Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Perf Tech II > Test 3 Immunity Part 2 > Flashcards

Test 3 Immunity Part 2 Flashcards

0
Q

Inflammation response to tissue damage

A

Pathogens, abrasions, chemical irritations, distortion/cell disturbance, extreme temps

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

Nonspecific inflammation

A

Response to is same as burn, radiation, infection, etc

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

4 signs of inflammation

A

Redness, pain, heat, swelling

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

Goal of inflammation

A

Dispose of microbes, toxins, foreign materials

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

Stages of inflammation

A
  1. Vasodilation: increase permeability of blood vessels
  2. Emigration: movement of phagocytes from blood to interstitial fluid
  3. Tissue repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Factors that cause vasodilation and increased permeability

A

Histamine, kinins, prostaglandins, leukotrienes, complement

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

Histamine release

A

Released by mast cells in the tissues
Release in blood is stimulated by basophils and platelets
Causes increased dilation and permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Kinins

A

Polypeptides
Increase permeability and vasodilation
Act as chemotactic phagocytes
Ex. Bradykinin a

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

Prostaglandins

A

Lipid released by damaged cells

Stimulated emigration of phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Leukotrienes

A

Produced by basophils and mast cells

Increase permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complement

A

Stimulate histamine release
Attract neutrophils
Promote phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clotting factors move into tissues causing

A

Initiation of clotting cascade

Fibrinogen converted to fibrin- forms fibrin mesh–localizes and traps invading organisms–blocks spread of organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When do phagocytes appear?

A

Within one hour of start of inflammatory process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes neutrophils to stick to blood vessel walls

A

Increased blood flow

  • squeeze through blood Vessel walls to tissues (emigration)
  • depends on chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Neutrophils attempt to destroy via…

A

Phagocytosis

  • monocytes follow neutrophils (transform into macrophages)
  • monocytes are more potent phagocytes than neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens when macrophages die?

A

Leave collection of dead cells and fluid (pus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

4 signs of inflammations due to vasodilation and increased permeability

A
  1. Heat
  2. Redness (large amount of blood in infected area, local temp increase, increased speed of metabolic process, more heat released)
  3. Swelling (increased permeability, more fluid in area)
  4. Pain (neuron injury or increased pressure (edema))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fever aids in…

A

Helps inhibit growth of microbes
Helps speed up body reactions
Aids in repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fever cause

A

Body toxins increase body temp

Trigger release of interleukin 1 (causes fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Two major components of inflammation

A

Vascular reaction and cellular reaction

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

Acute inflammation

A

Rapid onset, short duration, emigration of neutrophils

21
Q

Chronic inflammation

A

Long duration, lymphocyte involvement, proliferation of blood vessels, tissue necrosis

22
Q

Inflammation components

A
  1. Circulating white cells (neutrophils, monocytes, eosinophils, lymphocytes, basophils, platelets)
  2. Connective tissue cells (mast cells, fibroblasts, macrophages, lymphocytes)
  3. Extracellular matrix: structural fibrous proteins, adhesive glycoproteins, proteoglycans, basement membrane of capillary
23
Q

Chemical factors that mediate inflammation are derived from…

A

Plasma proteins/cells

Produced in response to or activated by inflammation

24
Q

Mediators at site of injury in acute inflammation

A

Leukocytes

Plasma proteins

25
Q

Components of acute inflammation

A
  1. Dilation ofcapillaries and surrounding blood vessels (increases flow)
  2. Structural changes in capillaries-allows plasma and leukocytes to enter interstitial space
  3. Emigration of leukocytes from capillaries where they accumulate in focus of injury –activation to eliminate offending agent
26
Q

Stimuli for acute inflammation

A
  1. Infections and microbial toxins (bacterial, girl, parasitic)
  2. Trauma
  3. Physical and chemical agents (thermal injury, irradiation, environmental chemicals)
  4. Tissue necrosis
  5. Foreign bodies (splinters, dirt, sutures)
  6. Immune reactions
27
Q

