DD Boyer Flashcards
1
Q
Inflammatory cells can come from 2 places. Name them
A
- tissue based/Sentinels within tissue, 2. vascular from bone marrow and lymphnodes
2
Q
What do Fibroblasts do in response to injury?
A
proliferate and produces collagen and other ECM to provide infrastructure
3
Q
What do endothelial cells (blood vessel lining) in response to injury?
A
proliferate and form new blood vessels
4
Q
Regenerative capacity of gastrointestinal system
A
epithelial cells have normal turnover and regenerate
5
Q
Regenerative capacity of respiratory system
A
epithelial cells have normal turnover and regenerate, but septa of alveoli cannot regenerate once damaged
6
Q
Regenerative capacity of liver
A
Great
7
Q
Tissue-based Macrophages in liver
A
Kupffer cells
8
Q
Regenerative capacity of Heart
A
absent
9
Q
Regenerative capacity of Kidney
A
epithelial cells have normal turnover and regenerate, but glomeruli do not regenerate
10
Q
local signs and symptoms of injury
A
Rubor, Calor, Tumor, Dolor
11
Q
systemic signs and symptoms of injury
A
Sleepiness, Anorexia, Fever, Elevated WBC, hypotension
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
13
Q
how fast does the acute inflammatory phase start and last
A
rapid initiation: minutes to hours. Short duration
14
Q
what cells are involved in acute inflammation
A
Neutrophils
15
Q
what do Neutrophils do during acute response
A
phagocytose bacteria, tissue debris, and damaged issue
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.
17
Q
what cells are involved with chronic inflammation
A
Macrophages and lymphocytes and Eosinophil
18
Q
Functions of macrophages
A
phagocytosis and regulate inflammatory response
19
Q
Functions of eosinophils
A
type-1 immune response, parasite difense, phagocytosis
20
Q
When is repair initiated
A
during chronic phase
21
Q
Critical features of acute inflammation - (hint: 3 things)
A
vasodilation, vascular permeability, and inflammatory cell infiltrate (neutrophils that make puss)
22
Q
transient chronic phase of inflammatory response begins when?
A
it is initiated with Acute phase response
23
Q
features prolonged/persistent chronic inammatory response (4 things)
A
- may or may not see acute phase 2. persistent infection 3. persistent damage/irritation (ie atheroschlerosis) 4. Antigen-Driven Immune-mediated process
24
Q
source of cells in acute response
A
peripheral blood
25
source of cells in chronic response
Sentinel/local cells in tissue and peripheral blood
26
vascular response in acute phase
dilation/increased flow, increased permeability that can be transudate or exudate
27
vascular response in chronic phase
variable persistense of dialation and leakiness, endothelial cells activated and ready to proliferate
28
repair in chronic phase
macrohphages release growth factors, fibroblasts cause fibrosis and scar, endothelial cells neovascularize
29
Fibrinopurulent Exudate
Anywhere, but usually a nonconfined space. Usually infectious. Mostly neutrophils
30
Abscess
within a parenchyma/confined space, cavity is newly formed by accumulation of inflammatory cells. Usually infectious. Mostly neutrophils
31
Empyema
location within an anatomic space of cavity. Usually infectious. Neutrophils early, MACs and lymphocytes late
32
Cellulitis
skin, fascia/deep connective tissue. Infectious or inflammatory
33
Granuloma
within parenchyma, rounded nodular appearance. MACs and lymphocytes. Infectious or foreign body. Mineralized on x-ray or CT scan
34
Common laboratory tests for inflammation
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
35
not typically evaluated lab tests for inflammation
chemical mediators (eg Prostaglandins, leukotrienes, thromboxanes, interleukins)
36
What cells make histamine?
Mast cells and Basophils, platelets
37
what does histamine do?
Vasodilate, Vascular Perm., constriction of smooth muscles
38
What cells make serotonin?
Plts
39
what does serotonin do?
Vascular perm
40
What cells make Prostaglandins (PG)?
