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Pharm > 05a: Acute Inflammation > Flashcards

05a: Acute Inflammation Flashcards

1
Q

Time frame of acute inflammation.

A

Few minutes/hours (resolves within few days)

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2
Q

List the leukocytes (from most to least numerous) and star the type that’s hallmark of acute inflammation.

A
  1. Neutrophils*
  2. Lymphocytes
  3. Monocytes
  4. Eosinophils
  5. Basophils
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3
Q

Normal WBC count.

A

4,000-11,000/microL blood

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4
Q

Which WBC types are granulocytes?

A

Neutrophils, eosinophils, basophils

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5
Q

Neutrophils have (short/long) half-life in blood and (can/cannot) recirculate back into blood after entering tissue site.

A

Short; cannot

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6
Q

Histologically, what’s the sign of inflamed tissue?

A

Leukocytes present where they’re not normally found

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7
Q

(X) leukocyte changes name when it leaves blood and enters peripheral tissues. What are some special names, based on location, for this cell type?

A

X = monocyte;
(Macrophage in tissue)

Microglia in CNS, Kupffer cell in liver

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8
Q

List the four cardinal signs of acute inflammation.

A
  1. Rubor (redness)
  2. Tumor (swelling)
  3. Calor (heat)
  4. Dolor (pain)
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9
Q

List the three steps of acute inflammation.

A
  1. Hyperemia (blood vessel dilation)
  2. Increased vascular permeability
  3. Emigration, accumulation, activation of leukocytes
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10
Q

List mediators that increase blood flow in acute inflammation.

A
  1. Vasoactive amines (His, SA)
  2. Arachidonic acid metabolites
  3. NO
  4. PAF (Platelet activating factor)
  5. Bradykinin
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11
Q

Acute inflammation: (X) are the earliest mediators of hyperemia. Where do they come from?

A

X = Vasoactive amines (His and SA)

Mast cells and Platelets (pre-formed in cytoplasmic granules)

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12
Q

List stimuli for His release from mast cells.

A
  1. Trauma/heat
  2. Ab binding
  3. C3a, C5a (anaphylatoxins)
  4. Neuropeptides (substance P)
  5. Cytokines (IL-1, 8)
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13
Q

Metabolites of arachidonic acid fall into which categories? Star those that are products of cyclooxygenase pathway.

A
  1. Prostaglandins*
  2. Leukotrienes
  3. Lipoxins
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14
Q

Formation of arachidonic acid from (X) is carried out by (Y). This step is known to be inhibited by (Z).

A 
X = membrane phospholipids
Y = phospholipases
Z = glucocorticoids
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15
Q

List products of the cyclooxygenase pathway that are important in inflammation. What’s the role of each?

A
  1. Prostaglandins (vasodilation)
  2. Prostacyclins (vasodilation)
  3. Thromboxane (vasoconstriction, platelet aggregation)
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16
Q

PAF (Platelet activating factor) derived from (X) and is produced by:

A

X = phospholipids

  1. Leukocytes
  2. Endothelial and mast cells
  3. Platelets
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17
Q

PAF main effect is (X). It also causes (vasoconstriction/vasodilation) and low levels and the opposite at high.

A

X = Platelet aggregation/activation

Vasodilation

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18
Q

NO synthesized from (X) by (Y) enzyme. List its effects.

A 
X = L-Arg and oxygen
Y = NO synthase
  1. Vasodilation
  2. Inhibits cell components (platelet aggr, WBC recruitment)
  3. Microbicidal (destructive to microorganisms)
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19
Q

iNOS stands for (X), found in (Y) cell types. What does the “i” indicate?

A 
X = inducible NO synthase
Y = macrophages and endothelial

Inducible by cytokines and bacterial breakdown products

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20
Q

Bradykinin formed by the proteolytic action of which enzymes?

A
  1. Factor XIIa (forms Kallikrein)

2. Kallikrein (forms Bradykinin)

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21
Q

List the actions of Bradykinin.

A
  1. Vasodilation
  2. Increased vascular permeability
  3. Contraction of nonvascular smooth muscle
  4. Pain
22
Q

Transudate has specific gravity (lower/higher) than (X) and exudate (lower/higher) than (X).

