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Pathophysiology > Inflammation, Inflammatory Response and Fever > Flashcards

Inflammation, Inflammatory Response and Fever Flashcards

1
Q

Inflammation: what are the two functions? What type of cells does it occur in? What is it controlled by?

A
  1. eliminates harmful agent.
  2. Sets stage for healing repair.
    - Occurs in necrotic cells/ tissue.
    - Controlled by cells and mediators (cytokines) two types: acute and chronic
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2
Q

acute inflammation: what is stimulates it? timeframe of action? process? what predominates?

A

trigger: harmful stimuli or conditions of infection/injury. time:comes on in min-hrs, lasts hrs-days.
process: exudation of fluid and plasma proteins, emigration of neutrophils.
NEUTROPHILS PREDOMINATE THIS

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3
Q

chronic inflammation: timeframe? process? what predominates?

A

time:lasts days to years.
process:proliferation of blood vessels, tissue necrosis + fibrosis.
MACROPHAGES, EOSINOPHILS, + MAST CELLS PREDOMINATE

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4
Q

types of inflammatory cells

A

endothelial (includes basophils, eosinophils, lymphocytes, platelets, neutrophils, monocytes.. aka all from myeloid stem cells).
platelets/thrombocytes,
leukocytes: (granulocytes-neutrophils, eosinophils, basophils, mast cells) + (agranulocytes-monocytes/macrophages)

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5
Q

cells in surrounding tissue (not endothelial)

A

mast cells, fibroblast, elastin, collagen, macrophage, proteoglycan filaments

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6
Q

endothelial cells: 3 general functions- then expand on each

A

“skin cells of the blood”
-barrier: to microbes and inflammatory mediators (cytokines)
-regulates…
…leukocyte extravasion via expression of adhesion molecules + receptors.
…immune response via releasing inflammatory mediators. …immune cell prolif. via secretion of hematopoietic colony stimulating factors
-helps repair process, producing GFs that stimulate angiogenesis + matrix formation.

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7
Q

platelets (thrombocytes) - critical for? activated by?

A
  • critical for normal hemostasis (blood flow ) + clotting
  • once activated, pLts(platelets) secrete >300 proteins- majority are inflamm. mediators.
  • pLts activated by PAF (platelet activating factor)
  • activated by injury (external and internal)
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8
Q

Leukocytes (WBCs): function in inflammation (3 stages). types of leukocytes?

A

MAJOR cell component in inflamm.

  • enter tissue then
    1. destroy infective organisms
    2. removing damaged cells
    3. releasing inflammatory mediator cells to control further infl. and healing
  • Types: granulocytes + agranulocytes
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9
Q

granulocytes include…

A

neutrophils, eosinophils, basophils, mast cells

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10
Q

neutrophils- function? timing for arrival?immature neutrophils? granules contain?

A

MOST important granulocytes: compose 60-70% of WBCs

  • arrive 1st, w/in 90min of inflammation + engulf pathogens
  • last up to 10hrs, need to be replenished quickly, all die in apoptosis 24-48hrs
  • bands (“baby” immature neutrophils) are in circulation but in very low amts
  • granules: contain enzymes that phagocytize microbes and dead tissue
  • O2 dependent metabolic pathways that generate toxic O2 and nitrogen (help phagocitize pathogens as well)
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11
Q

bands

A

immature “baby” neutrophils; these are in bone marrow but ineffective, only called out of bone marrow when there is a dire need- neutrophils are exhausted (like sepsis)

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12
Q

Eosinophils- timeline for arrival? granules contain? lifespan

A

compose 2-3% of all WBCs

  • arrive 3 hrs after neutrophils
  • longer lifespan - present in chronic inflammation
  • granules contain a protein highly toxic to worms that are too big to phagocytize.. elevated count of this means parasitic (or allergic rxn)
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13
Q

basophils - function? granules contain?

A

compose <1% of all WBCs

  • in allergic rxns esp. w/ IgE, causing vasodilation (redness, swelling, itching)
  • granules release histamine + other vasoactive substances
  • these are precursors to mast cells which develop when a basophil leaves the circulation
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14
Q

what are cytokines?

A

mediators help with cell movement

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15
Q

agranulocytes include?

