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HSC2008 Pathology & Pharmacology > Week 1 > Flashcards

Week 1 Flashcards

1
Q

body defense system

A
  1. non-specific / general
  2. specific
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2
Q

what mediates specific defense system

A

B-cells = humoral immunity = antigen specific ABs

T-cells = cell-mediated immunity = triggers apoptosis in infected cells

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3
Q

irreversible injury leads to __

A

necrosis & apoptosis

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4
Q

cellular adaptation types

A

Hand HM

  1. hyperplasia
  2. atrophy
  3. neoplasia
  4. dysplasia
  5. metaplasia
  6. hypertrophy
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5
Q

atrophy

A

size reduction

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6
Q

hyperplasia

A

increase in number of cells due to cell proliferation stimulation

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7
Q

hypertrophy

A

increase in cell size

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8
Q

metaplasia

A

healthy mature cells replaced by different kind of mature cells in same tissue such as changes in morphology & function

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9
Q

dysplasia

A

abnormal growth of other cells types within tissues

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10
Q

neoplasia

A

uncontrolled growth of tissues which may be malignant

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11
Q

cell injury causes

A

genetics, environment, infections, damage, foreign body, electrolyte imbalance

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12
Q

phases of repair in acute wound healing

A

hemostasis > inflammation > proliferation > remodeling

HIPR

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13
Q

how long does inflammation take

A

0.1 - 10 days after wounding

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14
Q

how long does cell proliferation & matrix deposition

A

1 - 30 days

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15
Q

how long does matrix remodeling occur

A

1 - 300 days

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16
Q

hemostasis

A

clot formation to stop bleeding

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17
Q

primary vs secondary hemostasis

A

primary = initial clot to form primary platelet plug

secondary = strengthening clot via coagulation cascade such as fibrinogen > fibrin

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18
Q

aim of inflammation

A
  1. eliminate initial cause of injury
  2. initiate repair process
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19
Q

inflammatory response steps

A
  1. injury
  2. chemical mediators released
  3. vasodilation
  4. increased capillary permeability
  5. leukocytes move to injury
  6. phagocytosis
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20
Q

list 2 hormones that promote inflammation

A

bradykinin & histamine

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21
Q

vascular events of acute inflammation

A

redness > head > swelling > pain

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22
Q

erythema

A

redness of skin

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23
Q

cellular events of acute inflammation

A

fluid exudation > stasis > margination > diapedesis > chemotaxis

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24
Q

stasis

A

RBC engorgement in vessels

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25
Q

margination

A

WBC accumulate & adhere to vessel wall

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26
Q

diapedesis

A

oozing of WBC out of blood vessel

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27
Q

chemotaxis

A

directional migration of WBC to injury site

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28
Q

leukocyte examples

A

neutrophils, basophils, eosinophils

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29
Q

neutrophil function

A

microbe phagocytosis

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30
Q

basophil function

A

histamine release causing inflammation

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31
Q

eosinophils function

A

enhances allergic response

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32
Q

lymphocyte examples

A

T-cells, B-cells, macrophages

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33
Q

T-cell function

A

activates cell mediated immune response

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34
Q

B-cell function

A

antibody production

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35
Q

macrophages function

A

matured monocytes for phagocytosis

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36
Q

how is injury cause eliminated during inflammation

A

degradation & removal of necrotic tissue via neutrophils & macrophages

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37
Q

how does differential count assist with inflammation diagnostic testing

A

distinguish type of bacterial infections

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38
Q

high eosinophil count indicates

A

allergic response

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39
Q

high neutrophil count indicates

A

pyogenic bacterial infection

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40
Q

high lymphocyte count indicates

A

viral infection

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41
Q

high basophil count indicates

A

parasitic infection

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42
Q

how does cell enzymes assist with inflammation diagnostic testing

A

locate site of necrotic cells

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43
Q

what parameters are monitored for inflammation screening

A

plasma proteins, C-reactive proteins, increased ESR

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44
Q

what parameters are unable to determine site of inflammation

A

plasma proteins, C-reactive proteins, increased ESR

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45
Q

when does C-reactive protein production increase in blood

A

24-48hrs

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46
Q

anorexia

A

appetite loss

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47
Q

characteristic differences between acute & chronic inflammation

A

A has more exudation & swelling than C
A involves migration of leukocytes but C has more presence of lymphocytes, macrophages, fibroblasts
C has more severe damage and scar tissue than A

