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BIOL 2200 > module 1 Adaption, Inflammation, & Healing > Flashcards

module 1 Adaption, Inflammation, & Healing Flashcards

1
Q

what is pathophysiology?

A

the study of functional changes in cells, tissues and organs altered by disease or injry

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2
Q

what is an acute illness

A

part of the innate (non-specific) immune response to tissue injury or microbial infection. Relatively severe, but short term

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3
Q

what is a chronic illness?

A

lasts longer than acute inflammation.Your body continues sending inflammatory cells even when there is no outside danger

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4
Q

how can cells be altered?

A
  1. adaptation
  2. injury: reversible or irreversible
  3. death: necrosis or apoptosis
  4. aging
  5. neoplasia
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5
Q

what are the 5 types fo cell adaptation?

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

what is cell atrophy?

A

a decrease in size

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7
Q

what is cell hypertrophy?

A

increase in size

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8
Q

what is hyperplasia?

A

increase in the number of cells

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9
Q

what is metaplasia?

A

reversible replacement of one mature cell type by another, sometimes less differentiated, cell type

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10
Q

what is dysplasia?

A

abnormal changes in size, shape, and organization of mature cells

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11
Q

what is a cell injury?

A

when the cell can no longer maintain homeostasis or cannot adapt

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12
Q

what are the 4 causes of cell injury?

A
  1. physical agents
  2. chemical
  3. biological microorganisms
  4. nutritional deficiences
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13
Q

what are 3 mechanisms/forms of cell injury?

A
  1. hypoxia
  2. impaired calcium homeostasis
  3. free radicals
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14
Q

what is hypoxia?

A

lack of sufficient oxygen for cells

  • the most common cause of cell injury
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15
Q

what causes hypoxia?

A
  • ischemia
  • arteriosclerosis (narrowing of arteries)
  • embolisms (sudden acute anoxia)
  • decreased oxygen in the air
  • loss of hemoglobin/RBC
  • diseases of respiratory/cardiovascular systems
  • poisons/toxins
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16
Q

what is ischemia?

A

reduced blood supple to cells in one area

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17
Q

what is arteriosclerosis?

A

gradual narrowing of arteries

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18
Q

what are embolisms?

A

sudden acute anoxia (something stuck in blood vessel)

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19
Q

Describe how loss of pump activity can lead to cellular swelling, cellular damage, and necrosis.

A
  • Na+/K+ pumps slow down due to the lack of ATP = no maintenance of Na+/K+ input/output
  • potassium will move out of the cell, sodium will move into the cell, drawing in water = swelling of the cell
  • endoplasmic reticulum (ER) will then start to swell and fragment mitochondria function = further reduction of ATP
  • lack of ATP results in an increased intracellular level of Calcium in the cell, leading to increased permeability and loss of mitochondrial membrane potential
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20
Q

Without adequate oxygen, cells are unable to produce sufficient levels of which critical energy-rich macromolecule? How does this affect cellular pH?

A
  • decreases amount of ATP = increased anaerobic respiration
  • increased anaerobic respiration = lactic acid buildup
  • lactic acid buildup = lower pH
  • lower pH = DNA clumping & decreased activity of many enzymes
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21
Q

Describe the mechanism whereby hypoxia leads to changes in cell membrane permeability

A
  • decreased amount of ATP = phospholipid synthesis reduced
  • phospholipid synthesis = less membranes and damaged membranes
    • lysosomal membrane damage = leakage of degradative enzymes that degrades macromolecoles = necrosis
    • mitochondiral membrane damage = change in membrane permeability = necrosis
    • plasma membrane damage = influx of fluids & ions = loss of cellular contents = necrosis
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22
Q

explain impaired calcium homeostasis

A
  1. activation of innapropriate enzymes causing
    1. breakdown membrane
    2. nuclear damage- breakdown nuclear & damaged DNA structure
    3. decreased ATP
  2. increased mitochondiral permeability causes:
    1. reduction in mitichondrial membrane = decrease ATP production
    2. leakage of proteins from inside of mitochondria into the cytosol = apoptosis
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23
Q

what are free radicals?

