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HLTH 341 - Pathobiology > Test 1 > Flashcards

Test 1 Flashcards

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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
# describe acute infection timeline ## Footnote L2
the state of the virus disappears after the disease ends
26
# describe chronic infection timeline ## Footnote L2
after initial infection, infectious virus is released from host w/o symptoms viral agent remains despite no signs/symptoms
27
# describe latent infection timeline ## Footnote L2
after initial infectious virus is kept in dormant state, which can be reactivated to produce new signs and symptoms
28
# define clinical parameters ## Footnote L2
measures that help determine extent of disease severity based on comparison to normal values often quantitative
29
# describe traits and uses of clinical parameters ## Footnote L2
used to screen, predict, diagnose, and determine disease progression can be structural, physiologic, biochemical, and genetic
30
what are clinical parameters assesed based/on? ## Footnote L2
1. direct observation/examination 2. direct measures 3. assessment of clinical samples
31
# describe the state and use of normal in clinical parameters ## Footnote L2
bell-shaped curve based on a collection of values in a normal population used to assess changes in the context of trends or patterns
32
# define and describe treatment (and what it involves) ## Footnote L2
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
33
# define prophylaxis ## Footnote L2
ongoing preventative treatment | i.e. antimalarial drugs, PrEP
34
# describe what is the difference between prophylaxis and immunization? ## Footnote L2
prophylaxis - not long-term if you stop taking the treatment immunization - antigen based to illicit antibody responses for long-term prevention via immunological memory
35
# define prognosis ## Footnote L2
probability or likelihood of recovery
36
# compare PrEP vs PEP ## Footnote L2
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
37
# define primary prevention ## Footnote L2
prevention of disease by altering susceptibility or reducing exposure for susceptible individuals
38
# define secondary prevention ## Footnote L2
applicable in early disease, early detection and disease management
39
# define tertiary prevention ## Footnote L2
in the stage of progressed disease or disability, attempts to alleviate disability and restore effective functioning
40
# define synaptic ## Footnote L2
signaling mechanism within the nervous system with the use of nt
41
# define paracrine ## Footnote L2
target cell and cell that produced the signaling molecule are located in the same area
42
# define endocrine ## Footnote L2
hormones produced by specialized cells travel through the bloodstream to impact target cells
43
# define autocrine ## Footnote L2
localized signaling mechanism in which target sell is the same cell that produced and secreted the small signaling molecule
44
what are types of reversible cell damage? ## Footnote L3
* cellular/hydropic swelling * intracellular communications
45
what are some types of irreversible cell damage/injury? ## Footnote L3
* necrosis * apoptosis
46
what are the 3 timelines of cell damage? ## Footnote L3
1. temporary, short lived, reversible 2. long term, adaptation 3. long term, irreversible, permanent and severe consequences
47
what are some types of infectious agents that can cause cell injury? ## Footnote L3
* bacteria * viruses * parasites * fungi
48
what are some types of bacteria that can cause cell injury? | * different classification systems ## Footnote L3
* gram-negative vs gram-positive * exotoxins vs endotoxins * via secretion systems, adhestions, and/or effectors
49
what are some considerations that should be made for cell injury caused by infectious agents ## Footnote L3
* infectious agent, virulence * reservoirs * route of transmission * host factors and susceptibility - human host factors and microbiome
50
what is the order of the timeline for cell damage/injury? ## Footnote L3
1. cell function deterioration 2. cell death 3. ultrastructural changes 4. light microscopic changes 5. gross morphological changes
51
what are some important considerations for determining the physiological impacts of a disease? ## Footnote L3
1. cell type 2. cell type in the context of the tissue
52
what are some cells that can withstand damage for a long time before experiencing severe damage? what about those that cannot? ## Footnote L3
hepatocytes (liver): can withstand damage for a long time cardiomyocytes: can only withstand short damage
53
what is tissue tropism? ## Footnote L3
the specificity in the types of tissue that can support/host a given pathogen
54
what are some things that determine the severity of disease by an infectious agent? ## Footnote L3
1. human host factors 2. human microbiome 3. environmental factors
55
what are the types of genetic causes of cell injury? ## Footnote L3
1. chromosomal abnormalities 2. mutations (loss or gain of function)
