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
What cells are involved in the intermediate lesions?
Foam cells T cells Smooth muscle cells Platelets begin to aggregate
26
What cells are involved in the formation of fibrous plaque
Foam cells T cells Smooth muscle cells Fibroblasts Lipids with necrotic core Fibrous cap over the top of lesion containing all the above
27
How does the fibrous plaque progress?
Stable angina: plaque is strong and less rupture prone Plaque prone to rupture-> prothrombotic state, platelet adhesion and accumulation, progressive luminal narrowing
28
Define apoptosis
Programmed cell death with the release of harmful products
29
Define necrosis
Traumatic cell death which induces inflammation and repair
30
what does p53 do?
Detects DNA damage and regulates apoptosis
31
What are the 3 mechanisms of apoptois?
Intrinsic Extrinsic Cytotoxic
32
Describe the intrinsic pathway of apoptosis
Bax acts on mitochondrial membrane to promote cytochrome C release Activates caspases-> induce apoptossis
33
Decribe the extrinsic pathway of apoptosis
FasL or TNFL binds to csm-> activates caspases-> apoptosis
34
Describe the cytotoxic pathway of apoptosis
CD8 cells release Granzyme B and perforin-> apoptosis
35
Define hypertrophy
Increase in cell size without cell division(LVH in athletes)
36
Define hyperplasia
Increase in cell number by mitosis(hyperplasia of prostate smooth muscle)
37
Define atrophy
Decrease in size of an organ/cell by reduction in cell size and/or reduction in cell numbers, often by apoptosis
38
Define metaplasia
Change in differentiation of a cell from one fully differentiated cell type to another fully differentiated cell type(Barretts)
39
Define dysplasia
Morphological changes seen in cells i progression to cancer
40
Define ischaemia
Reduction in blood flow to a tissue caused by a constriction/blockage of the blood vessels supplying it
41
Define infarction
Necrosis of part/whole of an organ that occurs when the artery supplying it is obstructed
42
Name 3 areas that have a dual blood supply
Liver Lungs Brain
43
Define a tumor
Any abnormal swelling
44
Define neoplasm
A lesion resulting form the autonomous abnormal growth of cells which persists after the initiating stimulus has been removed
45
Describe benign neoplasms
Localised Non invasive Low mitotic activity Close resemblance to normal tissue Normal nuclei Rarely cause ulceration or necoriss Exophytic growth
46
Describe malignant neoplasms
Invasive Metastasize High mitotic activity Some resemblance to normal tissue Poorly defined Can cause ulceration/necrosis Endophytic growth
47
How can benign neoplasms cause problems
Pressure on adjacent structures Obstruction of flow Can become malignant Anxiety
48
How can malignant neoplasms cause problems
Destruction of surrounding tissue Blood loss due to ulceration Pain Anxiety
49
Name the modes of tumour spread
Haematogenous Transcoelomic Lymphatic system
50
Which tumour metastasize to bone
BLTKP Breast lung thyroid kidney prostate
51
What does it mean if a neoplasm is well differentiated
Close resemblance to normal tissue Better prognosis, low grade
52
What is a tumour of unknown origin called?
Anaplastic
53
papilloma
benign non glandular non secretory epithelium
54
Carcinoma
malignant non glandular non secretoy
55
adenoma
benign Glandular/secretory epithelium
56
adenocarcinoma
malignant glandular epithelium
57
lipoma
benign adipocytes
58
liposarcoma
malignant adipocytes
59
chrondroma
benign cartilage
60
chrondrosarcome
malignant cartilage
61
osteoma
benign bone
62
osteosarcoma
malignant bone
63
angioma
benign vascular
64
angiosarcome
malignant vascular
65
rhabdomyoma
benign striated muscle
66
rhabdomyosarcoma
malignant striated muscle
67
leiomyoma
benign smooth muscle
68
leiomyosarcome
malignant smooth muscle
69
neuroma
beign nerves
70
neurosarcoma
malignant nerves
71
Define carcinogenesis
Transformation of normal cells to neoplastic cells through permanent genetic alterations/mutation Carcinogens increase probability of mutagenic affect
72
Name the different types of carcinogens
Chemical Viral Radiation Hormones Parasites Mycotoxins Miscellaneous
73
Give some examples of viral carccinogens
EBV-Burkitt's lymophoma HPV-cervical
74
Examples of how radiation us a carcinogen
ionisig radiation-lung, thyroidm skin cancer UV light-skin
75
How can hormones be carcinogenic
Oestrogen: increases breast an endometrial cancer Anabolic steroids-HCC
76
How can a parasite be carcinogenic
Schictosoma-squamous bladder cancer
77
How can mycotoxins be carcinogenic?
Aspergillus flavus-HCC
78
How can asbestos be carcinogenic
malignant mesothelioma lung carcinoma
79
What cancers are screened for int eh UK and how are they screened/
Colorectal -FIT >60yrs every 2 yrs Breast-mammography-50-71 every 3 yrs Cervical-pap smear >25