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Asad > Patho/Pharm > Flashcards

Patho/Pharm Flashcards

1
Q

Bradykinin

A

activates pain receptors

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2
Q

Sensation of pain stimulates ___

A

mast cells & basophils to release histamine

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3
Q

What causes capillary dilation?

A

histamine, bradykinin

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4
Q

Neutrophils

A

phagocytize bacteria

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5
Q

Chemical Mediators

A

histamine, sertonin, prostaglandins, leukotrienes

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6
Q

Cytokines

A

act as communicators in the tissue fluids

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7
Q

Histamine

A

From: Mast cell granules
Action: immediate vasodilation and increased capillary permeability to form exudate.

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8
Q

Cytokines

A

(interleukins, lymphokines)
From: T-lymphocytes, macrophages
Action: increase plasma proteins, ESR, induce fever, chemotaxis, leukocytosis

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9
Q

Leukotrienes

A

From: arachidonic acid in mast cells
Action: later response - vasodilation and increased capillary permeability, chemotaxis

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10
Q

Prostaglandins

A

From: arachidonic acid in mast cells
Action: vasodilation, increases capillary permeability, pain, fever, potentiate histamine effect

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11
Q

Kinins

A

activation of plasma protein

Action: vasodilation and increased capillary permeability, pain, chemotaxis

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12
Q

Leukocytes

A

neutrophils (phagocytosis), basophils (release of histamine), eosinophils(increased # in allergic reactions)

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13
Q

Lymphocytes

A

T (cell mediated immune response), B (produce antibodies), monocytes (phagocytosis), macrophages (active in phagocytosis - mature monocytes)

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14
Q

Serous exudate

A

watery, small amounts of protein & WBCs, (allergic reactions, burns)

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15
Q

Fibrinous exudate

A

thick and sticky, high cell and fibrin content (increase risk of scar tissue)

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16
Q

Purulent exudate

A

thick, yellowish green, more leukocytes and cell debris, microorganisms. (bacterial infection, pus)

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17
Q

Abcess

A

local pocket of purulent exudate in a solid tissue.

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18
Q

Non-specific changes related to inflammation

A

increased WBC, increased CRP, increased ESR, increased plasma protein and cell enzyme.

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19
Q

Characteristics of long term inflammation

A

less swelling and exudate, more lymphoctyes/macrophages and fibroblasts.

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20
Q

Aspirin (ASA)

A

decreases prostaglandin synthesis a the site of inflammation. reduces pain and fever. reduces platelet adhesion.

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21
Q

Acetaminophen (ibuprofin)

A

decreases fever and pain but not inflammation

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22
Q

NSAIDs (ibuprofin, advil, motrin)

A

treat many inflammatory conditions because they have anti-inflammatory, analgesic and antipyretic activities. Act by reducing number of prostaglandins.

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23
Q

Glucocorticoids

A

decrease capillary permeability, enahce effectiveness of epinephirine and norepi, stabilize vascular system, reduce number of leukocytes and mast cells decreasing release of histamine and PGs. Block immune response.

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24
Q

Resolution

A

minimal tissue damage, damaged cell recover and tissue returns to normal within short period of time

25
Q

Regeneration

A

damaged tissue in which cells are capable of mitosis.

26
Q

Replacement

A

by connective tissue or scar tissue when there is excessive damage or damage to tissue unable to go through mitosis

27
Q

Healing by first intention

A

process involved when the wound is clean, free of foreign material, and necrotic tissue and the edges are held together creating minimal gap.

28
Q

Healing by second intention

A

large brak in the tissue, more inflammation, longer hraling period, more scar tissue.

29
Q

Fibroblasts and macrophages___

A

produce growth factors (cytokines) for the purpose of attracting more fibroblasts which stimulate epithelial cell proliferation and migration and promote development of new blood vessels in the healing tissue.

30
Q

Factors promoting healing

A

youth, good nutrition, adequate hemoglobin, effective circulation, clean/undisturbed wound, no infection/further trauma to site

31
Q

Factors delaying healing

A

advanced age, reduced mitosis, poor nutrition/dehydration, anemia, circulatory issues, chronic diseases, other disorders present, irritation, bleeding or excessive mobility, infection/foreign material/exposure to radiation, chemo, glucocorticoids (prolonged use)

32
Q

partial thickness burns

A

epidermis and part of dermis

33
Q

Superficial partial thickness (1st degree)

A

damage epidermis and upper dermis, red and painful heal readily w/o scar tissue

34
Q

Deep partial thickness (2nd degree)

A

destruction of epidermis and pat of the dermis, area is red edematous, blistered, hypersensitive, painful during inflammatory stage. Healing occurs by regeneration from the edges of the blistered area and from epithelium lining the hair follicles and glands.

35
Q

Full thickness (3rd & 4th degree)

A

destruction of all skin layers and underlying tissues. hard and dry and charred. initally may be painless due to nerve damage but then VERY painful. require skin grafts for healing

36
Q

Rule of nines

A

with burns - the head and each arm 9%, each leg is 18%, anterior and posterior trunk each 18%, groin 1%.

