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Patho & Pharmo > Inflammation and Wound Healing > Flashcards

Inflammation and Wound Healing Flashcards

1
Q

Three lines of defense

A
  1. Mechanical barriers and body secretions.
  2. Phagocytosis, inflammation, and interferons.
  3. Immune response, very specific.
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2
Q

Phagocytosis

A

Process by which neutrophils and macrophages randomly engulf and destroy bacteria, cell debris, or foreign matter

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3
Q

Interferons

A

nonspecific agents that protect uninfected cells against viruses

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4
Q

Immune response

A

stimulates the production of unique antibodies or sensitized lymphocytes following exposure to specific substance

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5
Q

inflammation

A

Body’s nonspecific response to tissue injury, resulting in redness, swelling, warmth, pain, and sometimes the loss of function

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6
Q

suffix for inflammation

A

-itis

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7
Q

Acute inflammation

A

Occurs rapidly in reaction to cell injury, rids the body of the offending agent, enhances healing, and terminates after a short period. Hours or days.
Prevents the spread of infection with antibodies or other chemicals.
Attempts to wall off, destroy, and digest bacteria and dead or foreign tissue.
After insult is contained, repair can begin.

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8
Q

Chronic inflammation

A

May develop following an acute episode of inflammation when the cause is not completely eradicated.

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9
Q

Examples of chronic inflammation

A

Smoking, certain bacteria, or long-term abnormal immune response.

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10
Q

Granulocytes

A

Neutrophils
Basophils
Eosinophils

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11
Q

Agranulocytes

A

Lymphocytes
Monocytes

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12
Q

Arrive first at the site of cell injury, are the most numerous leukocyte, are part of the innate immune system.

A

Neutrophils

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13
Q

Active in allergic responses ,releasing their stores of inflammatory chemicals including histamine, serotonin, and leukotrienes. Contain heparin. Fight parasitic infections

A

Basophils

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14
Q

Active in larger parasitic infections, allergy responses, and some cancers

A

Eosinophils

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15
Q

B (humoral), T (cell mediated), and Natural Killer (NK) Cells
Identify and destroy foreign invaders
Found in lymph and blood
NK cells defend against tumors and viruses

A

Lymphocytes

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16
Q

Largest WBC; differentiates into macrophages that clean up cellular debris in the inflammatory process

A

Monocytes

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17
Q

Cytokines

A

short-lived proteins that are released by one cell as intracellular messengers

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18
Q

inflammatory mediators

A

send out signals, enabling the blood vessels to dilate and become more permeable, allowing fluids, WBC to enter

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19
Q

three stages of acute inflammation

A
  1. vascular permeability
  2. cellular chemotaxis
  3. systemic responses
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20
Q

WBC line up along endothelium when arriving at site of injury

A

margination

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21
Q

Three outcomes of acute inflammation

A

Complete resolution
Healing by connective tissue
Chronic, persistent inflammation that does not recede

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22
Q

Complete resolution of acute inflammation

A

normalization of vascular permeability
deactivation of chemical mediators
elimination of cellular debris and edema
apoptosis of WBC

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23
Q

Healing by connective tissue acute inflammation

A

In tissues that cannot regenerate cells or exudates and cellular debris cannot be adequately cleared.
Cellular debris and exudates are instead reabsorbed and fibrous scar tissue replaced damaged cells.

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24
Q

Characteristics of chronic inflammation

A

less swelling, more lymphocytes, macrophages, fibroblasts, more collagen

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25
Q

small mass of cells with necrotic center, covered by connective tissue

A

granuloma

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26
Q

local complications of chronic inflammation

A

depend on the site of the inflammation

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27
Q

infection complications of chronic inflammation

A

microorganisms can more easily penetrate when the skin or mucosa is damaged and the blood supply is impaired.

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28
Q

skeletal muscle spasms

A

result by inflammation from musculoskeletal injuries. can cause additional pressure on the nerves, increasing pain.

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29
Q

chemicals released during acute inflammation

A

histamine, kinins, prostaglandins

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30
Q

cardinal signs of inflammation

A
  1. Redness and heat- increased blood flow into the damaged area (erythema)
  2. Swelling- shift of protein and fluid into the interstitial space.
  3. Pain- increased pressure of fluid on the nerves and by local irritation of nerves by chemical mediators.
  4. Loss of function- cells lack nutrients or swelling interferes mechanically with function.
  5. Exudate- collection of interstitial fluid formed in the inflamed area. The characteristics of the exudate vary with the cause of the trauma.
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31
Q

Clinical cellulitis

A

Erysipelas

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32
Q

Exudation of inflammation (5)

A
  1. Serous
  2. Fibrinous
  3. Purulent
  4. Abscess
  5. Hemorrhagic
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33
Q

Examples of serous exudates

A

allergic reactions or burns. primarily of fluid with small amounts of protein and WBC.

