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Phase 2a fresh > ICS > Flashcards

ICS Flashcards

1
Q

what is acute inflammation

A

the initial and often transient series of tissue reactions to injury

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2
Q

what cells medicate acute inflammation

A

neutrophil polymorphs

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3
Q

describe the process of acute inflammation

A

-change in vessel calibre (gets wider) and increased vessel flow
-increased vascular permeability and formation of fluid exudate
-formation of cellular exudate- emigration of neutrophil polymorphs into extravascular space

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4
Q

what are the outcomes of acute inflammation

A

-resolution (normal)
-supportation (pus)
-organisation (granulation and fibrosis ,scar formation, )
-progression

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5
Q

examples of acute inflammation

A

infection eg acute appendecitis, hypersensitivity, physical agents, chemicals, bacteria, toxins, frostbite

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6
Q

what cells mediate chronic inflammation

A

macrophages and lymphocytes

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7
Q

examples of when chronic inflammation may occur

A

autoimmune diseases, recurring infections, TB

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8
Q

action of fibroblasts

A

produce collagenous connective tissue in scarring following some types of inflammation

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9
Q

what are granulomas

A

particular type of chronic inflammation with collections of macrophages/ histiocytes surrounded by lymphocytes. May be due to mycobacterial infection eg TB or leprosy

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10
Q

what are the 5 cardinal signs of inflammation

A

-Rubor (redness)
-Calor (heat)
-Dolor (pain)
-Tumor (swelling)
-Decreased function

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11
Q

what is hypertrophy

A

cell enlargement

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12
Q

what is hyperplasia

A

increase in number of cells

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13
Q

what is atrophy

A

decrease in number/ size of cells

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14
Q

what is metaplasia

A

change of one cell type to another eg Barrets oeophagus

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15
Q

what is dysplasia

A

change of a differentiated cell type to a poorly differentiated type

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16
Q

what is ischemia

A

decreased perfusion to tissue without infarction (eg TIA)

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17
Q

what is infarction

A

decreased perfusion to tissue with infarction (eg ischemic stroke)

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18
Q

what is thrombosis

A

when a solid mass forms from blood constituents in the intact vessel in a living person

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19
Q

what components make up Virchows triad for causes for thrombosis

A

-vessel wall injury
-hypercoagulability of blood
-stasis of blood

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20
Q

why are blood clots rare

A

-laminar flow of blood
-normal endothelial cells that line vessels are not sticky

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21
Q

what is the likely reason to thrombosis forming in the arterial system

A

formation of atheroslcerotic plaques

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22
Q

what is the likely reason to thrombosis forming in the venous system

A

slow blood flow

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23
Q

what is an embolism

A

the process of a solid mass in the blood being carried through circulation to a place where it gets stuck and blocks the vessel

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24
Q

if an embolus enters the venous system, where is it most likely to get stuck

A

pulmonary arteries due to capillary size at lungs

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25
Q

why are a lot of organs susceptible to infarction

A

because they are supplied by a single artery

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26
Q

what is atherosclerosis

A

plaque accumulation in high pressure arteries

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27
Q

risk factors for atherosclerosis

A

obesity, smoking, hypertension, hyperlipidemia, diabetes, old age, ethnicity (eg south Asian are at increased risk)

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28
Q

stages of atherosclerotic plaque formation

A

-endothelial injury
-this allows for increased LDLs in endothelium and phagocytosis by macrophages to form foam cells
-formation of fatty streak when foam cells die and their lipid contents are released
-inflammatory reaction- foam cells recruit other inflammatory cells (neutrophils, lymphocytes, macrophages) fibroblasts and platelets
-fibroblasts produce smooth muscle fibrous cap which covers internal lumen side of plaque
non rupture= stable
rupture= continuous platelet plug formation- lumen occlusion

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29
Q

what is apoptosis

A

programmed cell death

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30
Q

what is the importance of cell death

A

-removal of cells during development
-removal of cells during normal cell turnover

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31
Q

what is necrosis

A

wholesale death destruction of large number of cells by some external factor eg infarction or frostbite

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32
Q

metastasis pathway

A

-detachment from primary tumour
-invasion of other tissue
-invasion of blood vessels
-evasion of host defence, adherence to blood vessel wall
-extravasation to distant site

33
Q

methods of spread of tumours

A

-hematogenous (via blood)
-lymphatic
-transcolemic (via exudative fluid accumulation spread through pleural, peritoneal, pericardial infusions)

34
Q

what are carcinogens

A

agents known or suspected to cause tumours

35
Q

name some examples of carcinogens

A

chemical, viral, radiation, hormones, miscellaneous

36
Q

what is carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

37
Q

what is a neoplasm

A

a lesion resulting from the autonomous, abnormal growth of cells that persists after the initial stimulus has been removed.

