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PATH2220 > W2 > Flashcards

W2 Flashcards

1
Q

what is the definition of inflammation

A

the response of living tissue to injury (only living tissue)

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2
Q

describe inflammation

A

Goal is to bring leukocytes and plasma proteins normally circulating in blood to the site of infection or tissue damage to eliminate the agent and initiate healing

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3
Q

what is the desirable outcome of inflammation

A

to reverse tissue damage resulting from injury by enabling elimination of injurious material and organisms

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4
Q

what is the onset for acute inflammation

A

fast, minutes, hours

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5
Q

what is the onset for chronic inflammation

A

slow, days, months years,

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6
Q

what cells are involved in acute inflammation

A

mainly neutrophils

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7
Q

what cells are involved in chronic inflammation

A

monocytes, macrophages, lymphocytes

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8
Q

what sort of tissue damage or injury is involved in acute inflammation

A

mild, self-limited

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9
Q

what sort of tissue damage or injury is involved in chronic inflammation

A

often severe, progressive

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10
Q

is there local or systemic signs of acute inflammation

A

yes

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11
Q

is there local or systemic signs of chronic inflammation

A

no

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12
Q

what is an example of a common inflammatory condition

A

skin furuncle (boil), inflammation of the skin caused by staphylococcus

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13
Q

what are the four cardinal signs of inflammation

A

rubor (redness)-increased blood flow, calor (heat)-increased blood flow, tumour (swelling)- leakage of cells and fluid into tissues, dolor (pain)- increased nerve sensitivity due to chemical mediators

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14
Q

what is the 5th cardinal sign of inflammation and who was it added by

A

virchow in the 19th century, function laesa (loss of function

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15
Q

what are the causes of inflammation

A

physical agents, chemical agents, foreign bodies, infective agents, tissue necrosis (death), immune reactions

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16
Q

what are some examples of physical agents

A

trauma, heat, cold

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17
Q

what are some examples of foreign bodies

A

dirt, splinters, suture material

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18
Q

what are some examples of infective agents

A

bacteria, viruses and parasites

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19
Q

what are some examples of immune reactions

A

allergic, hypersensitivity

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20
Q

what is the first step in inflammation

A

harmful stimulus releases chemical agents, such as chemicals from damaged cells

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21
Q

what is the second step in inflammation

A

Recognition of signal by receptors on host cells (macrophages e.g.) initiates production of numerous proteins (mediators) which act on blood vessels and hot cells to produce inflammatory reaction

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22
Q

what is the third step in inflammation

A

response is down regulated, short-lived and self sustained

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23
Q

what are the two components of inflammation

A

vascular and cellular

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24
Q

increased blood flow is an example of vascular changes in inflammation (true or false)

A

true

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25
Q

what is swelling the result of

A

increase hydrostatic pressure, leads to increase permeability and active emigration of white blood cells

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26
Q

define exudate

A

protein and cell-rich fluid that accumulates in interstitial tissue in inflammation

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27
Q

what is the process of exudation

A

passage of fluid and protein from vessels to interstitial tissues

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28
Q

what are early mediators of acute inflammation

A

histamine and seretonin

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29
Q

what role does histamine and seretonin play

A

release brings about activation of endothelial cells and complement cascade

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30
Q

what occurs first out of vascular and cellular events

A

vascular but both happen together

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31
Q

what are cellular events in inflammation

A

recruitment of leukocytes to site of infection and injury, leukocyte migration through endothelium, migration of leukocytes to site of injury (chemotaxis), recognition by phagocytes of microbes and dead tissue, removal of offending agent (by phagocytosis, engufment, killing and degradation), other responses of leukocytes, initiation of repair process

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32
Q

what is chemotaxis

A

the movement of leukocytes after emigration towards an increasing concentration of a chemotactic agent (usually and protein or polypeptide)

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33
Q

what is phagocytosis

A

process by which neutrophils and macrophages ingest debris and foreign particles including bacteria

