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Phase 2a med mine > ICS > Flashcards

ICS Flashcards

1
Q

Primary cell in acute inflammation

A

Neutrophil polymorphs

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2
Q

Cells in chronic inflammation

A

Macrophages and lymphocytes

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3
Q

Cardinal signs of inflammation

A

Rubor
Dolor
Calor
Tumor
Loss of function

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4
Q

Stages of inflammation

A

1)Increase in vessel calibre->inflamamtory cytokines released like bradykinin and NO-> vasodilators
2)Fluid exudate-vessel becomes leaky and fluid forced out
3)Cellular exudate-> inflammatory cytokines released-> emigration of neutrophils into extravascular space

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5
Q

Neutrophil action in acute inflammation

A

1)Margination
2)Adhesion
3)Emigration
4)Diapadesis
5)Chemotaxis-> follow cytokines down concentration gradient to site of inflammation

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6
Q

Outcomes of inflammation

A

Resolution
Suppuration(pus)
Organisation(granulation and fibrosis)
Progression(chronic inflammation +fibrosis)

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7
Q

Granuloma definition

A

Aggregate of epithelioid histocytes

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8
Q

Name 4 conditions you would see granulomas in

A

TB
Leprosy
Crohns
Sarcoidosis

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9
Q

How are TB granulomas different to other granulomatous conditions

A

Caseating

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10
Q

What do granulomas secrete?

A

ACE

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11
Q

Thrombosis definition

A

Solidification of blood contents that forms within the vascular system during life

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12
Q

Embolism definition

A

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

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13
Q

Describe the primary platelet plug

A

1)Adhesion-VWF binds to exposed collagen
2)Activation
3)Aggregation and amplification

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14
Q

Describe the coagulation cascade

A

Intrinsic: 12-11-9-8
Extrinsic:3-7
Common: 10-2(with help of 5) 2 is thrombin
2-1: fibrin

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15
Q

Which pathway does aPTT reflect

A

Intrinsic

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16
Q

Which pathway does PT reflect

A

Extrinsic and common pathway

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17
Q

Name 2 vasodilators

A

Bradykinin
NO

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18
Q

What are the 3 stages for coagulation

A

1)Vasospasm
2)Primary platelet plug
3)Secondary platelet plug

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19
Q

Components of virchows triad

A

Hypercoagulability-cocp
Venous stasis-surgery
Endothelial injury-smoking

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20
Q

How is treatment for arterial thrombi different to venous thrombi

A

Arterial-aspirin-antiplatelets
Venous-anticoags-DOAC, warfarin

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21
Q

Define atherosclerosis

A

Accumulation of fibroid plaques in the intima of systemic arteries

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22
Q

Name the constituents of the fibroid plaque in atherosclerosis

A

Lipid
Smooth muscle cells
Foam cells
Inflammatory cells-macrophages, T cells
Platelets
Fibroblasts

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23
Q

Descrbe the formation of the atherosclerotic plaque

A

1)Fatty streak in intimal wall
2)Intermediate lesions
3)Fibroud plaque

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24
Q

What cells are involved int he fatty streak

A

T cells and lipid laden macrophages(foam cells)

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25
Q

What cells are involved in the intermediate lesions?

A

Foam cells
T cells
Smooth muscle cells
Platelets begin to aggregate

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26
Q

What cells are involved in the formation of fibrous plaque

A

Foam cells
T cells
Smooth muscle cells
Fibroblasts
Lipids with necrotic core
Fibrous cap over the top of lesion containing all the above

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27
Q

How does the fibrous plaque progress?

A

Stable angina: plaque is strong and less rupture prone
Plaque prone to rupture-> prothrombotic state, platelet adhesion and accumulation, progressive luminal narrowing

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28
Q

Define apoptosis

A

Programmed cell death with the release of harmful products

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29
Q

Define necrosis

A

Traumatic cell death which induces inflammation and repair

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30
Q

what does p53 do?

A

Detects DNA damage and regulates apoptosis

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31
Q

What are the 3 mechanisms of apoptois?

