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HLTH 341 - Pathobiology > Test 1 > Flashcards

Test 1 Flashcards

1
Q

define

health

L2

A

a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity

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2
Q

define

disease

L2

A

deviation from the normal structure or function of any part of an organ, system, or any deviation from a state of wellness

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3
Q

define

physiology

L2

A

the biological study of processes and mechanisms operating within an organism

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4
Q

define

pathophysiology

L2

A

study of abnormalities in physiologic functioning of living beings

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5
Q

what are some inclusions and considerations in pathophysiology?

L2

A
  • disturbances: mechanical, physical, biochemical
  • disturbance causes: internal and/or external factors
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6
Q

define

pathology

L2

A

medical discipline of study that examines organs, tissues, cells, and bodily fluids for the diagnosis of disease conditions during a state of disease

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7
Q

define

histology

L2

A

study of cells and tissues using microscopic investigation and examination

  • slicing an dstaining a tissue sample to look at markers
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8
Q

define

histopathology

L2

A

study of cells and tissues affected by disease using microscopic investigation and examination

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9
Q

define

pathobiology

L2

A

study of pathology with more emphasis on the biological aspects

biological > medical

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10
Q

explain

pathology framework

L2

A
  1. etiology: causes of disease
  2. pathogenesis: mechanisms of disease
  3. cellular damage
  4. clinical manifestations: signs and symptoms
  5. diagnosis
  6. treatment
  7. prevention
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11
Q

define

etiology

L2

A

the cause or reason for disease initiation and progression

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12
Q

define

risk factor

L2

A

a factor that increases the likelihood of a disease when present

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13
Q

explain

types of etiological factors

L2

A
  • intrinsic: from within the body (genetic, congential, immunological)
  • external: from outside the body (biological, chemical, physical agents, nutritional imbalances)
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14
Q

list

etiology classifications

L2

A
  1. congenital: in-born
  2. degenerative
  3. iatrogenic: physician induced
  4. idiopathic: unknown cause
  5. immunologic
  6. infectious
  7. inherited/genetic
  8. metabolic
  9. neuroplastic: cancers
  10. nutritional deficiency
  11. physical agent-induced
  12. psychogenic: mental
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15
Q

define

pathogenesis

L2

A

the disease process leading to the development or evolution of disease

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16
Q

describe

what type of changes occur during pathogenesis? what do they result in?

L2

A
  • cellular and molecular changes
  • result in structural and functional abnormalities
  • involves intra and intercellular communication
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17
Q

define

clinical manifestations

L2

A

the clinical signs and symptoms of a disease

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18
Q

define and describe

signs

L2

A

visible and/or measurable changes/disturbances
* objective and observed

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19
Q

define and describe

symptoms

L2

A

patient’s report of their feelings
* subjective and reported

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20
Q

define and describe

syndrome

L2

A

combination of characteristic signs and symptoms for a particular disease

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21
Q

define and describe

sequela

L2

A

pathologic condition resulting from an illness

*long-term or permanent

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22
Q

describe

stages/timeline of the clinical course of disease

L2

A
  1. onset: acute or insidious
  2. latent (subclinical/silent): time between exposure of tissue to injurious agent and first appearance of signs/symptoms
  3. prodromal stage: time during which first signs and symptoms appear (may be generic and non-specific)
  4. acute stage: full intensity and, often, specific signs and symptoms
  5. convalescence stage: recory stage
  6. remission: decrease in severity, subsiding of signs and symptoms
  7. exacerabtion: flare up, sudden increase in disease severity with return of signs and symptoms
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23
Q

define

acute

L2

A

short lived, quick and intense

typically includes most infectious diseases

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24
Q

define

chronic

L2

A

long-lived, slow and gradual

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25
Q

describe

acute infection timeline

L2

A

the state of the virus disappears after the disease ends

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26
Q

describe

chronic infection timeline

L2

A

after initial infection, infectious virus is released from host w/o symptoms

viral agent remains despite no signs/symptoms

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27
Q

describe

latent infection timeline

L2

A

after initial infectious virus is kept in dormant state, which can be reactivated to produce new signs and symptoms

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28
Q

define

clinical parameters

L2

A

measures that help determine extent of disease severity based on comparison to normal values

often quantitative

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29
Q

describe

traits and uses of clinical parameters

L2

A

used to screen, predict, diagnose, and determine disease progression

can be structural, physiologic, biochemical, and genetic

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30
Q

what are clinical parameters assesed based/on?

