Mason Exam 2 Flashcards
(153 cards)
1
Q
Hyperemia/Congestion
A
increased amount of blood in the vasculature of an organ or part of the body
2
Q
Active hyperemia
A
can be physiologic or pathologic
3
Q
Passive hyperemia
A
always pathologic
4
Q
Cellulitis
A
purulent, suppurative inflammation of connective tissues
5
Q
Phlegmon
A
fluctuant pocket of pus (suppurative inflammation) in subcutis
6
Q
Fasciitis
A
purulent/suppurative inflammation of fascia
7
Q
Abcess
A
Local collection of pus
8
Q
Empyema
A
accumulation of pus in body cavity (e.g. guttural pouches)
9
Q
Hypopyon
A
WBC’s in the anterior chamber of eye
10
Q
Atelectasis
A
complete or partial collapse of the lung/lung lobe
11
Q
Causes of hemorrhage
A
- local factors affecting blood vessels
- systemic factors affecting either vessels or blood
12
Q
Effects of hemorrhage
A
- external (loss of blood fluids, protein, iron)
- internal (blood components mostly recovered)
- Secondary
13
Q
What determines the severity of hemorrhage?
A
rate, amount, location
14
Q
secondary effects of hemorrhage
A
- resorption of fluid
- erythrocytes lysed and phagocytosed
- fibrinolysis
- potential scarring
15
Q
Hemostasis
A
- termination of blood loss from the vasculature
- stopping of blood flow
16
Q
What happens when control of hemostasis is lost?
A
thrombosis &/or hemorrhage
17
Q
How is hemostasis maintained?
A
Balance of pro & anti-coagulant mechanisms
18
Q
Events of hemostasis
A
- vasoconstriction (via neurogenic reflex)
- platelet plug (adherence, aggregation)
- coagulation (enzymatic cascade)
19
Q
Platelet contents
A
P-selectin (integrin membrane receptor) Thromboxane A2 (arachidonic acid) Alpha granules (Fibrinogen, fibronectin) Electron dense bodies (ADP, Ca, Histamine, Epi, Serotonin) - all vasoactive mediators
20
Q
Platelet activation steps
A
- adhesion & shape change
- Aggregation
- Secretion
21
Q
Platelet adhesion & shape change
A
- Von Willebrand’s factor binds to subendothelial collagen
- Platelets bind von Willebrand’s factor via gpIb surface integrins
- Undergo shape change
22
Q
Platelet aggregation
A
ADP & Thromboxane A2 produces temporary hemostatic plug (bricks)
Thrombin produced, promoting further aggregation & fibrin polymerization
Definitive hemostatic plug formed (mortar)
23
Q
Other platelet aggregators
A
collagen
epinephrine
immune complexes
platelet activating factor
24
Q
Platelet secretion
A
- Granule contents are secreted
- ADP promotes platelet aggregation
- Calcium is an important coagulation cofactor
- Phospholipid complex on platelet surface forms that binds and activates clotting factors
25
Anti-coagulants
Antithrombins (inactivate thrombin)
Proteins C & S (if deficient, cause thrombosis)
Plasminogen activator
NO & PGI2 (inhibit aggregation)
26
Pro-coagulants
```
von Willebrand's factor
Tissue factor
Activated clotting factors
Platelet activating factor
Plasminogen activator inhibitor
```
27
Types of bleeding disorders
1. hereditary
| 2. acquired (more common)
28
Examples of acquired bleeding disorders
1. infectious diseases
2. Intoxications
3. Disseminated Intravascular Coagulation (DIC)
29
DIC (disseminated intravascular coagulation)
Thrombo-hemorrhagic disorder
1. widespread activation of clotting mechanisms
2. consumption of all platelets & clotting factors
3. activation of fibrinolysis
4. widespread hemorrhage
= bleeding
30
Causes of DIC
infection
trauma
neoplastic disease
31
Pathogenesis of DIC
1. massive release of tissue factor (triggered by IL-1, TNF) into circulation
2. upregulates WBC binding to endothelial cells
3. WBC's damage endothelium by producing ROS
4. widespread endothelial injury & activation of clotting in microvasculature, activation of fibrinolysis
5. Platelets & clotting factors are consumed, FDP's inhibit further platelet aggregation/fibrin polymerization
6. terminal microvascular hemorrhage
32
Edema
accumulation of watery fluid in extravascular spaces
33
Appearance of edema
tissues are swollen & pit (can dent), appear gelatinous & shiny
34
Types of edema
1. Effusion – most watery
2. Transudate – more protein and cells present
3. Exudate – lots of plasma protein, more cloudy/opaque
35
Causes of generalized edema
1. cardiac edema
2. renal failure
3. hepatic failure or malnutrition/malabsorption
36
Causes of localized edema
1. venous obstruction
2. lymphatic obstruction
3. inflammatory edema or vascular injury
37
Causes of cerebral edema
hypoxia
hyperthermia
toxin
38
Hyperemia/Congestion
increased blood amount in the vasculature of an organ or part of the body due to local vascular dilation
39
Passive hyperemia
- blood not flowing through an organ in a timely fashion
- lose more oxygen
- causes hypoxia or complete anoxia
- always pathologic
40
causes of passive hyperemia
decreased venous return with pooling in blood tissue
- mechanical (e.g. obstruction)
- cardiac failure
- gravity
41
With right heart failure, what organ gets congested?