A

Intrinsic
Extrinsic
Cytotoxic

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32
Q

Describe the intrinsic pathway of apoptosis

A

Bax acts on mitochondrial membrane to promote cytochrome C release
Activates caspases-> induce apoptossis

33
Q

Decribe the extrinsic pathway of apoptosis

A

FasL or TNFL binds to csm-> activates caspases-> apoptosis

34
Q

Describe the cytotoxic pathway of apoptosis

A

CD8 cells release Granzyme B and perforin-> apoptosis

35
Q

Define hypertrophy

A

Increase in cell size without cell division(LVH in athletes)

36
Q

Define hyperplasia

A

Increase in cell number by mitosis(hyperplasia of prostate smooth muscle)

37
Q

Define atrophy

A

Decrease in size of an organ/cell by reduction in cell size and/or reduction in cell numbers, often by apoptosis

38
Q

Define metaplasia

A

Change in differentiation of a cell from one fully differentiated cell type to another fully differentiated cell type(Barretts)

39
Q

Define dysplasia

A

Morphological changes seen in cells i progression to cancer

40
Q

Define ischaemia

A

Reduction in blood flow to a tissue caused by a constriction/blockage of the blood vessels supplying it

41
Q

Define infarction

A

Necrosis of part/whole of an organ that occurs when the artery supplying it is obstructed

42
Q

Name 3 areas that have a dual blood supply

A

Liver
Lungs
Brain

43
Q

Define a tumor

A

Any abnormal swelling

44
Q

Define neoplasm

A

A lesion resulting form the autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

45
Q

Describe benign neoplasms

A

Localised
Non invasive
Low mitotic activity
Close resemblance to normal tissue
Normal nuclei
Rarely cause ulceration or necoriss
Exophytic growth

46
Q

Describe malignant neoplasms

A

Invasive
Metastasize
High mitotic activity
Some resemblance to normal tissue
Poorly defined
Can cause ulceration/necrosis
Endophytic growth

47
Q

How can benign neoplasms cause problems

A

Pressure on adjacent structures
Obstruction of flow
Can become malignant
Anxiety

48
Q

How can malignant neoplasms cause problems

A

Destruction of surrounding tissue
Blood loss due to ulceration
Pain
Anxiety

49
Q

Name the modes of tumour spread

A

Haematogenous
Transcoelomic
Lymphatic system

50
Q

Which tumour metastasize to bone

A

BLTKP
Breast
lung
thyroid
kidney
prostate

51
Q

What does it mean if a neoplasm is well differentiated

A

Close resemblance to normal tissue
Better prognosis, low grade

52
Q

What is a tumour of unknown origin called?

A

Anaplastic

53
Q

papilloma

A

benign
non glandular non secretory epithelium

54
Q

Carcinoma

A

malignant
non glandular non secretoy

55
Q

adenoma

A

benign
Glandular/secretory epithelium

56
Q

adenocarcinoma

A

malignant
glandular epithelium

57
Q

lipoma

A

benign
adipocytes

58
Q

liposarcoma

A

malignant
adipocytes

59
Q

chrondroma

A

benign
cartilage

60
Q

chrondrosarcome

A

malignant
cartilage

61
Q

osteoma

A

benign
bone

62
Q

osteosarcoma

A

malignant
bone

63
Q

angioma

A

benign
vascular

64
Q

angiosarcome

A

malignant
vascular

65
Q

rhabdomyoma

A

benign
striated muscle

66
Q

rhabdomyosarcoma

A

malignant
striated muscle

67
Q

leiomyoma

A

benign
smooth muscle

68
Q

leiomyosarcome

A

malignant
smooth muscle

69
Q

neuroma

A

beign
nerves

70
Q

neurosarcoma

A

malignant
nerves

71
Q

Define carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic alterations/mutation
Carcinogens increase probability of mutagenic affect

72
Q

Name the different types of carcinogens

A

Chemical
Viral
Radiation
Hormones
Parasites
Mycotoxins
Miscellaneous

73
Q

Give some examples of viral carccinogens

A

EBV-Burkitt’s lymophoma
HPV-cervical

74
Q

Examples of how radiation us a carcinogen

A

ionisig radiation-lung, thyroidm skin cancer
UV light-skin

75
Q

How can hormones be carcinogenic

A

Oestrogen: increases breast an endometrial cancer
Anabolic steroids-HCC

76
Q

How can a parasite be carcinogenic

A

Schictosoma-squamous bladder cancer

77
Q

How can mycotoxins be carcinogenic?

A

Aspergillus flavus-HCC

78
Q

How can asbestos be carcinogenic

A

malignant mesothelioma
lung carcinoma

79
Q

What cancers are screened for int eh UK and how are they screened/

A

Colorectal -FIT >60yrs every 2 yrs
Breast-mammography-50-71 every 3 yrs
Cervical-pap smear >25

Phase 2a med mine (11 decks)

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