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Pharmacology and Pathophysiology Own notes > Inflammation (week 3) > Flashcards

Inflammation (week 3) Flashcards

1
Q

alters cell function without causing death

A

sublethal injury

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2
Q

irreversible process that causes cell death

A

lethal injury

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3
Q

What are some ways in which sublethal cells are able to adapt to their environment and prevent cell death after injury?

A

hypertrophy
hyperplasia
atrophy
metaplasia

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4
Q

an increase in the size of cells, which results in increased tissue mass (no cell division)

A

hypertrophy

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5
Q

weightlifting or enlarged uterus during pregnancy is which type of sublethal cell adaptation?

A

hypertrophy

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6
Q

increase in the number of cells as a result of increased cellular division

A

hyperplasia

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7
Q

What areas of the body undergo hyperplasia?

A
  • liver regeneration
  • hormonal hyperplasia (endometrium)
  • breast development
  • uterus
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8
Q

A decrease in number or size of cell

A

atrophy

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9
Q

This adaptation occurs as a result of disease, lack of blood supply, nutritional deficiency, or the ageing process

A

atrophy

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10
Q

in this cell adaptation, there is a reversible transformation of one cell type into another

A

metaplasia

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11
Q

give an example of metaplasia?

A
  • Circulation of monocytes to macrophages as they migrate into inflamed tissues
  • pseudostratified columnar epithelium of the bronchi change to squamous epithelium when smoking
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12
Q

in the adaptation of sublethal cell injury, what adaptations are reversible?

A

metaplasia &

hyperplasia

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13
Q

Name some causes of lethal cell injury

A 
hypoxia 
physical agents: heat/cold
radiation
electrothermal injury
mechanical trauma
chemical injury
microbial injury
bacteria
immunological
neoplastic growth
normal substances: stomach acid, enzymes
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14
Q

What is hypoxia

A

a deficient amount of oxygen reaching tissues

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15
Q

what is apoptosis and is it normal?

A

Programmed cell death

it is a normal process in certain regenerating tissues, such as the skin and gut

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16
Q

what is necrosis?

A

large scale cellular death or portion of tissue with cellular reaction to dead cells

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17
Q

What are the four types of necrosis?

A
  • coagulative
  • liquefactive
  • caseous
  • gangrene
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18
Q

this type of necrosis is caused by ischemia, often resulting in myocardial infarct.

A

coagulative

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19
Q

this type of necrosis is caused by focal bacteria; it kills bacteria but dissolves tissue as it goes causing pus

A

liquefactive

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20
Q

this type of necrosis the form of coagulative necrosis that occurs in a myobacterial infections

A

caseous

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21
Q

necrosis of an appendage, usually a limb

A

gangrene

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22
Q

What are the four defence mechanisms against cell injury

A

Skin and mucous membranes
Mononuclear phagocyte system
Inflammatory response
immune system

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23
Q

This system consist of monocytes, macrophages, and precursor cells.

A

mononuclear phagocyte system

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24
Q

What are the two main cells that make up the mononuclear phagocyte system?

A

fixed phagocytic cells

free phagocytic cells

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25
Q

What tissues and organs have fixed phagocytes?

A

bone marrow
lungs
lymph nodes
nervous system

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26
Q

What tissues and organs are composed of free phagocytes?

A

monocytes (blood)

macrophages (connective tissue)

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27
Q

Where do monocytes and macrophages originate in the body?

A

the bone marrow

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28
Q

Once monocytes leave the blood and into the connective tissue they become these.

A

macrophages

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29
Q

What do macrophages do once in the connective tissue?

