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MEDSURG -FINALS (SIR ERICH > Inflammatory And Immunologic Disturbances > Flashcards

Inflammatory And Immunologic Disturbances Flashcards

1
Q

Three Lines of Defense

A

• Anatomical Barriers
• Acute Inflammatory Response
• Immune System

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2
Q

What are the layers of the skin?

A

Stratum Corneum
S.lucidum
S.Granulosum
S.Germinativum

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3
Q

3 Lines of Defense

A

First Line of Defense
Second line of Defense
Third Line of Defense

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4
Q

Mechanical Barriers and Chemical Barriers

A

First Line of Defense

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5
Q

Inflammation response and phagocytosis

A

Second line of defense

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6
Q

Specific immune response, Natural Killer cells (NK cells)

A

Third line of defense

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7
Q

Anatomical Barriers: First line of defense

A

Skin, Mucous Membrane, Normal Bacterial flora

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8
Q

1st line defense - Normal Bacterial flora are:

A

Clostridium difficile
Yeast Infections

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9
Q

multilayer barrier, shed outer layer, contains fatty acids that kills some bacteria

A

Skin

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10
Q

contain cilia in upper respiratory tract, macrophages

A

Lungs

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11
Q

flush action of urine washes away bacteria

A

Urinary Tract

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12
Q

Occurs in response to injury
• Localized
• Immediate
• Beneficial
• Appropriate level of
response
• Non Specific

A

Inflammatory Respons

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13
Q

Causes of Inflammation
Physical

A

Trauma, Lacerations, Burns

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14
Q

Causes of Inflammation
Chemical

A

BItes, Allergic response

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15
Q

Causes of Inflammation
Microorganisms

A

Bacteria.

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16
Q

Inflammatory Response (5 stages of response)

A

-REDNESS
• SWELLING
• PAIN
• HEAT
• LOSS OF FUNCTION

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17
Q

Purpose of inflammation (NRPA)

A

-Neutralizes and Dilutes Toxins
• Removes necrotic materials
• Provides an environment for healing
• Add “itis” to affected body part

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18
Q

4 Phases of Inflammation

A

Vascular
Cellular
Formation of Exudate
Healing

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19
Q

Think Blood Vessels

A

Vascular

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20
Q

Think WBC’s

A

Cellular

21
Q

Fluid and neutrophils

A

Formation of Exudate

22
Q

regeneration or repair of tissue

A

Healing

23
Q

Injury occurs
• Mediators intervene
• Vasodilation occurs
• Capillaries become more permeable
• Swelling and movement of fluid occurs

A

Vascular Phase: Blood Vessels

24
Q

Injury occurs
Chemotaxis begins
White blood cells rush in to help
Neutrophils Monocytes Macrophages

A

Cellular Phase – Think WBC’s

25
Q

Chemical Mediators

A

Coordinators of the inflammatory response
• Histamine
• Prostagladins
• Cytokines

26
Q

(ESR or sed rate)
<20 mm/hr

A

Erythrocyte sedimentation rate

27
Q

non specific test identifying the presence of inflammation <1.0 mg/dl

A

CRP – C reactive protein

28
Q

special long wave ultraviolet light produced by a Wood’s lamp that induvisible flourescence in certain skin lesions . Best seen in darkened room.

A

Wood’s Light examination- a special long wave ultraviolet light produced by

29
Q

obtain tissues for examination

A

Skin biopsy

30
Q

use to document contact sensitivity or allergy
– suspected allergens are placed on normal skin beneath patches of tape
– patches are removed and the skin under the patches is examined at specified intervals

A

Patch Test

31
Q

scales from a lesion are scraped with a scalpel and placed on a glass slides covered with potassium hydroxide and examined

A

Fungal Scraping

32
Q

for cytologic exam of blisterng diseases of the skin

A

Tzanck smear

33
Q

for suspected vesicle or pustule is opened and contents applied to a glass of slide.and scanning after

A

Tzanck smear

34
Q

reveal nature and extent of nature and show progress or improvement from treatment

A

clinical photograps

35
Q

Systemic Manifestations of Acute Inflammation

A

Fever/chills
Cytokines

Benefits
- Increased killing of microorganisms
- Increased phagocytosis by neutrophils
- Increased activity of interferon

Leukocytosis Neutrophils
- “left shift”…band cells

36
Q

Inhibits prostaglandin synthesis

A

NSAID’s ( Ibuprofen, Toradol)

37
Q

NSAID’s nursing implications

A
  • Give w/food
  • Elderly-high risk GI bleed
  • Prolongs bleeding times 1 day
  • Assess renal function-creatinine w/chronic use
38
Q

Inhibits production of prostaglandins Decreases platelet aggregation

A

NSAID’S (Salicylates – Aspirin)

39
Q

ASPIRIN Nursing implications

A

Give w/food
Prolongs bleeding times 4-7 days

40
Q

Block histamine at the receptor site
Decreases gastric acid secretion

A

ANTI-HISTAMINES
Benadryl, Ranitidine (Zantec), Famotidine (Pepcid)

41
Q

NURSING IMPLICATIONS OF ANTIHISTAMINE

A

With meals
Drowsiness/dizziness

42
Q
  • Decrease inflammation by stabilizing neutrophils and lysosomes Inhibit prostaglandin synthesis
  • Inhibits chemotactic cytokines
  • Decreases mast cell stimulation
A

Prednisone (Corticosteroids)

43
Q

Prednisone (Nursing Implications)

A

Meals

44
Q

Prednisone (Chronic Use complications)

A

Risk of infection
Hyperglycemia
SE

45
Q

Occurs when first line of defense is broken by cellular injury

A

Acute Inflammatory Response

46
Q

Injury can be caused by:

A

-trauma or surgery
• chemical agents
• temperature extremes
• invasion of micro-organisms
• oxygen/nutrient deprivation (ischemic damage)
• genetic/immune defects (e.g. autoimmune)

47
Q

A biochemical and cellular process that occurs in vascular tissues due to cellular injury

A

Acute Inflammatory Response

48
Q
  • Inflammation may precede an immune response
    or be caused by one
  • Occurs physiologically in the same manner
    whether initial or second exposure to antigen
A

Non- specific elimination of micro-organisms

49
Q

Momentary constriction followed by prolonged vasodilation of arterioles and venules
Vascular permeability increases d/t histamine release

A

VASCULAR RESPONSE
Hemodynamic changes in microcirculation:

MEDSURG -FINALS (SIR ERICH (13 decks)

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