Exam 2 Concept Review: Chapter 5 Flashcards

1
Q

What are the causes of inflammation and examples?

A

Direct physical damage.
Ex: cut, sprain

Caustic chemicals
Ex: acid, drain cleaner

Ischemia or infraction

Allergic reactions

Extremes of heat or cold

Foreign bodies
Ex: splinter, glass

Infection

I-FACED-Infection

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2
Q

What are the chemicals involved in inflammation?

A

Bradykinin: vasodilation and increased capillary permeability, pain, chemotaxis

Prostaglandins: vasodilation, increased capillary, pain, fever, potentiate, histamine effect

Histamine: Immediate vasodilation and increased capillary permeability to for exudate

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3
Q

What are the local effects of inflammation?

A

Redness and Warmth: caused by increased blood flow to the damaged area

Swelling (edema): shifts of protein and fluid into the interstitial space

Pain: increased pressure of fluid on nerves; release of chemical mediators (e.g Bradykinin)

Loss of function: may develop if cells lack nutrients; edema may interfere with movement

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4
Q

What are the systemic effects of inflammation?

A

Mild fever (pyrexia): common in inflammation is extensive (covering or affecting large area), release of pyrogens, and will be higher if the patient has infection present

Malaise: feeling unwell

Fatigue

Headache: inflammatory response in the body that doesn’t involve head and the patient still has an headache

Anorexia

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5
Q

What are the different types of exudate (drainage) in the inflammatory process?

A

Serous: watery, consist primarily of fluid, some proteins, and white blood cells

Fibrinous: thick, sticky, high cell and fibrin content (makes it thick and sticky). There will be a increase risk for scarring of the tissue in that area

Purulent (“Pus”): thick, yellow-green, contains more leukocytes, cell debris, and microorganisms. Indicated a bacterial infection

Abscess: localized pocket of purulent exudate or pus (pocket of infection)

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6
Q

What are the potential complications of inflammation?

A

Infection: Microorganisms can more easily penetrate edematous (swollen) tissues, Some microbes resist phagocytosis, and the inflammatory exudate also provides an excellent medium for microorganisms

Skeletal muscle spasm: May be initiated by inflammation and protective response to pain

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7
Q

What are the potential complications of chronic inflammation?

A

Deep ulcers may result from severe or prolonged inflammation: Caused by cell necrosis and lack of cell regeneration that causes erosion of the tissue (this can lead to complications such as perforation of viscera and cause extensive scar tissue formation)

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8
Q

What are the different kinds of treatment for inflammation?

A

Acetylsalicylic acid (ASA): aspirin (reduces pain and fever)

Acetaminophen- pain & fever only (does not impact the inflammatory response): Tylenol

Nonsteroidal anti-inflammatory drugs (NSAIDs) – (helps with everything- with pain, fever, inflammation: ibuprofen and COX-2 inhibitors - pain and inflammation

Glucocorticoids (“steroids”)- reduce inflammation: Corticosteroids

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9
Q

What are the anti-inflammatory effects of glucocorticoids?

A

Decreased capillary permeability: enhanced effectiveness of epinephrine and norepinephrine

Reduced number of leukocytes and mast cells at the time: decreased of histamine and prostaglandins

Reduces immune system

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10
Q

What are the adverse effects of Glucocorticoids?

A

Atrophy of lymphoid tissue; reduced number of WBC’s: increased risk of infection and decreased immune response

Catabolic effects: increased tissue breakdown; decreased protein synthesis (this put patients’ at risk for osteoporosis)

Delayed healing

Delayed growth in children

Retention of sodium and water because of aldosterone- like affect in the kidneys

Definition of Osteoporosis: a condition in which the bones become weak and brittle

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11
Q

What is the RICE therapy for injuries?

A

R - Relax

I - Ice (cause constriction- cold constricts vessels while heat dilates vessels which decrease swelling and pain)

C - Compression (helps with venous return)

E - Elevation (improve fluid flow away from the damaged area - help with excessive fluid)

Definition of venous return: the rate of blood flow back to the heart

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12
Q

What is the scar formation (HAULC)?

A

Hypertrophic scar tissue: overgrowth of fibrous tissue (excessive collagen that develop) - leads to hard ridges of scar tissue or keloid formation

Adhesions (sticking together): Bands of scar tissue joining two surfaces that are normally separated (result inflammation and infection)

Ulceration: Blood supply may be impaired around scar (results in further tissue breakdown and ulceration in future time)

Loss of function: result of loss of normal cells and specialized structures such as hair follicles, nerves, and receptors

Contractures and obstructions: Scar is no elastic (can restrict range of motion)

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13
Q

What are the classification of burns?

A

Superficial partial-thickness (first-degree) burns: involve the epidermis and part of the dermis and little, if any, blister

Deep partial-thickness (second-degree) burns: epidermis and part of dermis and blister formation

Full-thickness (third- and fourth-degree) burns: destruction of all skin layers and underlying tissues and require skin crafts for healing

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14
Q

What are the rule of nines?

A

Two legs together is 36% (each leg is 18% - front of the leg 9% and back of the leg 9%)

The head is 9% (front of the head is 4.5% and back of the head is 4.5%)

Entire trunk is 36% (the front half is 9%, front bottom is 9% - same in the back)

Entire arm meaning front and back is 9% (front is 4.5)

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15
Q

What is the first line of defense?

A

Nonspecific: it is going to have the same response regardless of the invader

Mechanical barrier: skin, mucous membranes, secretions: gastric juice or tears (they contain enzymes and chemicals that will inactive or destroy lots of different damaging material)

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16
Q

What is the second line of defense ?

A

Nonspecific

Phagocytosis: neutrophils and macrophages engulf and destroy antigens

Inflammation: there are sequence of events and these events are responsible for limit the effects of injury or dangerous agent

17
Q

What are the third line of defense?

A

Specific defense: target specific antigens (the body is going to change slightly due to the invader

Production of specific antibodies and cell-mediated immunity

18
Q

What is the role of Glucocorticoids in inflammation?

A

They are going to decrease capillary permeability

Decrease the number of leukocytes at the site by reducing the release of histamine (suppressing the immune system)

Blocks the immune system

19
Q

What are the effects of burn injury?

A

Both local and systemic

Dehydration and edema (fluid shifts)

Shock respiratory problems (due to inhaling air toxins)

Pain

Infection

Increased metabolic needs for healing period: Patient will need tons of protein, carbs, and calories

20
Q

During acute inflammation, how does chemical mediators affect blood vessels and nerves in the damaged area?

A

Vasodilation: the widening of the blood vessels

Hyperemia: increased amount of blood in the vessels of an organ or tissue in the body

Increase in capillary permeability

Chemotaxis to attract cells of the immune system