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phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

What is inflammation?

A

Local physiological response to tissue injury

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2
Q

What are 2 types of inflammation?

A

Acute and Chronic

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3
Q

Features of Acute Inflammation

A
  • Intial Response of tissue to injury
  • Early onset
  • Short Duration
  • Cells involved = Neutrophils and Monocytes
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4
Q

What are the steps of acute inflammation?

A

Vascular Component - Dilation of Vessels
Exudative component - Vascular leakage of protein-rich fluid (Exudate)
Neutrophil Polymorph - Cells type recruited to tissue

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5
Q

Causes of Acute inflammation

A

Microbial Infections
Hypersensitivity reactions - parasites
Physical agents - Trauma
Chemicals - Acids
Bacterial toxins
Tissue necrosis - Ischemic infarction

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6
Q

What are the 5 cardinal signs?

A

Rubor
Dolor
Calor
Tumor
Loss of function

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7
Q

How do you describe the appearance of redness?

A

Rubor (Due to dilation of small vessels)

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8
Q

How do you describe the appearance of heat?

A

Calor (only seen peripherally)

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9
Q

How do you describe the appearance of swelling?

A

Tumor (Results from oedema or physical mass)

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10
Q

How do you describe appearance of pain?

A

Dolor

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11
Q

What is the acute inflammatory response process?

A

Changes in vessel caliber (gets wider) -> Increased vessel flow
Increased vascular permeability -> Formation of fluid exudate
Formation of cellular exudate -> Emigration of neutrophil polymorphs

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12
Q

Steps of Neutrophil Polymorph Emigration

A
  1. Migration of neutrophils
    - Due to increase in plasma viscosity and slowing of flow due to injury, neutrophils migrate to plasmatic zone
  2. Adhesion of neutrophils
    - Adhesion to vascular endothelium occurs in venules called pavementing
  3. Neutrophil emigration
    - Neutrophils pass through endothelial cells, onto basal lamina and then the vessel wall
  4. Diapedesis
    - RBCs may also escape from vessels, this is a passive process and indicates severe vascular injury
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13
Q

Outcomes of acute inflammation

A

Resolution
Suppuration
Organisation
Progression

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14
Q

What happens in resolution of acute inflammation?

A

Complete restoration of tissues to normal

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15
Q

What happens in suppuration of acute inflammation?

A

Formation of pus
Becomes surrounded by a pyogenic membrane, which is start of healing
Leads to scaring

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16
Q

What happens in organisation of acute inflammation?

A

Replacement by granulation tissue

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17
Q

What happends in progression of acute inflammation?

A

Excessive recurrent inflammation -> Becomes chronic and fibrotic tissue

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18
Q

What is chronic inflammation?

A

Subsequent and prolonged response to tissue injury
Cells involved = Lymphocytes, macrophages and plasma cells
Longer onset, long last effects

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19
Q

What are granulomas?

A

Aggregates of epitheloid histocytes
Form granulomatous

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20
Q

what do granuloma and eosinophil indicate?

A

Parasite

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21
Q

What are the causes of primary chronic inflammation?

A
  • Resistance of infective agent (TB)
  • Endogenous materials (Necrotic tissue)
  • Exogenous materials (Asbetos)
  • Autoimmune conditions (Hashimoto)
  • Primary granulomatous diseases (Chron)
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22
Q

How do B lymphocytes cooperate in chronic inflammation?

A

Transform into plasma cells and produce antibodies

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23
Q

How do T lymphocytes cooperate in chronic inflammation?

A

Responsible for cell-mediate immunity

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24
Q

How do macrophages cooperate in chronic inflammation?

A

Responsible for cell-mediated immunity

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25
Q

How do you macrophages respond in chronic inflammation?

A

Respond to chemotatic stimuli
Produce cytokines

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26
Q

What is thrombosis?

A

Mass of blood constituents (mostly platelets) forming in vessels

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27
Q

How does thrombosis form?

A
  1. Vasospasm - Narrowing of arteries caused by persistent contraction of blood vessels
  2. Primary platelet plug - aggregation, adhesion, activation
  3. Coagulation cascade
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28
Q

What influences thrombosis?