A

monocytes/macrophages

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16
Q

monocytes/macrophages: produce? function? timeframe?

A

compose: 3-8% of WBCs
- are monocytes for about 1 day then macrophage in the tissues.
- produce: vasoactive mediators (prostoglandins, leukotrienes, PAF,inflammatory cytokines + GFs)
- help to: destroy all caustic agents, bacterial killing, signal process of immunity (as opposed to inflammation), resolve inflammatory process and initiate healing
- 24 to get to site of injury but then take over + stay
- important in chronic inflammation

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17
Q

CAMS (cell adhesion molecules): function? 3 types expanded

A

work to help with recruitment and adherence of WBCs of the endothelial wall

  • selectins: transmembrane proteins, found in endothelial cells (leukos and platelets) - help transport innate immune cells to where they are supposed to be.
  • integrins: proteins that attach to cytoskeleton of ECM
  • immunoglobin super family: cell surface proteins, recognition, binding and adhesion (antibodies and immunoglobulins)
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18
Q

LAD1 and LAD2 - too few or too many?

A

too few of different types:
LAD1- integrins: leukocytes cant get where where they need to be- typically genetic problems- have recurrent infections
LAD2: selectins: usually in middle eastern people (dont know why)- issue with recurrent infections

too many of either: chronic inflammation (i.e. autoimmune disorders)

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19
Q

what is venous dilation? what does it cause?

A

increase in blood flow- rubor (redness) and calor (heat)

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20
Q

increased vascular permeability causes…(3 things)

A

tumor (swelling), dolor (pain) functio laesa (loss of function)

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21
Q

acute inflammatory response:stages

A
  1. vascular stage 2. cellular stage
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22
Q

4 vascular stages

A
  1. momentary vasoconstriction
  2. vasodilation of arterioles and venules (warmth and redness) and then dilates capillaries
  3. increased permeability of capillaries
  4. extravasion of exudate (protein-rich fluid) into extravascular tissues (lead to swelling and pain)
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23
Q

vascular changes are one of the following…

A
  1. immediate transient (minor injury. i.e. papercut)
  2. immediate sustained (major injury)
  3. delayed hemodynamic response (occurs 2-12 hours after injury. ie. sunburn)
  • rapid swelling/tissue expansion causes pain
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24
Q

microcirculation consists of what?

A

arterioles, capillaries, venules

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25
Q

cellular phase- 4 phases

A

all WBCs start working

  1. marginations:lineup along endothelial wall surface- cytokines released, induce endothelial cells to produce CAMs and release cytokines, chemokines, and ROS. TNF alpha induces priming and aggregation of neutrophils
  2. transmigration: WBCs squeeze through junctions into vessel wall and into extravascular space
  3. chemotaxis: WBCs through extraCell space guided by cytokines, cellular debris and complement fragments
  4. phagocytosis: WBCs- recognition, engulfment, + intracellular killing

analogy: drunks lining up, going to bar, eating everything, wreaking havoc on those they dont know

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26
Q

phagocytosis expanded

A
  1. recognition and adherence : microbes can bind to specific receptors on phagocytic cells OR
    can be recognized by their coating on compliment or antibodies (opsinization)
    (2. engulfment then 3. intracellular killing)
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27
Q

types of inflammatory mediators

A

both short lived

  1. plasma-derived
  2. cell-derived
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28
Q

plasma-derived inflamm. mediators: where are they synthesized? what do they do?

A
  • synthesized in liver
  • includes: 1. acute phase proteins, 2. coagulation factors, 3. complement proteins

esentially: they bring more cytokines until the pathogen is killed. gradually decreasing number of CtKs its bringing, then inflammation resolves

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29
Q

interleukins and TNFs (tumor necrosis factors) are ____ kind of proteins

A

acute phase

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30
Q

mast cells produce —–

platelet cells produce —–

A

these are both types of cell derived mediators (subgroup: preformed mediators)
mast cells : histamine
platelet: serotonin
both important in inflammatory response

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31
Q

nitric oxide does what?

A

decreases inflammation (reduces the cellular phase of it), - works against overproduction of platelet (ex/ impaired production of NO is implied in infl. changes in arthresclerosis)

32
Q

histamine: where is it stored? function?