L2

A
  1. direct observation/examination
  2. direct measures
  3. assessment of clinical samples
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31
Q

describe

the state and use of normal in clinical parameters

L2

A

bell-shaped curve based on a collection of values in a normal population

used to assess changes in the context of trends or patterns

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32
Q

define and describe

treatment (and what it involves)

L2

A

utilizes evidence-based approach to either circumvent or mitigate disease progression and/or facilitate return abnormal physiological situations back to normal

can involve:
* medical intervention
* change in behaviour
* psychological attention

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33
Q

define

prophylaxis

L2

A

ongoing preventative treatment

i.e. antimalarial drugs, PrEP

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34
Q

describe

what is the difference between prophylaxis and immunization?

L2

A

prophylaxis - not long-term if you stop taking the treatment
immunization - antigen based to illicit antibody responses for long-term prevention via immunological memory

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35
Q

define

prognosis

L2

A

probability or likelihood of recovery

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36
Q

compare

PrEP vs PEP

L2

A

PrEP:
* 2 or more HIV antiretrovirals
* reduce risk of HIV infection
PEP:
* take within 72 hours of exposure
* prevent HIV infection in emergency situations
* not a long term solution

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37
Q

define

primary prevention

L2

A

prevention of disease by altering susceptibility or reducing exposure for susceptible individuals

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38
Q

define

secondary prevention

L2

A

applicable in early disease, early detection and disease management

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39
Q

define

tertiary prevention

L2

A

in the stage of progressed disease or disability, attempts to alleviate disability and restore effective functioning

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40
Q

define

synaptic

L2

A

signaling mechanism within the nervous system with the use of nt

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41
Q

define

paracrine

L2

A

target cell and cell that produced the signaling molecule are located in the same area

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42
Q

define

endocrine

L2

A

hormones produced by specialized cells travel through the bloodstream to impact target cells

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43
Q

define

autocrine

L2

A

localized signaling mechanism in which target sell is the same cell that produced and secreted the small signaling molecule

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44
Q

what are types of reversible cell damage?

L3

A
  • cellular/hydropic swelling
  • intracellular communications
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45
Q

what are some types of irreversible cell damage/injury?

L3

A
  • necrosis
  • apoptosis
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46
Q

what are the 3 timelines of cell damage?

L3

A
  1. temporary, short lived, reversible
  2. long term, adaptation
  3. long term, irreversible, permanent and severe consequences
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47
Q

what are some types of infectious agents that can cause cell injury?

L3

A
  • bacteria
  • viruses
  • parasites
  • fungi
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48
Q

what are some types of bacteria that can cause cell injury?

* different classification systems

L3

A
  • gram-negative vs gram-positive
  • exotoxins vs endotoxins
  • via secretion systems, adhestions, and/or effectors
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49
Q

what are some considerations that should be made for cell injury caused by infectious agents

L3

A
  • infectious agent, virulence
  • reservoirs
  • route of transmission
  • host factors and susceptibility - human host factors and microbiome
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50
Q

what is the order of the timeline for cell damage/injury?

L3

A
  1. cell function deterioration
  2. cell death
  3. ultrastructural changes
  4. light microscopic changes
  5. gross morphological changes
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51
Q

what are some important considerations for determining the physiological impacts of a disease?

L3

A
  1. cell type
  2. cell type in the context of the tissue
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52
Q

what are some cells that can withstand damage for a long time before experiencing severe damage?

what about those that cannot?

L3

A

hepatocytes (liver): can withstand damage for a long time
cardiomyocytes: can only withstand short damage

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53
Q

what is tissue tropism?

