05a: Acute Inflammation Flashcards

1
Q

Time frame of acute inflammation.

A

Few minutes/hours (resolves within few days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Normal WBC count.

A

4,000-11,000/microL blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which WBC types are granulocytes?

A

Neutrophils, eosinophils, basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Short; cannot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Histologically, what’s the sign of inflamed tissue?

A

Leukocytes present where they’re not normally found

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List the four cardinal signs of acute inflammation.

A
  1. Rubor (redness)
  2. Tumor (swelling)
  3. Calor (heat)
  4. Dolor (pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Bradykinin formed by the proteolytic action of which enzymes?

A
  1. Factor XIIa (forms Kallikrein)

2. Kallikrein (forms Bradykinin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
T/F: Transudate has low content of both cells and protein.
True
26
Edema is accumulation of fluid in (X) and is (transudate/exudate).
X = tissue interstitium | Either
27
Effusion is escape of fluid into (X) and is (transudate/exudate).
X = defined (sealed) body cavity | Either
28
(X) exudate contains few cells and is more clear than cloudy. Its presence suggests (Y) injury.
``` X = serous; Y = mild vascular ```
29
(X) exudate is pus; contains large concentration of (Y) cells.
``` X = Purulent Y = inflammatory (esp neutrophils) ```
30
(X) exudate contains RBC, implying (Y) injury/damage.
``` X = hemorrhagic Y = capillary ```
31
(X) exudate has a white layer of (Y) typically deposited on (Z) surfaces.
``` X = fibrinous Y = fibrin Z = serosal (i.e. pleural, pericardial) ```
32
"Bread and Butter" pericarditis gets its name from:
Fibrinous exudate deposited on pericardium
33
List steps of leukocyte recruitment to tissues.
1. Margination 2. Rolling 3. Tight adhesion 4. Migration (across vessel wall)
34
Leukocyte transmigration occurs most prominently in (X) vessels and, to lesser extent, (Y) vessels.
``` X = post-cap venules Y = capillaries ```
35
T/F: Leukocyte transmigration occurs in venules, cap's and arterioles, but not larger vessels.
False - only venules and cap's
36
Vascular leak of plasma proteins is beneficial for which reasons?
Plasma protiens kill invading pathogens and remove necrotic tissue
37
Transmigration of leukocytes: what's the function of margination?
Cells move to bloodstream margin to come into contact with vascular wall
38
Transmigration of leukocytes: initial adherence of cells to endothelium is mediated by (X) receptors on (leukocyte/endothelium).
X = selectin | Endothelium
39
Transmigration of leukocytes: tight adhesion of cells to endothelium is mediated by (X) receptors on (leukocyte/endothelium).
X = integrin | Leukocyte
40
Key points: Inflammation: Principal mediators of vasodilation.
His and prostaglandins
41
Key points: Inflammation: Principal mediators of increased vascular permeability.
1. His, SA 2. C3a, C5a 3. Leukotrienes (C4, D4, E4)
42
Key points: Inflammation: Principal mediators of chemotaxis/recruitment/activation.
1. TNF, IL-1 2. Chemokines 3. C3a, C5a 4. LTB4
43
Key points: Inflammation: Principal mediators of fever.
1. TNF, IL-1, IL-6 | 2. Prostaglandins
44
Key points: Inflammation: Principal mediators of pain.
Bradykinin and Prostaglandins
45
Key points: Inflammation: Principal mediators of tissue damage.
Lysosomal enzymes and ROS
46
List the systemic effects (signs) of acute inflammation.
1. Fever 2. Tachycardia 3. Tachypnea 4. Leukocytosis 5. Acute Phase Reactants
47
Major sources of endogenous pyrognes are (X), released from (Y) cells.
``` X = cytokines (IL-1, 6, TNF-alpa) Y = macrophages ```
48
Neutrophil extracellular nets: composed of (X) that contain (Y).
``` X = chromatin strands Y = antimicrobial peptides ```
49
Neutrophils use which tools/methods to carry out intracellular killing of bacteria?
1. Phagocytosis 2. Phagolysosome 3. Proteases 4. ROS and RNS
50
Tissue injury during acute inflammation is damage done by:
Release of ROS and proteases and/or inappropriate coagulation