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Phase 2a > ICS - Pathology COPY > Flashcards

ICS - Pathology COPY Flashcards

1
Q

What is inflammation?

A

Inflammation is the body’s process of fighting things that harm it such as infections, injuries and toxins.

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2
Q

What are the types of inflammation?

A

Acute and chronic inflammation.

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3
Q

What is acute inflammation?

A

The initial tissue reactions to injury which may last from a few hours to a few days.

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4
Q

What is acute inflammation mediated by?

A

Neutrophils

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5
Q

What is chronic inflammation?

A

The subsequent and prolonged tissue reactions to injury following acute inflammation.

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6
Q

What is chronic inflammation mediated by?

A

Macrophages and lymphocytes.

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7
Q

What is inflammation characterised by?

A

The 5 cardinal signs.

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8
Q

What are the 5 cardinal signs?

A
  1. Rubor (redness)
  2. Dalor (pain)
  3. Calor (heat)
  4. Tumor (swelling)
  5. Function loss
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9
Q

What are the 3 stages of acute inflammation?

A
  1. Increased vessel calibre - vasodilation by cytokines (bradykinin, NO, prostaglandins)
  2. Fluid exudate - Leaky vessel, fluid forced out
  3. Cellular exudate - Neutrophils become abundant
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10
Q

What do neutrophils do in acute inflammation?

A
  1. Margination - To edge of vessel
  2. Adhesion - Neutrophils bind to endothelium of vessel
  3. Emigration - Neutrophils move out of vessel
  4. Chemotaxis - phagocytosis, phagolysosome, macrophage clears debris.
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11
Q

What are the four outcomes of acute inflammation?

A
  1. Resolution - Tissue restored to normal
  2. Supportation - Pus formation
  3. Organisation - Granulation tissue and fibrosis.
  4. Progression - Excessive recurrent inflammation; becomes chronic and fibrotic tissue.
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12
Q

What are granulomas?

A

They’re aggregates of macrophages in response to chronic inflammation.

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13
Q

What is the significance of granuloma shape?

A
  1. Central necrosis - TB
  2. No central necrosis - Crohn’s, leprosy, sarcoidosis
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14
Q

What is the marker for granulomas?

A

ACE as they secrete it.

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15
Q

What is thrombus?

A

A mass of blood constituents (platelets) forming in vessels.

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16
Q

How does a thrombus form?

A
  1. Vasospasm
  2. Primary platelet plug - VWF binds to exposed collagen; platelets bind to this.
  3. Coagulation cascade
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17
Q

What is Virchow’s triad?

A

Three factors in the contribution of thrombosis. Only one is needed but it’s usually two or three.

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18
Q

What are the factors in Virchow’s triad (with examples)?

A
  1. Endothelial injury - Trauma, smoking, MI, surgery.
  2. Hypercoagulability - Sepsis, atherosclerosis, pregnancy, malignancy.
  3. Decreased blood flow - AF, immobility.
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19
Q

What are the different types of thrombosis?

A

Arterial and venous thrombi.

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20
Q

How does an arterial thrombus form?

A

Forms by atherogenesis.

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21
Q

How does a venous thrombus form?

A

Forms by venous stasis.

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22
Q

What are the fates of thrombi?

A
  1. Resolution - degrades
  2. Organisation - leaves behind scar tissue
  3. Embolism - fragments of thrombi break away and lodge in distal circulation
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23
Q

What is an embolus?

A

An embolus is a fragment of a thrombus which has broken off.

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24
Q

What are the types of emboli?

A

Arterial and venous.

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25
Q

What is an example of an arterial embolus?

A

A thrombus from AF embolises and lodges in the carotid artery causing an ischaemic stroke.

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26
Q

What is an example of a venous embolus?

A

A DVT thrombus embolises and lodges in the pulmonary artery causing a PE.

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27
Q

What is atherosclerosis?

A

Fatty plaque that forms in the intima and media of arteries, hardening and narrowing them over time.

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28
Q

What causes atherosclerosis?

A

Chronic inflammation and activation of the immune system in the artery wall.

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29
Q

What are the contents of an atherosclerotic plaque?

A

Lipids, smooth muscle, macrophages, platelets, fibroblasts.

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30
Q

What are the non-modifiable and modifiable risk factors for atherosclerosis?

A

Non-modifiable: age, family history, gender.
Modifiable: smoking, alcohol, poor diet, low exercise, obesity, poor sleep and stress.