L3

A

the specificity in the types of tissue that can support/host a given pathogen

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54
Q

what are some things that determine the severity of disease by an infectious agent?

L3

A
  1. human host factors
  2. human microbiome
  3. environmental factors
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55
Q

what are the types of genetic causes of cell injury?

L3

A
  1. chromosomal abnormalities
  2. mutations (loss or gain of function)
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56
Q

what are some things that nutritional injury may result from?

L3

A
  1. poor intake of nutrient rich sources
  2. altered absorption of nutrients across intestinal epithelium
  3. impaired distribution of nutrients by circulatory system
  4. inefficient cellular uptake of nutrients
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57
Q
A
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58
Q
A
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59
Q

what is vitamin K related to?

L3

A

coagulation cascade - made in the gut microbiome

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60
Q

what makes the essential amino acids ‘essential’?

L3

A

you need to derive them from your diet

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61
Q

what is autophagy?

L3

A

cellular response to nutritional depletion to gain nutrients by degrading and recycling intracellular content

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62
Q

what is the process of autophagy?

L3

A
  1. organelles and cytosolic portions captured in phagophore (ER derived double membrane structure, formation initiated by cytoplasmic proteins - ATG)
  2. matures into autophagic vesicle
  3. fusion with lysosomes froms autophagolysosome
  4. lysosomal enzymes digest the cellular components
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63
Q

what is autophagy notable with?

(types of injury)

L3

A

ischemic injury and some myopathies

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64
Q

what are some examples of toxins that can cause cell injury?

L3

A
  • air pollutants
  • insecticides
  • carbon monoxide
  • asbestos
  • cigarette smoke
  • ethanol
  • drugs
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65
Q

how does ionizing radiation induce physical/mechanical injury on a cell?

L3

A
  1. OH attaches to DNA
  2. prevents cell reproduction
  3. DNA mutations
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66
Q

what does the characteristic sequence of events for reversible cell injury include?

L3

A
  1. morphological changes - swelling and intracellular communications
  2. structural changes - membranes, proteins, nucleic acids
67
Q

what is reversible cell injury?

L3

A

cell injury where removal of injurious agent can restore cell morphology and function

68
Q

what type of membranes can damage occur to?

L3

A
  1. cytoplasmic
  2. mitochondrial
  3. lysosomal
69
Q

how can membrane damage occur?

via what?

L3

A
  1. reactive oxygen species
  2. decreased phospholipid biosynthesis (b/c of hypoxia nad nutrient deprivation)
  3. increased phophatase activity (degradation)
  4. cytoskeletal disruption abnormalities that disrupt the anchors for plasma membranes
70
Q

what is the mechanism of the unfolded protein response?

L3

A
  1. activation of IRE-1 sensor in ER membrane
  2. enhanced expression of chaperone proteins
  3. reduced protein translation processes
71
Q

via what pathway does excessive misfolded protein accumulatipon trigger apoptosis?

L3

A

intrinsic pathway
* activation of BH3 proteins and caspases

72
Q

what is the most common cause of cell injury?

L3

A

ischemia

73
Q

what is tissue hypoxia most often caused by?

L3

A

ischemia - lack of oxygen causes cells to undergo reduced mitochondrial oxidative phosphorylation (compromised ATP production)

74
Q

is ischemia and hypoxic injury reversible or irreversible?

L3

A

reversible once oxygen supplies are restored

75
Q

what is the process for ischemia cause hydrophic swelling?

L3

A
  1. lack of oxygen
  2. depletion of ATP

pathway one
1. dysregulated ATP-pumps (i.e. Na/K ATPase)
2. sodium accumulates in cells
3. water is retained/flows into cells

pathway two
1. calcium pumps
2. release of calcium stores
3. apoptosis triggered
4. activation of phospholipase and protease
5. degradation of phospholipids and proteins

76
Q

what does compensatory anaerobic metabolism result in?

