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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
why are a lot of organs susceptible to infarction
because they are supplied by a single artery
26
what is atherosclerosis
plaque accumulation in high pressure arteries
27
risk factors for atherosclerosis
obesity, smoking, hypertension, hyperlipidemia, diabetes, old age, ethnicity (eg south Asian are at increased risk)
28
stages of atherosclerotic plaque formation
-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
29
what is apoptosis
programmed cell death
30
what is the importance of cell death
-removal of cells during development -removal of cells during normal cell turnover
31
what is necrosis
wholesale death destruction of large number of cells by some external factor eg infarction or frostbite
32
metastasis pathway
-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
methods of spread of tumours
-hematogenous (via blood) -lymphatic -transcolemic (via exudative fluid accumulation spread through pleural, peritoneal, pericardial infusions)
34
what are carcinogens
agents known or suspected to cause tumours
35
name some examples of carcinogens
chemical, viral, radiation, hormones, miscellaneous
36
what is carcinogenesis
the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations
37
what is a neoplasm
a lesion resulting from the autonomous, abnormal growth of cells that persists after the initial stimulus has been removed.
38
cancers that metastasise to bone
breast cancer lung cancer kidney cancer prostate cancer thyroid cancer renal cell cancer
39
what is a papilloma
benign neoplasm of non-glandular/ non-secretory epithelium
40
what is an adenoma
benign neoplasm of glandular or secretory epithelium
41
characteristics of benign tumours
non invasive localised well-circumscribed bland cell morphology low mitotic activity necrosis usually absent
42
characteristics of malignant tumours
invasive local and distant spread (metastasis) poorly circumscribed abnormal cell morphology high mitotic activity necrosis may be present
43
what is a carcinoma
malignant epithelial neoplasm
44
what are adenocarcinomas
carcinomas of glandular tissue
45
lipomas, osteomas and neuromas are examples of what
benign connective tissue neoplasm (cell type of origin + -oma)
46
how to name malignant connective tissue neoplasms
cell type of origin + -sarcoma
47
how to stage tumours (TNM)
sizing of Tumour lymph Node Metestases
48
what are the primary lymphoid organs
bone marrow and thymus
49
what are the secondary lymphoid organs
lymph nodes and spleen
50
what is innate immunity
non specific, rapid initial response to a pathogen no memory killing usually complement activation neutrophil and macrophages mostly
51
what are some examples of physical barriers to infection
skin, mucus, cilia
52
what are some examples of chemical barriers to infection
lysozyme in tears, stomach acid
53
how does the complement system destroy foreign antigens
direct lysis - membrane attack complex (MAC) formation oponisation- increased phagocytosis inflammation- macrophage chemotaxis
54
what are the most common antigen presenting cells
dendritic cells
55
what is adaptive immunity
specific, slow, acquired/learned response to a pathogen needs activation and has memory
56
what is thymic tolerance
the process of eliminating any developing cells that are autoreactive
57
what is MHC
major histocompatibility complex- displays peptides from self or non self proteins. t cell receptors recognise foreign antigens in association with MHCs
58
in humans, what are MHCs coded for
Human leukocyte antigen (HLA) genes on chromosome 6
59
what are t helper cells also known as
CD4 positive cells
60
what are cytotoxic t cells also known as
CD8 cells
61
what is the role of t helper 1 cells
produce the cytokine interferon gamma (INF y) and interleukin 12 which activates natural killer cells and macrophages
62
what is the role of t helper 2 cells
produces the cytokine interleukin 4 (IL4) which activates b cells to differentiate into plasma cells
63
how do cytotoxic t cells work
-they secrete perforin which is mediated by granzyme B -cell lysis -express Fas ligand- activates caspases
64
what immunoglobulins are there
G,A,M,E,D
65
what is the most abundant Ig in the blood and is key in the immune response
IgG
66
what is the most abundant Ig in the total body
IgA
67
what is the first Ig released in the immune response
IgM
68
Function of IgE
activates mast cell and basophil degranulation in T1 hypersensitivity (allergic reaction)
69
what is T1 hypersensitivity reaction
anaphylaxis
70
what is atopy
exagerated IgE mediated response eg asthma
71
what does anaphylaxis cause
vasodilation, bronchoconstriction, rash etc
72
how do you use ABCDE for anaphylaxis
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
what drug is used to treat anaphylaxis
500mg intramuscular adrenaline
74
what is T2 hypersensitivity reaction
antigen-antibody complex -IgG/M binds to antigen and activates MAC (complement) at site of A-A BINDING
75
examples of T2 hypersensitivity reactions
goodpastures, rheumatic fever, autoimmune hemolytic anaemia
76
what is T3 hypersensitivity reaction
immune complex deposition -IgG/A binds to antigen and activates complement at site of A-A DEPOSITING
77
Examples of T3 hypersensitivity reaction
systemic lupus erythematous (SLE or lupus for short), post strep glomerulonephritis, IgA glomerulonephritis
78
what is T4 hypersensitivity reaction
cell mediated -TH1 activated by APCs which causes a response
79
examples of T4 hypersensitivity reactions
Tuberculosis, Multiple sclerosis, Guillan Barre

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