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PATHOLOGY I > quiz #2 - inflammation > Flashcards

quiz #2 - inflammation Flashcards

1
Q

INFLAMMATION

A

Non-specific response to injury
Purpose: start healing process
Interconnected events form coordinated reaction by cells
Involves blood vessels & cells, nerves & chemicals
May last minutes → years
Causes redness, swelling, warmth & pain
May be acute/ chronic

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2
Q

FUNCTION of inflammation

A

has protective role – serious side effects may go too far
-Inactivate injurious agent
-Breakdown & remove dead cells
-Initiate healing process

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3
Q

5 cardinal signs of inflammation & what they are caused by

A

HEAT: vasodilation & increased blood flow
ERYTHEMA (redness): vasodilation & increased blood flow
EDEMA (swelling): too much fluid & cells leak into interstitial spaces – imbalance
PAIN/ TENDERNESS: direct trauma, bradykinins, histamines, swelling of nerves
LOSS OF USE/ dysfunction: joint, ligament, mm, tendon damage

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4
Q

4 KEY COMPONENTS in response to injury

A
  1. Circulatory changes
  2. Vessel wall changes
  3. Immune response
  4. Cellular response
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5
Q

Circulatory changes (components in response to injury)

A

first response, increased blood flow: causes redness, swelling & warmth

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6
Q

Vessel wall changes (components in response to injury)

A

damage to endothelial lining in blood vessel walls causes them to become more permeable/ leakier via 4 processes

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7
Q

Vessel wall changes (components in response to injury): 4 processes

A

-increase in BP
-decrease in speed of circulation in area
-WBCs & platelets stick to endothelial lining (adhesion)
-release of mediators locally

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8
Q

Immune response (components in response to injury)

A

release of mediators/ chemicals → cytokines, histamines, bradykinins, arachidonic acid, activation of complement system

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9
Q

HISTAMINES (immune response)

A

released from platelets & mast cells, stimulates endothelial cells to contract making gaps between them wider & leakier

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10
Q

BRADYKININ (immune response)

A

released from plasma, accounts for pain with inflammation

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11
Q

COMPLEMENT SYSTEM (immune response)

A

proteins activated (by 3 different things) in cascade that forms membrane attack complex (MAC) that kills cell but also causes more histamine release

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12
Q

COMPLEMENT SYSTEM: 3 pathways

A

Classical pathway: activated by antibodies binding to antigens
Alternative pathway: activated by bacteria endotoxins (fungi, snake venom etc.) that are carbohydrates on surface of bacteria
Lectin pathway: activated by macrophages that digest bacteria, release chemicals that cause liver to produce lectins
*all 3 pathways lead to formation of the membrane attack complex (MAC) -> kills cells by boring hole in membrane

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13
Q

ARACHIDONIC ACID (immune response)

A

leukotrienes (promote chemotaxis & increased permeability) & prostaglandins (vasodilation, increased permeability, mediates pain & fever)

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14
Q

CYTOKINES (immune response)

A

produced by leukocytes (WBCs)
-Interleukin - 1
-Tumor Necrosis factor (TNF)

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15
Q

Cellular response (components in response to injury)

A

fluid imbalance, emigration of leukocytes, phagocytosis

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16
Q

CELLS of inflammation

A

Neutrophils
polymorphonuclear cells (PMN’s)
Eosinophils
Basophils
Macrophages
Platelets
Other cells

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17
Q

CAUSES of inflammation

A

Infections: bacteria, virus, fungus, protozoa, worms
Chemical: industrial, medicinal, exogenous & endogenous
Physical: heat, irradiation, trauma
Foreign bodies: thorn, bee sting
Immune: hypersensitivity reactions

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18
Q

TYPES of inflammation (by duration)

A

ACUTE: rapid onset, short duration, all 5 cardinal signs
-EXUDATE: full of PMNs, monocytes, eosinophils
CHRONIC: delayed onset, longer duration, may or may not have cardinal signs
-EXUDATE: full of lymphocytes, macrophages, plasma cells

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19
Q

TYPES of inflammation

A

Serous
Fibrinous
Purulent
Ulcerative
Pseudomembranous
Granulomatous

20
Q

SEROUS (types of inflammation)

A

mildest form, early stages
EXUDATE: clear fluid, no cells, lots of proteins
Common: viral infections (herpes)