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34
Q

what are the three steps of phagocytosis

A
  1. Recognition and attachment- specific receptors on surface of macrophages, mannose receptors binds to mannose, fructose on bacteria. 2. Engulfment- pseudopods form around organism, fusion with lysosomes and release of lysosomal contents 3. killing and degradation- reactive oxygen species, hydrogen peroxide, nitric oxide
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35
Q

describe neuotrophils in phagocytosis

A

last 1-2 days, lysosomal contents discharged into vacuole, oxidising agent kill or digest bacteria, neutrophil degranulated in process (released enzymes may causes injury), virulent bacteria may resist disintegration, bacteria liberated as cell dies and could cause more damage

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36
Q

describe macropahges in phagocytosis

A

successful kill may be accomplished, if bacteria persist may remain in site or move via lymphatic to other areas, all debris including dead polymorphs gradually removed, antigenic material presented to immune system, release of enzymes, oxidising agents into tissue may cause ongoing damage such as rheumatoid disease

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37
Q

what is the ideal outcome of inflammation

A

the harmful agent will be removed or killed and the damaged tissue will return to normal

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38
Q

when is resolution most likely to occur

A

when cell death and tissue damage is minimal, when damaged cells are capable of regeneration, when causative organism is rapidly eliminated, where local conditions favour removal or exudate

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39
Q

what is the process of resolution

A

fibrin and other proteins dissolved by fibrinolysin and enzymes from neutrophils and macrophages, fluid removed in blood and lymphatic vessels, removal of all debris by phagocytes to lymph nodes blood flow return to normal

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40
Q

what are the different classifications of inflammation

A

acute or chronic, according to the site such as appendix= appendicitis and according to predominate component of exudate that varies with what is causing reaction and the tissue involved.

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41
Q

what is the following exudate and where is it usually found: catarrhal

A

mucus, common cold

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42
Q

what is the following exudate and where is it usually found: serous

A

clear watery fluid, blister

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43
Q

what is the following exudate and where is it usually found: fibrinous

A

firbin, pleurisy

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44
Q

what is the following exudate and where is it usually found: suppurative

A

pus (otherwise known as purulent), abscess

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45
Q

what is the following exudate and where is it usually found: haemorhagic

A

red blood cells - fatal influenza

46
Q

what is the following exudate and where is it usually found: granulamatous

A

modified macrophages often with giant cells such as tuberculosis

47
Q

what is suppuration

A

formation of pus

48
Q

describe pus

A

an accumulation of dead and living neutrophils, dead and living bacteria (when inflammation caused by pyogenic bacteria), protein and other particulate matter

49
Q

what is an abcess

A

a pus-filled cavity

50
Q

what is an empyema

A

an accumulation of pus in a naturally occurring body cavity

51
Q

what is suppurative meningitis

A

pus found in sub-arachnoid space

52
Q

describe the evolution of an abscess

A

starts an an inflammatory exudate with many neutrophils.
proteins, bacteria and polymorphs aggregate to form a mass.
Tissue death ensues, new capillaries and fibroblasts develop at edge of accumulated material (process of organisation)., pus resorbed (if small amount) or can burst onto point to external surface (sinus) or adjacent body cavity (fistula) and may be discharged, collagen deposition process to formation of mature scar

53
Q

what are examples of acute inflammation in the lung

A

lobar pneumonia and bronchopneumonia

54
Q

describe lobar pneumonia

A

caused by streptococcus pneumonia, alveolar spaces file with exudate- neutrophils, crib, dead bacteria, it can return to normal

55
Q

what are the outcomes of lobar pneumonia

A

resolution, abscess formation, empyema, fibrosis and scarring, septicaemia and death

56
Q

what is septicaemia

A

blood poisoning, especially that caused by bacteria or their toxins.

57
Q

what is consolidation referring to pathology

A

filling up of lung area with inflammatory products

58
Q

what is bronchopneumonia

A

patchy distribution related to bronchi, abscess formation complicating pneumonia.

