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Pathophysiology > E1 Ch 5 Inflammation > Flashcards

E1 Ch 5 Inflammation Flashcards

1
Q

body defenses

A

first line of defense
- nonspecific
- mechanical barriers such as intact skin and mucous membranes block entry of bacteria and harmful substances into the tissues
- body secretions such as saliva or tears contain enzymes or chemicals that inactivate or destroy potentially damaging material
second line of defense
- nonspecific
- phagocytosis (neutrophils and macrophages randomly engulf and destroy bacteria, cell debris, or foreign matter)
- inflammation (sequence of events intended to limit the effects of an injury or a dangerous agent in the body)
- interferons (nonspecific agents that protect uninfected cells against viruses)
third line of defense
- specific
- antibody/lymphocyte production provides protection by stimulating the production of unique antibodies or sensitized lymphocytes following exposure to specific substances

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2
Q

normal capillary exchange

A
  • not all capillaries are open in a particular capillary bed unless the cell’s metabolic needs are not being met
  • movement of fluid, electrolytes, oxygen, and nutrients out of the capillary at the arteriolar end is based on the net hydrostatic pressure
  • at the venous end of the capillary, osmotic pressure facilitates the movement of fluid, carbon dioxide, and other wastes into the blood
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3
Q

physiology of inflammation

A
  • inflammation is the body’s response to a tissue injury
  • results in redness, swelling, warmth, pain, and sometimes loss of function
  • disorders are named using the ending -itis
  • normal defense mechanism in the body
  • intended to localize and remove an injurious agent
  • not the same as infection (infection has microbes present)
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4
Q

causes of inflammation

A
  • direct physical damage (cuts or sprains)
  • casuistic chemicals (acids or alkali)
  • ischemia
  • infarction
  • allergic reactions
  • extreme heat or cold
  • foreign bodies (splinters or glass)
  • infection
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5
Q

steps of inflammation

A
  • bradykinin is released from injured cells
  • bradykinin activates pain receptors
  • sensation of pain stimulates mast cells and basophils to release histamine
  • bradykinin and histamine cause capillary dilation
  • this results in an increase of blood flow and increased capillary permeability
  • break in skin allows bacteria to enter the tissue
  • this results in the migration of neutrophils and monocytes to the site of injury
  • neutrophils phagocytize bacteria
  • macrophages leave the bloodstream and phagocytose microbes
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6
Q

acute inflammation

A

rapid onset; severity of the inflammation varies with the specific cause and duration of exposure; chemical mediators affect blood vessels and nerves in the damaged area causing:
- vasodilation
- hyperemia
- increase in capillary permeability
- chemotaxis to attract cells of the immune system

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7
Q

chronic inflammation

A

may develop following an acute episode of inflammation; less swelling and exudate; more lymphocytes, macrophages, and fibroblasts; more tissue; more collagen is produced, causing more fibrous scar tissue forming

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8
Q

histamine

A

immediate vasodilation and increased capillary permeability

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9
Q

chemotactic factors

A

for example, attract neutrophils to site

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10
Q

platelet activating factor

A

activate neutrophils, platelet aggregation

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11
Q

cytokines (interleukins, lymphokines)

A

increase plasma proteins and erythrocyte sedimentation rate, induce fever, chemotaxis, leukocytosis

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12
Q

leukotrienes

A

later response; vasodilation and increased capillary permeability, chemotaxis, leukocytosis

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13
Q

prostaglandins

A

vasodilation, increased capillary permeability, pain, fever, potentiate histamine effect

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14
Q

kinins (ex. bradykinin)

A

vasodilation and increased capillary permeability, pain, chemotaxis

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15
Q

complement system

A

vasodilation and increased capillary permeability, chemotaxis, increased histamine release

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16
Q

cardinal signs of inflammation

A

redness and warmth
- caused by increased blood flow to damaged area
edema
- shift of protein and fluid into the interstitial space
pain
- increased pressure of fluid on nerves; release of chemical mediators (ex. bradykinin)
loss of function
- may develop if cells lack nutrients; edema may interfere with movement

17
Q

serous exudate

A

watery exudates, primarily of fluid with small amounts of protein and white blood cells; exudates of allergic reactions of burns

18
Q

fibrinous exudate

A

thick and sticky, high cell and fibrin content

19
Q

purulent exudate

A

thick, yellow green in color, more leukocytes and cell debris, as well as microorganisms, often malodorous, indicates bacterial infection