L3

A

lactice acidosis

77
Q

what are 3 ways ischemia-reperfusion causes cell injury?

L3

A
  1. calcium overload - unregulated influx of calcium can trigger apoptosis and activate enzymes
  2. formation of ROS - superoxide, hydrogen peroxide, hydroxyl radicals
  3. inflammation - increase in leukocytes and plasma proteins that activate complement cascade
78
Q

how are free radicals dealt with?

L3

A
  1. superoxide converted to hydrogen peroxide via superoxide dismutase
  2. hydrogen peroxide (more stable and can cross membranes) converted to water via glutathione peroxidase
79
Q

what are the main things that necrosis can result from?

L3

A
  1. ischemia
  2. toxins
  3. infectious agents
  4. trauma
80
Q

what is necrosis NOT marked by?

L3

A

biochemical signals or mechanisms

81
Q

describe some of the traits of general necrosis

L3

A
  1. loss of nuclei and tubule architecture
  2. leakage/spillage of cellular contents
82
Q

what are the cytoplasmic changes involved in necrosis?

L3

A
  1. breakdown of plasma membrane, organelles, and nucleus
  2. amorphous deposits in mitochondria
  3. leakage of contents
  4. inflammation
83
Q

what are the phases of the nuclear changes during necrosis?

L3

A
  1. pyknosis
  2. karyorrhexis
  3. karyolysis
84
Q

what are some of the key features of necrosis?

think:
cell size
nucleus
pl. mem.
cell contents
adj. inflammation
role

L3

A
  • cell size - enlarged (swelling)
  • nucleus - lysis pathway (pkk)
  • pl. mem - disrupted
  • cellular contents - intact
  • adj. inflammation - frequent (elicits immune responses)
  • role - pathologic
85
Q

what are some of the key features of apoptosis?

cell size
nucleus
pl. mem.
cell contents
adj. inflammation
role

L3

A
  • cell size - reduced (shrinkage)
  • nucleus - fragmentation
  • pl. mem - intact but altered structure
  • cellular contents - often released in apoptotic bodies
  • adj. inflammation - absent
  • role - commonly physiologic
86
Q

what is the most common type of necrosis?

L3

A

coagulative

87
Q

define and describe: coagulative necrosis

starts/ends with, speed, tissue structure, key trait

L3

A

starts with: ischemia
ends with: plasma membrane degradation, solid/firm mass
speed: slow
tissue structure/shape: kept
key trait: altered/denatured proteins (structural and enzymatic) causing coagulation, enzymatic destruction

88
Q

define and describe liquefactive necrosis

speed, cause, can result in, via, advances by

L3

A

speed :fast
cause : dissolution of dead cells via lysosomal enzymes
can result in : abscess or cyst from dissolved dead tissue
via: excessive enzymatic activity from dying cells and recruited immune cells
possible advanced by: bacteria and bacterial toxins

89
Q

define and describe fat necrosis

cause, appearance, what, key enzyme

L3

A

cause: trauma to abdominal cavity or pancreatitis
appearance: chalky white wlumps in peritineal cavity
what: death of adipose tissue
key enzyme: pancreatic lipase (breaks down triglycerides)

90
Q

define and describe caseous necrosis

appearance, characteristic of, process, surrounding tissue

L3

A

appearance: clumpy cheese tissue with thick yellow appearance
characteristic of: Tb infections (mycholic acid in conjunction with immune cells - macrophages)
process: death of granuloma cells causes enzymatic release and related death via enzymatic activity
surrounding tissue impacts: death of surrounding tissue

91
Q

define grangrenous necrosis

(what are the types)