59
Q

describe chronic inflammation

A

inflammation enduring longer than acute inflammation, may be primary but often results from acute inflammation when causative agent can be resolved, polymorphs (neutrophils) largely replaced by lymphocytes, plasma cells (and macrophages). Macrophages often fuse to form giant cells, often proliferation of vascular endothelium and fibroblasts, fibrosis

60
Q

what is an example of a chronic inflammatory reaction

A

chronic peptic ulcer and tuberculosis

61
Q

describe a chronic peptic ulcer

A

occurring in an area of acid pepsin digestion, commonly stomach, duodenum, oesophagus, often associated with helicobacter pyloric infection, inflamed area surrounded by mature collagen.

62
Q

what are the outcomes of a chronic peptic ulcer

A

resolution (rare without appropriate therapy), haemorrhage (due to erosion, usually shown by vomitting), fibrosis, perforation, penetration, malignant transformation can happen but very rare.

63
Q

what causes tuberculosis

A

mycobacterium tuberculosis

64
Q

what sort of inflammation is involved in tuberculosis

A

granulomatous inflammation, also giant cells and epithelia macrophages

65
Q

what is at the site of injury or infection first

A

neutrophils

66
Q

what do neutrophils looks like

A

the nucleus as three lobes

67
Q

what is pus

A

protein-rich fluid produced as a product of inflammation

68
Q

what comprises of pus

A

leuokocytes (white blood cells), debris from dead cells, tissue elements which have been liquified by the action of neutrophil enzymes

69
Q

what is the bateria that causes pus called

A

suppurative, pyogenic or purulent

70
Q

what is the stratum corneum

A

dead keratocytes (always shed and replaced)

71
Q

what is impetigo

A

acute superficial infection of the skin, most common bacterial skin infection of childhood,

72
Q

what adults are more susceptible to impetigo

A

athletes, military and institutions

73
Q

what are predisposing factors to impetigo

A

minor trauma, poor hygiene and warm, humid climate

74
Q

what is the organism that usually causes impetigo

A

staphylococcus aureus (may produce exfoliative toxins)

75
Q

what are the two types of impetigo

A

common impetigo and bullous impetigo

76
Q

describe common impetigo

A

school sores, thin walled vesicles or pustules, rupture to form thick golden crust and solitary or clustered, found in face or extremities

77
Q

describe bullous impetigo

A

erosions and flaccid ballae, caused by an exotoxin which results in karatinocytes falling apart and blister formation

78
Q

what is staphylococcal scalded skin syndrome

A

another blistering disorder caused by staphylococcus aureus, but different mechanism. widespread blisters that rupture easily,

79
Q

what does staphylococcal scalded skin syndrome occur in (who)

A

infants

80
Q

is there bacteria in blisters of staphylococcal scalded skin syndrome

A

no

81
Q

what is staphylococcal scalded skin syndrome caused by

A

an endotoxin that is made by the bacteria elsewhere and is transported via the bloodstream

82
Q

what is acne vulgaris

A

pimples, an inflammtory disorder of the pilosebaceous unit (the hair follicle and attached sebaceous gland),

83
Q

is acne vulgaris common

A

yes

84
Q

who does acne vulgaris usually affect

A

teenagers

85
Q

what are the clinical appearances of acne vulgaris

A

the lesions that make up acne are variable and include: comedones, papules, pustules, cysts, sinuses and scars

86
Q

what are comedones

A

widened hair follicles which are filled with keratin, other debris, bacteria and sebum. closed are whiteheads and open are blackheads.

87
Q

what are papules

A

lumbs

88
Q

what are pustules

A

lumbs and pus

89
Q

what are cysts

A

big bags of pus

90
Q

what are the the four interrelated factors of acne (pathogenesis of acne)

A

abnormal follicular keratinisation, with retention of keratin within the follicle (this process if the precursor for comedome formation, may be aided by bacterial ‘biofilm’). increased sebum production (androgens), presence of bacteria and inflammation

91
Q

what are the steps of acne development

A

ongoing dilution of the comedome leads to the wall becoming very thin, eventually ruptures. the keratin, sebum and bacteria incite an acute inflammatory response. Predominatly neutrophils first (pulsatile formation), followed by granulamatous inflammation and fibrosis (scarring), the acute inflammatory focus can enlarge into an abscess. Sinus tracts result when the epidermis grows down in an attempt to “wall off” the inflammation.