A

-Stored in mast cells at the scene
-Work by producing change in blood vessel tone
-Among the first mediators to be released
-Produces dilation of arterioles and increases permeability of venules.
Acts at the H1 receptors on endothelial cells and is considered the principle mediator of the immediate transient phase of increased vascular permeability in the acute inflammatory response.

33
Q

what do mediators secreted by platelets do? What if they are in excess?

A

increase vascular permeability and alter chemotactic, adhesive + proteolytic properties of endothelial cell.
- too many mediators in excess = problem (i.e. migraines, lupus, arthresclerosis)

34
Q

opsonization

A

Opsonization involves the binding of an opsonin, e.g., antibody, to an epitope (binding side for antibody) on a pathogen. After opsonin binds to the membrane, phagocytes are attracted to the pathogen

35
Q

serotonin: found where? released when?

A

Similar to histamine - involved in inflammation.

Found in the granules of platelets and is released during platelet aggregation.

36
Q

Arachnidonic Acid Metabolites: where is it found? This Acid initiates events that follow what two pathways?

A

Arachidonic Acid:found in the phospholipids of cell membranes
pathways
1- lipoxygenase pathway to produce leukotrienes
2- Cyclooxygenase pathway to produce Prostaglandins and thromboxane
Prostaglandins induce inflammation and potentiate the effects of histamine and other inflammatory mediators

37
Q

What is an example of a leukotriene blocker?

A

singulair/montelukast

38
Q

What is the Cox pathway?

A

makes prostaglandins from arachidonic acid (which induce inflammation, potentiating the effects of histamine and other infl. mediators). Subsequently, causes pain (i.e. menstrual cramps). BUT you need them b/c they keep stomach acid in check. prostoglandins—> inflammation—> pain — > excessive Midol —> pain goes away—> stomach acid persists—> stomach ulcers

39
Q

why are Omega 3 Fatty acids good for you?

A

Omega 6 in cell membrane (produce infl. mediators). Eat O3 and replace the O6, reduces # of infl. mediators produced = reduced overall infl.

40
Q

What are Lymphocytes?

A

Tcells + Bcells. Adaptive Immune System components. Loop of infl. communication (one cell doesn’t do everything) - macrophages produce Tcells that produce CdKs that activate macrophages

41
Q

What can overactivity of adaptive immune system cause?

A

can come from chronic infl. -accumulation of lymphocytes —> scarification (i.e. arthritis pts.)

42
Q

What are memory B cells?

A

adaptive immune system: if you get sick w/ something, body remembers it and is able to fight it off quickly the second time. *These take longer to arrive on site of injury but are VERY effective once they do

43
Q

What are plasma cells?

A

made from activated B lymphocytes, produce antibodies against offending agent

44
Q

what is platelet activating factor (PAF)? where does it come from and what does it cause?

A

Causes platelet aggregation and degranulation but . . .
A phospholipid-derived mediator with a broad spectrum of inflammatory effects- releases serotonin, increases vascular permeability- chemotaxis of WBCs-( too much = anaphylaxis )
Generated by the membrane phospholipids of all the activated inflammatory cells

45
Q

what are two cytokines that are important for inflammation?

A

TNF alpha and IL1 (tumor necrosis factor and interleukin 1). stimulated by bacterial toxins, injury and and immune cells. come from macrophages

46
Q

TNF alpha and IL1 properties and 3 functions

A

hormone-like, low molecular weight proteins (type os CtKs). 1. mediate BP and temp in acute phase response. 2.induce endothelial cells to produce adhesion molecules and release CtKs, chemokines and ROS
3.TNF alpha induces priming and aggregation of neutrophils

47
Q

what are chemokines?

A

type of CtK that recruit and direct migration of infl. immune cells. Generate a chemotaxic gradient by binding to proteoglycans on endothelial cell wall or in ECM.2 types

48
Q

what are the 2 types of chemokines?

A

Inflammatory
Produced in response to bacterial toxins and inflammatory cytokines
Homing
Are made all the time, but are up-regulated during inflammatory reactions

49
Q

ROS- 2 ways they can be released

A

“O2 derived free radicals “
Two ways
Can be released extracellularly with exposure to microbes, cytokines, and immune complexes
(Release of low levels amplify the inflammatory response)
Phagocytic process during cellular phase of inflammatory process

50
Q

what do higher levels of free radicals do? (3 things)

A

Produce endothelial damage
Inactivate antiproteases
Injury to other cell types

51
Q

when does chronic inflammation occur? what is it? two types?