L3

A

cellular death in a large area of tissue that has undergone necrosis for multiple layers due to loss of blood supply (perfusion) for an extended period of time

types: dry, wet, gas

92
Q

describe dry gangrene

L3

A
  • coagulative necrosis
  • blackened, dry, wrinkled skin, foul smell
  • line of demarcation
  • slow
93
Q

describe wet gangrene

L3

A
  • liquefactive necrosis
  • typicall in internal organs
  • can be fatal
  • fast
  • often in conjunction with internal organ infection
94
Q

describe gas gangrene

L3

A
  • infection of necrotic tissue by Clostridium (anaerobic bacteria)
  • formation of gas bubbles in damaged muscle tissue
  • can be fatal
95
Q

define and describe fibrinoid necrosis

L3

A

visualization requirement: microscopic investigation
histopathology: bright pink via H&E staining
result of: immune response with antigen-antibody complexed
process: plaques conglomerate on vessel walls
common in: hypertension, vasculitis, transplant rejection

96
Q

describe atrophy

L3

A
  • decrease in cell size
  • often due to reduced use (denervation, ischemia, nutrient starvation, endocrine interruption)
  • can be a normal aging process
97
Q

what is often associated with atrophy?

L3

A

thinning of skin and hair loss in the affected area

98
Q

describe hypertrophy

L3

A
  • increase in cell size
  • accompanied by augmented functional capacity (response to increased demands)
  • caused by increased cellular protein content, hormones, or persistent injury
99
Q

what can hypertrophy be combined with?

L3

A

hyperplasia

100
Q

describe hyperplasia

L3

A
  • increase in cell number to allow increased functional capacity
  • possible causes: increased demand, persistent cell injury, chronic epithelial cell irritation
  • can be normal (puberty)
101
Q

describe metaplasia

L3

A

when a mature cell type is replaced by another differentiated mature cell type
* via injury, pressure, assault

102
Q

describe Barrett’s esophagus

what type of cellular adaptation is it?

L3

A

replacement of squamous cells with columnar cells
* risk of adenocarcinoma (glandular cancer)
* in cells lining bronchi

103
Q

describe dysplasia

L3

A

cells appear disorganized, vary in shape and size within a tissue

104
Q

describe neoplasia

L3

A

new cell growth (tumor)

105
Q

describe hydrophic swelling

L3

A
  • reversible cell damage
  • accumulation of water due to defective Na/K pump
  • megaly: general swelling of cells in organs leading to an increase in size and weight
106
Q

describe intracellular accumulation

L3

A

an excess of:
* normal intracellular substance
* faulty metabolism or synthesis
* pigments or particles unable to be degraded

107
Q

caseation necrosis refers to an area where:
a. cells are liquefied by enzymes
b. cell proteins have been denatured
c. dead cells form a thick cheesy substance
d. neoplastic invasion has occurred

A

c. dead cells form a thick cheesy substance

108
Q

which of the following would be the most likely cause of an iatrogenic disease?
a. an unwanted effect of a prescribed drug
b. a combination of specific etiological factors
c. prolonged exposure to toxic chemicals in the environment
d. an inherited disorder

A

a. an unwanted effect of a prescribed drug

109
Q

with reference to a single signaling molecule, which statement is correct?
a. will always elicit the same response regardless of the target cell type
b. will alway elicit the same response regardless of the receptor type
c. may elicit different responses in different target cells or after binding with different receptor type
d. none of the above

A

c. may elicit different responses in different target cells or after binding with different receptor type

110
Q

what are the main cells of the immune system?

A
  1. erythrocytes
  2. thrombocytes
  3. granulocytes
  4. mast cells
  5. macrophages
  6. B cells
  7. T cells
111
Q

what are some examples of non-specific physical barriers?

A
  • epithelial layers and barriers
  • cell junctions
  • cilia/mucociliary escalator
  • mucous
  • defacation/urination
112
Q

what are some examples of non-specific chemical barriers?

A
  • tears, saliva, earwax, sweat glands, sebum
  • antimicrobial substances
  • stomach acid and mucous
  • defacation/urination
  • sneezing, coughing, vomiting
113
Q

what are the main cells of the immune system?

