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DD Unit I > DD Boyer > Flashcards

DD Boyer Flashcards

1
Q

Inflammatory cells can come from 2 places. Name them

A
  1. tissue based/Sentinels within tissue, 2. vascular from bone marrow and lymphnodes
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2
Q

What do Fibroblasts do in response to injury?

A

proliferate and produces collagen and other ECM to provide infrastructure

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3
Q

What do endothelial cells (blood vessel lining) in response to injury?

A

proliferate and form new blood vessels

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4
Q

Regenerative capacity of gastrointestinal system

A

epithelial cells have normal turnover and regenerate

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5
Q

Regenerative capacity of respiratory system

A

epithelial cells have normal turnover and regenerate, but septa of alveoli cannot regenerate once damaged

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6
Q

Regenerative capacity of liver

A

Great

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7
Q

Tissue-based Macrophages in liver

A

Kupffer cells

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8
Q

Regenerative capacity of Heart

A

absent

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9
Q

Regenerative capacity of Kidney

A

epithelial cells have normal turnover and regenerate, but glomeruli do not regenerate

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10
Q

local signs and symptoms of injury

A

Rubor, Calor, Tumor, Dolor

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11
Q

systemic signs and symptoms of injury

A

Sleepiness, Anorexia, Fever, Elevated WBC, hypotension

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12
Q

7 basic steps to injury response

A

Recruit help, increase blood flow, increase vascular permeability, recognition of problems, clear/remove/wall off offending material, collateral damage, stimulate repair and remodeling

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13
Q

how fast does the acute inflammatory phase start and last

A

rapid initiation: minutes to hours. Short duration

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14
Q

what cells are involved in acute inflammation

A

Neutrophils

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15
Q

what do Neutrophils do during acute response

A

phagocytose bacteria, tissue debris, and damaged issue

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16
Q

how fast does the chronic inflammatory phase start and last

A

initiation is slower (days or longer), but can lask anywhere from days to years.

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17
Q

what cells are involved with chronic inflammation

A

Macrophages and lymphocytes and Eosinophil

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18
Q

Functions of macrophages

A

phagocytosis and regulate inflammatory response

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19
Q

Functions of eosinophils

A

type-1 immune response, parasite difense, phagocytosis

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20
Q

When is repair initiated

A

during chronic phase

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21
Q

Critical features of acute inflammation - (hint: 3 things)

A

vasodilation, vascular permeability, and inflammatory cell infiltrate (neutrophils that make puss)

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22
Q

transient chronic phase of inflammatory response begins when?

A

it is initiated with Acute phase response

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23
Q

features prolonged/persistent chronic inammatory response (4 things)

A
  1. may or may not see acute phase 2. persistent infection 3. persistent damage/irritation (ie atheroschlerosis) 4. Antigen-Driven Immune-mediated process
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24
Q

source of cells in acute response

A

peripheral blood

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25
Q

source of cells in chronic response

A

Sentinel/local cells in tissue and peripheral blood

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26
Q

vascular response in acute phase

A

dilation/increased flow, increased permeability that can be transudate or exudate

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27
Q

vascular response in chronic phase

A

variable persistense of dialation and leakiness, endothelial cells activated and ready to proliferate

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28
Q

repair in chronic phase

A

macrohphages release growth factors, fibroblasts cause fibrosis and scar, endothelial cells neovascularize

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29
Q

Fibrinopurulent Exudate

A

Anywhere, but usually a nonconfined space. Usually infectious. Mostly neutrophils

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30
Q

Abscess

A

within a parenchyma/confined space, cavity is newly formed by accumulation of inflammatory cells. Usually infectious. Mostly neutrophils

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31
Q

Empyema

A

location within an anatomic space of cavity. Usually infectious. Neutrophils early, MACs and lymphocytes late

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32
Q

Cellulitis

A

skin, fascia/deep connective tissue. Infectious or inflammatory

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33
Q

Granuloma

A

within parenchyma, rounded nodular appearance. MACs and lymphocytes. Infectious or foreign body. Mineralized on x-ray or CT scan

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34
Q

Common laboratory tests for inflammation

A

WBC, Erythrocyte sedimentation rate and C-reactive proteins (acute phase), firbin split/degradation products and platelet count (DIC-related markers), repid ID testing, cultures and serology, Ig quantification

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35
Q

not typically evaluated lab tests for inflammation

A

chemical mediators (eg Prostaglandins, leukotrienes, thromboxanes, interleukins)

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36
Q

What cells make histamine?

A

Mast cells and Basophils, platelets

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37
Q

what does histamine do?

A

Vasodilate, Vascular Perm., constriction of smooth muscles

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38
Q

What cells make serotonin?

A

Plts

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39
Q

what does serotonin do?