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31
Q

What is the name of the formation of a plaque?

A

Atherogenesis.

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32
Q

What are the four steps of atherogenesis?

A
  1. Endothelial injury
  2. Fatty streak
  3. Inflammatory reaction
  4. Fibrous cap
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33
Q

How does a fibrous cap in atherosclerosis cause further narrowing?

A

If the fibrous cap ruptures, there is continuous plug formation which occludes the lumen leading to narrowing.

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34
Q

What is apoptosis?

A

Apoptosis is non-inflammatory genetically programmed cell death without any harmful product release.

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35
Q

How do cells appear in apoptosis?

A

Cells shrink, organalles are retained, cytoplasm stays intact, chromatin is unaltered, fragmented for phagocytosis.

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36
Q

What are the mechanisms for apoptosis?

A
  1. Intrinsic
  2. Extrinsic
  3. Cytotoxic
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37
Q

What is necrosis and what causes it?

A

Inflammatory unprogrammed cell death due to adverse event such as infarction, burn, frostbite, infection and trauma.

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38
Q

How do cells appear in necrosis?

A

Cells burst, organelles splurge, cytoplasm is damaged, chromatin is altered, and the cell is FUCKED.

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39
Q

What are the different patterns of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Gangrene
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40
Q

What is hypertrophy?

A

Cell gets bigger without cell division.

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41
Q

What is hyperplasia?

A

Number of cells increase via mitosis.

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42
Q

What is atrophy?

A

Number or size of cells decreases

43
Q

What is metaplasia?

A

Replacement of one cell type to another.

44
Q

What is dysplasia?

A

Morphological changes seen in cells progressing to become cancerous.

45
Q

What is ischaemia?

A

Decreased perfusion to tissue without infarction.

46
Q

What is infarction?

A

Death of tissue due to severe and prolonged ischaemia.

47
Q

What is carcinogenesis?

A

Transformation of normal cells to neoplastic cells through permanent mutation.

48
Q

What is a neoplasm?

A

An abnormal and persistent new growth which can only arise from nucleated cells (not RBCs).

49
Q

What is a tumour?

A

Any abnormal swelling.

50
Q

How can tumours be classified?

A

By behaviour and histogenesis.

51
Q

How can tumours be divided by their behaviour?

A

Benign or malignant.

52
Q

What are the differences between benign and malignant cells?

A

Benign - slow growing, localised, well circumscription, outward growing, rare ulceration and necrosis.

Malignant - Very fast growing, poor circumscription, invade nearby tissues, inward growing, common ulceration and necrosis.

53
Q

What does tumour histogenesis measure?

A

The origin cell of tumours.

54
Q

What are carcinomas?

A

Tumours of epithelia.

55
Q

What are sarcomas?

A

Tumours of connective tissue.

56
Q

What are lymphoid tumours?

A

Leukeamia and lymphoma (always malignant).

57
Q

Which cancers are screened for?

A

Cervical - Swab
Breast - Mammograms
Colorectal - Fecal sample

58
Q

How are most tumours staged?

A

By TNM (tumour, nodes, metastases)

-Primary tumour measured (T1-4)
-Nearby lymph nodes measured for cancer (NX, N0, N1)
-Metastases measured (MX, M0, M1)

59
Q

What are the classes of carcinogens?

A
  1. Chemicals (paints).
  2. Viruses (HPV).
  3. Ionising/non-ionising radiation (UVB light),
  4. Hormones (oestrogen).
  5. Miscellaneous (asbestos).
60
Q

Which tumours are pathological?

A

Malignant and benign. Benign tumours can also put pressure on local structures, secrete hormones and cause obstruction like malignant tumours.

61
Q

What are the five main cancers that metastasise to bone?

A

BLTKP - Breast, lung, thyroid, kidney, prostate

62
Q

What are the methods of tumour spread?

A
  1. Haematogenesis - Via blood.
  2. Lymphatic - Secondary formation in lymph nodes.
  3. Transcolemic - Via exudate fluid accumulation.
63
Q

What is the pathway of metastasis?

A
  1. Detachment from primary tumour
  2. Invasion of other tissue
  3. Invasion of blood vessels
  4. Evasion of host defence and adherence to blood vessel endothelium
  5. Extravasation and colonisation
64
Q

What is the name of a non-glandular benign tumour?

A

Papilloma

65
Q

What is the name of a non-glandular malignant tumour?