A

result of a recurrent/progressive acute infl. or a low grade, smoldering response that failed to evoke an acute response
Nonspecific vs. granulomatous
Diffuse accumulation of macrophages and lymphocytes.
–>fibroblast proliferation with scar of the connective tissue or the parenchymal tissue of the involved structures

52
Q

what is a granuloma?

A

massing of macrophages surrounded by lymphocytes. modified macrophages resemble epithelial cells (sometimes called epitheloid) - eventually surrounded by connective tissue and isolated

53
Q

Granulomatous inflammation arises when?

A

associated with foreign bodies (splinters, sutures, silica, and asbestos and with microorganisms that cause tuberculosis, syphilis, sarcoidosis, etc.) Things that are hard to “digest” and are not well controlled by other inflammatory mechanisms

54
Q

epitheloid cells in granulomatous inflammation

A

Epithelioid cells in granulomatous inflammation may surround the foreign agent and clump in a mass, with eventual encapsulation (foreign body response) of connective tissue

55
Q

4 types of manifestations of inflammation

A

Acute-phase response
Leukocytosis
Fever
Systemic Inflammatory response -SIR0 (sepsis & septic shock)

56
Q

acute phase response- inflamm. manifestation

7 parts

A

within hrs/days of insult.
Mediated by the release of Cytokines (IL-1, IL-6, and TNFα)
which do the following:
-Change in the conc. of plasma proteins- Liver increases production of acute-phase proteins (w/nonspecific protective functions)
-Increased Erythrocyte Sedimentation Rate (ESR)- b/c of increased proteins
-Fever- secondary to CtKs on thermoregulatory part of hypothalamus
-Increased WBC count- stimulates the bone marrow to produce
-Skeletal muscle catabolism- amino acids used for tissue repair
-Negative nitrogen balance (more released than taken in and used)
-Lethargy- central nervous system reacting to cytokines

57
Q

inflammatory exudates- 5 types

A

Serous- clear protein rich fluid
Hemorrhagic- injury to tissues or lots of RBC leaking from vessels
Fibrinous- thick and sticky with a lot of meshwork
Membranous or pseudomembranous- develop on mucous membranes
Purulent or suppurative degraded WBCs, protein tissue debris

58
Q

WBC accumulation (inflamm. manifestation) expanded

A

accumulation of WBCs-
left shift/bandemia:- elevated white count and they are seeing bands (immature neutrophils) - (lab needed to shift the specimen to see the bands)

  • Bacterial infection- increase in neutrophils
  • Parasitic and allergic- increase in eosinophilia
  • Viral infection –decrease in neutrophils and increase in lymphocytes
59
Q

SIRS expanded

A

Sepsis
Overwhelming infections is resulting in an uncontrolled inflammatory response with large amounts of cytokines being released
- vasodilation, increased vascular permeability, intravascular fluid loss, myocardial depression, and circulatory shock
-*old people may not have fever (body isnt as good at fighting back

60
Q

lymphadenitis

A

Reaction of lymph nodes that drain the area.
Reaction to mediators released from injured tissue or to immunologic response to specific antigen
Painful is usually infectious
Non-painful-think neoplasm ( nodes contain macrophages and lymphoctyes- theyre doing there is swelling)

61
Q

Body Temp: regulated by what? what is the thermostatic set point?

A

Body temperature is regulated by the thermoregulatory center in the hypothalamus.–nervous system feedback and sensors throughout the body

Thermostatic set point- level at which the core temperature is maintained within a normal range
When gets too high heat dissipating measures are taken; too low heat production is increased.
Core > 41 C (105.8F) or < 34C (93.2 F)

62
Q

dramatic changes in temp increase risk for?