Purpose of vascular changes

A

Maximize movement of plasma proteins and appropriate circulating cells into site of injury or infection
Happens by vasodilation and increased capillary permeability

28
Q

Mechanism of vasodilation

A
  • Early manifestation
  • arterioles involved first, followed by openings of new capillary beds
  • induced by histamine and NO
29
Q

Mechanism of increased capillary permeability

A
  • movement of protein rich fluid into intravascular tissue and concentration of RBCs (viscosity change)
  • physical changes in endothelial structure of capillaries
30
Q

Result of increased capillary permeability

A

Osmotic and hemodynamic changes force fluid into interstitial space (results stasis)
Neutrophils begin adhering to endothelium and moving into interstitial space
Physical openings in endothelium allow more fluid, protein, and cells to migrate

31
Q

Result of vasodilation

A

Increased blood flow which leads to increased redness and warmth of tissue

32
Q

Extravasation

A

Movement of leukocytes from vessel lumen to interstitial space

33
Q

Margination

A

Movement of leukocytes toward wall of capillary

34
Q

Rolling

A

Leukocytes tumble along endothelium, adhere transiently, then attached. Endothelium completely lined with white cells

35
Q

Transmigration (diapedesis)

A

Insert pseudopods into junctions between endothelial cells- move through junction

36
Q

Chemotaxis

A
  • Locomotion along chemical gradient

- most common exogenous agents are bacterial products

37
Q

Order of cellular events

A
  1. Extravasation
  2. Margination
  3. Rolling
  4. Transmigration (diapedesis)
  5. Chemotaxis
38
Q

Endogenous agents for chemotaxis

A

Components of complement (C5a)
Products of lipoxygenase pathway (leukotriene B4)
Cytokines

39
Q

Leukocyte activation induced by…

A

Microbes
Necrotic cells
Antigen/antibody complexes
Cytokines

40
Q

Results of leukocyte activation

A

Production of arachnidonic acid metabolites
Degranulation and secretion of lysosomal enzymes
Secretion of cytokines
Modulation of surface receptors
Phagocytosis

41
Q

Origin of clinical mediators

A

Plasma or cells
-plasma derived must be activated
-cell derived stored in intra cellular granules
Production triggered by microbial products or host proteins (complement)

42
Q

Chemical mediators actions

A

Bind to specific receptors on target cells
One mediator may stimulate release of other mediator
Can act on more than one target
Short lived
Potential to cause GREAT HARM

43
Q

Systemic inflammatory response to CPB: SIRS

A

common systemic response to wide variety of insults
Induced in all patients on bypass
-incidence and severity is variable
-degree and type of response is unpredictable
-risk factor is length of CPB

44
Q

Indications of SIRS

A 
Body temp below 36 or above 38
HR>90bpm
Respiratory rate >20/min 
PaCO2 12000 cells/mm2
    -or <10% immature neutrophils

Need two of the above to diagnose SIRS

45
Q

SIRAB

A

Systemic inflammatory response after bypass
CPB produces whole body inflammation
Injuries: pulmonary, renal, gut, CNS, myocardial dysfunction, coagulopathy, hemolysis, fever, increased susceptibility to infection, leukocytosis

46
Q

Most common culprits for SIRAB

A

Contact with foreign surface area
Other factors: altered arterial blood flow patterns, sheer stress, cardiotomy suction, tissue ischemia, reperfusion, hypothermia, relative anemia, anticoagulants

47
Q

Contact activation

A

Blood passes through ECC

Activation of contact proteins (coagulation factors XI and XII, prekallikriens, high molecular weigh kininogen)

48
Q

End result of contact activation

A

Formation of bradykinin
Conversion of plasminogen into plasmin
Initiate fibrinolysis
Triggers classical complement cascade

49
Q

Immune system and bypass

A

Postop: patients more acceptable to infection
Serum immunoglobulins and complement decreased
Decreased chemotaxis ability of granuloyctes
Decreased NK cells
Decreased CD3+ and CD4+ cells
Increased CD8+ cells
Leukocyte numbers decreased for up to a week post bypass

Perf Tech II (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions