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Pathology I > Inflammation Two > Flashcards

Inflammation Two Flashcards

1
Q

Inflammation

A

A non-specific response to any agent that causes cell injury.

Absolutely necessary for healing, but potentially harmful to body as well.

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2
Q

Agents of inflammation

A

Can be:
Physical
Chemical
Biologic

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3
Q

Non-Specific Response

A

Same response regardless of cause
Amount of response can vary

Variable to:
Virulence of agent
Size
Severity
Host factors
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4
Q

Suffix for -itis

A

Inflammation

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5
Q

Are cardinal signs on inflammation always visible?

A

No, not always.

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6
Q

Presentations of Loss of Function

A

Decreased ROM
Decreased performance
Decreased ability

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7
Q

PRICE

A

Old theory to treatment of inflammation
Some studies still support

Protect
Rest
Ice
Compress
Elevate
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8
Q

SHARP Mnemonic

A 
S - Swelling
H - Heat
A - Abnormal function 
R - Redness
P - Pain
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9
Q

PT Actions When Swelling Presents

A

Generally, do not treat.

If significantly worsens, very uncomfortable, puts pressure on other structures, or makes ADL’s too challenging then should be treated for.

Acute = leave it, chronic = treat it

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10
Q

Local Manifestations of Inflammation

A

Exudate formation; many potential types

Abscess formation

Ulceration

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11
Q

Exudate

& Types

A

A local manifestation of inflammation
Appearance associated with name

Serous
Fibrinous
Sanguinous
Serosanguinos
Seropurulent/Prurulent
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12
Q

Serous Exudate

A

Clear

Healthy response, normal

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13
Q

Fibrinous Exudate

A

Yellow

Occurs later in healing, normal

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14
Q

Sanguinous Exudate

A

Red

Indicative of blood, normal

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15
Q

Serosanguinous Exudate

A

Pink

Indicative of minor blood, normal

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16
Q

Seropurulent/Prurulent Exudate

A

Pus

Indicative of infection, abnormal

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17
Q

Abscess formation

A

A local manifestation of inflammation
When exudate occurs in solid tissue
“Walled off” by fibroblasts & macrophages
Inhibits body from releasing infections

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18
Q

Ulceration

A

A local manifestation of inflammation
When inflammation erodes epithelial surface
May require surgical intervention

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19
Q

Hypothalamus function in inflammation

A

Directs body to increase temperature to fight off infection

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20
Q

Systemic manifestations in inflammation

A

Occurs only in large injuries, infections, or autoimmune diseases

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21
Q

Signs of systemic manifestations

A 
Fever
Leukocytosis
Malaise
Lymphadenitis
Leukopenia
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22
Q

What is the hallmark sign of systemic inflammation?

A

Fever

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23
Q

Leukocytosis

A

Sign of systemic manifestation of inflammation
WBC growth
Potential leukopenia if overwhelming condition

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24
Q

Malaise

A

Sign of systemic manifestation of inflammation

Unwell feeling

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25
Q

Lymphadenitis

A

Sign of systemic manifestation of inflammation

Lymph nodes swelling

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26
Q

Leukopenia

A

Sign of systemic manifestation of inflammation
Low WBC count
Fight is using more cells than can produce

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27
Q

Leuko-

A

white

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28
Q

Cyto-

A

cells

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29
Q

-osis

A

growth of

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30
Q

Categories of Inflammation

A

Acute = short (less than a week)
Subacute = closer to healing, sign that still in inflammatory process but progressing
Chronic = long, need to intervene
Acute on Chronic = has existence of a chronic disease

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31
Q

Self-perpetuating

A

Viscous cycles of inflammatory response
Individual leaks cells to fight off
Usually severe exposure
Lasts weeks, months, years

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32
Q

Why can self-perpetuating cycles occur?

A

Cause still present
Chronic low intensity irritant, infection
Altered function of inflammatory/immune system response

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33
Q

How is chronic inflammation identified?