20
Q

abcess

A

localized pocket of purulent exudate in a solid tissue

21
Q

hemorrhagic

A

bloody type drainage; may be present if blood vessels have been damaged

22
Q

systemic effects of inflammation

A
  • fever or pyrexia (low grade or mild); common if inflammation is extensive
  • malaise (feeling unwell)
  • fatigue
  • headache
  • anorexia
23
Q

course of a fever

A
  • fever may be severe if inflammation is caused by infection
  • high fever can be beneficial if it impairs the growth and reproduction of a pathogenic organism
  • fever results from the release of pyrogens or fever-producing substances (ex. interleukin-1) from white blood cells or macrophages
  • pyrogens circulate in the blood and cause the body temperature control system in the hypothalamus to be reset at a higher level
  • heat production mechanisms such as shivering are activated to increase cell metabolism
  • involuntary cutaneous vasoconstriction characterized by pallor and cool skin reduces heat loss from the body
  • voluntary actions such as curling up or covering the body conserve heat
  • these mechanisms continue until the body reaches the new, higher setting
  • following removal of the cause, body temperature returns to normal by reversing the mechanisms
24
Q

diagnostic tests indicating inflammation

A
  • complete blood count with differential (differential meaning showing the different types of WBCs that are present)
  • c-reactive protein (increased c-reactive protein indicates inflammation)
  • erythrocyte sedimentation rate (ESR) (increased ESR indicates inflammation)
  • increased WBCs indicates infection
    • leukocytosis (increased WBCs)
    • band neutrophils (shift to the left)
    • eosinophils (allergic reaction)
  • plasma proteins (fibrinogen, prothrombin, and alpha-antitrypsin
  • tissue specific (increased creatine kinase w/ myocardial component (CK-MB): myocardial infarction; increased alanine aminotransferase (ALT): liver)
25
Q

potential complications of inflammation

A

local complications depend on the site of inflammation; infection; skeletal muscle spasms or strong muscle contractions

26
Q

treatment of inflammation

A

medications:
- acetylsalicylic acid (ASA/aspirin)
- acetaminophen
- nonsteroidal anti-inflammatory drugs (NSAIDs)
- glucocorticoids (steroids)
RICE:
- rest
- ice (first 48 hours)
- compression
- elevation

27
Q

types of healing (3 Rs)

A
  • resolution: minimal damage
    regeneration: damaged tissue
  • replaced with cells that are functional
  • replacement: functional tissue replaced by scar tissue, loss of function
28
Q

factors that promote healing

A

youth, good nutrition (proteins, vitamins a and c), adequate hemoglobin, effective circulation, clean/undisturbed wound, no infection or further trauma to the site

29
Q

factors that delay healing

A

advanced age, reduced mitosis, poor nutrition, dehydration, anemia (low hemoglobin), circulatory problems, certain chronic diseases, presence of other disorders such as diabetes or cancer, irritation, bleeding, excessive mobility, infection, foreign material, exposure to radiation, chemotherapy treatment, prolonged use of glucocorticoids

30
Q

types of burn injuries

A

thermal, chemical, smoke and inhalation injury (metabolic asphyxiation, upper airway injury, lower airway injury), electrical, radiation

31
Q

classification of burns

A
  • superficial partial thickness (first-degree) burns: involve epidermis only, generally no blister formation
  • superficial or deep partial thickness (second-degree) burns: involve epidermis and part of dermis, may or may not have blister formation
  • full thickness (third-degree) burns: destruction of all skin layers into subcutaneous tissue
  • deep full thickness (fourth-degree) burns: destruction of all skin layers and into underlying tissues (muscle, bone)
32
Q

effects of burn injury

A
  • both local and systemic
  • dehydration and edema
  • shock
  • respiratory problems
  • pain
  • infection
  • hypermetabolism during healing period after burn
33
Q

complications of burns

A

loss of function, contractures and obstructions, adhesions, hypertrophic scar tissue, ulceration

34
Q

emergency care of burns

A

pre-hospital:
- remove clothing unless adhered
- rinse with tepid water
- apply a clean, dry covering
ED:
- fluids to maintain perfusion until capillary permeability is restored
- monitoring airway due to edema
- pain and infection control
- nutritional support due to hypermetabolism

35
Q

healing of burns

A
  • hypermetabolism occurs during healing period
  • immediate covering of a clean wound is needed to prevent infection
  • healing is a prolonged process
  • scar tissue develops, even with skin grafting
  • physiotherapy and occupational therapy may be necessary
  • surgery may be necessary to release restrictive scar tissue
36
Q
A

first intention

37
Q
A

second intention

38
Q

capillary exchange

A

Pathophysiology (7 decks)

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