A

seizure (lower threshold for it)

63
Q

sources of body heat: metabolism and shivering

A

Metabolism: main source of heat production
Increase of 0.56 C in body temperature for each 7% rise in metabolism
Sympathetic neurotransmitters are released when increase in heat is needed

Shivering controlled by hypothalamus
-Increases the body temperature 3 to 5-fold

64
Q

goose bumps and AV shunt

A

rxn to heat loss:
“Goose bumps”
Lessens the surface area to prevent heat loss

AV shunt- shift the blood flow to more central locations when the shunt is closed (when it’s open you have more heat loss)

65
Q

4 ways the body loses heat

A
  • Radiation - transfer of heat through the air; 60-70% of heat loss
  • Conduction to skin surface – direct transfer of heat from one molecule to another ; inner body to outer
  • Convection – heat transfer through the circulation of air currents
  • Evaporation of sweat – converts water on the skin to water vapor
66
Q

pyrexia and pyrogens

A

Pyrexia- elevation in body temp caused by a CtK induced upward displacement of the set point of the hypothalamic thermoregulatory center.

Pyrogens- substances that cause fever
Endogenous- fever producing mediators from host cells
Exogenous- things that are external that when broken down, for example, will work to increase set point.

67
Q

mechanism of fever

A
  • Release of endogenous pyrogen from inflammatory cells
  • Resetting of hypothalamic thermostatic set point to a higher level (prodrome)
  • Generation of hypo-thalamus-mediated responses that raise body temp (chill)
  • Development of fever with elevation of body temperature to new thermostatic set point
  • Production of temperature lowering responses and return of body temperature to a lower level (flush and defervescence)
68
Q

prodrome

A

just not feeling well before the fever sets in

69
Q

neurogenic fever: what is it? causes? characterized by what?

A

A fever that is produced from injury to the hypothalamus caused by:
CNS trauma
Intracranial bleeding
Increased intracranial pressure
Characterized by high temperature resistant to antipyretic therapy and not associated with sweating. (ibuprofen)
wont help to treat- rapid cooling that is controlled until we get them to normal level and then fix injury

70
Q

4 stages of fever

A

Four stages
1.Prodromal period-
mild nonspecific complaints
2.Second stage (chills)- w/ pyrogen entering the circulation
Chilled and shaking , vasoconstriction/pilo-erection, skin pale and covered with goose flesh
3.Third stage (flush)- vasodilation : Skin warm and flushed
4. Fourth stage (defervescense)- sweating
Initiation of sweating
how quickly you reached fever is more worrisome than how high it is

71
Q

4 types of fever

A

1.Intermittent- temperature returns to normal at least once every 24 hours
Gram neg/pos sepsis, abscesses, acute bacterial endocarditis
2.Remittent- the temperature does not return to normal and varies a few degrees in either direction
3.Sustained- temperature remains above normal with minimal variation
4.Relapsing- one or more episodes of fever, each as long as several days, with one or more days of normal temp in between

72
Q

fever in children

A

Children
Younger than 3 months –fever is dangerous!!!!!
Occult bacteremia or meningitis
Fever defined as rectal temp over 100.4 F or 38 C
Overbundling should be considered as a cause
Classify as high or low risk on the probability of progression to bacteremia of meningitis

Signs of toxicity
Lethargy
Poor feeding
Hypoventilation
Poor tissue oxygenation
Cyanosis

Diagnosis
CXR, blood cx, WBC count, urine, LP

73
Q

fever of 104 in child versus adult

A

less indicative of danger in child- they dont have strong immune system set up yet, more understable they would have high fever

74
Q

probable mechanisms for why elderly dont mount fever response as easily

A
  • Disturbance in sensing of temperature by hypothalamus
  • Alterations in release of endogenous pyrogens
  • Failure to elicit responses that would increase the body temp- i.e.shivering (bad at it)
75
Q

diagnosis and treatment (4) of fever

A 
Diagnosis and treatmentDetermine cause: unknown origin- 101F or higher that is present for 3 weeks or longer look for...
Malignancies
Infections
Drug fever
Cirrhosis

Treatment:

  1. External environment
  2. Support hypermetobolic state (malnourished from shivering/fever calorie burning)
  3. Protections of vulnerable organs and systems
  4. Treatment of causative agent
76
Q

1 C of temperature produces a _____ in heart rate

A

15 bpm increase in heart rate (1F- 10bpm)

Pathophysiology (28 decks)

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