A

Virchow’s Triad

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29
Q

What are the components of Virchows’ triad?

A

Endothelial injury
Hypercoagulability
Decreased blood flow

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30
Q

What is atherosclerosis?

A

Plaques forming in intima and media of high pressure vessels
ARTERIES

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31
Q

What is in a plaque?

A

Lipid
Smooth muscle
Macrophages
Platelets
Fibroblasts

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32
Q

How does atherosclerosis form?

A
  1. Endothelial cell dysfunction
  2. Fatty Streak - Precursor to plaque
  3. Platelet aggregation - Plaque protrudes into artery lumen, disrupts laminar flow. THINNING OF MEDIA
  4. Fibrin mesh + RBC trapping - Platelet plug forms fibrin mesh over itself causing RBCS to be trapped within
  5. Fibrous Cap - Fibroblasts form smooth muscle cap over 2o platelet plug
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33
Q

What is the difference between a stable and unstable atheromas?

A

In an unstable artheroma, the fibrous cap is damaged and there is continuous platelet plug formation over the cap
Therefore, NARROWED

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34
Q

What are the risk factors of atherosclerosis?

A

Diabetes
Smoking
Obesity
Increasing age
Male
Hypertension

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35
Q

How do arterial thromobosis occur?

A

Atherogenesis

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36
Q

How does venous thrombosis occur?

A

Venous stasis

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37
Q

What are the fates of thrombi

A

Resolution - Degrades, returns normal
Organisation - Leaves scar tissue
Embolism - Fragments of thrombi break off and lodge in distal circulation

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38
Q

What is an embolism?

A

Mass of material in vascular system able to lodge in a vessela and block its lumen

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39
Q

Where are arterial emboli lodged?

A

System circulation (From left heart)

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40
Q

Where are venous emboli lodged?

A

In pulmonary circulation (From right heart)

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41
Q

Where does embolus lodge causing ischemic stroke?

A

In carotid artery

42
Q

Where does embolus lodge causing pulmonary embolism?

A

Lodges in pulmonary artery

43
Q

What is apoptosis?

A

Non inflammatory controlled cell death
Cells shrink, organelles retained + CSM intact
Chromatin unaltered

44
Q

What are the mechanisms of apoptosis?

A

Intrinsic
Extrinsic
Cytotoxic

45
Q

What happens in the intrinsic mechanism of apoptosis?

A

BAX (Protein) acts in mitochondrial membran to promote cytochrome C release
Activates CASPASES -> Apoptosis

46
Q

What happens in extrinsic mechanism of apoptosis?

A

Fas-Ligand or TNF-Ligand binds to CSM receptor which activate caspases -> apoptosis

47
Q

What happens in cytotoxic mechanism of apoptosis?

A

CD8+ binding releases granzyme B from CD8+ cell; granzyme B -> performin -> caspases -> apoptosis

48
Q

What is necrosis?

A

Inflammatory traumatic cell death
Cells burst, organelles splurge, CSM damaged
Chromatin altered; cell is fucked

49
Q

What is Hypertrophy?

A

Increase in size of tissue caused by increase in number of constituent cells

50
Q

What is hyperplasia?

A

Number of cells increases via mitosis

51
Q

What is atrophy?

A

Number or size of cell decrease

52
Q

What is metaplasia?

A

Change of one cell type to another type

53
Q

What is dysplasia?

A

Change of differentiated cell type to poorly differentiated cell type

54
Q

What is ischemia?

A

Decreased perfusion to tissue without infarction

55
Q

Does basal cell carcinoma of skin invade globally or locally?

A

Locally - Never spreads to other parts of body

56
Q

How do you cure basal cell carcinoma?

A

Complete local excision

57
Q

What is carcinogenesis?

A

Transformation of normal cells to neoplastic cells through permanent mutation

58
Q

What are neoplasms?

A

Autonomous, Abnormal, Persistent New Growth

59
Q

What type of neoplasms do carcinogenesis only apply to?

A

Malignant

60
Q

What do both carcinogenic and oncogenic act on?

A

DNA (Mutagenic)

61
Q

What is the difference between carcinogenic and oncogenic?

A

Carcinogenic is cancer causing and oncogenic is tumour causing

62
Q

What are tumours classified by?