liver
42
With left heart failure, what organ gets congested?
lungs
43
Effects of passive hyperemia
- relative hypoxia or complete anoxia
- hemorrhage
- thrombosis
- edema
- fibrosis
44
acute passive congestion
- occurs due to sudden occlusion of vessels
| - get congestion +/- severe anoxia
45
chronic passive congestion
- occurs with long standing interference (hypoxia) that doesn't cause complete ischemia
46
Hypostatic congestion
- ante or post mortem gravitational settling of blood in tissue
- down side becomes congested
47
Causes of liver congestion
1. Right heart failure
2. Valvular insufficiency or stenosis (narrowing)
3. Obstruction of blood flow through lung
4. Obstruction of posterior vena cava
48
Acute vs. Chronic passive congestion in the liver
Acute - liver looks enlarged, rounded edges, dark red to purple with prominent architecture
chronic - liver looks smaller
49
Pathogenesis of liver congestion
- hypoxic cell injury leads to loss of hepatocytes and fibrosis
- congestion usually involves central vein (most severe hypoxic injury at this level vs. portal vein) b/c closer to heart
50
Causes of lung congestion
- left ventricular failure due to valvular insufficiency or stenosis
- leads to pulmonary edema, fibrosis
51
Causes of spleen congestion
- barbiturate euthanasia
| - incidental finding
52
Thrombi
- excessive clot formation in vessel lumen, always pathologic
- lesion forms during life
- attached to endothelium +/- trailing tail
- looks like cranberry sauce
53
Post-mortem clot
- incidental, not a lesion
- forms after death
- not attached to endothelium
- e.g. chicken fat clot
54
Arterial thrombus
- usually pale, dry (only things of high affinity can stick in high P, high flow system - fibrin, platelets)
- firm but friable
55
venous thrombus
- large, dark red
- soft, gelatinous, shiny
- entrapped RBC's
- can be mistaken as PM clot (not always recognized on necropsy)
56
Virchow's Triad for the Pathogenesis of thrombosis
1. Changes in the blood itself (hypercoagulability)
2. Hemodynamic and rheological changes (blood flow rate and direction change)
3. Damage to vessel wall and endothelium
2 or 3 out of 3 = thrombosis likely
57
Fate of Thrombi
1. propagation
2. Fibrinolysis (best outcome)
3. Organization & Recanalization (conversion into scar)
4. Embolism (worst outcome) - can cause ischemia, infarction
58
Embolus/Embolism
- physical mass of material which is carried in bloodstream & lodges in dependent vascular bed
- often produce infarcts
59
Infarct
localized area of tissue necrosis caused by ischemia (a lesion)
60
Infarction
the process of infarct formation
61
Causes of infarction
blockage of blood flow due to thrombi, emboli, vasospasm, volvulus, torsion, strangulation or other external compression
62
Appearance of an infarct
- irregularly shaped
- sharply demarcated
- peripheral zone of hyperemia
- raised (hemorrhage) or depressed (old, scarring) lesion
- can be anemic or hemorrhagic infarcts
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Organs most susceptible to infarction
- single vessel perfusion
| - brain, renal cortex, heart
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Organs moderately susceptible to infarction
- tissues with parallel systems
| - skeletal muscle, viscera
65
Organs least susceptible to infarction
- tissues with dual blood supply - would need dual infarction
- liver, lung
66
Pyogranulomatous
neutrophils and macrophages
67
Eosinophilic granulomatous
eosinophils and macrophages
68
Lymphogranulomatous
lymphocytes and macrophages
69
-itis
inflammation
70
-angitis
inflammatory process of a channel
| e.g. cholangitis = bile duct inflammation
71
-adenitis
inflammation of an excretory or lymph gland
72
Cystitis
inflammation of urinary bladder
73
Cholecystitis
inflammation of gall bladder
74
inflammation of lung (if exudative)
pneumonia
75
inflammation of vein
phlebitis
76
inflammation
graded reaction of living tissue to injury
| innate defense mechanism
77
Primary goal of tissue repair
regeneration of tissue
| most commonly, see a combo of tissue regeneration and scarring
78
cardinal signs of inflammation
```
calor
rubor
dolor
tumor
loss of function
```
79