A

Vascular perm

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40
Q

What cells make Prostaglandins (PG)?

A

Mast cells, plts, Macs, Lymphs, PMNs, Endo cells

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41
Q

what do Prostaglandins (PG) do?

A

Vasodialate (PGI2), Plt ag. (+/-), constrict smooth muscle, fever, pain (PGE2, PGI2)

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42
Q

What cells make Leukotrienes LT C4, D4, E4?

A

Mast cells and Basos, Macs, Lymphs, PMNs

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43
Q

what do Leukotrienes LT C4, D4, E4 do?

A

Vascular Perm, constrict smooth muscle

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44
Q

What cells make Leukotrienes LT B4?

A

Mast cells and Basos, Macs, Lymphs, PMNs

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45
Q

what does Leukotrienes LT B4 do?

A

WBC chemotaxis

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46
Q

What cells make Thromboxanes TXA2?

A

Plts

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47
Q

what does Thromboxanes TXA2 do?

A

Vasoconstriction, Plt ag.

48
Q

What cells make PAF (platelet-activating factor)?

A

Mast cells and Basos, plts, Macs, PMNs, Endo Cells

49
Q

what does PAF (platelet-activating factor) do?

A

Vasodialation (low []s), vasoconstriction, vascular perm, WBC Chemotaxis, plt ag., constrict smooth muscle

50
Q

What cells make Reactive Oxygen Species?

A

Macs, Lymphs, PMNs

51
Q

what does Reactive Oxygen Species do?

A

Tissue/Microbe Damage

52
Q

What cells make Nitric Oxide (NO)?

A

Macs (iNOs), endo cells (eNOs)

53
Q

what does Nitric Oxide (NO) do?

A

vasodialation, WBC Chemotaxis (iNOs), relax smooth muscles, tissue/microbe damage (iNOs)

54
Q

What cells make TNF (tumor necrosis factor)?

A

Mast Cells and Basos, Macs, Lymphs

55
Q

what does TNF (tumor necrosis factor) do?

A

WBC chemotaxis, Fever

56
Q

What cells make Interleukins (1, 6, ?)?

A

Macs, Endo Cells

57
Q

what does Interleukins (1, 6, ?) do?

A

WBC chemotaxis, Fever

58
Q

What cells make Chemokines?

A

Mast cells, Macs, Lymphs, Endo Cells

59
Q

what does Chemokines do?

A

WBC chemotaxis

60
Q

What cells make Cytoplasmic Granule Content?

A

Macs, PMNs

61
Q

what does Cytoplasmic Granule Content do?

A

WBC chemotaxis, tissue/microbe damage

62
Q

What cells make Substance P?

A

Nerve Fibers

63
Q

what does Substance P do?

A

vascular perm, Pain

64
Q

What cells make C3a, C5a?

A

liver

65
Q

what does C3a, C5a do?

A

Vasodialation and Vascular perm (through Mast cell stim.), WBC chemotaxis, Tissue/microbe damage (Mac effect on microbes)

66
Q

What cells make Bradykinin?

A

liver

67
Q

what does Bradykinin do?

A

Vasodialate, Vascular Perm, constrict smooth muscle, Pain

68
Q

What cells make Thrombin?

A

liver

69
Q

what does Thrombin do?

A

WBC Chemotaxis

70
Q

What cells make Plasmin?

A

liver

71
Q

what does Plasmin do?

A

Vasodialation

72
Q

What cellular chem. Mediators are in secretory granules?

A

Histamine, serotonin, lysosomal enzymes

73
Q

What cellular chem. Mediators are newly synthesized?

A

prostaglandins, Leukotrienes, Platelet-activating factors, ROS, NO, cytokines

74
Q

Why are Macrophages so critical?

A

They make most chemical mediators! Except histamine, serotonin and substance P

75
Q

Which mediators tend to have a systemic effect?

A

Substances P, Prostaglandins, IL-1, TNF, Bradykinin

76
Q

Arachidonic Acid + lipoxygenase

A

leukotrienes, lipoxin, and HETE

77
Q

Arachidonic Acid + cyclooxygenase

A

Prostaglandins and Thromboxane A

78
Q

Basic Kinin system pathway

A

Factor XII => Factor XIIa => kallikrein => bradykinin

79
Q

Factor XII function

A

“Hageman Factor”. Important for pain, coagulation, antimicrobial activity, and inflammation

80
Q

What does Factor XII help produce?

A

Bradykinin, Plasmin, C3a, C5a, Thrombin, and Fibrin. All use Kallikrein in pathway except Thrombin

81
Q

Describe the Proliferative Phase

A

Fibroblasts proliferate and produce collagen and ECM, Endothelial cells proliferate and form new blood vessels.

