial and peritoneal cavities

59
Q

What tumours commonly metastasise to the liver?

A

Colon, stomach, pancreas, intestine (portal system)

60
Q

Give 2 promoters of tumour angiogenesis

A
  1. Vascular endothelial growth factors

2. Fibroblast growth factors

61
Q

Give 3 inhibitors of tumour angiogenesis

A
  1. Angiostatin
  2. Endostatin
  3. Vasculostatin
62
Q

Give 3 endogenous chemical mediators of acute inflammation

A
  1. Bradykinin
  2. Histamine
  3. Nitric Oxide
63
Q

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

A

Angiotensin converting enzyme

64
Q

Define abscess

A

Acute inflammation with a fibrotic wall

65
Q

what are the steps of acute inflammation?

A
  • Initial reaction of tissue to injury
  • Vascular component: dilation of vessels
  • Exudative component: vascular leakage of protein-rich fluid
66
Q

what is the role of p53 protein?

A

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

67
Q

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

A

p53 protein

68
Q

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

A

Caspases.

69
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor.

70
Q

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

A
  1. Collagenases.

2. Cell motility.

71
Q

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

A
  1. Adhesion receptors.
  2. Collagenases.
  3. Cell motility.
72
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.
73
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.
74
Q

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

A

Lung cancer and skin cancer.

75
Q

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

A

Smoking cigarettes and mineral oils.

76
Q

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

A

Bladder cancer.

77
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.

78
Q

Chemical carcinogens: what type of cancer do nitrosamines cause?

A

Gut cancer.

79
Q

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

A

Leukaemia; the risk is small in humans.

Phase 2A revision (38 decks)

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