21
Q

FIBRINOUS (types of inflammation)

A

caused by severe inflammation, does not resolve easy
EXUDATE: lots of proteins (fibrin), dead neutrophils
Common: bacterial infections (strep throat)

22
Q

PURULENT (types of inflammation)

A

caused by pus forming bacteria, may accumulate & form an abscess
EXUDATE: viscous, yellow fluid, dead PMNs, dead tissue, lytic enzymes
Common: bacteria (streptococci, staphylococci)

23
Q

ULCERATIVE (types of inflammation)

A

on body surfaces or mucosa of hollow organs (stomach, small intestine), epithelial lining lost or ulcerated creating a hole

24
Q

PSEUDOMEMBRANOUS (types of inflammation)

A

combination of ulcerative, purulent & fibrinous
EXUDATE: made of fibrin, pus & cellular debris form membrane on surface of ulcer
Common: diphtheria (throat)

25
Q

GRANULOMATOUS (types of inflammation)

A

formation of granulomas made of T lymphocytes, macrophages & multinucleated giant cells that clump together into small nodules that destroy tissues over long period of time
Common: tuberculosis, hypersensitivity reactions

26
Q

SYSTEMIC CLINICAL FINDINGS with inflammation

A

Fever: caused by pyrogenic cytokines
Leukocytes: increase in circulating WBCs
General symptoms: fatigue, weakness, depression, malaise, lack of appetite, achiness

27
Q

Wound healing

A

sequence of events that occur after skin injury

28
Q

CELLS in wound healing

A

leukocytes, macrophages, CT cells, epithelial cells, PMN’s

29
Q

Leukocytes (WBCs) / POLYMORPHONUCLEAR (PMNs)

A

act as scavengers at site

30
Q

Macrophages (most important)

A

stay the longest, produce cytokines, growth factors, mediators, myofibroblasts, angioblasts, fibroblasts

31
Q

Connective tissue

A

produce scar tissue:
Myofibroblasts – smooth mm & fibroblasts combined, holds wound margins together
Angioblasts – precursor to blood vessels, form new blood vessels & blood supply
Fibroblasts – produce extracellular matrix & two most important proteins:
-Fibronectin → forms scab
-Collagen type III → scar tissue

32
Q

Epithelial cells

A

undergo mitosis & duplicate to extend to cross gap over wound to fill gap

33
Q

1st intention healing

A

clean wound edges close together

34
Q

2nd intention healing

A

wound left open due to too much tissue damage, more scar & granulation tissue allowed to build up before closing wound

35
Q

delayed wound healing

A

wound left open

36
Q

angioblasts

A

precursors to blood vessels, proliferate like sprouts from close-by blood vessels at margins of wound
-appear 2-3 days after injury, provide new blood supply

37
Q

DETERMINANTS of wound healing

A

Site of wound: skin heals well, brain does not
Mechanical factors: if margins are close, no tension around wound, not over joint
Size of wound: small wounds heal faster
Presence/ absence of infection: sterile wounds heal faster
Circulatory status: if wound is in ischemic tissue, will heal slower (diabetes mellitus)
Nutritional & metabolic factors: if healthy, wounds heal faster
Age: wounds heal fastest in children

38
Q

EPIDERMAL wound healing

A

effects dermis, minimal damage

39
Q

DEEP wound healing

A

effects epidermis, dermis & subcutaneous layers

40
Q

clot formation - INTRINSIC pathway

A

blood vessel wall damage, activated by exposed collagen fibers in wall, activates clotting factor XIII

41
Q

clot formation - EXTRINSIC pathway

A

tissue damage, activated by presence of tissue factor (TF), releases thromboplastin & activates clotting factor VIII

42
Q

clot formation - what do both pathways require?

A

require Ca2+ to produce prothrombinase then prothrombin → thrombin → fibrin thread → fibrin clot (scab)

43
Q

COMPLICATIONS of wound healing

A

Deficient scar formation
Excessive scar formation
Loss of function
Infection

44
Q

Hypertrophic scar

A

elevated scar within original boundaries of wound

45
Q

Keloid scar

A

elevated scar that exceeds original boundaries of wound

46
Q

Contracture

A

over joint, fixation/ deformity

47
Q

Adhesions

A

bands of scar tissue that join two normally separated surfaces

PATHOLOGY I (17 decks)

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