acute inflammation events
hemodynamic changes
increased vascular permeability
efflux of WBC's
80
hemodynamic changes
1. transient arteriolar constriction
2. followed by vasodilation (histamine, bradykinin, PG's, neurogenic reflex)
3. increased hydrostatic pressure (= get edema)
4. hemoconcentration & slowing or stasis of blood flow
81
increase in vascular permeability results in
increased protein leakage
| leads to further osmotic pull, edema
82
ways to increase vascular permeability
- direct injury that incites inflammation
- injury mediated by active leukocytes
- endothelial cell borders separate during injury
83
chemical mediators of vascular permeability
- vasoactive amines
- kinins
- complement fragments
- arachidonic acid mediators
- cytokines
- platelet activating factor
84
serous inflammation
- exudate is thin, watery fluid
- goal: dilute/wash away injurious agent
- due to envenomation, irritants, trauma, early infectious process
- fluid occupies space or flows from mucous membranes
85
Catarrhal inflammation
- exudate contains abundant mucous
- goal: dilute, wash away injurious agent
- due to irritants, infectious processes
86
fibrinous inflammation
- exudate contains strands/sheets of polymerized fibrin
| - goal: wall off injurious agent, form network for WBC migration
87
fibrinogen
- plasma clotting protein from liver
- present in the blood
- makes fibrin
88
fibroblast
makes collage, not fibrin
| secretes ECM components
89
cell type expected in an inflammatory reaction to pyogenic bacteria
neutrophils
| suppurative exudate
90
cell type expected in an inflammatory reaction to allergy & hypersensitivity reactions, fungal, or parasitic infections
```
eosinophils
Mast cells (allergy & hypersensitivity)
```
91
cell type expected in an inflammatory reaction to persistent stimulus
macrophages/monocytes
92
Heterophils
avian/reptile equivalent to neutrophils
| often cause caseated leasions (don't have myeloperoxidase to liquify)
93
eosinophil granules
- inactivate mast cell-derived mediators
- Major Basic Protein (punched hole in wall)
- Histaminase (inactivates histamine)
- Phospholipase D (inactivates PAF)
- Arylsulfatase
94
mast cell granules
- histamine
- proteloytic enzymes
- heparin, chondroitein sulfate (anti-coagulants)
- chemotactic factors for eosinophils and neutrophils
95
specialized macrophage subtypes
- alveolar
- pulmonary intravascular
- microglia (brain)
- kuppfer (liver)
96
inflammatory macrophage subtypes
- epithelial
| - multinucleate giant cell
97
Macrophage/monocyte products
- lysosomal proteases, hydrolases
- ROs
- complement components
- arachidonic acid mediators
- cytokines
- growth factors
98
Platelet products
- inflammatory mediators
- growth factors
- proteases
99
Types of platelet inflammatory mediators
- histamine
- thromboxane A2
- P-selectin
- PDGF, FGF, TGF
100
endothelial cells do what during injury?
regulate clotting
101
Steps of leukocyte efflux from vasculature
1. margination
2. rolling
3. Adhesion & pavementing
4. Transmigration
102
adhesion molecules involved in rolling
Selectins E & P on endothelial cells
Selectin L on leukocytes
103
adhesion molecules involved in adhesion & pavementing
Integrins (LFA1 & Mac1 on leukocytes)
Ig family of adhesins (ICAM & VCAM on endothelial cells)
Addressins (MadCAM-1 etc)
104
Control of adhesion
- Redistribution of Receptor: P-selectin & integrins
- Induction of Expression: E-selectin
- Increased binding avidity: Integrins
105
adhesion molecules involved in transmigration
CD31:CD31 (syn PECAM) homotypic binding on WBC and endothelial cell is the exit signal
Integrins
Chemotaxins
Ig
106
Chemotaxin types
- C5a
- Bacterial products
- Leukotrienes (LTB4, 5-HETE)
- Fibrin degradation products
- WBC products (IL-8, MCP-1, PAF)
107
Top phagocytic cell types
macrophages and neutrophils
108
Process of phagocytosis
1. opsonization
2. attachment
3. ingestion
4. killing & degradation
109
opsonizing agents
- C3b, C3bi
- Immunoglobulin
- Lysozyme
- Fibronectin
110
Plasma-derived chemical mediators of inflammation
Circulating precursors (Hageman factor, complement, kinongens)
111
When intrinsic and extrinsic coagulation pathways combine...