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48
Q

causes of chronic inflammation

A

persistent infection, persistent indigestible material, immune mediated reactions, repeated/continuous acute inflammation

PRIP

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49
Q

acute management of inflammation

A

RICE = rest, ice, compression, elevation

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50
Q

non selective COX inhibitors

A

Naproxen + ibuprofen

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51
Q

selective COX inhibitors

A

Diclofenac, Etoricoxib

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52
Q

Arachidonic Acid breaks down into

A

COX-1 & COX-2

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53
Q

which COX is present in normal tissues

A

COX-1

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54
Q

which COX is induced during inflammation

A

COX-2

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55
Q

what are the products of COX-1

A

PGI2 & TXA2

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56
Q

PGI2 function

A

Gastric protection

57
Q

TXA2 function

A

platelet function

58
Q

what are the products of COX-2

59
Q

PGE2 effects

A

pain, inflammation, fever

60
Q

which inflammatory stimuli stimulates COX-2

61
Q

which anti-inflammatory stimuli controls COX-2

62
Q

pharmacological effects of NSAIDs

A

anti-inflammatory, anti-pyretic, analgesic

63
Q

how do NSAIDs have anti-inflammatory effect

A

decrease synthesis of prostaglandins involved in increasing vasodilation

64
Q

how do NSAIDs have anti-pyretic effect

A
  • inhibits COX-2 in hypothalamus
  • IL-1 stimulates prostaglandins in hypothalamus which increases body temp
65
Q

how do NSAIDs have analgesic effect

A

reduces peripheral prostaglandin synthesis which sensitizes nociceptors to inflammatory mediators

66
Q

diff ways to administer glucocorticoids

A
  • PO; orally
  • intramuscularly
  • intravenous
  • topical
  • inhalation
  • rectal
  • inject into joints
67
Q

anti-inflammatory mechanisms of glucocorticoids

A

inhibits NKfB = inhibits production of inflammatory cytokines, chemokines, adhesion molecules

inhibits phospholipase A2 & cox enzyme = decreases PG, thromboxane production

increases transcription of anti-inflammatory

68
Q

ASA

A

aminosalicyclic acid

69
Q

ASA mechanism of anti-inflammatory action

A

irreversibly inhibits COX-1 & 2

weakly selective to COX-1

70
Q

Acetaminophen mechanism of anti-inflammatory action

A

selective COX-2 inhibitor property

71
Q

NSAID mechanism of anti-inflammatory action

A

competitive inhibitor of COX-1 & 2

both ibuprofen & naproxen weakly selective to COX-1

72
Q

glucocorticoids mechanism of anti-inflammatory action

A

inhibits NFkB

increases transcription of anti-inflammatory proteins, IL-1 antagonist, & IL-10

73
Q

COX-2 mechanism of anti-inflammatory action

A

competitive COX-2 inhibitor at therapeutic dose

74
Q

NSAID

A

non-steroid anti-inflammatory drug

75
Q

common synthetic corticosteroids

A

cortisone/hydrocortisone
prednisone/prednisolone
dexamethasone
betamethsaone

76
Q

half life of cortisone/hydrocortisone

77
Q

half life of prednisone / prednisolone

A

12 - 36 hrs; 5x more potent than hydrocortisone

78
Q

half life of dexamethasone

A

36 - 72 hrs; 25x more potent than hydrocortisone

79
Q

half life of betamethasone

A

36 - 72 hrs; used topically to manage skin inflammation

80
Q

3 Rs of healing

A

resolution, regeneration, replacement

81
Q

tissue healing is achieved by __

A

cell regeneration & replacement process

82
Q

resolution happens in tissues that are ___

A

capable of regeneration with intact extracellular matrix framework

83
Q

regeneration occurs by

A

replacement of damaged tissue by identical tissue via mitosis

84
Q

replacement occurs when __

A

tissues cannot regenerate and replaced by connective tissue scars

85
Q

types of tissues

A

labile, stable, permanent

86
Q

what are labile tissues

A

stem/undifferentiated cells

87
Q

what are stable tissues

A

normally low proliferative activity unless stimulated to

88
Q

what are permanent tissues

A

left cell cycle and cannot proliferate

89
Q

cell proliferation process

A

granulation tissue formation > collagen synthesis + laydown by fibroblasts

90
Q

what is granulation tissue metabolically active with

A

angiogenesis & fibroblast proliferation

91
Q

key building blocks of tissue healing

A

fibronectin, proteoglycans, elastin, collagen

92
Q

function of fibronectin + proteglycans

A

forms scaffolding that provides tensile strength and glues cells together

93
Q

function of elastin

A

cross linking to form fibrils that provide tissue elasticity

94
Q

function of collagen

A

structural support & tensile strength; main determinant of structural stability of extracellular matrix

