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KN-Pathology Block 1 > Inflammation 1 > Flashcards

Inflammation 1 Flashcards

1
Q

What are the causes of inflammation? (6)

A

infection, tissue necrosis, immune reaction trauma, foreign bodies, physical and chemical agents

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2
Q

What are the four cardinal signs and symptoms of acute inflammation?

A

redness, swelling, heat and pain

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3
Q

Which of these is subjective: sign or symptom?

A

symptoms are subjective experiences, signs are objective physical manifestation of a disease

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4
Q

What are the 5 forms of inflammation?

A

purulent (suppurative), abscessing (necrotizing, fibrinous, serous and granulamatous.
(they are not mutually exclusive)

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5
Q

What are the 3 components of inflammation response?

A

vascular - dilation and increased permeability
leukocyte-primarily neutrophils flow into site

systemic - fever, tachycardia, hyperventilation, leukocytosis for acute infl.

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6
Q

What is serum?

A

thin liquid portion of blood that has low protein content and no cells.

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7
Q

What is blood plasma?

A

portion of blood that has been anticoagulated and centrifuged, leaving protein-rich liquid that has blood clotting factors, including fibrin

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8
Q

What is serous inflammation?

A

a form of usually acute inflammation marked by an outpouring of a thin fluid from blood vessels or mesothelium

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9
Q

What is fibrinous inflammation?

A

a form of usually acute inflammation featuring deposition of fibrin-rich exudate, on pleura, pericardium, peritoneum or meninges, or in the interstitium of any tissue.

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10
Q

What is an exudate?

A

an inflammatory extracellular fluid with high protein content, cells, cellular debris, and specific gravity > 1.02

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11
Q

What is trasudate?

A

a thin, acellular serous edema fluid

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12
Q

What is edema?

A

swelling of tissue due to accumulation of water

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13
Q

What is purulent inflammation?

A

Suppurative inflammation. usually acute and features production of abundant pus (neutrophils, necrotic cellular debris and edema fluid). It is commonly caused by infection with pyogenic bacteria.

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14
Q

What does pyogenic mean?

A

pus-producing

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15
Q

What is pus?

A

a purulent exudate rich in neutrophils, cellular debris and commonly microbes. It is thick , opaque and variably colored. It can be mixed with mucus or blood.

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16
Q

What is mucus?

A

grey, slimy, and stringy secretion.

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17
Q

What should you do with pus once it is recognized?

A

send it to lab for culture to identify invading organism.

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18
Q

What are diabetes mellitus, hemodialysis, malnutrition and leukemia all common causes of?

A

acquired leukocyte deficiency

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19
Q

What are some causes of congenital leukocyte defects?

A

leukocyte adhesion deficiency-1 and -2, chronic granulomatous disease, myeloperoxidase deficiency, Chediak-Higashi syndrome, and cryopyrin-associated periodic fever syndromes.

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20
Q

What are the 4 main systemic signs of acute inflammation?

A

fever, tachycardia, hyperventilation, leukocytosis (elevated WBC).

There is usually also a change in plasma protein levels, lipid metabolism, hormone synthesis, decreased RBC production, elevated WBC and platelets, decreased serum iron and zinc, and a negative nitrogen balance.

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21
Q

What plasma protein levels rise during acute inflammation response?

A

C-reactive protein, amyloid A, and fibrinogen

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22
Q

What plasma protein levels drop during acute inflammation response?

A

Albumin mainly

23
Q

What are the cytokines that mediate acute phase response?

A

IL-1, TNF, and IL-6

24
Q

What happens to epinephrine, norepinephrine, cortisol and glucagon levels in the acute phase response?

A

all go up

25
Q

During inflammation, is the body in a state of anabolism or catabolsim?

A

catabolism and hypermetabolism.

26
Q

Why is there a negative nitrogen balance during acute phase response?

A

muscle is broken down faster than it is built so nitrogen is lost in urine.

27
Q

What type of infection/invasions is neutrophilia associated with?

A

bacterial infections

28
Q

What type of infections/invasions is lymphocytosis associated with?

A

viral infections

29
Q

What type of infections/invasions is eosinophilia associated with?

A

allergies, parasites

30
Q

What are Dohle bodies?