37
Q

Major burns include

A

burns involving large surface area, young children, elderly, genitalia, hands feet face ears, inhalation injury, chemical burns, other injuries/complications present, electrical injuries

38
Q

What happens with a large burn area?

A

massive shift of water, protein, electrolytes into the tissues causing fluid excess (edema). Loss of water and protein from the blood leads to decreased circulating volume, low blood pressure, hypervolemic shock, increased hematocrit. protein shift out of the capillaries lower osmotic pressure in the blood hard to maintain blood volume. Prolonged or recurrent shock may cause kidney failure or other organ damage.

39
Q

effects of burn injury

A

shock, respiratory problems, pain, infection, metabolic needs (hypermetabolism)

40
Q

During burn shock K is moving ___ and Na and H20 is moving ____

A

out, in

41
Q

Defenses of the body

A

First - the barriers (skin, mucous membrane, secretions like tears and saliva, second - phagocytosis third specific defeses, the immune response.

42
Q

Specific immune responses

A

responding to particular substances, cells, toxins, or proteins which are perceived as foreign to teh body and therefore unwanted or potentially dangerous.

43
Q

Components of the immune system

A

lymphoid structures (lymph nodes, spleen, tonsils, intestinal lymphoid tissue, lymphatic circulation), immune cells (lymphocytes, macropahges), tissues concerned with immune development, chemical mediators.

44
Q

antigens

A

foreign substances or human cell surface antigens that are unique in each individual. complex proteins or polysaccharides or glycoproteins. activate the immune system to produce specific antibodies.

45
Q

Major histocompatibility complex

A

MHC, detecting changes in the cell membrane altered by virus’ or cancerous changes and alerting teh immune system to their presence.

46
Q

Macrophage

A

critical in the initiation of the immune response. develop from monocytes. large phagocytic cells that intercept and engulf foreign materials, then process and display the antigens from the foreign material on their cell membranes. lymphocytes respond to the display to initiate immune response. secrete monokines & interleukins to activate additional lymphocytes.

47
Q

What is the primary cell in the immune response?

A

lymphocyte, produced by the bone marrow.

48
Q

T-lymphocytes

A

arise from stem cells, Cell mediated immunity develops when T-lymphocytes with protein receptors on the cell surface recognize antigens on the surface of target cells and directly destroy the invading antigen. T cells reproduce to create army to fight the invader. & activate other T & B lymphocytes. Primarily effective against virus infected cells, fungal and protozoal infections, cancer cells, foreign cells such as transplants.

49
Q

Cytotoxic CD8 positive T-killer cell

A

destroy target cell by binding to the antigen and releasing damaging enzymes or chemicals (monokines, lymphokines) which may destroy foreign cell membranes or cause inflammation response attracting macrophages to the site.. stimulate more lymphocyte production, hematopoiesis, phagocytes clean up debris.

50
Q

Helper CD4 positive T cell

A

facilitates the immune response

51
Q

Memory T cells

A

remain in the lymph nodes for years, ready to activate the response again if same invader comes.

52
Q

In pts with aids have increased levels of

A

CD4 molecules to CD8T lymphocytes

53
Q

B lymphocytes

A

humoral immunity through production of antibodies mature in bone marrow and go to spleen and lymphoid tissue. After exposure to the antigen they become antibody producing plasma cells. (with help of t lymphocytes)act primarily against bacteria and virus that are outside body cells.

54
Q

Natural killer cells

A

destroy without prior exposure and sensitization tumor cells and cells infected with virus’.

55
Q

Complement system

A

frequently activated with immune reaction involving IgG or IgM class immunoglobulins (antibodies)

56
Q

Type I hypersensitivity

A

Allergic Reaction, IgE bound to mast cells; release of histamine and chemical mediators, immediate inflammation and pruritis. begins when an individual is exposed to a specific allergen and for some reason develops IgE antibodies from B lymphocytes. The antibodies attach to mast cells making sensitized mast cells. On reexposure, the allergen attaches to the IgE antibody on the mast cell stimulating chemical mediator release (histamine from granules in the mast cell), prostaglanding and leukotrienes are released at the site in a second phase of the reaction and cause similar effects.

57
Q

Type II hypersensitivity

A

Cytotoxic Hypersensitivty, antigen is present on the cell membrane. may be normal body antigen or foreign. circulating IgG antibodies react with the antigen causing destruction of the cell by phagocytosis or cytolytic enzymes. (incompatible blood transfusion), complement activated.

58
Q

Type III hypersensitivity

A

Immune complex hypersensitivity - antigen combines with antibody forming a complex deposited into tissue and activates complement. causes inflammation and tissue damage.

59
Q

Type IV hypersensitivity

A

Cell mediated or delayed hypersensitivity - delayed response by sensitized T-lymphocytes to antigens resulting in release of lymphokines or other inflammatory mediators and destruction of antigen.

Asad (3 decks)

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