A

chemical species with an unpaired outer electron that makes chemicals really unstable & highly reactive

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24
Q

what are reactive oxygen species (ROS)?

A
  • mostly endogenous products (ex: metabolic processes, WBC)
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25
Q

what are commonly produced ROS?

A
  • superoxide
  • hydrogen peroxide
  • hydroxy radical
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26
Q

how are ROS kept in check?

A

ROS scavengers

  • enzymes reacts with the free radical and neutralize them
  • antioxidants
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27
Q

how are free radicals produced?

A

can be exogenous (from environment) or endogenous (our own chemical reactions

  • produced by phagocytic leukocytes to use them to kill pathogens
  • generated by absorption of radiation from X-rays or UV light
  • generated during the metabolism of many drugs
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28
Q

explain the process of apoptosis

A
  1. destruction of nucleus = release of DNA fragments into intracellular environment = DNA chopped up
  2. cell is going to dhrink from its neighbours and remove itself easily
  3. blebs start to form on membrane
  4. blebs pinch off and enclose components of intracellular environments as apoptotic bodies
  5. apoptotic bodies cleaned away from phagocytes
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29
Q

what is the purpose of apoptosis?

A
  • so old cells can be replaced with new cells
  • remove those cells during normal development
  • cell is infected, don’t want to cause additional harm
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30
Q

how does apoptosis and necrosis differ?

A
  • apoptosis only happens on cells that been activated for the apothotic pathway
  • no inflammation is involved since everything is contains in apoptotic bodies that the phagocytes remove easily
  • necrosis is messy
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31
Q

what is necrosis?

A

unregulated cell death = messy

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32
Q

what is apoptosis?

A

programmed cell death caused by both normal and pathologic tissue changes (cell suicide)

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33
Q

explain the process of necrosis

A
  1. interference of tissue regeneration/healing of the area = distinctive changes in tissue appearance due to messyness
  2. cell swells/bursts causing leakage of enzymes into the environment and self-digestion = autolysis
  3. there is damage to nearby tissues due to the leakage into environment and self-digestion
  4. during autolysis, enzymes start to degrade the cell itself because of leakage of digestive enzymes and damage to nearby cells = inflammatory response
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34
Q

what are the different types of necrosis?

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. caseous necrosis
  4. fat necrosis
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35
Q

Describe the causes, locations and appearance of the following types of necrosis: coagulative

A
  • cause: hypoxia and characteristics of infarcts (lack of blood flow to area), manifesting of protein denaturation
  • location: kidneys, heart, and adrenal glands
  • appearance: tissue firm and opaque (clear, white-ish colour)
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36
Q

Describe the causes, locations and appearance of the following types of necrosis: liquefactive

A
  • cause: tissues soften and liquefy in abscess: cells completely digested
  • location: focal bacterial or fungal infections, and brain
  • appearance: an abscess (pus-filled pocket)
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37
Q

Describe the causes, locations and appearance of the following types of necrosis: caseous

A
  • cause: a combination of coagulative and liquefactive necrosis
  • location: lungs due to tuberculosis infections
  • appearance: tissue is “cheese-like”, crumble yellowish appearance
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38
Q

Describe the causes, locations and appearance of the following types of necrosis: fat

A
  • cause: leakage of pancreatic lipases into peritoneal cavity causing “saponification”
  • location: breast, or anywhere with fatty tissue
  • appearance: tissue appears opaque and white
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39
Q

what is gangrene?

A
  • results from severe hypoxic injury
  • significant tissue area whose cells have undergone necrosis
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40
Q

what are the different types of gangrene?

