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PATH1000 > cell injury and inflammation > Flashcards

cell injury and inflammation Flashcards

1
Q

Pathophysiology

A

study of underlying changes in body physiology that results from disease or injury

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2
Q

signs

A

observed, what you can see

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3
Q

symptoms

A

subjective experiences
- different for everyone

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4
Q

type 1 diabetes

A

insulin producing cells have been destroyed so they can no longer produce insulin

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5
Q

type 2 diabetes

A

pancreas produces insulin but the body doesn’t respond to it

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6
Q

symptoms of diabetes

A

polyuria - excessive urination
polydipsia - excessive thirst
polyphagia - excessive hunger

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7
Q

common cold signs

A

eyes - watery itchy red
nose - runny sneezing red
cough
swollen gland

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8
Q

common cold symptoms

A

pain
eyes - itchy
nose - nasal congestion, runny, loss of smell
head - congestion headache
cough
tightness of chest, sore throat

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9
Q

complication

A

onset of a disease in a person who is already coping with another disease

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10
Q

insidious symptoms

A

lack of awareness
appears to be no symptoms
often healthy for years until it has caused irreversible damage

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11
Q

risk factors / predisposing factors

A

increase the probability that disease will occur but not the cause of the disease

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12
Q

acute condition

A

sudden appearance of signs and symptoms and last short amount of time
- broken bone
- acute asthma attack

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13
Q

chronic condition

A

develops slowly and last long time eg diabetes, COPD

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14
Q

incidence of disease

A

number of new cases

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15
Q

prevalence of disease

A

number of existing cases

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16
Q

reversible cell injury

A

alters in structure and function
eg atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

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17
Q

irreversible cell injury

A

lethal, cell death then necrosis

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17
Q

irreversible cell injury

A

lethal, cell death then necrosis

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18
Q

atrophy

A

reduction in size and function and shrinkage of organ

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19
Q

hypertrophy

A

increase in size and output increase in organ size

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20
Q

hyperplasia

A

increase in cell number

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21
Q

metaplasia

A

changes in cell morphology and function
reversible replacement of one mature cell with another

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22
Q

dysplasia

A

increased cell number, changed morphology and differentiation

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23
Q

biological cell injury

A

ischaemia
hypoxic injury
oxidative stress

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24
Q

ischaemia

A

decreased blood supply therefore decrease in oxygen which leads to hypoxia

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25
Q

physical cell injury

A

burn, cut, fracture

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26
Q

hypoxia

A

decreased aerobic production of ATP in mitochondria
failure of Na/K pump
Na and water accumulation in cell

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27
Q

oxidative stress

A

occurs after reperfusion (removal of a blockage)
- damage all parts of cell

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28
Q

necrosis

A
  • infammatory response
  • membrane not in tact
    can affect numerous cells
    swells
    spontaneously occuring
    normally harmful
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29
Q

apoptosis

A

single cell death
clean death
- shrinking of cell structure
- do not elicit inflammation
- membrane in tact
- not harmful

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30
Q

immunity

A

ability to resist damage from foreign substances eg microbes
2 types
- innate and adaptive

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31
Q

innate immunity

A
  • physical barriers
  • inflammation
  • chemical mediators
  • white blood cells
  • non specific, present at birth
  • no memory
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31
Q

adaptive immunity

A
  • cell mediated immunity - t cells
  • antibody mediated immunity - b cells
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32
Q

function of the immune system

A
  • homeostasis: maintenance of optimal body/cell function
  • defence against microbes and foreign bodies
  • defence against growth of tumour cells
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33
Q

how many types of white blood cells and what are they

A

5
granulocytes: basophils neutrophils and eosinophils
agranulocytes: lymphocytes and monocytes

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34
Q

role of white blood cells

A

coordinate with one another to fight off infection, cancer and cell injury

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35
Q

granulocytes

A
  • have visible granules
    include basophils neutrophils and eosinophils
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36
Q

agranulocytes

A

free of visible grains under the microscope
include lymphocytes and monocytes

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37
Q

neutrophils

A

Granulated leucokytes,
- highest concentration in the blood
- first responders to inflammation.
- most abundant.
Release cytokines which are pro inflammatory and drive inflammatory response and chemotaxis and facilitate the recruitment of white blood cells.
- Granules contain lysosomes enzymes to help clear any dead cell debris.

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38
Q

eosinophils

A

principal defender against parasites
granularsites and have large granules which release toxins to the target parasites and help to defend against worms. Associated with allergic reactions, in response to hypersensitivity they will be released

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39
Q

basophils

A

Release anti coagulants which maintain hemostasis, they are granulasites. Within white blood cells they are the least amount
Contain gradules packed with antibodies to facilitate hypersensitivity and enhance the immune system. When granules are released they can be explosive

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40
Q

monocytes

A

leucocytes that circulate in the blood stream
- later responders and longer acting
- precursors of tissue macrophages
- once they have migrated through vessels walls they become macrophages
- produce cytokines and destroy offending agents
- release monotones
- turn into macrophages