Mast cells, plts, Macs, Lymphs, PMNs, Endo cells
41
what do Prostaglandins (PG) do?
Vasodialate (PGI2), Plt ag. (+/-), constrict smooth muscle, fever, pain (PGE2, PGI2)
42
What cells make Leukotrienes LT C4, D4, E4?
Mast cells and Basos, Macs, Lymphs, PMNs
43
what do Leukotrienes LT C4, D4, E4 do?
Vascular Perm, constrict smooth muscle
44
What cells make Leukotrienes LT B4?
Mast cells and Basos, Macs, Lymphs, PMNs
45
what does Leukotrienes LT B4 do?
WBC chemotaxis
46
What cells make Thromboxanes TXA2?
Plts
47
what does Thromboxanes TXA2 do?
Vasoconstriction, Plt ag.
48
What cells make PAF (platelet-activating factor)?
Mast cells and Basos, plts, Macs, PMNs, Endo Cells
49
what does PAF (platelet-activating factor) do?
Vasodialation (low []s), vasoconstriction, vascular perm, WBC Chemotaxis, plt ag., constrict smooth muscle
50
What cells make Reactive Oxygen Species?
Macs, Lymphs, PMNs
51
what does Reactive Oxygen Species do?
Tissue/Microbe Damage
52
What cells make Nitric Oxide (NO)?
Macs (iNOs), endo cells (eNOs)
53
what does Nitric Oxide (NO) do?
vasodialation, WBC Chemotaxis (iNOs), relax smooth muscles, tissue/microbe damage (iNOs)
54
What cells make TNF (tumor necrosis factor)?
Mast Cells and Basos, Macs, Lymphs
55
what does TNF (tumor necrosis factor) do?
WBC chemotaxis, Fever
56
What cells make Interleukins (1, 6, ?)?
Macs, Endo Cells
57
what does Interleukins (1, 6, ?) do?
WBC chemotaxis, Fever
58
What cells make Chemokines?
Mast cells, Macs, Lymphs, Endo Cells
59
what does Chemokines do?
WBC chemotaxis
60
What cells make Cytoplasmic Granule Content?
Macs, PMNs
61
what does Cytoplasmic Granule Content do?
WBC chemotaxis, tissue/microbe damage
62
What cells make Substance P?
Nerve Fibers
63
what does Substance P do?
vascular perm, Pain
64
What cells make C3a, C5a?
liver
65
what does C3a, C5a do?
Vasodialation and Vascular perm (through Mast cell stim.), WBC chemotaxis, Tissue/microbe damage (Mac effect on microbes)
66
What cells make Bradykinin?
liver
67
what does Bradykinin do?
Vasodialate, Vascular Perm, constrict smooth muscle, Pain
68
What cells make Thrombin?
liver
69
what does Thrombin do?
WBC Chemotaxis
70
What cells make Plasmin?
liver
71
what does Plasmin do?
Vasodialation
72
What cellular chem. Mediators are in secretory granules?
Histamine, serotonin, lysosomal enzymes
73
What cellular chem. Mediators are newly synthesized?
prostaglandins, Leukotrienes, Platelet-activating factors, ROS, NO, cytokines
74
Why are Macrophages so critical?
They make most chemical mediators! Except histamine, serotonin and substance P
75
Which mediators tend to have a systemic effect?
Substances P, Prostaglandins, IL-1, TNF, Bradykinin
76
Arachidonic Acid + lipoxygenase
leukotrienes, lipoxin, and HETE
77
Arachidonic Acid + cyclooxygenase
Prostaglandins and Thromboxane A
78
Basic Kinin system pathway
Factor XII => Factor XIIa => kallikrein => bradykinin
79
Factor XII function
"Hageman Factor". Important for pain, coagulation, antimicrobial activity, and inflammation
80
What does Factor XII help produce?
Bradykinin, Plasmin, C3a, C5a, Thrombin, and Fibrin. All use Kallikrein in pathway except Thrombin
81
Describe the Proliferative Phase
Fibroblasts proliferate and produce collagen and ECM, Endothelial cells proliferate and form new blood vessels.