A

they recognize bad cells and destroy them (phagocytosis)

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30
Q

name of macrophage found in the connective tissue

A

histocytes

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31
Q

name of macrophage found in the liver

A

kupffer cells

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32
Q

name of macrophage found in the lung

A

alveolar macrophages

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33
Q

name of macrophage found in the spleen

A

free and fixed macrophages

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34
Q

name of macrophage found in the bone marrow

A

fixed macrophages

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35
Q

name of macrophage found in the lymph nodes

A

free and fixed macrophages

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36
Q

name of macrophage found in the bone tissue

A

osteoclasts

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37
Q

name of macrophage found in the CNS

A

microglial cells

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38
Q

name of macrophage found in the peritoneal cavity

A

peritoneal macrophages

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39
Q

name of macrophage found in the pleural cavity

A

pleural macrophages

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40
Q

name of macrophage found in the skin

A

histiocytes, langerhans cells

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41
Q

name of macrophage found in the synovium

A

type A cells

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42
Q

what is an Inflammatory response?

A

a response to pathogens that neutralize and dilute inflammatory agents, removes necrotic material and establishes an environment for healing and repair.

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43
Q

What type of person may not mount an inflammatory response to infection?

A

a neutropenic person; someone who has an abnormally low level of neutrophils

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44
Q

What is the initial response during a vascular response to injury?

A

the SNS stimulates vasoconstriction

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45
Q

during vascular response, platelets adhere to vessels and aggregate to seal the injured area forming these

A

fibrin-platelet clot

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46
Q

The release of this pro inflammatory mediator causes vasodilation

A

histamine

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47
Q

a mass of cells and fluid that seep out of a blood vessel or an organ especially during inflammation

A

exudate

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48
Q

what are the 5 types of inflammatory exudate?

A 
serous
catarrhal
fibrinous
purulent (pus)
hemorrhagic
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49
Q

exudate where fluid that has low sell in protein content seen in the early stages of information or when injury is mild

give an example

A

serous

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50
Q

exudate found in tissues in which cells produce mucus

give an example

A

catarrhal

runny nose

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51
Q

exudate that increases vascular probability and fibrinogen leakage into interstitial spaces

give an example

A

fibrinous

adhesion SBO

52
Q

in fibrinous exudate, excessive amounts of this may cause tissues to adhere

A

fibrin coating

53
Q

exudate that consists of white blood cells, microorganisms, liquified dead cells and other debris’s

give an example

A

purulent (pus)

bases

54
Q

exudate that results from rupture or necrosis of blood vessel walls; consist of red blood cells that escaping to the tissue

give an example

A

hemorrhagic

hematoma

55
Q

what are the local manifestations (or signs) of inflammation?

A 
redness
heat
pain
swelling
loss of function
56
Q

what causes redness?

A

hyperaemia from vasodilation

57
Q

what causes the area to heat up during inflammation?

A

increased metabolism at inflammatory rate

58
Q

what causes Pain during inflammation

A
  • change in pH
  • change in local ionic concentrations
  • never stimulation
  • pressure from fluid exudates
59
Q

What occurs during swelling when inflammation is happening

A

fluid shift to interstitial spaces

60
Q

What happens when there is a loss of function during inflammation?

A

swelling and pain

61
Q

What are the stages of a febrile response?

A

prodromal
chill
flush
defervescence

62
Q

What happens during the prodromal stage of a febrile response?

A

mild headache, fatigue, general malaise, muscle aches

63
Q

what happens during the chill stage of a febrile response?

A

pale skin; feeling of being cold; generalized shaking; chill; shivering causing the body to reach new temperature set by control centre in hypothalamus

64
Q

what happens during the flush stage of a febrile response?

A

sensation of warmth throughout the body, cutaneous vasodilation, warming and flushing of skin

65
Q

what happens during the defervescence stage of a febrile response

A

sweating; decrease in body temperature

66
Q

what are the stages in primary intention healing?

A
  1. initial (3-5 days)
  2. granulation (5 days-4 weeks)
  3. scar contracture (7 days to several months)
67
Q

What is the medical term for pus and what is it composed of?

A

purulent exudate

neutrophils and other debris

68
Q

Which white blood cell is the first to arrive at site of inflammation and what do they do?

A

neutrophils

phagocytize bacteria, foreign material, damaged cells

69
Q

What produces neutrophils?

A

bone marrow

70
Q

What is leukocytosis?