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41
Q

macrophages

A
  • mononuclear phagocytic cells that move out into affect lesioned tissues
  • participate in innate and adaptive immunity
  • able to ingest
  • release cytokines and growth factors that drive immune response
  • able to call for help and recruit other WBC
42
Q

mast cells

A
  • present in tissue that surround neuromuscular tissue
  • initial immune / inflammatory responce
  • rapidly degranuolate and release histamine and other chemical mediators
  • help drive vascular responses
  • release reparative mediators and enzymes
43
Q

haemostasis

A

blood clotting

44
Q

how to remember white blood cells

A

Never - neutrophils
Let - lymphocytes
Monkey - monocytes
Eat - eosinophils
Bananas - basophils

45
Q

coagulation cascade

A

two pathways
1. intrinsic
2. extrinsic
pathways converge with activation of factor X
- thrombin cleaves fibrinogen to form fibrin
- coagulation is controlled by enzyme inhibitors

46
Q

5 clinical indicators of acute inflammation

A
  1. redness - vasodilation
  2. heat - vasodilation
  3. swelling - increased blood flow and exudate/ transudate
  4. loss of function
  5. pain - nerve ending stimulation
47
Q

itis

A

= inflammation
eg appendicitis
pancreatitis

48
Q

vascular changes

A

changes associated with vessels

49
Q

cellular changes

A

changes as a result of action of WBC

50
Q

tissue cells

A

mast cells and macrophages

51
Q

phagocytosis

A

by ingestion or eating

52
Q

diapedesis

A

migration of cells through vessels

53
Q

transudate

A

fluid only leak out of vessels

54
Q

exudate

A

plasma protein rich fluid and cells leak out of vessels to get to the site of injury

55
Q

acute vs chronic inflammation

A

respond: immediate vs persistant
onset: rapid vs slow
immunity: innate vs adaptive
prominent cell type: neutrophils vs myphocytes macrophages, fibroblasts
during: hours vs months/years

56
Q

mast cell degranulation

A
  • degranulation and synthesis of new mediators
  • histamine and other mediators initiate vascular changes and chemotaxis
57
Q

vascular phase

A

caused by release of histamine
1. very brief vasoconstriction
2. followed by rapid vasodilation (hyperaemia)
- more blood to area = heat and redness, expansion of capitally beds
3. increased hydrostatic pressure = transudate
- pain, swelling and impaired function
4. increased concentration of cells in blood
5. slowing of blood = blood clotting
6. endothelial cell walls become adhesive to white blood cells
7. endothelial cell activation = retraction = gaps = increases vascular permeability = exudate

58
Q

edema / effusion

A

combination of exudate and transudate

59
Q

chemical mediators roles

A
  • cause vasodilation and cellular changes
  • ## histamine, bradykinin, serotonin, endothelial activation factors
60
Q

kinins

A
  • bradykinins
  • plasma derived mediator
  • small vasoactive peptides
  • increase vascular permeability
  • increase sensitivity of señor nerve endings = pain
61
Q

arachidonic acid, prostaglandins and leukotrienes

A
  • arachidonic acid catalysed by 5-lipoxygenase to form leukotrienes
  • arachidonic acid catalysed by cyclooxygenase to form prostaglandins
  • anti inflammatory drugs inhibit synthesis of prostaglandins
62
Q

platelet activation factors

A
  • released from mast cells and neutrophils during degranulation
  • induce lately aggregation and degranulation
  • increase vascular permeability
  • induce leucocyte adhesion to the endothelium
  • stimulate synthesis or arachidonic acid derivatives
63
Q

cytokines

A
  • family of chemical messengers
  • released by activated T lymphocytes and macrophages
    include
  • lymphokines
  • monokines
  • interleukins
  • interferons
  • growth factors
64
Q

lymphokines

A

cytokine produced by lymphocytes

65
Q

monokine

A

cytokine produced by monocytes and macrophages

66
Q

interferons

A

inhibit replication of virus within cell and activate macrophages and natural killer cells

67
Q

acute phase proteins

A
  • increase during acute inflammation
  • induce by circulating interleukins
  • produce and release from liver
    CRP - blood test to detect infection and inflammatory conditions
68
Q

neutrophil and monocyte attracted to site of injury

A
  • adhesion and margination = diapedesis = chemotaxis towards high chemotactic factor gradient = immobilise at site of injury = phagocytosis
  • destroy offending agents
69
Q

4 steps of phagocytosis

A
  1. recognition and adherence to target - attachment of particle to surface = opsonisation
  2. engulfment and formation of phagosome
  3. fusion with lysosome, degranulation of enzymes
  4. killing and degradation of ingested microbe
70
Q

healing and repair of slight tissue damage

A
  • removal of causative agent
  • destroyed tissue able to regenerate
  • solution back to normal
71
Q

healing and repair of substantial tissue damage

A
  • non regenerative tissue or lots of fibrin exudate
  • replacement of destroyed tissue with scar tissue
  • healing by scarring
72
Q

healing and repair of extensive tissue damage

A
  • necrosis and bacterial / fungal infection
  • formation of granulation
  • abscess
73
Q

pus

A

formation and accumulation of dead material

74
Q

chronic inflammation

A

persistant unsuccessful acute inflammation

75
Q

asthma - chronic inflammation

A
  • activation of mast cells
  • cytokines released
  • triggers inflammation
    = constriction of airways and increased mucus secretion
76
Q

atherosclerosis - chronic inflammation

A
  • accumulation of lipids on artery
  • triggers inflammation
    = artery becomes stiff and less flexible = lumen narrows
  • forming fibrous plaque = thrombus
77
Q

how are cytokines pro inflammatory

A
  • chemotaxic
  • activate B cells
  • active endothelium adhesion
  • cause more cytokine release
  • active neutrophils
  • attract fibroblasts
  • activate T cells
78
Q

regeneration

A

replacement of damage tissue with healthy tissue, limited to cells which can undergo mitosis