A

May result in further tissue destruction
More macrophages, lymphocytes, plasma cells
More fibroblasts
Little/no edema, exudate

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34
Q

Greater fibroblast proliferation

A 
Scar tissue
Lack original tissue properties
Can interfere with tissue function
ROM decreased
Lack of function
35
Q

Medical concerns with chronic inflammation

A 
"Recurring systemic inflammation"
Alzheimers
Diabetes Mellitus
Athersclerosis (heart disease)
Some cancers
Some autoimmune disease
36
Q

Atherosclerosis

A

Wearing down on lumen and plaque forms

37
Q

Parenchymal Tissue

A

Actual function tissue

38
Q

Stromal Tissue

A

Support structures

Give stability

39
Q

Tissue regeneration

A

Repair by same parenchymal type cells
Depends on cell proliferation and ability to move through cell cycle:
Labile, Stable, Fixed cells

40
Q

Labile cells

A

Always replicating
They are used to dividing and do it easily
Ex: smooth tissue repair
Ex: skin, GI tract

41
Q

Stable cells

A

Can be triggered to replicate/re-grow

Ex: liver

42
Q

Permanent or Fixed Cells

A

Will never proliferate or re-grow
Ex: neurons, cardiac, and skeletal
Think “expensive”

43
Q

Phases of tissue healing and repair

A

Inflammatory phase
Proliferation phase
Maturation phase

44
Q

Proliferation phase

A

“Fibroblastic phase”, Granulation, Granular phase
If better vasculature, better healing
Generally days 3-20
Rebuilding stage done by fibroblasts
Has four major components
*First phase PT’s can start to really help

45
Q

Maturation phase

A

“Remodeling phase”
Can last months or years

New tissue laid down, but changing
MOST progress occurs here
Day 7 - or Years 1-2

Longest phase in healing
# of macrophages, fibroblasts, capillaries decrease
Scar whitens and collagen aligns
Capillaries decrease
Collagen fiber synthesis

No pain
No swelling

46
Q

Components of Proliferative phase

A

Collagen production
Wound contraction
Revascularization
Epithelialization

47
Q

Collagen production

in Tissue Regeneration

A

First gets laid down
Basis for nearly all tissues
Produced by fibroblasts
Provides support/strength to tissue

Encourages correct “lay down”

48
Q

Wound contraction

in Tissue Regeneration

A 
Make wounds smaller
Only for large defects
Edges of wound pull together
Similar to the way sutures work
From outside in
49
Q

Revascularization

in Tissue Regeneration

A 
Good blood supply returns to area
"Angiogenesis"
Vessels from wound periphery migrate inward, providing blood
New scars often pink or bright red
Blood provides nutrients, O2

Bone fractures = quick
Ligaments = long

50
Q

Epithelialization

in Tissue Regeneration

A

Wound edges start to heal

Cells start at wound edge and migrate along granulation tissue

51
Q

Stages of healing in proliferation phase

A 
Epidermal layer reestablished
Epithelialization
Collagen & fibroblasts proliferation continues
WBC leave
Edema decreases
Small blood vessels degenerate 
Tissue blanches
Collagen production
Wound contraction 
Revascularization

Variable time based on size of wound

52
Q

Primary intention

A

Small wound
Easy to heal
Minimal scar tissue

No initial tissue loss
Little or no scar formation

53
Q

Secondary intention

A

Larger injuries
Occurs if:
larger amount tissue loss
contamination or infection

Larger amount of scar/fibrotic tissue

54
Q

Collagen fiber synthesis

A

Occurs in maturation phase

Reaches homeostasis during phase
Collagen fiber orientation resembles original tissue
Synthesis and lysis of collagen to reorient scar to increase tensile strength
70-80% of normal tissue strength at best

55
Q

Maturation phase: regeneration

A

Injured tissue replaced with new tissue of same kind and properties
Begins with granulation tissue

56
Q

Maturation phase: fibrosis

A

Scar tissue present
With more severe inflammation or larger tissue insults

Scar tissue not same as original tissue:
Lacks original strength
Lacks flexibility
Lacks original function

57
Q

Impaired healing can occur due to what 12 factors?

A 
Impaired blood flow, O2
Cardiac conditions
Respiratory conditions
Vascular conditions
Blood conditions
Malnutrition
Edema
Age (extremes = young and old)
Impaired inflammatory function
Impaired immune function
Foreign bodies
Some medications
58
Q

Malnutrition

A

Many micro and macro nutrients needed for adequate tissue function and healing

59
Q

Impaired inflammatory and immune function

A

Too much or too little action

Can be primary or secondary conditions

60
Q

What kind of system does the body work on?