A

an increase in the total number of WBCs due to any cause

71
Q

What causes the release of bands or banded neutrophils?

A

during infection or inflammation, there is a high demand for neutrophils resulting in the release of immature neutrophils from the bone marrow to keep up with demands. These are known as bands

72
Q

What is the “left shift” in patients with acute bacterial infections?

A

there are a high number of immature neutrophils present in the blood. the bone marrow is producing more WBCs and releasing them into the blood before they are fully mature

73
Q

What WBC arrives second at the site of inflammation and how?

A

monocytes; by chemotaxis

74
Q

briefly describe a monocyte.

A

They transform into macrophages upon arrival. They phagocytize inflammatory debris and clean up area. They have long life spans and can accumulate and form multinucleated giant cells to phagocytize larger particles of debris.

75
Q

What are the maladaptive responses to post injury?

A

dysplasia

anaplasia

76
Q

What is dysplasia?

A

abnormalities in cellular shape, size and appearance

typically seen in cervical dysplasia

77
Q

What is anaplasia?

A

differentiation of cells to immature or embryonic form

IE: malignant tumors

78
Q

What is the mononuclear phagocyte system?

A

a system that is composed of monocytes and macrophages. the system recognizes and phagocytes foreign material and participates in immune response

79
Q

Briefly describe what happens in a vascular response.

A

Vasoconstriction>Vasodilation> Increased permeability> exudate

When tissue is first injured, the small blood vessels in the damaged area constrict momentarily, a process called vasoconstriction. Following this event, the blood vessels dilate (vasodilation), increasing blood flow into the area.

Next, the walls of the blood vessels, become more permeable. Protein-rich fluid, called exudate, is now able to exit into the tissues. Platelet aggregation occurs and seals off the area. WBC’s then adhere to the blood vessel walls and emigrate into extravascular space.

80
Q

What is hyperemia?

A

an excess of blood in the vessels supplying an organ or other part of the body due to increased filtration pressure and increased capillary permeability

81
Q

What is hyperaemia caused by?

A

vasodilation

82
Q

What causes edema?

A

Plasma proteins, such as albumin, exert oncotic pressure (pulling pressure) which pulls fluid from the blood vessels into the interstitial space causing edema

83
Q

What is albumin?

A

is the main plasma protein found in blood. it plays a major role in regulating oncotic pressure

84
Q

What s oncotic pressure?

A

is a form of osmotic pressure exerted by proteins, notably albumin, in a blood vessel’s plasma (blood/liquid) that usually tends to pull water into the circulatory system

85
Q

describe the relationship between hydrostatic pressure and oncotic pressure.

A

Hydrostatic pressure within blood vessels tends to cause water to filter out into the tissue. This leads to a difference in protein concentration between blood plasma and tissue. As a result, ther oncotic pressure of the higher level of protein in the plasma tends to draw water back into the blood vessels from the tissue, causing edema.

86
Q

Briefly describe what happens in a cellular response during inflammation.

A

phagocytes produce nitric oxide inhibiting vascular smooth muscle contraction and growth. platelet aggregation occur; leukocytes attach to the endothelium walls.

Macrophages release cytokines, causing endothelial cells to express cellular adhesion. Capillary blood flow into area slows, fluid is lost and viscosity thickens.

neutrophils and monocytes move to the inner surface of capillaries (margination) and then through the walls of the capillary (diapedesis) to the site of injury.

87
Q

What is the accumulation and adhesion of leukocytes to the epithelial cells of blood vessel walls at the site of injury in the early stages of inflammation.

A

margination

88
Q

what is known as the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.

A

diapedesis

89
Q

What is chemotaxis?

A

It is the directional migration of WBCs against concentration gradient of chemotactic factors

90
Q

These attract WBC’s to site of injury during inflammation.

A

chemotactic factors

91
Q

What are chemotactic factors?

A

any molecule that acts as a chemical stimulant along a concentration gradient attracting macrophages and other phagocytic cells to site of injury

92
Q

This white blood cell arrives later during inflammation. It’s role is related to humeral and cell mediated immunity.