A
  • dry grangrene
  • wet grangrene
  • gas gangrene
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41
Q

Describe the causes, locations and appearance of the following types of gangrene: dry

A
  • cause: coagulative necrosis
  • location: in extremities
  • appearance: skin becomes dry, wrinkles, and dark
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42
Q

Describe the causes, locations and appearance of the following types of gangrene: wet

A
  • cause: liquefactive gangrene
  • location: internal organs, can easily spread to other tissues
  • appearance: cold, swollen, and black with foul odour due to bacterial action
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43
Q

Describe the causes, locations and appearance of the following types of gangrene: gas

A
  • cause: infection with a species of bacteria (clostridium)
  • location: connective tissue
  • appearance: bubbles of gas formation
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44
Q

Outline two main categories of theory for the aging process

A
  1. programmed (moelcular) theories
  2. damage (senescence) theories
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45
Q

what are the inflammatory cells involved with acute inflammation?

A
  • endothelial cells
  • platelets
  • neutrophil
  • macrophages
  • mast cells
  • basophils
  • eosinphil
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46
Q

what are the key chemical mediators for acute inflammation?

A
  • histamine
  • prostaglandine & leukotrienes
  • nitric oxide & reactive oxygen species
  • cytokines
  • chemokines
    *
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47
Q

describe the sequence of cellular-chemical interactions that produce the cellular response

A
  • leukocytes (neutrophils/monocytes/macrophages) come in contact with inflammatory chemicals in the blood stream at site of injury
  • margination: leukocytes move to edge of blood vessels and accumulate at the endothelium to get ready to move to damaged tissue
  • adhesion: leukocytes stick to endothelial cells by adhesion molecules, to stick to the edge so they can start to move through blood vessels
  • transmigration: leukocytes move out of blood vessel, into tissue, to site of injury
  • chemotaxis: chemical signals recuit the leukocytes to exactly where they need to be to deal with infection
  • leukocytes migrate over and phagocytose (ingest) foreign material
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48
Q

describe the sequence of cellular-chemical interaction that produce the vascular response

A
  • damaged tissue cells release cytokines (signals) and chomokines into intertistitial fluid to bring WBC to the area and get in contact with othr cells in the immune system
  • mast cells become activated. by cytokines, bacterial PAMPs, other antigens, physical stress
  • mast cells release histamine (key mediation in getting infammatory response happening) = vasodilation of blood vessels and increase permeability of capillaries
  • fluid and blood proteins leak into interstitial fluid of tissues = edema (swelling)
  • edema and vasodilation = heat, swelling, redness, loss of function, pain brought on by bradykinin
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49
Q

what part of the vascular response causes heat and redness?

A

increased blood vessel dilation slows flow rate (or velocity) but increases volume in area

50
Q

what part of the vascular response causes swelling?

A

increased vascular permeability protein-rich exudate moves into interstitial space

51
Q

what part of the vascular response causes pain?

A

released prostaglandina and bradykinin stimulates pain receptos of neurons

52
Q

what is exudate?

A

the fluid that moves from vessels into the tissues, combines with neutrophils and the debris from phagocytosis

53
Q

what are the 4 types of exudate?

A
  1. serous exudate
  2. fibrinous exudate
  3. purulent exudate
  4. hemorrhagic exudate
54
Q

describe serous exudate

A
  • low protein content
  • similar to fluid under a blister
  • mild inflammation
55
Q

describe fibrinous exudate

A
  • greater injury
  • increased inflammation
  • vessels become more permeable
  • more proteins released out into tisue
  • fluid sticky and thick, may have to be removed for healing
56
Q

describe purulent exudate

A
  • “pus”
  • severe inflammation
  • infection = neutrophils, protein and tissue debris
  • large pockets may have to be drained for healing
57
Q

describe hemorrhagic exudate

A
  • contains large amount of RBS
  • severe inflammation
  • severe leakage, or necrosis of blood vessels
58
Q

Define chronic inflammation

A

inflammation lasting over 2 weeks and can last for years

59
Q

what are the three main causes of chronic inflammation?

A
  1. low grade, persistent infection- minor bacteria/virus we can’t get rid of
  2. irritants that the body is unable to dispose of
  3. autoimmune in origin- body attacking itself instead of pathogen
60
Q

what are the characteristics of chronic inflammation?