82
Describe the Remodeling Phase
Regenerative processes fade, followed by reorganization of connective tissue and contractile response
83
How does Infrastructure repair occur?
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
Where do new cells for Angiogenesis come from?
Pre-existing blood vessels, bone-marrow derived endothelial precursor cells, smooth muscle cells, and pericytes.
85
What does Suprastructure repair include?
Re-epithelialization via epidermal stem cells in skin/Bulge stem cells in hair follicles/crypt cells in intestine, and regeneration of liver cells.
86
What do you do when you can't repair Suprastructure?
Scar tissue that can rupture. (ie after necrosis of myocardium in MI)
87
What are the big chemical mediators of repair and what releases them?
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
What causes abnormal scar formation?
Inadequate granulation tissue formation or excess/exuberant scar formation/repair
89
Define cirrhosis
persistent injury overcomes regeneration potential.
90
What is a Hypertrophic scar?
remains relatively limited to affected area and regression. Indented scar
91
What is a Keloid?
raised beyond boundary of wound without regression. Protruding scar
92
What is a Desmoid tumor?
aggressive fibromatoses and benign neoplasm
93
What is a contracture?
joint deformity when scar crosses a joint.
94
What is in the Portal triad? How important is repair?
Hepatic artery, portal vein, and bile duct. Restoration during during repair is critical
95
What are 3 histologic findings of Cirrhosis?
Bridging fibrous bands, regenerative nodules, and altered architecture
96
What are systemic factors (3) affecting repair?
Nutritional, Metabolic, and Vascular issues
97
What are local factors (5) affecting repair?
Infection, Persistence of Insult (eg Hep C), Trama with early movement before repair, trama with foreign material, Size/Location of injury
98
What is Virchow's Triad?
Endothelial Injury, abnormal blood flow, and hypercoagulability are the three big contributing factors to Thrombosis
99
What is Edema?
Fluid accumulation in interstitial tissue
100
What is Effusion?
Fluid accumulation in a body cavity, includes Pleural Effusion and Ascites. Can be transudate and Exudate
101
What is Anasarca?
Systemic edema and effusions due to one or mixed causes. Usually a transudate
102
What is Transudate?
accumulated fluid leakage from vessels. Associated with Increased hydrostatic pressure/reduced oncotic pressure
103
What is exudate?
accumulated fluid and protein leakage from vessels, also usually has WBC. Associated with inflammation
104
Describe Active Congestion
Dialation of arteries results in increased blood flow. Creates redness of acute inflammation
105
Describe Passive Congestion
Impaired venous drainage results in stasis and accumulation of deoxygenated blood. Has bluish/dusky tinge. Can be caused by right sided heart failure
106
What is a hemorrhage?
Burst blood vessel. On skin from smallest to largest they are Petechiae, Purpura, Echymoses. Also can be hematoma and hemothorax/hemopericardium/hemoperitoneum
107
What causes Infarct?
Ischemia and hypoxia
108
What is Thrombosis?
Intravascular, mass coagulation of blood (platelets, fibrin, and entrapped cells), adherent to luminal surface of vessel
109
Predisposing factors for Thrombosis (5 things)
Stasis, non-laminar blood flow, increased blood viscosity (dehydration), damage to endothelium (atherosclerosis), hypercoagulable state
110
Complications of Thrombosis? (2 things)
reduced blood flow to tissue, fragments causing embolism
111
Define Embolism
Some material carried in blood, it can be lodged at a point and obstructs a vessel
112
Embolism variations (6 things)
Thromboembolus, Atheroemboli, fat/bone marrow emboli, tumor emboli, amniotic fluid emboli, air/gas emboli
113
Define Shock
systemic hypoperfusion of cells and tissue. Seen with lactic acidosis, hypotension, and tachycardia
114
What is Disseminated intravascular coagulation (DIC)
complication in many disease states where clotting factors become activated in blood vessels.
115
Tests for DIC
fibrin split products, D-Dimer, Platelet count