1. Prothrombin converts to Thrombin
2. Thrombin and fibrinogen interact to form Fibrin
3. Fibrin forms a network of insoluble protein
112
Plasminogen activator
helps form plasmin, which digests polymerized fibrin (fibrinolysis)
113
Hageman factor
activated in 1st step of intrinsic coagulation cascade
| Concurrently initiates clotting, fibrinolysis, kinin generation, complement cascade
114
complement fragments that are opsonins
C3b, C3bi
115
complement fragments that are anaphylotoxins
C3a, C5a
116
Kininogens
form kinins that cause vasodilation, increase vascular permeability, pain
117
Cell-derived pre-formed inflammatory mediators
Histamine, Serotonin
118
Cell-derived de novo inflammatory mediators
- Arachidonic acid derivatives
- Platelet activating factors
- ROS
- Cytokines & Chemokines
119
Cox-1 (cyclooxygenase)
maintains homeostasis
120
Cox-2 (cyclooxygenase)
induced in inflammation
121
Arachidonic acid derivatives
```
Cyclooxygenase pathway (Cox, PG's)
Lipoxygenase pathway (leukotrienes, lypoxins)
```
122
IL-1, TNF
- increase leukocyte adherence
| - increase pro-coagulent potential of endothelium (favors thrombosis)
123
IL-8
- produced by macrophages & other cells
| - strongly chemotactic for neutrophils
124
What cytokines mediated the acute phase response of inflammation?
TNF
IL-1
IL-6 & 8
125
Low quantities of cytokines trigger what kind of inflammation
- local inflammation
- monocyte/macrophage inflammation
- endothelial cell & complement activation
126
Moderate quantities of cytokines trigger what kind of inflammation
- systemic effects
- fever
- acute phase reactants from liver
127
High quantities of cytokines trigger what kind of inflammation
- septic shock
- low cardiac output
- low peripheral resistance
- DIC, ARDS
128
Types of neutrophil-mediated inflammatory damage
- lysosomal suicide
- frustrated phagocytosis
- regurgitation while feeding
129
Outcomes of acute inflammation
- complete resolution (goal)
- scarring
- abcessation
- chronic inflammation
130
Hallmark of chronic inflammation
neovascularization & fibrosis
131
Key cell type involved in chronic inflammation
macrophages (granulomatous inflammation)
132
Granuloma vs. granulomatous inflammation
Granulomatous inflammation = chronic inflammation where macrophages predominate
Granuloma - aggregate of macrophages & lymphoid cells + peripheral fibrosis surrounding a persistent stimulus
133
Other characteristics a granuloma may have
- Central necrotic debris – often caseous
- Mineralized debris - dystrophic
- Multinucleate giant cells (macrophages fuse with one another)
134
Granuloma types
foreign body or immune (T cell response)
135
Factors that affect healing
Stromal Integrity (tissue framework)
Regenerative capacity of tissue (labile or stable cells)
136
Mechanisms of tissue healing & repair
1. parenchymal regeneration
2. Replacement by fibrous tissue (fibrosis) when framework destroyed or permanent cell pop damaged
3. combo of these two
137
Labile cell populations
- turn over all the time
- GI/oral mucosa, skin, blood
- regeneration possible
138
Stable cell populations
- capable of mitosis, but don't turn over often
- hepatocytes, bone, all cT of body, epithelium anywhere, etc.
- regeneration possible
139
Permanent cell populations
- limited ability to regenerate
| - striated muscle, neurons/nervous tissue
140
Proud Flesh
Granulation tissue grows faster than epithelium can cover it, so it extends above the epithelium
Horse hooves, oral cavity of cats
141
3 phases of granulation tissue formation
- inflammatory phase (healing initiated)
- proliferative phase (fibrovascular tissue growth)
- remodeling phase (scar tissue)
142
Granulation tissue cells
- macrophages (clean up, trigger fibroblasts)
- fibroblasts (lay down collagen matrix, reduce wound volume)
- endothelial cells (vascular supply)
143
Zones of tissue recovery
- Zone of CT maturation (deepest layer)
- Zone of capillary proliferation
- Zone of capillary sprouts and arches
- Zone of necrotic debris (at skin surface)
144
Primary/First Intention Healing
- Wound edges opposed
- Rapid healing with minimal scar tissue
- E.g. seen in surgery
145
Second Intention Healing
- Defect filled with granulation tissue
- Prolonged course
- Potential for scarring is significant
- More commonly seen in clinics
146
Adverse consequences of healing
Adhesion
Ankylosis
Stricture
Contracture
147
Ankylosis
join fixed in space
148
Stricture
circumferential scarring around a tubular structure
149
Contracture
same as stricture, but occurs in the musculoskeletal system (can occur with ankylosis as well)
150
Shock
cardiovascular collapse
| peripheral circulatory failure
151
Types of shock
- Hypovolemic
- Neurogenic
- Cardiogenic
- Septic
152
Phases of Shock
1. non-progressive
2. Reversible
3. Irreversible
153
Critical players in shock
- PAMPs, DAMPs, PRRs
- Cytokines, other mediators
- Neutrophils, macrophages, platelets, vasculature
- Complement & coagulation cascades