A
  1. erythrocytes
  2. thrombocytes
  3. granulocytes
  4. mast cells
  5. macrophages
  6. B cells
  7. T cells
114
Q

define leukocytes

A

primary cells of the immune system (wbc)

115
Q

list the types of leukocytes

A
  • granulocytes - neutrophils, eosinophils, basophils (mast cells)
  • monocytes and macrophages (dendritic cells)
  • lymphocytes (NKC, T-cells, B-cells)
116
Q

describe neutrophils

A
  • polymorphonuclear leukocytes (PMNs)
  • important for acute bacterial infections
  • get recruited to areas of inflammation
  • release toxins during defense - free radicals, defensins, proteolytic enzymes (elastase), can cause damage to normal tissue when in excess (degrade & destroy rather than defense)
117
Q

describe eosinophils

A
  • circulating granulocytes
  • stain red-orange with eosin
  • increased # during allergic reactions and intestinal parasite infections
  • major function: kill intestinal worms
118
Q

define basophils

A

granulocytes that when mature circulate in vascular system but then can migrate into connective tissue and do not reenter bloodstream

119
Q

define and describe mast cells

A

definition: basophils that have migrated into connective tissue
* typically live for weeks to months
* contain histamines that contribute to inflammatory response
* degranulation of basophils and mast cells - begin inflammatory response
* involved with wound healing and chronic inflammatory conditions

120
Q

describe the breakdown of different leukocytes (%)

A
  • neutrophils - 60-80%
  • lymphocytes - 20-30%
  • monocytes - 3-8%
  • eosinophils - 1-6%
  • basophils - 0-2%
121
Q

describe the role in inflammation of different leukocytes

A
  • neutrophils - phagocytosis (first to appear after injury)
  • lymphocytes - immune response
  • monocytes - phagocytosis
  • eosinophils - allergic reactions, parasite infection
  • basophils - initiate inflammation and mediate type I allergic reactions
122
Q

describe macrophages

A
  • undergo maturation from monocytes in circulation
  • major role in phagocytosis
  • can proliferate at site of inflammation
  • identify foreing entities via cell surface receptors
  • function in antigen presentation via MHC-II (adaptive immunity)
  • secrete cytokines
123
Q

what cytokines do macrophages secrete?

A

IL-1, IL-6, IL-12, TNF-alpha

124
Q

what are the macrophages of the following tissues:
* lung
* brain
* liver
* connective tissue

A
  • lung - alveolar macrophages
  • brain - microglial cells
  • liver - Kupffer cells
  • connective tissue: histiocytes
125
Q

describe dendritic cells

A
  • located throughout body within mucous membrane
  • major role in phagocytosis and antigen presentation via MHC-II
  • can produce IFN-alpha and IFN-beta, and cytokines
126
Q

what are some of the components of dendritic cells and their functions (8)?

A
  1. IL-12 - stimulate helper T and NK cells
  2. fibroblast - growth factor simtulates wound healing
  3. IL-10 - promotes expresison of MHC II
  4. IL-6 - stimulates B-cell growth and inflammation
  5. IL-1 - promotes inflammation
  6. colony sitmulating factors - promote hemtopoeisis
  7. IL-15 and 18 - promote NK profliferation
  8. tumor necrosis factor-alpha - promotes inflammation
127
Q

describe natural killer cells

A
  • innate immunity function
  • released into circulation
  • don’t contain B or T cell markers (no adaptive immunity)
  • kill tumors and virally infected cells w/o previous exposure
  • use Fc receptors to recognize antibody coated cells
  • respond to numerous antigens
  • action: antibody-dependent cell mediated cytotoxicity (ADCC)
128
Q

describe T cells and their types

A

t-cells: mature in thymus and have a specific role in adaptive immunity
cytotoxic: have CD8 protein markers
helper: have CD4 protein markers - active other T cells and macrophages, stimulate B cell proliferation and antibody production, secrete pro-inflammatory cytokines

129
Q

describe B-lymphocytes

A
  • produce antibodies and have antibody like receptors
  • carry many copies of identical B receptors
  • respond to one antigen per epitope - form reserve that quickly mount immune response
130
Q

define and describe phagocytosis

A
  • process of cell engulfment of large materials
  • can be facilitated by cell surface receptors (Mannose)
  • cell surface receptors can include pattern recognition receptors (TLR, Mannose)
  • key : phagolysosome fusion
131
Q

define phagocytes and describe their roles

A

cells that perform phagocytosis
* routinely monitor and survey for foreing entities
* engulf and digest foreign entities
* cells: macrophages (slow and long), dendritic cells, neutrophils (rapid and short)

132
Q

what are some things that can avoid phagolysosomal fusion?