A

lymphocytes

93
Q

These white blood cells are released in large quantities in an allergic reaction.

A

eosinophils

94
Q

These white blood cells

control the affects of histamine and serotonin.

A

eosinophils

95
Q

These white blood cells can phagocytize the antigen-antibody complex and destroy parasite cell surfaces.

A

eosinophils

96
Q

This white blood cell carries histamine and heparin that are released during inflammation

A

Basophils

97
Q

What does histamine do during inflammation?

A

Histamine increases the permeability of the capillaries to white blood cells and some proteins, to allow them to engage pathogens in the infected tissues.

98
Q

What does heparin do during inflammation?

A

heparin has anticoagulant properties and possesses anti-inflammatory effects

99
Q

What are the functions of the chemical mediators?

A
  • enhanced phagocytosis
  • increased vascular permeability
  • chemotaxis
  • cellular lysis
100
Q

What is required for cellular lysis (cell destruction)

A

The complements C1-C9 need to be activated in sequential order for cellular lysis to occur.

101
Q

Where is histamine stored?

A

in the granules of circulating mast cells and basophils

102
Q

These two compounds are synthesized from phospholipids on the cell membrane of most body tissues including blood.

A

prostaglandins

leukotrienes

103
Q

stimulation from chemotactic factors, phagocytosis or cell injury causes the phospholipids to be converted into this.

A

arachidonic acid

104
Q

What do prostaglandins do in the body during inflammation?

A
  • Cause vasodilation and increased vascular permeability

- increase blood flow causing edema

105
Q

This pathway is a potent pyrogen and acts on the hypothalamus to raise temperatures in the body.

A

Prostaglandin E2 (PGE2)

106
Q

What causes hyperalgesia, which is excessive pain or sensitivity to pain?

A

Prostaglandin E2 (PGE2)

107
Q

this pathway constricts the smooth muscles of the bronchi causing bronchospasm (asthma)

A

leukotriene pathways

108
Q

What are some benefits of having a fever?

A
  • killing of microorganisms, increased
  • phagocytosis by neutrophils
  • increased T cells
  • increased interferon (virus-fighting substance
109
Q

what do phagocytes produce that inhibits vascular smooth muscle contraction and growth

A

nitric oxide

110
Q

Macrophages release cytokine which causes this. endothelial cells to express cellular adhesion

A

endothelial cells to express cellular adhesion

111
Q

After cellular response, where do neutrophils and monocytes move to and where do they end up?

A

The inner surface of capillaries (margination) and then through the capillary wall (diapedesis) to the site of injury

112
Q

This WBC’s role is related to humeral and cell mediated immunity

A

lymphocytes

113
Q

this white blood cells controls the affects of histamine and serotonin.

A

eosinophils

114
Q

this WBC phagocytes the antigen-antibody complex

A

eosinophils

115
Q

these cells carry histamine and heparin that are released during inflammation

A

basophils

116
Q

this system is a major mediator of the inflammatory response

A

complement system

117
Q

What sequence is required for cellular lysis?

A

the entire sequence of C1-C9

118
Q

These chemical mediators are synthesized from phospholipids on the cell membrane of most body tissues.

A

prostaglandins and leukotrienes

119
Q

What is arachidonic acid synthesized?

A

on the prostaglandin pathway or the leukotriene pathway

120
Q

these chemical mediators are considered proinflammatory

A

prostaglandins

121
Q

these chemical mediators cause vasodilation and increased vascular permeability

A

prostaglandin pathways

122
Q

This potent pyrogen acts on the hypothalamus to raise temperatures

A

PGE2

123
Q

this chemical mediator causes hyperalgesia (excessive pain)

A

prostaglandins

124
Q

this chemical mediator constricts smooth muscles of bronchi, resulting in brochospamss

A

leukotriene pathway

125
Q

this pathway causes oedema due to increased capillary permeability

A

leukotriene

Pharmacology and Pathophysiology Own notes (9 decks)

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