Lecture 2 Flashcards

1
Q

First line of defense

A

skin and mucous membranes

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2
Q

second line of defense

A

inflammation

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3
Q

third line of defense

A

immune response

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4
Q

cellular response steps (4)

A

marginization/adhesion
migration
chemotaxis
phagocytosis

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5
Q

marginalization/adhesion

A
  1. cytokines released leads sto increase in selectins
  2. leukocytes slow down *stick to vessel walls
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6
Q

migration

A

leukocytes extend pseudopods PASS thru cell wall via ameboid movement

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7
Q

chemotaxis

A

leukocytes travel thru tissues to injury

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8
Q

phagocytosis

A
  1. recognition *adherence
  2. engulfment
  3. intercellular killing
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9
Q

3 vascular response patterns

A
  1. immediate transient
  2. immediate sustained
  3. delayed hemodynamic
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10
Q

immediate transient

A

follows minor injury (ex. being snapped)

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11
Q

immediate sustained

A

follows major injury (surgical incision)

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12
Q

delayed hemodynamic

A

4 to 24 hours after injury (ex sunburn, vaccine)

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13
Q

types of white blood cells

A

neutrophils, eosinophils, basophils, mast cells, monocytes

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14
Q

neutrophils

A

1st responder! arrives approximately 90 minutes and stay / live for approximately 10 hours.
Bands or left shift=immature neutrophil
Primary phagocyte
neutrophilia due to bacterial infection.

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15
Q

Eosinophils

A

Red under microscope
parasitic

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16
Q

basophils

A

inflammation x allergic rxns
release histamine & bonds with IGE

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17
Q

mast cells

A

last basophils but In connective tissues & mucosal surfaces
allergic rxn and parasitic
“sentinel position” -immediately releases anti-histamine

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18
Q

monocytes

A

Swat team
acts like macrophage
slowest to respond (approximately 24 hours) but last 48 hours

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19
Q

What do inflammatory mediators do?

A

modify and enhance inflammatory response

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20
Q

types of inflammatory mediators

A

plasma protein systems, histamines, cytokines, cyclooxygenase pathway, nitric oxide

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21
Q

Plasma Protein systems

A

Kinins, clotting system, complements

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22
Q

What do kinins do?

A

inflammatory mediators that do vasodilstion + increased permeability
feel pain via smooth muscle contraction
bradykinin
kinins broken down by 1. ace inhibitors
2. Kininase

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23
Q

What breaks down kinins?

A
  1. ACE inhibitors
  2. Kininase
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24
Q

Clotting system

A

expresses adhesion molecules and produces prostaglandins and chemokines
key clotting enzyme: thombin

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25
Q

Complements-what do they do?

A

vasodilation + inc. permeability
adhesion and chemotaxis
leukocute activation
augmentation of phagocytes

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26
Q

what do histamines help with?

A

helps with vasodilation and permeability via H1 receptor

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27
Q

What cells release histamines?

A

released by mast cells, platelets, and basophils

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28
Q

what do cytokines consist of?

A
  1. niterferons (IFNs)
  2. intereukins (ILs)
  3. chemokines
  4. lympohkines
  5. tumor necrosis factor (TNF)
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29
Q

what are the 5 actions–>

A
  1. fever
  2. adhesion of leukosytes
  3. pain
  4. chemotaxis
  5. acute phase response
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30
Q

2 major cytokines (major mediators of early inflammatory response

A

IL-1 and TNF-alpha

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31
Q

what is arachidonic acid

A

it is a fatty acid precursor derived from phospholipids in cell membrane

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32
Q

3 types of granulocytes

A

eosinophils, basophils, and mast cells

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33
Q

pathway that converts arachidonic acid to prostaglandins and thromboxane

A

cyclooxygenase pathway

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34
Q

pathway that converts arachidonic acid to leukotrienes

A

lipoxygenase pathway

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35
Q

What is a leukotriene antagonist

A

5-lipoxygenase inhibitor
IE: singulair–used to treat asthma

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36
Q

fxn of leukotreienes

A

induces smooth muscle contraction
constricts pulmonary airway (with smooth muscle contraction)
increases microvascular permeability
adhesion of endothelial cells
chemotaxis
further histamine release

37
Q

fxn of prostaglandins

A

vascular permeability and vasodilation
induces inflammation
involved in pain response
potentiate effects of other inflammatory mediators (especially histamine)

38
Q

fxn of thromboxane A2

A

promotes platelet aggregation and vasoconstriction
NSAIDs and Aspirin–inhibit enzyme in cyclooxygenase pathway for prostaglandin synthesis

39
Q

Nitric oxide

A

slows/stops inflammation:
smooth muscle relaxation
antagonism of platelet functions (adhesion, aggregation, degranulation)

40
Q

5 cardinal signs of inflammation

A

erythema, heat, swelling, pain, loss of function

41
Q

erythema

A

redness due to vasodilation, increase in RBC, and increase in blood flow

42
Q

heat

A

vasodilation, increased blood flow

43
Q

Swelling

A

also known as edema or tumor
increase vascular permeability
increase fluid in extracellular space

44
Q

Pain

A

compression in tissues due to swelling, direct elicitation of pain due to inflammatory mediators

45
Q

loss of fxn

A

direct damage or due to pain or swelling

46
Q

Types of local manifestations of inflammation (3)

A

exudates, abscess, ulceration

47
Q

What is a exudate?