38
Q

cancers that metastasise to bone

A

breast cancer
lung cancer
kidney cancer
prostate cancer
thyroid cancer
renal cell cancer

39
Q

what is a papilloma

A

benign neoplasm of non-glandular/ non-secretory epithelium

40
Q

what is an adenoma

A

benign neoplasm of glandular or secretory epithelium

41
Q

characteristics of benign tumours

A

non invasive
localised
well-circumscribed
bland cell morphology
low mitotic activity
necrosis usually absent

42
Q

characteristics of malignant tumours

A

invasive
local and distant spread (metastasis)
poorly circumscribed
abnormal cell morphology
high mitotic activity
necrosis may be present

43
Q

what is a carcinoma

A

malignant epithelial neoplasm

44
Q

what are adenocarcinomas

A

carcinomas of glandular tissue

45
Q

lipomas, osteomas and neuromas are examples of what

A

benign connective tissue neoplasm
(cell type of origin + -oma)

46
Q

how to name malignant connective tissue neoplasms

A

cell type of origin + -sarcoma

47
Q

how to stage tumours (TNM)

A

sizing of Tumour
lymph Node
Metestases

48
Q

what are the primary lymphoid organs

A

bone marrow and thymus

49
Q

what are the secondary lymphoid organs

A

lymph nodes and spleen

50
Q

what is innate immunity

A

non specific, rapid initial response to a pathogen
no memory
killing usually complement activation
neutrophil and macrophages mostly

51
Q

what are some examples of physical barriers to infection

A

skin, mucus, cilia

52
Q

what are some examples of chemical barriers to infection

A

lysozyme in tears, stomach acid

53
Q

how does the complement system destroy foreign antigens

A

direct lysis - membrane attack complex (MAC) formation
oponisation- increased phagocytosis
inflammation- macrophage chemotaxis

54
Q

what are the most common antigen presenting cells

A

dendritic cells

55
Q

what is adaptive immunity

A

specific, slow, acquired/learned response to a pathogen
needs activation and has memory

56
Q

what is thymic tolerance

A

the process of eliminating any developing cells that are autoreactive

57
Q

what is MHC

A

major histocompatibility complex- displays peptides from self or non self proteins. t cell receptors recognise foreign antigens in association with MHCs

58
Q

in humans, what are MHCs coded for

A

Human leukocyte antigen (HLA) genes on chromosome 6

59
Q

what are t helper cells also known as

A

CD4 positive cells

60
Q

what are cytotoxic t cells also known as

A

CD8 cells

61
Q

what is the role of t helper 1 cells

A

produce the cytokine interferon gamma (INF y) and interleukin 12 which activates natural killer cells and macrophages

62
Q

what is the role of t helper 2 cells

A

produces the cytokine interleukin 4 (IL4) which activates b cells to differentiate into plasma cells

63
Q

how do cytotoxic t cells work

A

-they secrete perforin which is mediated by granzyme B
-cell lysis
-express Fas ligand- activates caspases

64
Q

what immunoglobulins are there

A

G,A,M,E,D

65
Q

what is the most abundant Ig in the blood and is key in the immune response

A

IgG

66
Q

what is the most abundant Ig in the total body

A

IgA

67
Q

what is the first Ig released in the immune response

A

IgM

68
Q

Function of IgE

A

activates mast cell and basophil degranulation in T1 hypersensitivity (allergic reaction)

69
Q

what is T1 hypersensitivity reaction

A

anaphylaxis

70
Q

what is atopy

A

exagerated IgE mediated response eg asthma

71
Q

what does anaphylaxis cause

A

vasodilation, bronchoconstriction, rash etc

72
Q

how do you use ABCDE for anaphylaxis

A

Airways- swelling of mouth, airway obstruction
Breathing- wheezing, cough, chest tightness, dyspnea (SOB), hypoxia
Circulation- tachycardia, clammy skin, hypotension
Disability- loss of consciousness, dizziness, collapse, D&V
Exposure- skin changes eg pruritis (rash)

73
Q

what drug is used to treat anaphylaxis

A

500mg intramuscular adrenaline

74
Q

what is T2 hypersensitivity reaction

A

antigen-antibody complex
-IgG/M binds to antigen and activates MAC (complement) at site of A-A BINDING

75
Q

examples of T2 hypersensitivity reactions

A

goodpastures, rheumatic fever, autoimmune hemolytic anaemia

76
Q

what is T3 hypersensitivity reaction

A

immune complex deposition
-IgG/A binds to antigen and activates complement at site of A-A DEPOSITING

77
Q

Examples of T3 hypersensitivity reaction

A

systemic lupus erythematous (SLE or lupus for short), post strep glomerulonephritis, IgA glomerulonephritis

78
Q

what is T4 hypersensitivity reaction

A

cell mediated
-TH1 activated by APCs which causes a response

79
Q

examples of T4 hypersensitivity reactions

A

Tuberculosis, Multiple sclerosis, Guillan Barre

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