79
Q

4 overlapping phases of wound healing

A
  1. haemostasis
    - damaged vessel = vasoconstrictor = vasodilation = coagulation cascade
  2. inflammatory phase = can occur immediately with infiltration of neutrophils
    - macrophages clear debris and release mediators
  3. proliferative phase
    - 3-14 days after injury
    - macrophages secrete growth factors
    = growth of granulation tissue and fibroblasts activation, collagen deposition = wound contraction
  4. remodelling phase
    - several weeks after injury complete within 2 years
    - continuation of regeneration and wound contraction
    - fibroblasts kept cells for tissue remodelling
80
Q

primary wound healing

A
  • clean incision
  • margin surgically clean
  • uninfected
  • rapid healing
  • more epithelial regeneration
  • scar is smooth
81
Q

secondary wound healing

A
  • extensive tissue lost
  • margin is irregular
  • usually infected
  • slower healing
  • fibrosis healing
  • scar is thick
82
Q

is there a cure for diabetes

A

no

83
Q

complications of diabetes

A

hypertension, stroke, kidney failure, blindness, amputation of foot/leg

84
Q

risk factors of type 2 diabetes

A

family history, high cholesterol, high blood pressure, obesity, race, ethnicity

85
Q

what diabetes is more common

A

type 2

85
Q

what diabetes is more common

A

type 2

86
Q

how does hypertension affect the heart

A

thickening of heart muscles and narrowing of blood vessels
- can cut off blood supply to the heart = heart attack

87
Q

how does hypertension affect the kidneys

A
  • affects ability to filter and clean blood = kidney failure
  • affects glomerular filtration
88
Q

how does hypertension affect the eye

A

affects the arteries supplying the retina can lead to complications such as blurred vision

89
Q

how does hypertension affect the brain

A

stroke, slurred speach, paralysis, loss of consciousness

90
Q

signs and symptoms of asthma

A
  • cough, wheeze, tight chest, shallow breathing
  • increased mucus production
91
Q

chemical cell injury

A

toxins, metabolic, medications, drugs

92
Q

key stages of cell apoptosis

A
  1. Cell not functioning adequately, activating suicide genes
  2. Chromatin condensation in nucleus, cell shrinks
  3. Biochemical breakdown of enzymes
  4. Blebs are formed
  5. Fragmentation leading to formation of apototic bodies
  6. Cell breaks down into fragments, is clean and doesn’t affect surrounding cells
  7. Release of chemical mediators to attract phagocytes
  8. Phagocytes contain apototic bodies and remove it from the area
  9. Cell loses survival signals and can no longer function
93
Q

what are the blood constituents involved in clotting

A

platelets and prothrombin

94
Q

keys stages in clotting

A
  1. Vasospasm reduces blood flow and facilitates platelet aggregation and coagulation
  2. Platelet aggregation and the formation of a platelet plug to arrest bleeding
  3. Fibrin clot arrests bleeding until the vessel is repaired
  4. After vessel repair clot is removed by the process of fibrinolysis (dissolution of fibrin)
95
Q

vasospasm

A

narrowing of the arteries caused by persistant contraction of the blood vessel

96
Q

vitamin K and clotting

A

Vitamin K = more clotting factor = more clotting
Increase in vit k = increase in clots
Decrease in vit k = hemorrage

97
Q

key features of acute inflammation

A
  1. Increased blood flow:
  2. Increased capillary permeability:
  3. Migration of neutrophils:
  4. Chemotaxis:
  5. Leukocyte recruitment & activation
98
Q

key features of chronic inflammation

A
  1. Infiltration of Mononuclear phagocytic cells:

Activated by numerous cytokines
Infiltration of lymphocytes- T & B cells:

  1. Tissue destruction:
  2. Tissue repair Angiogenesis at the injured sites Formation of granulomas
    Fibrosis
99
Q

chemotaxis

A

movement of neutrophils to the injurious agent

100
Q

The chemotactic factor affects the inflammatory process by:

A

Directing leukocytes to the inflamed area

101
Q

two chemotactic factors

A

neutrophil chemotactic factor (NCF) and eosinophil chemotactic factor of anaphylaxis (ECF-A), are released during mast cell degranulation. NCF attracts neutrophils (a type of leukocytes), and ECF-A attracts eosinophils to the site of inflammation.

102
Q

what type of immunity Is acute inflammation

A

innate immunity

PATH1000 (8 decks)

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