A

fluid excreted from site of injury

48
Q

what is an absess?

A

localized collection of purulent (PUS) walled off by fibroblasts

49
Q

what is an ulceration?

A

necrotic or eroded epithelium due to Trauma or Vascular compromise

50
Q

Types of exudates?

A

serous, sanguinous, fibrinous, purulent, hemorrhagic, membranous/pseudomembranous

51
Q

describe serous exudate

A

yellow and watery, derived from plasma. Lower in protein

52
Q

describe sanguinous exudate

A

thin, red or pink, watery; plasma with a few RBCs mixed in

53
Q

describe fibrinous exuate

A

large amounts of fibringen-thick sticky meshwork (adhesions) usually inside the body

54
Q

describe Purulent/Suppurative exudate

A

pus (degraded WBC, proteins, tissue debris)

55
Q

describe a hemorrhagic exudate

A

severe tissue injury causing damage to blood vessels or significant leakage of RBCs from capillaries (hematoma)

56
Q

describe a membranous/pseudomembranous

A

form on mucous membranes; necrotic cells in fibropurulent base

57
Q

3 types of capillaries

A

continuous, fenestrated, sinusoid

58
Q

Systemic manifestations of inflammation

A

fever, increase in leukocytes, lethargy, skeletal muscle catabolism, increase in erythrocyte sedimentation rate (ESR)

59
Q

What is leukocytosis?

A

increase in overall number of WBCs in the serum

60
Q

if someone has a bacterial infection, they would see an increase in what kind of leukocyte? and what would that be called?

A

increase in neutrophil
would be called neutrophilia

61
Q

if someone has a parasitic infection, they would see an increase in what kind of leukocyte? and what would that be called?

A

eosinophilic cells would increase to site

would be called eosinophilia

62
Q

if someone has an allergic reaction, they would see an increase in what kind of leukocyte? and what would that be called?

A

eosinophilic cells would increase to site

would be called eosinophilia

63
Q

if someone has a viral infection, they would see an increase in what kind of leukocyte? and what would that be called?

A

neutrophils or lymphocytes would increase

would be called neutropenia and/or lymphocytosis

64
Q

what are an increase in left shift cells suggestive of?

A

an infection

65
Q

what is lymphadenitis?

A

inflammatory reaction in lymph nodes draining an injured area

66
Q

what causes lymphadenitis?

A

caused by filtering lymph fluid with infectious and/or necrotic material draining from local injured or infected area

67
Q

What is the treatment for lymphadenitis?

A

antimicrobial therapy, analgesics, anti-inflammatories, cool compress

+abscessed nodes may require drainage

68
Q

what is lymphangitis?

A

inflammation or infection of lymph channels draining an injured area

69
Q

most common cause of lymphangitis?

A

streptococcus pyogeneses

70
Q

characteristics of lymphangitis?

A

red, tender streaks extending proximally

71
Q

how is lymphangitis treated?

A

antimicrobial therapy, analgesics, anti-inflammatories, cool compress

72
Q

what causes shock?

A

lack of O2 and circulation

73
Q

what are the fatality rates if you have a patient in septic shock?

A

35-60% mortality rate

74
Q

what are the fatality rates if a patient presents themselves with cardiogenic shock?

A

60-90% mortality

75
Q

Major symptoms of shock

A

extremely low blood pressure (hypotension)
decreased urine output (oliguria)
pale, cool, clammy skin
altered mental status:
early-agitation, irritabily, and or anxiety
late-confusion, delirium, coma
metabolic acidosis

76
Q

What causes cardiogenic shock?

A

inability of heart to pump the required amount of blood

causes include: cardiac arrhythmia, damaged heart muscle or valves, rupture of heart muscle

77
Q

hypovolemic shock causes?

A

decreased intravascular volume leading to decreased perfusion of vital organs.

can be caused by hemorrhage or fluid loss

78
Q

types of distributive shock?

A

anaphylactic shock, neutrogenic shock, septic shock

79
Q

what causes anaphylactic shock?

A

severe, rapid allergic or hypersensitivity reaction with potential to be fatal

80
Q

what causes neurogenic shock?

A

damage to the autonomic pathways within the CNS?

sudden loss of sympathetic stimulation to blood vessels–>massive vasodilation–>sudden hypotension

81
Q

what causes septic shock?

A

systemic vasodilation secondary to infection and dysregulation of inflammatory response

Most common cause- G+ bacteria, followed by G- endotoxin-producing bacteria

82
Q

Systemic inflammatory response syndrome (SIRS)

A

systemic uncontrolled inflammatory response

happens when exaggerated, unregulated, self sustaining inflammatory response to an infection

largely mediated by IL-1 and TNF-alpha

83
Q

how does septic shock affect the circulatory system?

A

severe hypotension and hypoperfusion

84
Q

how does septic shock affect the lungs?

A

pulmonary edema and hypoxemia

85
Q

how does septic shock affect the GI tract?

A

increased intestinal permeability allowing bacterial in gut to enter systemic circulation

86
Q

how does septic shock affect the Liver?

A

impaired elimination of bacteria and endotoxins from gut due to hypoperfusion and direct renal damage

87
Q

how does septic shock affect the kidneys?

A

impaired filtration of toxins and waste products from blood due to thypoperfusion and direct renal damage

88
Q

how does septic shock affect the nervous system?

A

encephalopathy due to changes in cell signaling caused by inflammatory mediators; dysfunction of blood-brain barrier?