A

Negative Feedback Mechanism

61
Q

Anti-Inflammatory medications

A

Common prescription for inflammation

62
Q

Is inflammation normal?

A

Yes - normal response to cellular injury

Vital for normal healing

63
Q

Dangers of excessive inflammation

A

Prolonged or excessive inflammation can cause more damage than the initial cellular injury

64
Q

Types of Anti-inflammatory meds

A

Analgesics
Non-steroidal anti-inflammatories
Corticosteroids
DMARD’s

65
Q

Analgesics

A

Strictly pain inhibitors
Symptom relief
“Not feeling”
Ex: acetaminophens, opiates, narcotics

66
Q

Non-Steroidal Anti-inflammatories

A

Prescription or OTC
Interrupt pathway to prostaglandin production
NSAID, non-NSAID’s, anti-feveretics
Ex: aspirin, ibuprofen, naprosyn, Celebrex

67
Q

Corticosteroids

A 
Sugar based
NOT anabolic
Either hormone from adrenal cortex (cortisol) or a synthetic derivative
Very potent anti-inflammatory properties
Many different kinds

-one’s
Ex: cortisone, prednisone, hydrocortisone, dexamethasone

68
Q

DMARD’s

A

Disease modifying anti-rheumatic drugs
Symptom relief
Affect underlying disease processes
Most common for autoimmune conditions

Ex: methotrexate, Enbrel, Humira

69
Q

Corticosteroid Potential Adverse Effects in Major systems

A 
Muskuloskeletal
Immunological
Cardiovascular
Integumentary
Metabolic & Endocrine 
Psychological
70
Q

How are corticosteroids delivered?

A

Injection (tissue or IV)
Topical
Inhaled (nebuligens)

71
Q

Conditions corticosteroids used for

A

Reduce inflammation for local OR systemic
Especially chronic

Allergies
Autoimmune disorders
-itis conditions (arthritis)

72
Q

Adverse Musculoskeletal Effects Corticosteroids

A

Muscle, tendon, cartilage weakening
Myopathy, muscular atrophy
Osteoporosis
Osteonecrosis

73
Q

Adverse Immunological Effects Corticosteroids

A

Immunosuppression
Bone marrow suppression

> intervene with RBC, WBC, platelet production

74
Q

Adverse Cardiovascular Effects Corticosteroids

A

HTN
Elevated blood lipids
Atherosclerosis
High blood pressure

75
Q

Adverse Integumentary Effects Corticosteroids

A 
Acne
Stretch marks (breakdown of collagen)
Hair loss
Easy bruising/bleeding
Skin atrophy
Poor wound healing
"skin tears" - friction causes skin to rip
76
Q

Adverse Metabolic & Endocrine Effects Corticosteroids

A 
Fluid retention
Electrolyte imbalances
Obesity
Growth retardation in children
Elevates BP (cause diabetes)

Excess sugar means pancreas malfunction

77
Q

Adverse Psychological Effects Corticosteroids

A

Mood changes
Behavioral changes

Can occur even in short doses;
anger, can’t sleep, hungry

78
Q

Adverse Psychological Effects Corticosteroids

A

Mood changes
Behavioral changes

Can occur even in short doses;
anger, can’t sleep, hungry

79
Q

PT Implications for Corticosteroids

A

Be aware of adverse effects with long term use
Systemic effects more likely when used for systemic conditions
Four major effects

80
Q

Four major effects for PT implications and corticosteroid usage

A

1) Weakness, may not tolerate activity well
2) Immunosupression
Standard precautions, risk of infection, may need neutropenic precautions
3) Poor skin quality, poor wound healing
4) Edema, weight gain

= Everything with awareness!

81
Q

Intra-cellular injections

A

Few months of effectiveness
Control acute pain and inflammation
Not to treat muscular, tendinous, or ligamentous injury
Less likely to result in systemic effects

Used as a bridge prior to surgery

Ex: cortisone shots

82
Q

Erythrocyte Sedimation Rate (ESR)

A

“sed rate”
Nonspecific test for inflammation
Positive result if elevated

83
Q

C-reactive protein (CRP)

A

Nonspecific test for inflammation

Positive result if elevated

84
Q

Current Considerations for Inflammation

A

Traditional Rx
-Halt/Limit inflammation following injury

Some newer proponents

  • Calling RICE into question
  • Allow normal inflammation to occur

Pathology I (9 decks)

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