A
  1. dense infiltration (rush) of lymphocytes, macrophages, and fibroblasts = more scar tissue
  2. little or no exudate (fluid) compared to acute inflammation
  3. more tissue damage
  4. can be in association with cancer development since enzymes can also damage our own cell, which can damage DNA and hit a gene that produces tumor
61
Q

what are the two patterns of chronic inflammation?

A
  1. general/non-granulomatous
  2. granulomatous
62
Q

describe general/non-granulomatous inflammation

A
  1. still have an increase of chemotaxis = consistent recruitment of macrophages
  2. macrophages stimulate TGF-beta
  3. TGF-beta recruit fibroblasts = formation of scar tissue
  4. too much collagen = too much scar tissue
63
Q

describe granulomatous

A
  1. cells build up around particles your body can’t get rid of = macrophages and lymphocytes surround it
  2. macrophages change physiology = epitheloid cells
  3. epitheloid cells fuse together to become multinucleate “giant cells”
  4. “giant cells” try to engulf large particles = gain connective tissue around the large mass of cells
  5. granuloma is formed
64
Q

Describe the acute phase response as systemic characteristics of inflammation

A

jacking up inflammatory signals to cause systematic response (everywhere)

  • release of IL-1, IL6, and TNF-beta
  • ex: fever, the overall feeling of sickness
65
Q

Describe leukocytosis as systemic characteristics of inflammation

A

increase in immune cells when you have an inflection

  • neutrophils
  • eosinophils
  • lymphocytes
66
Q

Describe two detrimental effects of inflammation

A
  1. edema can get so bad, it blocks blood vessels to the area = loses oxygen = no energy (ATP) for healing & waste removal
  2. neutrophils rush to the area to kill pathogens = release hydrolytic enzymes
    1. hydrolytic enzymes can start attacking normal cells
67
Q

what 2 things can happen during healing?

A
  1. regeneration
  2. replacement
68
Q

what is regeneration?

A

injured tissue is returned to almost original structure and function if tissue is capable of regeneration

69
Q

what is replacement?

A

destroyed tissue gets replaced with scar tissue

70
Q

define labile cells and give an example

A
  • continually dividing
  • ex: epithelial and bone marrow cells
71
Q

define stable cells and give an example

A
  • normally stop dividing at some point in time
  • ex: smooth muscle cells
72
Q

define fixed cells and give an example

A
  • cannot regenerate and will be replaced with scar tissue
  • ex: nerve cells
73
Q

what cells are capable of regeneration?

A
  • labile
  • stable
  • fixed
74
Q

describe phase 1 (inflammation) stage of healing

A
  • begins during acute inflammation - lasts 1-2 days
  1. platelets will start to form blood clots, acting as scaffolds to lay down new material = release PDGF
  2. macrophages produce growth factors and TGF-beta = recruit fibroblasts
  3. fibroblasts generate collagen for healing
  4. growth factors help with regenesis (new blood vessels)
75
Q

describe phase 2 (proliferation & new tissue formation) healing phase

A
  1. the wound has been plugged by blood clots & broken down by enzymes
  2. macrophages get rid of tissue debris/damaged cells = release cytokines (TGF-beta)
  3. TGF-beta recruit fibroblasts = make collagen and growth of blood vessels
  4. granulation tissue is formed from connective tissue at edges of the wound
  5. myofibroblasts (from granulation) contracts the wound
  6. epithelial tissue grows over granulation tissue
76
Q

describe phase 3 (remodeling and maturation) of healing

A
  • starts before reconstructive phase ends
  • begins around 3 weeks after injury, completed withing 6 months- 2 years
  1. scar tissue gets replaced by tougher scar tissue made by tougher collagen
  2. capillaries disappear
77
Q

what type of healing are clean incisions and what are the characteristics?

A
  • primary intention
  • an area where you can pull the edges together to heal nicely alone lines
  • not much contraction or sealing required
78
Q

what type of healing are open wounds and what are some characteristics?

A
  • secondary intention
  • there is an open wound (gauge), no thin line to pull back together
  • requires a lot of sealing, filling in, and contraction
79
Q

what are some local problems with healing?

A
  1. ischemia
  2. large blood clots
  3. excessive fibrin
  4. excessive collagen
  5. excessive contraction of wound
  6. wound disruption
80
Q

why is ischemia a local problem with healing?

A
  • lowers ATP production = lower protein synthesis
  • lower wound strength that has higher chance for infection
81
Q

why are large blood clots a local problem with healing?

A
  • delays granulation
  • lowers oxygen diffusion
82
Q

why is excessive fibrin a local problem with healing?

A
  • adhesions = fibrous bands of tissue that attaches to internal organs
    • not able to move as well as they should
83
Q

why is excessive collagen a local problem with healing?

A

surface over-healing = keloid scarring

84
Q

why is an excessive contraction of the wound a local problem with healing?

A

causes deformity and restricted movement = contracture

85
Q

why is wound disruption a local problem with healing?

A

dehiscence = when the sutured wound is pulled apart prematurely

86
Q

what are some systematic problems with healing?

A
  • inadequate nutrients
  • diabetes mellitus
  • medications
  • age
87
Q

why is diabetes mellitus a systemic problem with healing?

A
  • lower capillary circulation to extremities
  • glycosylated hemoglobin = lower oxygen release in tissues, lower macrophage activation (so much sugar in body, so hemoglobin binds to sugar and no oxygen to tissues)
88
Q

why are medications a systemic problem with healing?

A

corticosteroids, NSAIDs, anticancer drugs can delay the healing process

89
Q

what is a thrombus?

A

a blood clot that occurs inside the vascular system

90
Q

what is thrombosis?

A

occurs when blood clots block veins or arteries

91
Q

what is an embolus?

A

a blood clot, air bubble, piece of fatty deposit, or other object which has been carried in the bloodstream to lodge in a vessel and cause an embolism

92
Q

what is thromboembolism

A

a blood clot (thrombus) that forms in a blood vessel, breaks loose and is carried by the bloodstream to block another blood vessel

93
Q

what is atherosclerosis

A

gradual narrowing of arteries

94
Q

what is hypoxemia

A

a below-normal level of oxygen in your blood

95
Q

what is a communicable disease?

A

a disease that can be transferred between individuals

96
Q

what is congenital?

A

a disease that is present from birth

97
Q

what is a degenerative disease?

A

when the structure/function worsens overtime

98
Q

what is etiology?

A

the. study of the cause of disease

99
Q

what is exacerbation?

A

severity of disease made worse

100
Q

what is iatrogenic?

A

diseases that occur as a result of medical treatment

101
Q

what is idiopathic

A

diseases with no identifiable cause

102
Q

what is genetic?

A

a disease that is passed down through genes

103
Q

what is pathogenesis?

A

how a disease develops

104
Q

what is a prognosis?

A

the expected outcome of a disease

105
Q

what is remission?

A

period during which there is a decrease in severity of disease

106
Q

what is a syndrome?

A

a combination of signs and symptoms that are characteristics of a disease

107
Q

what does systemic mean?

A

affecting the whole body

108
Q

Four days post-trauma, the patient presented to a urologist complaining of blood in his urine and shortness of breath secondary to severe scrotal pain. On physical examination his scrotum was enlarged, warm, tender, and firm. He was admitted to the hospital with a WBC of 38,600/mm3 with a left shift, a temperature of 38.8°C, C-reactive protein (CRP) of 20 mg/dl, and an erythrocyte sedimentation rate of 80 mm/hour. Ultrasound showed findings of bilateral epididymitis and swelling of both testes. Although no microbiological organism was cultured from the patient’s blood or urine, he was given a broad range antibiotics.