92
Q

what is superficial folliculitis

A

typically affects the superficial part of the hair follicle , called the infundibulum (thus perhaps more correctly should be called infundibulitis). may be related to bacterial infection. neutrophils under the status corneum and around the infundibulum, pseudofolliculitis is a term used to describe a foreign body response to hair shafts that have ruptured out of the follicle into surrounding dermis

93
Q

what is furnacle

A

boils, a deeper infectious inflammatory process centered on the pilosebaceous unit,

94
Q

where is the typical location of a furnacle

A

the back of the neck, buttocks and thighs (sites of friction with clothing),

95
Q

how does furnacle start

A

painful papule with surrounding erythema (redness) and swelling, the centre becomes soft and yellow and may discharge pus

96
Q

what are the causes of furnacle

A

often bacterial, usually staphylococcus aureus, pseudomonas, aeruginosa is associated with hot rub folliculitis (develops 8-48 hours after recreational exposure to the organisms, which is found contaminated spas

97
Q

what is erysipelas

A

erysipelas s an acute inflammatory process within the dermis which is usually caused by streptococcus progenies, often accompanied by a fever,

98
Q

what are the most affected in erysipelas

A

face, feet, hand and lower limbs are most affected,

99
Q

what is cellulitis

A

same as erysipelas but a bit deeper, more often occurs in the legs

100
Q

what are the causing factors of erysipelas and cellulitis

A

minor trauma, peripheral vascular disease, diabetes, lymphoedema, alcohol disease,

101
Q

explain resolution

A

removal of exudate, regeneration of tissue if possible, complete return to normal

102
Q

explain repair

A

occurs when resolution impossible (severe, ongoing damage, or tissue cannot regenerate), involves formation of granulation tissue (organisation). Maturation of granulation tissue to scar tissue (fibrosis)

103
Q

what is the definition of organisation

A

the growth of new capillaries and fibroblasts into the damaged tissue together with migration of macrophages. Macrophages remove debris, fibroblast lay down collagen

104
Q

what is the healing by primary intention

A

occurs in clean incised wound with apposed edges (e.g. surgical wounds). Results minimal scarring, occurs in shorter time (mainly healed in a week or two - stitches removed), strengthening, devascularization continues longer

105
Q

what is healing by secondary intention

A

occurs in open wounds (loss of tissue, necrosis or infection), often results in significant scarring (fibrosis), process may continue for months to years

106
Q

outline the process in healing by primary intention

A

immediate: cavity fills with fibrin and blood. 2-3 hours: minor inflammation. 2-3 days: macrophages, fibroblast activity, new vessels oration (i.e. minimal granulation tissue). 10-14 days: re-epithelialisation complete, weak fibrosis union, weeks: good fibrous union continues strengthening for months to years. Devasculariztion. minimal scarring

107
Q

outline the process in healing by secondary intention

A

immediate: large cavity fills with blood and fibrin. Acute inflammation begins. days: epithelium begins to regenerate to cover lesion. overlying scab. Contraction of wound. New capillary loops form, bring macrophages, neutrophils (prominent granulation tissue). Fibroblasts proliferate. weeks- months- epithelium restored, collagen bundles thickened. Often extensive scarring

108
Q

what is fibrosis

A

end result of organisation in would healing and chronic inflammation

109
Q

what is the process of fibrosis

A

fibrocytes stimulated by polypeptides from surrounding damaged cells become active fibroblasts. Commence protein synthesis. Secretion of ground substance including fibrinonectins. Secretion of procallage. condensation to fine reticulin fibres, binding and weaving to form scar tissue, fibroblasts revert to fibrocytes

110
Q

what are the local factors that adversely affect wound healing

A

poor blood supply, infection, excessive movement or irritation, foreign material

111
Q

what are the general factors that adversely affect would healing

A

defiency of vitamin C, essential amino acids and zinc. Excess adrenal corticosteriod, intercurrent debilitating chronic disease

112
Q

what are complications of wound healing

A

excess collagen formation (keloid) and excess epithelial proliferation

PATH2220 (14 decks)

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