A

Lower;
X = 1.015
Higher

23
Q

Presence of (transudate/exudate) implies that (X) is generally intact and (Y) cannot pass through.

A

Transudate;
X = endothelial barrier
Y = plasma proteins

24
Q

T/F: Transudate, to a small degree, occurs normally across capillary beds.

25
Q

T/F: Transudate has low content of both cells and protein.

26
Q

Edema is accumulation of fluid in (X) and is (transudate/exudate).

A

X = tissue interstitium

Either

27
Q

Effusion is escape of fluid into (X) and is (transudate/exudate).

A

X = defined (sealed) body cavity

Either

28
Q

(X) exudate contains few cells and is more clear than cloudy. Its presence suggests (Y) injury.

A 
X = serous;
Y = mild vascular
29
Q

(X) exudate is pus; contains large concentration of (Y) cells.

A 
X = Purulent
Y = inflammatory (esp neutrophils)
30
Q

(X) exudate contains RBC, implying (Y) injury/damage.

A 
X = hemorrhagic
Y = capillary
31
Q

(X) exudate has a white layer of (Y) typically deposited on (Z) surfaces.

A 
X = fibrinous
Y = fibrin
Z = serosal (i.e. pleural, pericardial)
32
Q

“Bread and Butter” pericarditis gets its name from:

A

Fibrinous exudate deposited on pericardium

33
Q

List steps of leukocyte recruitment to tissues.

A
  1. Margination
  2. Rolling
  3. Tight adhesion
  4. Migration (across vessel wall)
34
Q

Leukocyte transmigration occurs most prominently in (X) vessels and, to lesser extent, (Y) vessels.

A 
X = post-cap venules
Y = capillaries
35
Q

T/F: Leukocyte transmigration occurs in venules, cap’s and arterioles, but not larger vessels.

A

False - only venules and cap’s

36
Q

Vascular leak of plasma proteins is beneficial for which reasons?

A

Plasma protiens kill invading pathogens and remove necrotic tissue

37
Q

Transmigration of leukocytes: what’s the function of margination?

A

Cells move to bloodstream margin to come into contact with vascular wall

38
Q

Transmigration of leukocytes: initial adherence of cells to endothelium is mediated by (X) receptors on (leukocyte/endothelium).

A

X = selectin

Endothelium

39
Q

Transmigration of leukocytes: tight adhesion of cells to endothelium is mediated by (X) receptors on (leukocyte/endothelium).

A

X = integrin

Leukocyte

40
Q

Key points: Inflammation: Principal mediators of vasodilation.

A

His and prostaglandins

41
Q

Key points: Inflammation: Principal mediators of increased vascular permeability.

A
  1. His, SA
  2. C3a, C5a
  3. Leukotrienes (C4, D4, E4)
42
Q

Key points: Inflammation: Principal mediators of chemotaxis/recruitment/activation.

A
  1. TNF, IL-1
  2. Chemokines
  3. C3a, C5a
  4. LTB4
43
Q

Key points: Inflammation: Principal mediators of fever.

A
  1. TNF, IL-1, IL-6

2. Prostaglandins

44
Q

Key points: Inflammation: Principal mediators of pain.

A

Bradykinin and Prostaglandins

45
Q

Key points: Inflammation: Principal mediators of tissue damage.

A

Lysosomal enzymes and ROS

46
Q

List the systemic effects (signs) of acute inflammation.

A
  1. Fever
  2. Tachycardia
  3. Tachypnea
  4. Leukocytosis
  5. Acute Phase Reactants
47
Q

Major sources of endogenous pyrognes are (X), released from (Y) cells.

A 
X = cytokines (IL-1, 6, TNF-alpa)
Y = macrophages
48
Q

Neutrophil extracellular nets: composed of (X) that contain (Y).

A 
X = chromatin strands
Y = antimicrobial peptides
49
Q

Neutrophils use which tools/methods to carry out intracellular killing of bacteria?

A
  1. Phagocytosis
  2. Phagolysosome
  3. Proteases
  4. ROS and RNS
50
Q

Tissue injury during acute inflammation is damage done by:

A

Release of ROS and proteases and/or inappropriate coagulation

Pharm (16 decks)

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