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foundations exam 2 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

3 types of inflammation and key differences

A

acute: neutrophil-mediated, regeneration of normal tissue architecture

chronic: mononuclear cell-mediated, tissue cell death and architecture destruction, repair includes new blood vessels/connective tissue (scars)

granulomatous: mediated by specialized macrophages, circumscribed chronic inflammation, when causative agent can’t be removed so it is sequestered instead

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2
Q

granulomatous inflammation

A

mediated by specialized macrophages, circumscribed chronic inflammation, when causative agent can’t be removed so it is sequestered instead

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3
Q

describe what occurs during acute inflammation

A

macrophages release histamine, serotonin —> vascular dilation, plasma leakage to interstitium

later - neutrophil emigration (diapedesis) and phagocytosis, recruitment of macrophages which clean up neutrophil lysis

resolution: macrophages transition to anti-inflammatory (IL-10, TGF-b) and leave the field

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4
Q

what occurs during “red hepatization” of the lung?

A

due to inflammation of the lung from lobar pneumonia

lung has heavy and dark red appearance - neutrophils have filled in the alveolar spaces

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5
Q

what typically occurs in viral pneumonia presenting with pulmonary inflammation?

A

mononuclear inflammatory infiltrate, characteristically seen in interstitium

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6
Q

upon activation, mast cells release effector molecules in a time-dependent fashion. describe this (and what is released)

A

within second: degranulation - histamines, TNF-a, amines

within minutes: eicosanoids - luekotrienes and prostaglandins

within hours: cytokines, chemokines, growth factors

result: vasodilation, vascular leakage, inflammatory cel activation

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7
Q

contrast histamine release from mast cells to cytokines and eicosanoiods release

A

histamine: already present in granules, released in response to injury/immune reaction/C3a and C5a complement (anaphylatoxins)

cytokines and eicosanoids: synthesized de novo, secreted in response to viruses/bacterial LPS/TLR activation/immune reaction

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8
Q

_____ cytokine mediates an increase in endothelial transcytosis during microvascular leakage in inflammation

A

VEGF: vascular endothelial growth factor

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9
Q

T/F: histamine- mediated vascular leakage follows a stereotypic time course

A

TRUE: histamine mediated leakage is gated

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10
Q

what is the major mechanism of inter-endothelial leakage during inflammation, induced by histamine

A

endothelial shape change, induced by histamine

results in opening of inter-endothelial junctions, allowing for leakage

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11
Q

how is inflammatory edema different than general edema

A

inflammatory edema has fluid that is localized and has a high protein concentration (exudate)

general edema occurs form imbalance of hydrostatic and osmotic pressures

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12
Q

stasis

A

as fluid leaves vascular use, blood in microcirculation has increased hematocrit (ratio of RBC volume to total blood volume)

as a result, blood flow slows down (stasis)

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13
Q

what are the roles of each of these endothelial molecules in leukocyte infiltration?
a. P-selectin
b. E-selectin
c. GlyCam-1, CD34
d. ICAM-1
e. VCAM

A

a. P-selectin: rolling
b. E-selectin: rolling/adhesion
c. GlyCam-1, CD34: rolling (CAM = cell adhesion molecule)
d. ICAM-1: adhesion
e. VCAM: adhesion

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14
Q

two main groups of opsonization factors

A
  1. IgG (heat stable): recognized by Fc receptors
  2. C3b complement proteins (heat labile): recognized by complement receptors (CR)
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15
Q

how do cells produce more energy for phagocytosis, an energy-requiring process accompanied by a burst of metabolic activity and oxygen consumption?

What is the outcome of this process?

A

glucose metabolized via the hexose monophosphate shunt (HMS): converts glucose phosphate to ribulose 5-phosphate and oxygen
—> generates NADH, NADPH

NADH oxidase converts oxygen to hydrogen peroxidase (required for bacterial killing)
NADPH oxidase generates superoxidase

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16
Q

chronic granulomatous disease

A

X-linked or AR, affects males mostly - recurrent infections with granulomas

lack of NADPH oxidase activity —> leukocytes do not show burst of metabolic activity that occurs with phagocytosis

remember that NADPH oxidase generates superoxide

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17
Q

Chediak-Higashi syndrome

A

decreased leukocyte functions because of mutations affecting proteins involved in lysosomal membrane traffic

causes increased CNS infections

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18
Q

pt presents with recurrent CNS infections. PMH includes genetic testing that showed mutation in a protein involved in lysosomal memrbane trafficking. FHx includes a grand-parent who suffered similar recurrent infections

what is your diagnosis

A

Chediak-Higashi syndrome (AR): decreased leukocyte function due to mutations affecting proteins involved in lysosomal membrane trafficking

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19
Q

name the effect of each:
a. histamine
b. serotonin
c. NO
d. prostaglandins
e. IL-1

A

a. histamine: vasodilation and increased vascular permeability
b. serotonin: increased vascular permeability
c. NO: vasodilation
d. prostaglandins: vasodilation, fever (pyrogenic), and pain
e. IL-1: leukocyte activation and fever (pyrogenic)

20
Q

what is the effect of C-reactive protein (CRP), serum amyloid A (SAA), serum amyloid P (SAP), fibrinogen, and haptoglobin?