A

Carcinoma

66
Q

What is the name of a glandular benign tumour?

A

Adenoma

67
Q

What is the name of a glandular malignant tumour?

A

Adenocarcinoma

68
Q

What is the name of benign and malignant adipocyte tumours?

A

Benign - lipoma
Malignant - liposarcoma

69
Q

What is the name of benign and malignant striated muscle tumours?

A

Benign - rhabdomyoma
Malignant - rhabdomyosarcoma

70
Q

What is the name of benign and malignant smooth muscle tumours?

A

Benign - leiomyoma
Malignant - leiomyosarcoma

71
Q

What is the name of benign and malignant cartilage tumours?

A

Benign - chrondroma
Malignant - chondrosarcoma

72
Q

What is the name of benign and malignant bone tumours?

A

Benign - osteoma
Malignant - osteosarcoma

73
Q

What is a melanoma?

A

Malignancy of melanocytes

74
Q

Which cancer never spreads to other parts of the body?

A

Basal cell carcinoma

75
Q

What is a suitable treatment for leukaemia and why?

A

Chemotherapy as leukaemia is systemic

76
Q

What is an example of a carcinoma that spreads to the axillary lymph nodes?

A

Breast carcinomas

77
Q

What is a pro and con of conventional chemotherapy?

A

Pro: Effective against fast dividing tumours.

Con: Non-selective for tumour cells, normal cells also get killed (diarrhoea, N+V, hair loss)

78
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.

79
Q

Which type of cancers is targeted chemotherapy most suited to?

A

Slow growing cancers.

80
Q

What is myeloma?

A

Cancer of plasma cells.

81
Q

What is multiple myeloma?

A

When a myeloma affects multiple parts of the body.

82
Q

What is carcinoma in situ?

A

When a carcinoma is still contained and hasn’t invaded the basement membrane.
Often referred to as stage 0 cancer.

83
Q

What is a mesothelioma?

A

Malignancy of mesothelial cells of pleura.

84
Q

What is a major risk factor and features of mesothelioma?

A

Asbestos inhalation.
Very large latent period (up to 45 years).
Very poor prognosis.

85
Q

How long does acute inflammation last for?

A

Hours to days.

86
Q

How long does chronic inflammation last for?

A

Months to years.

87
Q

Give two examples of things that may cause acute inflammation.

A

Infections and hypersenstivity.

88
Q

Give two examples of things that may cause chronic inflammation.

A

Autoimmunity and recurrent infections.

89
Q

Which two tissues never resolve?

A

Cardiac tissue and neurons - most become granular tissue and fibrotic.

90
Q

What would raised eosinophils and granulomas indicate?

A

A parasite infection.

91
Q

What can arterial thrombi cause?

A

MI, angina, ischaemic strokes and PVD.

92
Q

What are the three signs of an arterial thrombi?

A

Cold, pale and loss of pulse.

93
Q

What do venous thrombi cause?

A

Mainly DVTs which can cause PEs.

94
Q

What are the three signs of a venous thrombi?

A

Tender, swollen and red.

95
Q

How are thrombi treated?

A

Antiplatelets (aspirin) and anticoagulants (warfarin, DOACs).

96
Q

What causes endothelial injuries at the start of atherogenesis?

A

Due to smoking, T2DM, hypertension, and increased LDL in blood.

97
Q

Describe a fatty streak in atherogenesis.

A

Plaque precursor, LDL phagocytosed by macrophages to form foam cells in intima; this builds up over time.

98
Q

What are foam cells?

A

LDL phagocytosed by macrophages which accumulate in a fatty streak.

99
Q

Describe the inflammatory reaction in atherogenesis.

A

WBCs infiltrate the fatty streak and it gets larger.

100
Q

Describe a fibrous cap in atherogenesis.

A

Fibroblasts produce smooth muscle fibrous cap which covers internal lumen of plaque.

101
Q

What happens when a fibrous cap is damaged?

A

There is continuous platelet plug formation over the damaged fibrous cap, forming a large thrombus.
-This occludes the artery and if in the heart - MI.

102
Q

To which tissues does hypertrophy most commonly occur?

A

Muscles (including the heart).

103
Q

What is an example of metaplasia?

A

Barrett’s oesophagus.
-From simple squamous to columnar epithelia.

104
Q

How are leukaemias and lymphomas staged?

A

Ann arbor staging.

Phase 2a (14 decks)

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