56
what are some things that nutritional injury may result from? ## Footnote L3
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
57
58
59
what is vitamin K related to? ## Footnote L3
coagulation cascade - made in the gut microbiome
60
what makes the essential amino acids 'essential'? ## Footnote L3
you need to derive them from your diet
61
what is autophagy? ## Footnote L3
cellular response to nutritional depletion to gain nutrients by degrading and recycling intracellular content
62
what is the process of autophagy? ## Footnote L3
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
63
what is autophagy notable with? | (types of injury) ## Footnote L3
ischemic injury and some myopathies
64
what are some examples of toxins that can cause cell injury? ## Footnote L3
* air pollutants * insecticides * carbon monoxide * asbestos * cigarette smoke * ethanol * drugs
65
how does ionizing radiation induce physical/mechanical injury on a cell? ## Footnote L3
1. OH attaches to DNA 2. prevents cell reproduction 3. DNA mutations
66
what does the characteristic sequence of events for reversible cell injury include? ## Footnote L3
1. morphological changes - swelling and intracellular communications 2. structural changes - membranes, proteins, nucleic acids
67
what is reversible cell injury? ## Footnote L3
cell injury where removal of injurious agent can restore cell morphology and function
68
what type of membranes can damage occur to? ## Footnote L3
1. cytoplasmic 2. mitochondrial 3. lysosomal
69
how can membrane damage occur? | via what? ## Footnote L3
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
what is the mechanism of the unfolded protein response? ## Footnote L3
1. activation of IRE-1 sensor in ER membrane 2. enhanced expression of chaperone proteins 3. reduced protein translation processes
71
via what pathway does excessive misfolded protein accumulatipon trigger apoptosis? ## Footnote L3
intrinsic pathway * activation of BH3 proteins and caspases
72
what is the most common cause of cell injury? ## Footnote L3
ischemia
73
what is tissue hypoxia most often caused by? ## Footnote L3
ischemia - lack of oxygen causes cells to undergo reduced mitochondrial oxidative phosphorylation (compromised ATP production)
74
is ischemia and hypoxic injury reversible or irreversible? ## Footnote L3
reversible once oxygen supplies are restored
75
what is the process for ischemia cause hydrophic swelling? ## Footnote L3
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
what does compensatory anaerobic metabolism result in? ## Footnote L3
lactice acidosis
77
what are 3 ways ischemia-reperfusion causes cell injury? ## Footnote L3
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
how are free radicals dealt with? ## Footnote L3
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
what are the main things that necrosis can result from? ## Footnote L3
1. ischemia 2. toxins 3. infectious agents 4. trauma
80
what is necrosis NOT marked by? ## Footnote L3
biochemical signals or mechanisms
81
describe some of the traits of **general** necrosis ## Footnote L3
1. loss of nuclei and tubule architecture 2. leakage/spillage of cellular contents
82
what are the cytoplasmic changes involved in necrosis? ## Footnote L3
1. breakdown of plasma membrane, organelles, and nucleus 2. amorphous deposits in mitochondria 3. leakage of contents 4. inflammation
83
what are the phases of the nuclear changes during necrosis? ## Footnote L3
1. pyknosis 2. karyorrhexis 3. karyolysis
84
what are some of the key features of necrosis? | think: cell size nucleus pl. mem. cell contents adj. inflammation role ## Footnote L3
* cell size - enlarged (swelling) * nucleus - lysis pathway (pkk) * pl. mem - disrupted * cellular contents - intact * adj. inflammation - frequent (elicits immune responses) * role - pathologic
85
what are some of the key features of apoptosis? cell size nucleus pl. mem. cell contents adj. inflammation role ## Footnote L3
* 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
what is the most common type of necrosis? ## Footnote L3
coagulative
87
define and describe: coagulative necrosis | starts/ends with, speed, tissue structure, key trait ## Footnote L3
**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
define and describe liquefactive necrosis | speed, cause, can result in, via, advances by ## Footnote L3
**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
define and describe fat necrosis | cause, appearance, what, key enzyme ## Footnote L3
**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
define and describe caseous necrosis | appearance, characteristic of, process, surrounding tissue ## Footnote L3
**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
define grangrenous necrosis | (what are the types) ## Footnote L3
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
describe dry gangrene ## Footnote L3
* coagulative necrosis * blackened, dry, wrinkled skin, foul smell * line of demarcation * slow
93
describe wet gangrene ## Footnote L3