A

acute phase response of inflammation

released by hepatocytes (liver)

21
Q

describe process of chronic inflammation

A
  1. mononuclear emigration
  2. angiogenesis and fibroblast invasion
  3. granulation tissue (precursor to scar) - ingrowth of new capillaries and fibroblasts
22
Q

process of fibrosis (scar formation)

A

quiescent fibroblasts become active myofibroblasts which secrete ECM

activated by TGF-b, IL-13, IL-1

as fibrosis progresses, number of microvessels and cells decreases, becoming relatively acellular tissue

23
Q

acute respiratory distress syndrome (ARDS)

A

widespread lung injury from pneumonias, sepsis, aspiration, inhaled toxins (high fatality rate)

results in inability of alveoli to gas exchange

inflammatory response, Type II pneumocyte proliferation, necrotic debris accumulates at alveolar/air interface —> hyaline membranes form

24
Q

formation of hyaline membranes at the alveolar/air interface is a distinctive histological feature of the initial state of _____

A

ARDS (acute respiratory distress syndrome)

inflammation due to widespread lung injury leads to inability of alveolar to exchange gas

following initial phase is proliferation and fibrotic phase

25
Q

purulent inflammation

A

encapsulated accumulation of pus (neutrophilic exudate) with tissue destruction and formation of a cavity

26
Q

empyema

A

accumulation of pus in existing body cavity (purulent inflammation that is not walled off)

can be seen following inflammation of pleura or pericardium

27
Q

type of chronic inflammation that occurs in response to localized inciting agent that can be sequestered by inflammatory tissue, but not easily removed

A

granulomatous inflammation

macrophages (foamy) are prominent, along with mononuclear cells and giant cells

granuloma surrounded by cuff of B/T cells

28
Q

which of the following is most suggestive of ARDS?
a. bacterial pneumonia
b. hyaline membranes
c. diffuse collagenous fibrosis
d. organizing pneumonia

A

b. hyaline membrane

*ARDS = acute respiratory distress syndrome (alveoli can’t gas exchange)

29
Q

what is the enzyme that generates superoxide from molecular oxygen?

A

NADPH oxidase

30
Q

the pain experienced during inflammation is most likely the result of the formation of which of the following two chemical mediators?
a. complement C3b and IgG
b. Interleukin-1 and TNF
c. prostaglandin and bradykinin
d. histamine and serotonin

A

c. prostaglandin and bradykinin

a. C3B/IgG - opsonization
b. IL-1/TNF - chemotaxis
d. histamine/5HT - vascular permeability

31
Q

a women with a breast implant that has ruptured experiences a foreign body reaction to the silicone particles. This would lead to what kind of reaction?
a. acute inflammation
b. hypertrophic (raised) scar
c. chronic inflammation
d. granulation
e. granulomatous inflammation

A

e. granulomatous inflammation - when invading material becomes sequestered in granuloma because the body can’t get rid of it

32
Q

what types of cell aggregates form multinucleated giant cells seen in granulomas in granulomatous inflammation?

A

macrophages

33
Q

which of the following stimulates collagen and fibronectin production in fibrosis?
a. matrix metalloproteinase
b. NO (nitric oxide)
c. TGF-b
d. TNF
e. VEGF

A

c. TGF-b (transforming growth factor beta)

a. matrix metalloproteinase - ECM degradation
b. NO - vasodilation
d. TNF (tumor necrosis factor) - chemotaxis, fever
e. VEGF (vascular endothelial growth factor) - angiogenesis

34
Q

local defect of the surface of a tissue or organ caused by sloughing of inflammatory or necrotic tissue

A

ulcers

can be caused by H. pylori (helicobacter), steroids, NSAIDs

35
Q

Helicobacter pylori, steroids, and NSAIDs are all possible causes of

A

ulcers

36
Q

what is the order of events leading to neutrophil infiltration? order these steps:
rolling, migration across vessel wall, margination, adhesion, migration through tissues

A

margination
rolling
adhesion
migration across vessel wall
migration through tissues

37
Q

initial rolling interactions of neutrophils during infiltration are mediated by:
a. arachidonic acid metabolites
b. cadherins
c. integrins
d. selectins

A

selectins

(selectin phase, then integrin phase)

38
Q

presence of WBC and epithelial casts, along with bacteria, in urine indicates infection in ____

A

infection in kidney proper, not just lower urinary tract

39
Q

autopsy of a lung shows fibrinous exudates over the pleural surfaces, and innumerable small, grey-white nodules, as well as a large caseous tubercle which eroded into a large pulmonary vessel

what is the likely causative organism? diagnosis?

A

agent: mycobacterium tuberculosis

diagnosis: miliary (disseminated) tuberculosis

40
Q

serous inflammation

A

aka blister

outpouring of fluid (effusion) derived for either plasma or secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities

41
Q

fibrinous inflammation

A

fibrinous exudate is characteristic of inflammation in the lining of the body cavities (ex- meninges, pericardium, pleura)

exudate develops when vascular leakage allows fibrinogen to traverse vascular barrier (appears eosinophilic histologically)

42
Q

pus is made of mostly

A

neutrophils

43
Q

chronic inflammation is characterized by tissue infiltration by ______

A

mononuclear cells (macrophages and lymphocytes)

acute inflammation - neutrophils
chronic inflammation - macrophages/lymphocytes replace neutrophils

44
Q

Cachexia (“wasting”) is caused by chronic inflammation, which induces extensive catabolism of fat and muscle. Which cytokine listed plays the largest role?
a. IL-8
b. IFN-y
c. TNF
d. IL-2

A

c. Tumor Necrosis Factor (TNF)

45
Q

which mechanism is predominately response for pain during infection?
a. humoral immune response
b. cell-mediated immune response
c. local production of inflammatory mediators

A

c. local production of inflammatory mediators —> increases responsiveness of sensory nerve endings

46
Q

what process causes the experience of flu symptoms such as muscle/joint pain, fever, sleepiness, loss of appetite, malaise

A

secretion of cytokines by monocytes and T cells (most notably IFN)

47
Q

in a histological section of a biopsy from an infected portion of a lung, what immune cells would be most abundant?

A

lymphocytes and macrophages —> granulomatous inflammation

foundations exam 2 (42 decks)

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