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34
Q

Fibrinous exudate

A

thick and sticky, have high cell and fibrin content. Increases the risk of scar tissue in the area.

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35
Q

Purulent exudates

A

thick, yellow-green in color, contain more leukocytes and cell debris and microorganisms. Indicates bacterial infection.

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36
Q

Abscess

A

Localized pocket of purulent exudate or pus in a solid tissue. Around a tooth or in the brain

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37
Q

Hemorrhagic exudate

A

present if blood vessels have been damaged.

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38
Q

Systemic responses of inflammation

A

Pyrexia.
Malaise.
Fatigue.
Headache.
Anorexia.
Weight loss.
Lethargy/sleepiness.
Lymphadenopathy.

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39
Q

Common systemic effect if inflammation is extensive, microbial organisms bacterial products and cytokines act as pyrogens

A

Pyrexia

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40
Q

Agents that cause fever

A

Pyrogens

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41
Q

Where is the body temperature control system

A

Hypothalamus

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42
Q

Cells that mature inside the lymph nodes

A

Lymphocytes

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43
Q

Increased number of white cells in the blood

A

leukocytosis

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44
Q

measures the rate at which red blood cells precipitate out of the plasma, indicating damage to these cells during the inflammation process

A

erythrocyte sedimentation rate (ESR)/ sed rate

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45
Q

C-reactive protein (CRP)

A

produced by the liver, also indicating presence of inflammation

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46
Q

High WBC, 90% neutrophils

A

bacterial infection

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47
Q

High WBC, 90% lymphocytes

A

viral infection

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48
Q

immature neutrophils

A

bands - present in patients with leukocytosis

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49
Q

increased number of bands

A

acute inflammatory process

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50
Q

increased number of white blood cells, especially neutrophils

A

leukocytosis

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51
Q

proportion of each type of white blood cell altered, depending on the cause

A

differential count

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52
Q

Increased fibrinogen and prothrombin

A

plasma proteins

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53
Q

a protein not normally in the blood, but appears with acute inflammation and necrosis within 24-48 hours.

A

C-reactive protein

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54
Q

Elevated plasma proteins increase the rate at which red blood cells settle in a sample

A

Increased erythrocyte sedimentation rate

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55
Q

released from necrotic cells and enter tissue fluids and blood: may indicate the site of inflammation

A

cell enzymes

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56
Q

COX-1 inhibitors protect against

A

myocardial infarction and stroke

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57
Q

other first-generation NSAIDs inhibit

A

COX-1 and COX-2

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58
Q

Non-aspirin NSAIDs cause __ inhibition

A

reversible

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59
Q

Ibuprofen is the prototype of

A

Propionic acid derivatives

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60
Q

severe hypersensitivity reaction that causes blistering of the skin and mucous membranes, can result in scarring, blindness, and death

A

Stevens-Johnson syndrome

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61
Q

rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, mild pain, primary dysmenorrhea, and migraine

A

diclofenac

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62
Q

This NSAID can cause fluid retention, which can exacerbate hypertension and heart failure.

A

Diclofenac

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63
Q

NSAID for arthritis, bursitis, tendinitis, and acute gouty arthritis

A

Indomethacin

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64
Q

Given IV to preterm infants to promote closure of the ductus arteriosus

A

Indomethacin

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65
Q

Can cause frontal headache, CNS effects, seizures and psychiatric changes, GI effects, hematologic reaction

A

Indomethacin

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66
Q

Powerful analgesic with minimum anti-inflammatory actions

A

Keterolac

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67
Q

Pain relief is equivalent to morphine and other opioids

A

ketorolac

68
Q

Usual indication for ketorolac

A

Postoperative pain

69
Q

Approved only for rheumatoid arthritis and osteoarthritis

A

piroxicam

70
Q

Half-life of 50 hours

A

Piroxicam

71
Q

inhibits COX-1, selectivity for COX-2 at low doses

A

meloxicam

72
Q

Derivative of salicylic acid

A

Diflunisal

73
Q

Should not be given to children with chickenpox or influenza, for Reye’s syndrome precipitation

A

Nonacelytated salicylates

74
Q

should be avoided in patients on a sodium-restricted diet

A

sodium salicylate

75
Q

may accumulate to toxic levels in patients with chronic renal insufficiency

A

magnesium salicylates

76
Q

prodrug that breaks down to release two molecules of salicylate in the alkaline environment