* liquefactive necrosis * typicall in internal organs * can be fatal * fast * often in conjunction with internal organ infection
94
describe gas gangrene ## Footnote L3
* infection of necrotic tissue by Clostridium (anaerobic bacteria) * formation of gas bubbles in damaged muscle tissue * can be fatal
95
define and describe fibrinoid necrosis ## Footnote L3
**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
describe atrophy ## Footnote L3
* decrease in cell size * often due to reduced use (denervation, ischemia, nutrient starvation, endocrine interruption) * can be a normal aging process
97
what is often associated with atrophy? ## Footnote L3
thinning of skin and hair loss in the affected area
98
describe hypertrophy ## Footnote L3
* increase in cell size * accompanied by augmented functional capacity (response to increased demands) * caused by increased cellular protein content, hormones, or persistent injury
99
what can hypertrophy be combined with? ## Footnote L3
hyperplasia
100
describe hyperplasia ## Footnote L3
* 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
describe metaplasia ## Footnote L3
when a mature cell type is replaced by another differentiated mature cell type * via injury, pressure, assault
102
describe Barrett's esophagus | what type of cellular adaptation is it? ## Footnote L3
replacement of squamous cells with columnar cells * risk of adenocarcinoma (glandular cancer) * in cells lining bronchi
103
describe dysplasia ## Footnote L3
cells appear disorganized, vary in shape and size within a tissue
104
describe neoplasia ## Footnote L3
new cell growth (tumor)
105
describe hydrophic swelling ## Footnote L3
* 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
describe intracellular accumulation ## Footnote L3
an excess of: * normal intracellular substance * faulty metabolism or synthesis * pigments or particles unable to be degraded
107
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
c. dead cells form a thick cheesy substance
108
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. an unwanted effect of a prescribed drug
109
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
c. may elicit different responses in different target cells or after binding with different receptor type
110
what are the main cells of the immune system?
1. erythrocytes 2. thrombocytes 3. granulocytes 4. mast cells 5. macrophages 6. B cells 7. T cells
111
what are some examples of non-specific physical barriers?
* epithelial layers and barriers * cell junctions * cilia/mucociliary escalator * mucous * defacation/urination
112
what are some examples of non-specific chemical barriers?
* tears, saliva, earwax, sweat glands, sebum * antimicrobial substances * stomach acid and mucous * defacation/urination * sneezing, coughing, vomiting
113
what are the main cells of the immune system?
1. erythrocytes 2. thrombocytes 3. granulocytes 4. mast cells 5. macrophages 6. B cells 7. T cells
114
define leukocytes
primary cells of the immune system (wbc)
115
list the types of leukocytes
* granulocytes - neutrophils, eosinophils, basophils (mast cells) * monocytes and macrophages (dendritic cells) * lymphocytes (NKC, T-cells, B-cells)
116
describe neutrophils
* 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
describe eosinophils
* circulating granulocytes * stain red-orange with eosin * increased # during allergic reactions and intestinal parasite infections * major function: kill intestinal worms
118
define basophils
granulocytes that when mature circulate in vascular system but then can migrate into connective tissue and do not reenter bloodstream
119
define and describe mast cells
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
describe the breakdown of different leukocytes (%)
* neutrophils - 60-80% * lymphocytes - 20-30% * monocytes - 3-8% * eosinophils - 1-6% * basophils - 0-2%
121
describe the role in inflammation of different leukocytes
* 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
describe macrophages
* 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
what cytokines do macrophages secrete?
IL-1, IL-6, IL-12, TNF-alpha
124
what are the macrophages of the following tissues: * lung * brain * liver * connective tissue
* lung - alveolar macrophages * brain - microglial cells * liver - Kupffer cells * connective tissue: histiocytes
125
describe dendritic cells
* 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
what are some of the components of dendritic cells and their functions (8)?
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
describe natural killer cells
* 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
describe T cells and their types
**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
describe B-lymphocytes
* 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
define and describe phagocytosis
* 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
define phagocytes and describe their roles
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
what are some things that can avoid phagolysosomal fusion?
