Brainscape's Knowledge GenomeTM

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


See full index

NURS 2500 > Class 6 - Inflammation > Flashcards

Class 6 - Inflammation Flashcards

1
Q

What is inflammation?

A

A protective process that is initiated to minimize or remove the pathologic agent or stimulus triggering the inflammation and to promote healing

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

Inflammation and infection relationship

A

Inflammation is always present with inflammation, but inflammation can occur in the absence of infection

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

Causes of inflammation

A

Infection and immunity

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

Inflammation can be:

A

Acute or Chronic or Repair/Restorative

Local or Systemic

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

Inflammation is triggered by:

A
  • Mechanical trauma
  • Thermal, electrical or chemical injury
  • Radiation damage
  • Biological assault (infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The goal of a normal inflammatory response

A
  • Restore normal cell function
  • Fibrous repair when cells can’t be restored
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Physiological process of a normal inflammatory response

A

White blood cells and chemicals that serve to protect the body from invaders or cellular/tissue damage are involved

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

Types of WBCs

A

Granulocytes (mature, around 8-15 days = segmented [segs], immature = bands)
Agranulocytes

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

Granulocytes

A

Neutrophils (helps in phagocytosis)
Eosinophils (fights against parasitic infections)
Basophils (produces inflammatory and allergic reactions)
Tissue mast cells (signal for more neutrophils)

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

Agranulocytes

A

Lymphocytes (produce specific immune responses - B lymphocytes, T lymphocytes, Natural Killer Cells)
Monocytes (fights off bacteria, viruses, and fungi)

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

Chemotaxis

A

Proinflammatory response - WBCs head towards inflammation when chemotaxis occurs

Stimulated by:
- Bacterial or viral extoxins
- Degenerative by-products of inflammation
- Products of complement system activation
- Reactive products of plasma clotting

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

Proinflammatory hormones

A

Prostaglandins
Histamines
Cytokines

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

Functions of proinflammatory hormones

A
  • Increase blood flow to the area of injury
  • Attract leukocytes to area of injury
  • Increase vascular permeability
  • Activate components of an immune response
  • Promote angiogenesis
  • Stimulate connective tissue growth
  • Cause fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stage 1 of vascular response

A
  • Injured tissues, local granulocytes, and tissue masts secrete proinflammatory hormones
  • Macrophages secrete proinflammatory hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do injured tissues, local granulocytes, and tissue masts secreting proinflamamtory hormones do?

A

Small veins constrict and aerterioles dilate (blood flow increases delivering nutirents like O2 and glucose to injured tissues)
- Hyperemia/redness, warmth, edema

Capillary leak/permeability (swelling/edema and pain)

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

What do macrophages that secrete proinflammatory hormones do?

A

Mature WBCs quicker and promote neutrophil invasion

17
Q

Stage 2 of vascular response

Cellular response

A
  • Granulocytes and tissue mast cells become activated
  • Exudate forms
  • Macrophages increase and stimulate monocyte production
  • Arachidonic acid cascade
18
Q

Granulocytes and tissue mast cells become activated

A
  • Neutrophilia occurs 12 hrs after injury & Phagocytosis
  • Eosinophils, basophils, and mast cells promote continuous inflammatory response
19
Q

Exudate forms

A

Dead WBCs, necrotic tissue, leaked cell fluid

20
Q

Arachidonic acid cascade

A

Increases inflammation
- Fatty acids in membrance of injured cells turn into arachidonic acid which is then converted (by COX enzyme) into substances (histamine, leukotrienes, prostaglandins, serotonin, kinins) that promote more inflammation

21
Q

Stage 3 of vascular response

Tissue repair and replacement

A
  • All WBCs involved start the replacement of lost/damaged tissues by stimulating healthy cells to divide
  • WBCs trigger blood vessel growth and scar tissue formation for those cells that cannot divide
    • Function of these cells are lost

The stages can overlap - they are not discrete

22
Q

Local responses

A

Swelling
Pain
Heat
Redness
Exudate/impaired function - serous/fibrinous/purulent/hemorrhagic

23
Q

Chronic inflammation

A
  • Macropages are the star
    • Release tissue thromboplastin - facilitates hemostasis, promotes fibroblasts
    • Removes necrotic tissue and pathogens (debridement) continuous release of proinflammatory cells
  • Thickening and scarring of connective tissue
  • May be subclinical
24
Q

What is subclinical?

A
  • No overt symptoms (more systemic manifestations)
  • Investigate through blood tests: CRP and ESR
  • May need a WBC scan to identify areas of inflammation
25
Q

Systemic responses

A

Neutrophilia
Fever
Malaise
Loss of appetite
Muscle catabolism

26
Q

What is ESR?

A

Fibrinogen levels go up in the serum which causes RBCs to clump.
**CHRONIC INFLAMMATION MARKER **

Erythrocyte sedimentation rate

27
Q

What is hs-CRP?

A

Dead and dying cells release chemical factors, which cause the liver to produce CRP.
PROTEIN LIVER MAKES HS-CRP DURING ACUTE INFLAMMATION

Highly sensitive C-reactive protein

28
Q

Drugs that reduce inflammation

A

Steroidal agents = glucocorticoids (Prednisone)
Non-steroidal anti-inflammatory drugs (NSAIDs) = Ibuprofen

29
Q

Drugs that manage fever

A

Antipyretics
- Acetaminiphen
- Aspirin (almost never because of anti-coagulant properties)
- NSAIDs

30
Q

Drugs for pain relief

A

Analgesics
- Acetaminophen
- Aspirin (rarely)
- NSAIDs
- Opioids for severe pain

31
Q

MOA of Glucocorticoids (Prednisone)

A

Inhibit synthesis of chemical mediators (prostaglandins, leukotrienes, histamines)
- They suppress infiltration of phagocytes so damage from lysosomal enzymes is averted
- The suppress proliferation of lymphocytes and therby reduce the immune components of inflammation

32
Q

Glucocorticoids (Prednisone) adverse effects

A

Hyperglycemia
Fluid and electrolyte imbalances (Na/K)
Psychological disturbances (anxiety/agitation/insomnia)
Peptic ulcer disease
Adrenal insufficiency
Osteoporosis
Cushings

33
Q

Glucocorticoids (Prednisone) Nursing Considerations

A

Monitor:
BP
Weight gain
Lab values
Abdominal pain
Signs and symptoms of infection

Adminster with antacid
Tapering required
Caution with NSAIDs
Give in the morning

34
Q

Sudden withdrawal and adrenal crisis

A

Exogenous cortisol stops pituitary release of ACTH which controls adrenal glands thus stopping them from working
Adrenal crisis = hypotension, fly-like symptos, seizures, shock

NURS 2500 (8 decks)

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