A

salsalate

77
Q

Developed on the theory that selective inhibition of COX-2 should be able to suppress pain and inflammation with no gastric ulceration

A

COX-2 inhibitors/coxibs

78
Q

First selective COX-2 inhibitor to reach market

A

Celecoxib

79
Q

Off-label use for familial adenomatous polyposis - predisposes colorectal cancer

A

Celecoxib

80
Q

devoid of clinically useful anti-inflammatory and anti rheumatic actions

A

acetaminophen

81
Q

does not suppress platelet aggregation, cause gastric ulceration, decrease renal blood flow, cause renal impairment

A

acetaminophen

82
Q

used more than any other analgesic

A

acetaminophen

83
Q

inhibition of CNS is limited to CNS

A

acetaminophen

84
Q

decreases prostaglandin synthesis in the CNS

A

acetaminophen

85
Q

regular alcohol consumption increases the risk of liver injury when taken at excessive doses

A

acetaminophen

86
Q

evidence that there is increased risk of bleeding in patients taking

A

warfarin

87
Q

routine use of these drugs to prevent vaccination-associated pain/fever is discouraged

A

acetaminophen

88
Q

preferred NSAID for children suspected of having chickenpox or influenza

A

acetaminophen

89
Q

preferred NSAID for patients with peptic ulcer

A

acetaminophen

90
Q

not preferred for arthritis or rheumatic fever

A

acetaminophen

91
Q

principal feature of overdose is hepatic necrosis

A

acetaminophen

92
Q

drug used to minimize liver damage

A

acetylcysteine - acetaminophen antidote

93
Q

NSAIDs are contraindicated for patients with a history of

A

severe NSAID hypersensitivity

94
Q

NSAIDs (especially aspirin) are contraindicated for children with

A

chickenpox or influenza

95
Q

Celecoxib is contraindicated for patients with

A

sulfa allergy

96
Q

synthetic chemicals related to the naturally occurring glucocorticoids

A

corticosteroids

97
Q

hormones produced by the adrenal cortex gland in the body

A

glucocorticoids

98
Q

beneficial anti-inflammatory effects of glucocorticoids

A
  1. decreasing capillary permeability - epinephrine and norepinephrine - vascular systems stabilized.
  2. reducing the number of leukocytes and mast cells at the site - decreases release of histamine and prostaglandins.
  3. Blocks immune response - common cause of inflammation.
99
Q

increased intake reduces normal hormone secretion and adrenal gland atrophy

A

glucocorticoids

100
Q

glucocorticoids influence the metabolism of

A

carbohydrates, proteins, and fats

101
Q

principal effect of carbohydrate metabolism

A

elevation of blood glucose - promoting synthesis of glucose from amino acids, reducing peripheral glucose utilization, reducing glucose update by muscle and adipose tissue.

102
Q

protein metabolism with glucocorticoids

A

suppress synthesis of proteins from amino acids and divert amino acids for production of glucose. Reduce muscle mass, decrease protein matrix of bone, thinning of skin, nitrogen balance is negative.

103
Q

low endogenous glucocorticoid levels

A

capillaries are more permeable, vasoconstriction is suppressed, bp falls

104
Q

increase the number of circulating red blood cells and polymorphonuclear leukocytes

A

glucocorticoids

105
Q

Decrease counts of lymphocytes, eosinophils, basophils, and monocytes

A

glucocorticoids

106
Q

physiologic stress releases which two hormones

A

glucocorticoid and epinephrine

107
Q

synthesis and release regulated by negative feedback loop

A

glucocorticoids

108
Q

components of negative feedback loop of synthesis and release of glucocorticouds

A

hypothalamus, anterior pituitary, adrenal cortex

109
Q

ways in which glucocorticoids differ from most drugs

A
  1. receptors are located inside the cell, not on surface.
  2. modulate the production of regulatory proteins, not signaling pathway.c
110
Q

ironic disease similar to RA, not limited to just joints

A

systemic lupus erythematosus (SLE)

111
Q

can be used to treat severe cases of ulcerative colitis and Crohn’s disease

A

glucocorticoids

112
Q

most effective antiasthma agent

A

glucocorticoids

113
Q

Adverse effects of glucocorticoids

A

adrenal insufficiency, osteoporosis, infection, glucose intolerance, myopathy, fluid and electrolyte disturbance, growth delay, psychologic disturbances, cataracts, glaucoma, peptic ulcer disease, Cushing’s syndrome

114
Q

induce hypokalemia, when used with digoxin can cause dysthymia

A

glucocorticoids

115
Q

when a microbe or parasite is able to reproduce in or on the body’s tissues

A

infection

116
Q

proteins produced by human host cells in response to viral invasion of the cell

A

interferons

117
Q

factors that decrease host resistance

A

-age
-genetic susceptibility
-immunodeficiency of any type
- malnutrition
-chronic disease
-severe physical or emotional stress
-inflammation or trauma affecting the integrity of skin or mucosa
-impaired inflammatory response

118
Q

capacity of microbes to cause disease

A

pathogenicity

119
Q

percentage of deaths occurring in the number of persons who develop the disease

A

case fatality rate

120
Q

time the body is expose to the organism and the appearance of clinical signs of disease

A

incubation period

121
Q

early symptoms stage when the infected person may feel fatigued, lose appetite, or have headache

A

prodromal period

122
Q

stage where infectious disease develops fully and the clinical manifestations reach a peak

A

acute period

123
Q

organism enters the Boyd and remains confined to a specific location

A

local infections

124
Q

pathogen spreads from a local infection to other tissues

A

focal infection

125
Q

infection spreads to several sites and tissue fluids, typically through the circulatory system

A

systemic infection

126
Q

caused by multiplication of pathogenic organisms in the blood and the cause of sepsis

A

septicemia

127
Q

presence of bacteria in the blood

A

bacteremia

128
Q

presence of toxins in the blood

A

toxemia

129
Q

presence of viruses in the blood

A

viremia

130
Q

several infectious agents concurrently establish themselves path these are site

A

mixed infections

131
Q

appear rapidly with severe symptoms but are short lived

A

acure infections

132
Q

less severe symptoms than acute but persist for a long period

A

chronic infections

133
Q

initial or fist time exposure/infection

A

primary infection

134
Q

follows a primary infection caused by a microbe other than the causing the primary infection - usually opportunistic pathogens

A

secondary infections

135
Q

do not cause apparent signs or symptoms, although they may persist over long periods of time

A

subclinical infection

136
Q

Local signs of infection

A

pain/tenderness, swelling, redness, and warmth

137
Q

swollen and tender lymph nodes

A

lymphadenopathy

138
Q

hospital-acquired infection

A

nosocomial

139
Q

agent applies to living tissue

A

antiseptic

140
Q

preparations applied to

A

objects

141
Q

complete destruction of all microorganisms

A

sterilization

142
Q

drug that suppresses the growth and replication of microorganisms but does not kill them

A

germistatic drug

143
Q

inactive against bacterial spores and has erratic behavior with lungi

A

ethanol

144
Q

somewhat more germicidal than ethanol, vasodilation properties

A

70%-100% isopropanol

145
Q

lethal to all microorganisms, must be immersed for 10 hours

A

glutaraldehyde

146
Q

reasons formaldehyde is less desirable than glutaraldehyde

A

acts slowly, more volatile than glutaraldehyde

147
Q

most widely germicidal agents

A

iodine

148
Q

preferred for intact skin - iodine

A

tincture

149
Q

treatment of wounds and abrasions - iodine

A

solution

150
Q

rod-shaped organisms, include vibrio, and pleomorphic

A

bacilli

151
Q

spirochetes and spirilla, wavy-like

A

spirals

152
Q

spherical forms

A

cocci

153
Q

pairs of bacteria, prefix

A

diplo-

154
Q

chains of bacteria, prefix

A

strep(to)

155
Q

irregular, grapelike clusters of bacteria

A

staph(ylo)

156
Q

cells groups in a packet or square of four cells bacteria

A

tetrads

157
Q

cells lying together with the long sides parallel bacteria

A

palisade

158
Q

present in the cell wall of gram-negative organisms and released after the bacterium dies

A

endotoxins

159
Q

produced by gram-positive organisms and diffuse through body fluids

A

exotoxins

160
Q

small obligate intracellular parasite that requires a living host for replication

A

virus

161
Q

protein-like agents that are transmitted by consumption of contaminated tissues such as muscle or use of donor tissues

A

prions

162
Q

creutzfeld-jakob disease

A

prion disease - degenerative disease of the nervous system

163
Q

drugs or substances that can kill or inhibit the growth of microorganisms. Originally derived from organisms, such as penicillin from mold, many drugs are now synthetic or semisynthetic.

A

antibiotics

164
Q

classified by the type of microbe against which the drug is active, such as antibacterials, antivirals, and antifungals. These drugs are unique to the type of organism and are not interchangeable.

A

antimicrobials

165
Q

drugs that kill organisms, whereas bacteriostatic applies to drugs that inhibit reproduction and rely on the host’s defenses to destroy the organisms.

A

bactericidal

166
Q

antibacterials that are effective against both gram-negative and gram-positive organisms

A

broad-spectrum antibiotics

167
Q
A

Patho & Pharmo (3 decks)

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