* salmonella - avoids enzymatic damage so stays intact in the cells * mycobacterium - cell wall too thick to be degraded
133
how can phagocytosis be efficiency enhanced?
via opsonization (speckling of foreign bacteria with complement features)
134
what are the granular contents of a phagocyte?
* enzymes * oxidase * MPO (myelperoxidase)
135
what are the stages of phagocytosis?
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
what are the 3 types of complement cascades? what do they differentiate by?
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
how can autoimmune disorders occur due to complement cascades?
gene deficiency in inhibitors resulting in an unregulated pathway and self-destruction
138
what denotes the active version of a component of the complement cascade?
designation with a letter
139
define the complement components with the following roles: * opsonization * mast cell degradation * vascular permeability * MAC (lysis) * bronchospasm (anaphylatoxins) * chemotaxis * neutrophil recruitment and activation
* **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
what is the complement pathway of the classical complement cascade?
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
what are the effector functions of the following complement components: * C5a, C3a * C3b * MAC
* **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
what are the pro-inflammatory mediators? (just list)
* histamine * leukotrienes * prostaglandins * kinins (bradykinin)
143
describe the function of histamine as a pro-inflammatory mediator
* 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
describe the function of leukotrienes as a pro-inflammatory mediator
* synthesized from arachidonic acid in mast cells via **lipooxygenase** * cause vasodilation, capillary permeability, **chemotaxis**, bronchospasm * LTB4 is a chemotactic
145
describe the function of prostaglandins as a pro-inflammatory mediator
* synthesized from arachidonic acid in mast cells via **cyclooxygenase** (COX1, COX2) * cause vasodilation, capillary permeability, **pain, fever, increases effects of histamine**
146
describe the functions of kinins as a pro-inflammatory mediator
* activates plasma proteins * linked with clotting mechanisms (coagulation cascade) * causes vasodilation, capillary permeability, pain, chemotaxis
147
describe the role of lipoxins in inflammation
* anti-inflammatory mediator * inhibits chemotaxis, and recruitment/adhestion to the endothelium * provides 'reset' of inflammatory response
148
what is the role of COX-inhibitors in mediating inflammation?
* inhibit COX1 and COX2 * inhibit prostaglandin synthesis * i.e. aspirin and NSAIDs (ibuprofen)
149
what is the role of lipoxygenase inhibitors in mediating inflammation?
* inhibit leulotriene production * asthma treatment * i.e. zileuton
150
what is the role of corticosteroids in mediating inflammation?
reduce transcription of genes for: * COX2 * phospholipase A2 * proinflammatory cytokines (Il-1, TNF) * iNOS
151
what is the role of leukotriene receptor agonists in mediating inflammation?
* block leukotriene receptors and prevent the actions of leukotrienes * treatment of allergic asthma and allergic rhinitis * i.e. zarfirlukast
152
what types of cells are cytokines released by?
immune: activated lymphocytes, macrophages, DCs non-immune: endothelial, epithelial, CT
153
what are the factors of cytokines?
* IFNs * ILs (1-33) * TNF * TGF * CSF factors * chemokines
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describe cytokines and their functions
* 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
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what types of cytokines are used in acute inflammation? chronic?
acute - TNF, IL-6, IL-1, chemokines chronic - IL-12, IFN-gamma, IL-17
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what are the effects of cytokines on local inflammation? what components are used to do this?
**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
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what are the systemic protective effects of cytokines in the brain?
stimulation by TNF and IL-1 causes fever response to facilitate clearing of foreign entities
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what are the systemic protective effects of cytokines in the liver?
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
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what are the systemic protective effects of cytokines in the bone marrow?
stimulation by TNF, IL-1 and IL-6 causes increased leukocyte production and release to circulation * results in some immature leukocytes being released
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what are the systemic pathological effects of TNF and IL-1?
* risk of systemic inflammatory response syndrom (SIRS) * sustained vasodilation * reduced cardiac output via reduced myocardial contractility * reduced blood pressure * cachexia
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what is cachexia?
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
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what are the 4 main groups of chemokines?
1. CXC 2. CC 3. C 4. CX3C
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what is bradykinin and what effects does it have?
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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