List (define, if necessary) and explain the cause of each of the abnormal signs and symptoms exhibited by Bobby four days post-trauma.

A
  • Blood in urine – due to injury, inflammation of epididymis
  • Pain – bradykinin (part of kinin system)
  • Swelling, warm, tender and firm – release of histamine causing acute inflammation with increased vasodilation and increased permeability – the vascular phase
  • Left shift – increased amount of immature neutrophils in the blood – part of acute phase response – shows inflammation is systemic
  • Leukocytosis – increased amount of white blood cells in blood – part of acute phase response – shows inflammation is systemic
  • Fever – due to release of IL-1, IL-6 and TNF – part of acute phase response – shows inflammation is systemic
  • CRP – C reactive protein – this is an opsonin (makes phagocytosis easier) – part of acute phase response – shows inflammation is systemic
  • ESR – erythrocyte sedimentation rate – increased rate of RBC settling out due to presence of fibrinogen (what type of protein is this?) – part of acute phase response – shows inflammation is systemic
109
Q

Explain the changes in blood pressure and heart rate that Bobby exhibited by the fifth-day post-trauma

A
  • Mast cells have released histamine, causing increased vasodilation.
  • If enough can cause system-wide vasodilation, causing a decrease in BP
  • Heart rate will increase to compensate for decreased BP
110
Q

Why was Bobby prescribed antibiotics throughout his treatment, even though no cultures revealed positive results?

A

The inflammatory response is the same, whether from trauma or infection. Can’t be sure that nothing is there, so antibiotics are given “just in case”

111
Q

What is the “post inflammatory increased nodularity” noted in the final ultrasound taken three months post-trauma? (Bobby’s case)

A

after 3 months, it should be scar tissue

112
Q

Samuel Dawes is a 72-year-old, obese, white, diabetic male who underwent an emergency appendectomy five days ago. He had a small incision, approximately 6 cm in length, which was secured with staples. Eight days after the operation, the staples were removed, at which point, the wound opened and pus was visible. The wound margins were red, and the more internal portions of the wound appeared to be closed.

Identify and describe the type of healing that a surgical incision should undergo.

A

Primary intention – edges of wound are close together, minimal scarring

113
Q

Describe the actions of platelets and macrophages during the inflammatory phase of the healing process.

A
  • Platelets – make blood clots (can be used as a scaffold) and release growth factors
  • Macrophages – release growth factors
114
Q

Describe the actions of macrophages, fibroblasts and myofibroblasts during the proliferation phase of the healing process.

A
  • Macrophages – clean up the area and release TGF-β that attracts fibroblasts
  • Fibroblasts – secrete collagen, growth factors that increase blood vessel growth
  • Myofibroblasts – contract wound edges
115
Q

Describe granulation tissue.

A

Contains blood vessels, fibroblasts and collagen. Delicate and easily broken down (infected) by bacteria

116
Q

How is epithelialization accomplished?

A

Epithelial tissue grows in from edges of wound, meet in the middle, stop growing, then differentiate into layers.

117
Q

Describe changes that occur in scar tissue during the remodeling phase of the healing process.

A
  • The collagen in scar tissue is broken down and a stronger type of collagen is built up along the lines of stress.
  • Blood vessels decrease.
118
Q

What terms can be applied to the two problems that developed during the attempted healing of Mr. Dawes’ wound? Justify your choice by matching the definition of the terms with the final appearance of the wound.

A
  • Infection – appearance of pus / purulent exudate
  • Dehiscence – disruption of a surgical wound along the suture line
119
Q

What is the technical term for the exudate that appeared after removing the staples? Of what does this exudate consist?

A

Purulent exudate – neutrophils, tissue debris and some protein

120
Q

In Mr. Dawes’ case, what factors may delay wound healing? What influence does each factor have on wound healing?

A
  • Age – decreases powers of regeneration and immunity
  • Obesity – fat tissue can put strain on sutures
  • Diabetes – decreased circulation
  • Infection – presence of pus

BIOL 2200 (12 decks)

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