A

Behaviour
Histogenesis

63
Q

What are the 2 behaviours of a tumour?

A

Benign or Malignant

64
Q

what are the features of a benign tumour?

A
  • localised (No BM invasion)
  • Slow growing
  • Exophytic (Outward growth)
  • Rare ulceration and necrosis
  • Close resemblance to normal tissue
65
Q

What are the features of malignant tumour?

A

-BM invading
- very fast mitotic growth
- Endophytic (Inward growth)
- Common necrosis and ulceration
- Poorly differentiated (little resemblance to normal tissue)

66
Q

What is histogenesis?

A

Origin cell of tumour or based on the specific cell

67
Q

What cells form carcinomas?

A

Epithelial cells

68
Q

What tissues form sarcomas?

A

Connective tissue

69
Q

What is metastasis?

A

Process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites

70
Q

What is the pathway of metastasis?

A
  1. Detachment (From primary)
  2. Invasion of other tissue
  3. Intravasation of BV
  4. Evasion of host defence, ADHERENCE to BV wall
  5. Extravasation to distant site
71
Q

What are the 3 methods of spread in metastasis?

A
  1. Haematogenous
  2. Lymphatic
  3. Transcoelomic
72
Q

What happens in haematogenous spread?

A

Spreads to bone via lung, breast, kidney, thyroid, prostate

73
Q

What happens in lymphatic spread?

A

secondary formation in lymph nodes e.g. lymphoma

74
Q

What happens in Transcoelomic spread?

A

Via exudative fluid accumulation, spread through pleural, pericardial + peritoneal effusions

75
Q

What method of spread do carcinomas prefer?

A

Lymphatic spread

76
Q

What method of spread do sarcomas prefer?

A

Haematogenous spread

77
Q

What are 2 components of neoplams?

A

Neoplastic cells and Stroma

78
Q

What are the characteristics of neoplastic cell?

A
  • Derived from nucleated cells
  • Usually monoclonal
  • Growth pattern related to parent cell
  • Synthetic activity related to parent cell
79
Q

What are the characteristics of a stroma?

A
  • Connective tissue framework
  • Mechanical support
  • Nutrition
80
Q

What is essential for neoplasm growth?

A

Angiogenesis

81
Q

What does a neoplasm release in order to initiate angiogenesis?

A

Vascular endothelial growth factor

82
Q

What is a benign tumour of non-glandular, non-secretory epithelium called?

A

Papilloma

83
Q

What is a benign tumour of glandular or secretory epithelium called?

A

Adenoma

84
Q

What is a malignant tumour of epithelial cells called?

A

Carcinoma

85
Q

What are carcinomas of glandular epithelium called?

A

Adenocarcinomas

86
Q

What is a benign adipocyte tissue neoplasm called?

A

Lipoma

87
Q

What is a benign cartilage tissue neoplasm called?

A

Chondroma

88
Q

What is a benign bone tissue neoplasm called?

A

Osteoma

89
Q

What is a benign vascular tissue neoplasm called?

A

Angioma

90
Q

What is a benign striated muscle tissue neoplasm called?

A

Rhabdomyoma

91
Q

What is a benign smooth muscle tissue neoplasm called?

A

Leiomyoma

92
Q

What is benign nerve tissue neoplasm callled?

A

Neuroma

93
Q

What is a malignant adipose tissue neoplasm called?

A

Liposarcoma

94
Q

What is a malignant striated muscle tissue neoplasm called?

A

Rhabdomyosarcoma

95
Q

What is a malignant smooth muscle tissue neoplasm called?

A

Leiomyosarcoma

96
Q

What is malignant cartilage tissue neoplasm called?

A

Chondrosarcoma

97
Q

What is a malignant bone tissue neoplasm called?

A

Osteosarcoma

98
Q

What is a malignant blood vessel tissue neoplasm called?

A

Angiosarcoma

99
Q

What do you call a tumour which its cell-type of origin is unknown?

A

Anaplastic

100
Q

What exceptions are there to nomenclature of neoplasia?

A
  • Not all ‘-omas’ are neoplasms
  • Not all malignant tumours are carcinoma or sarcoma

phase 2a (2 decks)

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