82
Q

Describe the Remodeling Phase

A

Regenerative processes fade, followed by reorganization of connective tissue and contractile response

83
Q

How does Infrastructure repair occur?

A

Granulation of tissue occurs via ECM and collagen depositing by fibroblasts, neovascularization, and the presense of macrophages and lymphocytes providing growth factors and cytokines

84
Q

Where do new cells for Angiogenesis come from?

A

Pre-existing blood vessels, bone-marrow derived endothelial precursor cells, smooth muscle cells, and pericytes.

85
Q

What does Suprastructure repair include?

A

Re-epithelialization via epidermal stem cells in skin/Bulge stem cells in hair follicles/crypt cells in intestine, and regeneration of liver cells.

86
Q

What do you do when you can’t repair Suprastructure?

A

Scar tissue that can rupture. (ie after necrosis of myocardium in MI)

87
Q

What are the big chemical mediators of repair and what releases them?

A

Macrophages are the big players here. TNF and IL-1 promote fibroblast recruitment and other inflammation. Macs also release Growth Factors (look for the letters GF)

88
Q

What causes abnormal scar formation?

A

Inadequate granulation tissue formation or excess/exuberant scar formation/repair

89
Q

Define cirrhosis

A

persistent injury overcomes regeneration potential.

90
Q

What is a Hypertrophic scar?

A

remains relatively limited to affected area and regression. Indented scar

91
Q

What is a Keloid?

A

raised beyond boundary of wound without regression. Protruding scar

92
Q

What is a Desmoid tumor?

A

aggressive fibromatoses and benign neoplasm

93
Q

What is a contracture?

A

joint deformity when scar crosses a joint.

94
Q

What is in the Portal triad? How important is repair?

A

Hepatic artery, portal vein, and bile duct. Restoration during during repair is critical

95
Q

What are 3 histologic findings of Cirrhosis?

A

Bridging fibrous bands, regenerative nodules, and altered architecture

96
Q

What are systemic factors (3) affecting repair?

A

Nutritional, Metabolic, and Vascular issues

97
Q

What are local factors (5) affecting repair?

A

Infection, Persistence of Insult (eg Hep C), Trama with early movement before repair, trama with foreign material, Size/Location of injury

98
Q

What is Virchow’s Triad?

A

Endothelial Injury, abnormal blood flow, and hypercoagulability are the three big contributing factors to Thrombosis

99
Q

What is Edema?

A

Fluid accumulation in interstitial tissue

100
Q

What is Effusion?

A

Fluid accumulation in a body cavity, includes Pleural Effusion and Ascites. Can be transudate and Exudate

101
Q

What is Anasarca?

A

Systemic edema and effusions due to one or mixed causes. Usually a transudate

102
Q

What is Transudate?

A

accumulated fluid leakage from vessels. Associated with Increased hydrostatic pressure/reduced oncotic pressure

103
Q

What is exudate?

A

accumulated fluid and protein leakage from vessels, also usually has WBC. Associated with inflammation

104
Q

Describe Active Congestion

A

Dialation of arteries results in increased blood flow. Creates redness of acute inflammation

105
Q

Describe Passive Congestion

A

Impaired venous drainage results in stasis and accumulation of deoxygenated blood. Has bluish/dusky tinge. Can be caused by right sided heart failure

106
Q

What is a hemorrhage?

A

Burst blood vessel. On skin from smallest to largest they are Petechiae, Purpura, Echymoses. Also can be hematoma and hemothorax/hemopericardium/hemoperitoneum

107
Q

What causes Infarct?

A

Ischemia and hypoxia

108
Q

What is Thrombosis?

A

Intravascular, mass coagulation of blood (platelets, fibrin, and entrapped cells), adherent to luminal surface of vessel

109
Q

Predisposing factors for Thrombosis (5 things)

A

Stasis, non-laminar blood flow, increased blood viscosity (dehydration), damage to endothelium (atherosclerosis), hypercoagulable state

110
Q

Complications of Thrombosis? (2 things)

A

reduced blood flow to tissue, fragments causing embolism

111
Q

Define Embolism

A

Some material carried in blood, it can be lodged at a point and obstructs a vessel

112
Q

Embolism variations (6 things)

A

Thromboembolus, Atheroemboli, fat/bone marrow emboli, tumor emboli, amniotic fluid emboli, air/gas emboli

113
Q

Define Shock

A

systemic hypoperfusion of cells and tissue. Seen with lactic acidosis, hypotension, and tachycardia

114
Q

What is Disseminated intravascular coagulation (DIC)

A

complication in many disease states where clotting factors become activated in blood vessels.

115
Q

Tests for DIC

A

fibrin split products, D-Dimer, Platelet count

DD Unit I (10 decks)

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