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PATHOLOGY I > inflammtion - KAHOOT & HINTS > Flashcards

inflammtion - KAHOOT & HINTS Flashcards

1
Q

what is one cardinal sign of inflammation?

A

heat & redness

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2
Q

what can cause inflammation?

A

infection
thorn
heat/ burn

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3
Q

T/F - endorphins are released into bloodstreams by platelets & mast cells in response to injury?

A

FALSE
=histamines released

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4
Q

what cell is most prominent in allergic & parasitic reactions?

A

eosinophils

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5
Q

T/F - RBCs are directly involved with inflammation

A

FALSE
cells involved: neutrophils, PMNs, eosinophils, basophils, macrophages, platelets

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6
Q

phagocytosis is…

A

a process where macrophages engulf & digest foreign objects

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7
Q

what type of inflammation produces exudate rich in fibrin?

A

fibrinous

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8
Q

T/F - a popped blister is an example of purulent inflammation

A

FALSE

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9
Q

5 stages of deep wound healing in order

A

inflammatory, migratory, proliferative, maturation, scar formation

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10
Q

a keloid scar…

A

is elevated & exceeds boundary of original wound

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11
Q

T/F - intrinsic & extrinsic pathways both merge to form fibrin which then turns into fibrin clot

A

FALSE
= prothrombinase then prothrombin → thrombin → fibrin thread → fibrin clot

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12
Q

purpose of inflammation

A

Start the healing process
FUNCTION: protective role
-inactivate injurious agent
-breakdown & remove dead cells
-initiate healing of tissues

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13
Q

Cardinal signs/ symptoms of inflammation

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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14
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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15
Q

HISTAMINES

A

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

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16
Q

BRADYKININ

A

released from plasma, slower reaction, accounts for pain with inflammation

17
Q

COMPLEMENT SYSTEM

A

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

18
Q

ARACHIDONIC ACID

A

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

19
Q

CYTOKINES

A

produced by leukocytes (WBCs)
-Interleukin-1: promotes inflammatory reaction
-Tumor Necrosis factor (TNF)

20
Q

NEUTROPHILS / POLYMORPHONUCLEAR cells (PMNs)

A

60-70% of all WBCs – most numerous, first to arrive, highly mobile, phagocytes (engulfing cells), contain bactericidal lysosomes, produce cytokines

21
Q

EOSINOPHILS

A

2-3% of all WBCs, arrive 2-3 days after, phagocytes, bactericidal, in chronic, in allergies & parasitic reactions

22
Q

BASOPHILS

A

less than 1%, IgE reactions, release histamine, morph into mast cells

23
Q

MACROPHAGES

A

arrive 3-4 days after onset, in chronic, derived from monocytes, in tissues NOT blood stream, phagocytes, secrete cytokines that produce inflammatory mediators

24
Q

PLATELETS / THROMBOCYTES

A

early to arrive with PMNs, contain many substances: histamine, clotting proteins, growth factor – released if damage to endothelial lining/ ECM, cause coagulation

25
Q

complement system - activated in 3 ways

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 that release chemicals that cause liver to produce lectins

26
Q

SEROUS (types of inflammation)

A

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

27
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)

28
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)

29
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

30
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)

31
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

32
Q

wound healing stages

A

-1st intention: clean wound edges close together
-2nd intention: wound left open due to too much tissue damage, more scar & granulation tissue allowed to build up before closing wound
-Delayed: wound left open

33
Q

CELLS in wound healing

A

Leukocytes, macrophages, connective tissue cells, epithelial cells, PMN’s.

*macrophages are most important - stay long time & contribute by producing cytokines, growth factors, mediators, myofibroblasts, angioblasts, fibroblasts

34
Q

EXTRINSIC pathway

A

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

35
Q

INTRINSIC pathway

A

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

36
Q

clot formation - intrinsic & extrinsic pathway

A

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

PATHOLOGY I (17 decks)

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