95
Q

MMP

A

matrix metalloproteinases

96
Q

type of collagen for early & late scars

A

early = type III
late = type I

97
Q

3 determinants of complete healing

A

tissue type, injury nature, extent of injury

98
Q

difference between necrosis & apoptosis in terms of cell size

A

n = enlarged
a = reduced

99
Q

difference between necrosis & apoptosis in terms of nucleus

A

n = clumped
a = fragmented

100
Q

difference between necrosis & apoptosis in terms of plasma membrane

A

n = disrupted
a = intact

101
Q

difference between necrosis & apoptosis in terms of cellular content

A

n = enzymatic digestion
a = intact & packaged into apoptatic body

102
Q

difference between necrosis & apoptosis in terms of inflammation

A

n = frequent
a = none

103
Q

difference between necrosis & apoptosis in terms of causes

A

n = pathological
a = physiological & pathological

104
Q

coagulate necrosis

A

coagulation of dead cells

105
Q

liquefactive

A

liquidifcation of dead cells

106
Q

gangrenous

A

lack of blood supply

107
Q

caseous

A

cheese-like necrosis

108
Q

factors affecting healing

A

age, nutrition, circulation, existing tissues

109
Q

when does collagen synthesis & fibroblast laydown occur

A

3-5 days post injury & continues for weeks depending on wound size

110
Q

as collagen mass increases, cellularity & vascularity __

111
Q

what specific plasma proteins do we look out for during diagnostic testing for inflammation

A

fibrinogen & prothrombin

112
Q

what happens when COX-2 selective NSAIDs inhibit COX-2

A

decreased gastric & platelet function

113
Q

analgesic

A

pain relief

114
Q

pyretic

115
Q

other effects of glucosteroids

A
  • increased blood sugar
  • decreased serotonin, immunity, Ca2+ absorption
  • regulates metabolism
  • retains Na+
116
Q

vascular events of injury

A

vasodilation & capillary permeability

117
Q

cellular events of injury

A

leukocyte migration, phagocytosis

118
Q

which process is important for recovery & mobility

A

cell proliferation

119
Q

examples of labile cells

A

epithelial, hemopoietic stem cells

120
Q

examples of stable cells

A

parenchymal / mesenchymal cells

121
Q

examples of permanent tissues

A

skeletal / cardiac cells

122
Q

what are essentials for recovery

A

Protein, Vitamin A & C

123
Q

exacerbation

A

disease worsens

124
Q

sequelae

A

unwanted outcome of primary condition

125
Q

healing process

A

blood clot > inflammation > granulation tissue formation > epithelial regeneration > fibroblast laying collagen fibers > angiogenesis > cross-linking & realigning collagen fibers

126
Q

pyknosis

127
Q

karyorrhexis

A

fragmented

128
Q

karyolysis

A

dissolution

129
Q

clean vs dirty cell death

A

clean = apoptosis
dirty = necrosis

130
Q

remodelling primarily mediated by __

A

matrix metalloproteinases

131
Q

which enzyme indicates myocardial infarction

A

CK-MB isoenzyme

132
Q

which enzyme indicates liver

133
Q

adverse effects of NSAIDs

A

GI distress, stomach ulceration, allergies, blood clot delays

134
Q

adverse effects of ASA

A

GI distress, stomach ulceration, allergies, blood clot delays

135
Q

adverse effects of glucocorticoids

A

GI distress, stomach ulceration, allergies, blood clot delays, increased risk of infection, edema, increased BP

136
Q

adverse effects of acetaminophen

137
Q

which drug has no anti-inflammatory effect

A

acetaminophen

138
Q

which drug has no anti-pyretic & anti-analgesia

A

glucocorticoids

139
Q

which synthetic glucocorticoid is used topically for skin condition

A

betamethasone

HSC2008 Pathology & Pharmacology (14 decks)

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