A
  • salmonella - avoids enzymatic damage so stays intact in the cells
  • mycobacterium - cell wall too thick to be degraded
133
Q

how can phagocytosis be efficiency enhanced?

A

via opsonization (speckling of foreign bacteria with complement features)

134
Q

what are the granular contents of a phagocyte?

A
  • enzymes
  • oxidase
  • MPO (myelperoxidase)
135
Q

what are the stages of phagocytosis?

A
  1. recognition and attachment - microbes bind to phagocyte receptors
  2. engulfment - phagocyte membrane zips up around microbe
  3. killing and degradation - degradation by lysosomal enzymes
136
Q

what are the 3 types of complement cascades? what do they differentiate by?

A

differentiate by initiation
1. classical - antibody-antigen complexes (Ag+Ab)
2. alternative - identifies microbial antigens (lipopolysaccharide) and endotoxins (C3 activation)
3. lectin - binding to mannose

137
Q

how can autoimmune disorders occur due to complement cascades?

A

gene deficiency in inhibitors resulting in an unregulated pathway and self-destruction

138
Q

what denotes the active version of a component of the complement cascade?

A

designation with a letter

139
Q

define the complement components with the following roles:
* opsonization
* mast cell degradation
* vascular permeability
* MAC (lysis)
* bronchospasm (anaphylatoxins)
* chemotaxis
* neutrophil recruitment and activation

A
  • opsonization - C3b
  • mast cell degradation - C3a
  • vascular permeability - C2a, C5a
  • MAC (lysis) - C5b, C6, C7, C8
  • bronchospasm (anaphylatoxins) - C3a
  • chemotaxis - C5b67
  • neutrophil recruitment and activation - C5a
140
Q

what is the complement pathway of the classical complement cascade?

A
  1. C1
  2. combination of C2 and C4 into an enzyme
  3. C3 activation
  4. C3 split to C3a and C3b
  5. C3b joins to C5 splitting it to C5a and C5b
  6. C5b forms MAC complex
  7. insertion of large pore in membrane, cell lysis
141
Q

what are the effector functions of the following complement components:
* C5a, C3a
* C3b
* MAC

A
  • C5a, C3a - inflammation: recruitment and activation of leukocytes, destruction of microbes
  • C3b - phagocytosis: recognition of bound C3b by phagocyte C3b receptor, phagocytosis of microbe
  • MAC - lysis
142
Q

what are the pro-inflammatory mediators? (just list)

A
  • histamine
  • leukotrienes
  • prostaglandins
  • kinins (bradykinin)
143
Q

describe the function of histamine as a pro-inflammatory mediator

A
  • is a vasoactive amine
  • secreted from granules of mast cells
  • causes vasodilation and capillary permeability that results in exudate formation
  • exudate - fluid cell mix that seeps from vessels (part of reason for swelling)
  • can occur due to: IL-1, IL-8, injury, allergic response
144
Q

describe the function of leukotrienes as a pro-inflammatory mediator

A
  • synthesized from arachidonic acid in mast cells via lipooxygenase
  • cause vasodilation, capillary permeability, chemotaxis, bronchospasm
  • LTB4 is a chemotactic
145
Q

describe the function of prostaglandins as a pro-inflammatory mediator

A
  • synthesized from arachidonic acid in mast cells via cyclooxygenase (COX1, COX2)
  • cause vasodilation, capillary permeability, pain, fever, increases effects of histamine
146
Q

describe the functions of kinins as a pro-inflammatory mediator

A
  • activates plasma proteins
  • linked with clotting mechanisms (coagulation cascade)
  • causes vasodilation, capillary permeability, pain, chemotaxis
147
Q

describe the role of lipoxins in inflammation

A
  • anti-inflammatory mediator
  • inhibits chemotaxis, and recruitment/adhestion to the endothelium
  • provides ‘reset’ of inflammatory response
148
Q

what is the role of COX-inhibitors in mediating inflammation?