A

pathes of dilated ER that appear as sky-blue peripheral cytoplasmic puddles

31
Q

What are toxic granulations?

A

immature primary cytoplasmic granules characteristic of less mature granulocytes. They are dark blue or purple, bigger and coarser than the small, faintly stained neutral granules characteristic of segmented neutrophils.

32
Q

What are acute phase reactants?

A

proteins produced in abundance with inflammation. Include fibinogen, clotting factors, complement proteins, amyloid A, C-reactive protein, alpha-1-antitrypsin and other antiprotesases, hepcidin and ferritin.

33
Q

What does amyloid A do?

A

plays a role in recylcling and reusing cholesterol from destroyed and damaged cells by replacing apolipoprotein A in high density lipprotein and targeting delivery of HDL to macrophages, supressing ACAT and enhancing neutral cholesterol esterase and ABC transporters in macrophases.

34
Q

What does fibrinogen do?

A

causes sticky erythrocytes and an increased erythrocyte sedimentation rate (ESR, “sed rate”)

35
Q

What does CRP (C-reactive protein) do?

A

binds to phosphocholine residues uniquely found on bacteria and becomes a ligand for complement C1 binding, initiating classical complement cascade. Its synthesis is induced by cytokines, chiefly IL-6.

36
Q

Will CRP levels rise with acute inflammation? With viral infections?

A

During acute inflammation it will skyrocket, but will do nothing during viral infections.

37
Q

What are the criteria for SIRS (systemic inflammatory response syndrome)?

A
  1. Temp>38 (100.4) or 90/min
  2. RR > 20/min or pCO2 < 32 mmHg
    WBC > 12,000/cu mm or < 4,000 cu mm or > 10% bands
38
Q

Can you determine if a patient is septic or has SIRS based off a negative blood culture?

A

NO. the majority of septic patients will have negative blood cultures.

39
Q

What is somnolence?

A

constant desire to sleep, independent of circadian rhythm

40
Q

What is margination?

A

leukocyte accumulation at the periphery of blood vessels

41
Q

What is leukocyte rolling?

A

leukocytes are pushed out of the central axial column by flowing blood, mediated by selectins

42
Q

What is pavementing?

A

leukocytes line up along the lbood vessel wall.

43
Q

What are selectins?

A

a family of surface receptors that bind to selected sugar domains (lectins). They the account for the relatively loose and transient adhesions involved in rolling

44
Q

What is E-selectin? P-selectin? L-selectin?

A 
E = endothelium
P = endothelium and platelets
L = most leukocytes
45
Q

What is leukocyte adhesion?

A

leukocytes firmly stick to endothelial surfaces

46
Q

What is diapedesis?

A

leukocytes move between edothelial cells and through the basement membrane into extravascular spaces. IT is mediated by molecules of the Ig superfamily on endothelial cells that interact with integrins expressed on leukocyte cell surfaces.

47
Q

What are ICAM-1 and VCAM-1? What induces them?

A

They are intercellular adhesion molecule 1 and vascular adhesion molecule 1. They are induced by TNF and IL-1

48
Q

What are integrins?

A

leukocyte transmembrane heterodimeric glycoproteins that bind to ICAM-1 and VCAM-1.
Examples: LFA-1, VLA-1

49
Q

Which integrin binds to ICAM-1? which binds to VCAM-1?

A

LFA-1 for ICAM-1

VCAM-1 is VLA-1

50
Q

What is the molecular foundation for chemotaxis?

A

chemotactic molecules bind to cell surface receptors.
G proteins mediate activation of phospholipase C.
Membrane PIP2 is hydrolyzed into DAG and IP3.
IP3 increases intracellular Ca, which causes pseudopod assembly.

51
Q

What are opsonins? What do they bind to?

A

Opsonins are IG FC, C3b and collectins.

They bind to FcR; CR 1,2 and 3; and C1q, respectively.

52
Q

What triggers engulfment?

A

binding of opsonized particles.

53
Q

What happens during the killing and degradation phase of phagocytosis?

A

oxidative burs forms reactive oxygen metabolites (H2O2).
Azurophilic granules contain MPO: (HOCl)
Dead microorganisms are degraded by lysosomal acid hydrolases.

KN-Pathology Block 1 (11 decks)

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