Systemic features of inflammation chronic inflammation Flashcards

(40 cards)

1
Q

Fever

A

hypothalamic thermoregulatory center

  • preoptic area of hypothalamus
  • “set point”
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2
Q

regulation of temperature

A

thermoreceptors monitor temperature

-increase in heat loss/conservation of heat/increase in heat production

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3
Q

Nonpyrogenic hyperthermia

A

NOT fever, overcome bodies ability to keep set point, and body temperature goes up
-physiological mechanism unable to increase heat loss sufficiently to offset increased temperature

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4
Q

what cause non-pyrogenic hyperthermia

A

high environmental temperature
increased heat production
exercise/seizures/metabolic diseases
malfunctioning regulatory centers (CNS lesions)

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5
Q

Pyrogenic hyperthermia

A

changes in thermoregulatory set point

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6
Q

causes of Pyrogenic hyperthermia

A
toxins from bacteria such as endotoxin
inflammation
immune responses
cancer
some pharmocological agents
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7
Q

what stimulates a fever?

A
  • stimulation of macrophages by exposure to endotoxin, viruses, inflammation or lymphocyte products
  • production of “endogenous pyrogens” from mononuclear cells (monocytes, macrophages, Kupfer cells) IL1/6 TNF
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8
Q

how do endogenous factors start a fever?

A

endogenous pyrogens (IL-1/6/TNF)-> enter the brain and act directly on hypothalamus to cause local production of PG’s by COX-3-> physiological conservation of heat to raise temperature set point

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9
Q

adverse affects of having a fever?

A

inactivity, chills, sweats, anorexia, discomfort, seizures

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10
Q

Lymphadenitis

A

inflammatory mediators, debris and infectious organisms drain into local and regional lymph nodes-> cause hyperplasia of lymph nodes and cause stimulation of immune system

  • lymph nodes are tender, not hard and squeeze-able
  • inflammation of lymphatic channels-> red streaks
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11
Q

difference between lymphoma and lymphadenitis?

A

in lymphoma-> lymph nodes are NOT tender and very hard

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12
Q

what are acute phase proteins?

A

proteins in which appear in plasma early in the inflammation
(not normally present or in small amounts)
-inflammation-> IL-1/6/TNF signal liver to increase production of plasma proteins by liver

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13
Q

positive acute phase proteins?

A

complement proteins, coagulation, proteases, metal-binding proteins, other proteins

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14
Q

negative acute phase proteins?

A

albumin

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15
Q

C-reactive protein

A

is an acute phase protein

  • binds surface of cells (Mac, Platelets, and lymphocytes) and results in increased binding of complement proteins/bacteria
  • activates alternate complement pathway
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16
Q

what does C-reactive protein indicate?

A

chronic inflammation

-measures degree of inflammation

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17
Q

serum amyloid A

A

may be involved in secondary amyloidosis which occurs with chronic disease

18
Q

with inflammation, why does increased erythrocyte sedimentation rate occur?

A

red cells fall more quickly with settling of blood due to present of increased fibrinogen as an acute phase protein
-indicator of chronic inflammation

19
Q

Leukocytosis

A

release of white cells from marginated pools-> WBC get trapped in places with sinusoids-> spleen and liver (marginated pools)

  • requires just a few hours
  • primarily released from marginated pool, then released from BM
20
Q

accompanying an infection, WBC count goes up or down?

A

Up, increased production of leukocytes

21
Q

what do IL-1/6/TNF induce early on in leukocytosis?

A

first induce early release of cell from BM-> early forms of neurtrophils “bands” may be present

  • increased synthesis due to CSF released from M and Lymphocytes
  • 2-3 fold increase in 72 hours
22
Q

normal and abnormal Neutrophil values

A

N: 40-80%, A: < 1,500; >8,000

23
Q

normal and abnormal band values

A

0-5%, A: > 5% or 500

24
Q

normal and abnormal lymphocytes values

A

N: 15-50%, A: < 1,500, > 5,000

25
normal and abnormal Eosinophils values
N: 1-5%, > 5% or 500
26
what does an increased peripheral leukocyte count?
leukocytosis | -increased due to inflammatory mediators (IL-1, TNF, IL-8)
27
an increase primarily in neutrophils?
bacterial infection | -total white count > 10,000, neutrophil account for > 80%
28
increased bands means?
acute bacterial infection -in acute bacterial infections, young neutrophils are kicked out of the bone marrow early (nucleus is band shaped instead of multi-lobed)
29
increased in eosinpohils means?
allergies or parasites - greater than 5% of the differential count or > 500 per microliter - due to IL-5, Th1 response with increased IgE to IL-4 - mast cell activation results in increased eosinophil recruitment to attack parasites
30
anaphylaxis is mediated by?
mast cell degranulation all over the body at the same time
31
DIC
stimulating coagulation all over the body, not uncommon to see septic shock as well
32
vascular leakage syndrome
man-made condition, would give massive amount of IL-1-> edema (mainly in the lungs)
33
SIRS
burns-> increase vascular permeability (as mainly in lungs)
34
septic shock
mediated by toll like receptors
35
variation in inflammation response
depends on 1. signals that trigger the inflammatory response 2. degree of edema and vasodilation 3. types of cellular infiltrates 4. persistence of inflammatory process 5. role of immune response
36
triggers of inflammation
trauma, toxins, infection, venoms, necrosis
37
resolution of inflammation
- apoptosis of neutrophils - production of anti-inflammatory mediators (Lipoxins, resolvins, and protectins, acute phase reactants) - continued activation of Macrophages - participation of immune response
38
outcomes of inflammation
-removal or neutralization of agent: complete resolution -repair of injured tissue: healing and regeneration persistence of injury or stimulus: chronic inflammation
39
chronic inflammation is caused by
- chronic activation of Macrophages - stimulation of immune response - stimulation of fibroblast with fibrosis-> collagen formation and cross-linking of collagen, determine by chronic activation macrophages, "scar" tissue - chronic tissue damage, NO production, can be associated with cancer
40
pathology of chronic inflammation
metaplasia lymphocyte infiltrate fibrosis-> exuberant production of collagen, alteration of normal tissue architecture, thickening of tissue layers -atrophy-> chronic necrosis