A
  • inhibit COX1 and COX2
  • inhibit prostaglandin synthesis
  • i.e. aspirin and NSAIDs (ibuprofen)
149
Q

what is the role of lipoxygenase inhibitors in mediating inflammation?

A
  • inhibit leulotriene production
  • asthma treatment
  • i.e. zileuton
150
Q

what is the role of corticosteroids in mediating inflammation?

A

reduce transcription of genes for:
* COX2
* phospholipase A2
* proinflammatory cytokines (Il-1, TNF)
* iNOS

151
Q

what is the role of leukotriene receptor agonists in mediating inflammation?

A
  • block leukotriene receptors and prevent the actions of leukotrienes
  • treatment of allergic asthma and allergic rhinitis
  • i.e. zarfirlukast
152
Q

what types of cells are cytokines released by?

A

immune: activated lymphocytes, macrophages, DCs
non-immune: endothelial, epithelial, CT

153
Q

what are the factors of cytokines?

A
  • IFNs
  • ILs (1-33)
  • TNF
  • TGF
  • CSF factors
  • chemokines
154
Q

describe cytokines and their functions

A
  • small peptide molecules that bind to cell surface receptors
  • impact the functioning of other cells
  • involved in intercellular communication network
  • enhance and coordinate innate and specific immune defenses
  • grouped according to source and function - proinflammatory, antiinflammatory, coagulatory
155
Q

what types of cytokines are used in acute inflammation? chronic?

A

acute - TNF, IL-6, IL-1, chemokines
chronic - IL-12, IFN-gamma, IL-17

156
Q

what are the effects of cytokines on local inflammation? what components are used to do this?

A

effect
* macrophages: cytokine and chemokine secretion (T-cells -> IL-17 -> acute inflammation)
* neutrophils: enhanced response
* fibroblasts: collagen production (hardening with production of basement membrane)

process
* E and P-selectin: endothelial cell adhesion molecules
* integrins: leukocyte recruitment

  1. increased expression of adhesion molecule and endothelial activation causes activation of leukocytes and other cells
157
Q

what are the systemic protective effects of cytokines in the brain?

A

stimulation by TNF and IL-1 causes fever response to facilitate clearing of foreign entities

158
Q

what are the systemic protective effects of cytokines in the liver?

A

stimulation by IL-1 and IL-6 causes production of acute phase proteins
* C-reactive protein - increased levels in myocardial infarction
* fibrinogen - ESR (erythrocyte sedimentation rate)
* serum amyloid A - increased levels with acute inflammation

159
Q

what are the systemic protective effects of cytokines in the bone marrow?

A

stimulation by TNF, IL-1 and IL-6 causes increased leukocyte production and release to circulation
* results in some immature leukocytes being released

160
Q

what are the systemic pathological effects of TNF and IL-1?

A
  • risk of systemic inflammatory response syndrom (SIRS)
  • sustained vasodilation
  • reduced cardiac output via reduced myocardial contractility
  • reduced blood pressure
  • cachexia
161
Q

what is cachexia?

A

loss of weight and anorexia
* often when you have cancer or long term infectious agent
* protein mobilization and metabolism
* lipid mobilization and metabolism
* loss of appetite
* severe depletion of musculature

162
Q

what are the 4 main groups of chemokines?

A
  1. CXC
  2. CC
  3. C
  4. CX3C
163
Q

what is bradykinin and what effects does it have?

A

polypeptide with vasodilation effects
* active in inflammation
* linked with clotting mechanisms/ helps initiate clotting
* increased vacular permeability
* smooth muscle contractions
* can contribute to localized pain

HLTH 341 - Pathobiology (3 decks)

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