(01) Lecture 1

Question 1

(Cardinal Signs of Acute Inflammation)

(Give what each of these means)

1. rubor
2. calor
3. dolor
4. tumor
5. functio laesa

Answer 1

1. redness
2. heat
3. pain
4. swelling
5. loss of function

Question 2

1-4. What are the four phases of acute inflammation?

5-6 Chronic Inflammation consists of what two phases?

Answer 2

1. fluidic (exudative)
2. necrosis
3. cellular (prinipally neutrophilic)
4. reparative
5. cellular (macrophages and lymphocytes)
6. healing (fibrosis, granulation tissue formation)

Question 3

1-2. What are the functions of inflammation?

Answer 3

1. dilute, sequester, kill
2. repair (removal of damaged tissue, wound healing factors, restrict appendages)

Question 4

1-3. Three times when inflammation is harmful

Answer 4

1. inflammation itself
2. infectious disease made worse by inflammation
3. post-inflammatory fibrosis

Question 5

1-3. What are the three phases of initiation and exudative phase of inflammation?

Answer 5

1. tissue damage (exo and endogenous)
2. hyperemia due to vasodilation
3. endothelial changes (postcapillary venules) –> leakage of plasma fluid and plasma proteins

Question 6

(Acute inflammation: endothelial cell dynamics)

(endothelial gaps widening)

1-2. caused by what two things?

(injury to endothelial cells)

3. leads to what?

(leukocyte induced injury)

(increased transcytosis)

4. is what?

Answer 6

1. endothelial cell contraction (postcaplliary venules; vasoactive amines)
2. cytoskeletal organization (venules and capillaries; cytokines, hypoxia)
3. necrosis and detachment from basement membrane
4. molecule transport

Question 7

(Acute Inflammation: Overview)

(Initiation and Exudative phase)

1. changes of what type of cell? produce what? up-regulate receptors for what?
2. What is first fluid?
3. later?

Answer 7

1. perivascular cells (mast cells, dendritic cells, etc)

cytokines

inflammatory mediators and adhesion molecules

2. transudate (ultrafiltrate of plasma)
3. exudate (larger plasma proteins and cells (neutrophils))

Question 8

(Acute Inflammation: Fluidic Phase)

1. normal vascular protein exchange: up to size of what?
2. osmotic colloid pressure <–> ?
3. inflammation results in net inflow or outflow of fluid (and proteins)?
4. will dilation and increase permeability lead to slower or faster blood flow?

Answer 8

1. albumin
2. hydrostatic pressure
3. outflow
4. slowed

Question 9

(Vascular Events)

1. Vasodilation caused by what three things?
2. do what?

Answer 9

1. Histamine, NO, PG
2. increase permeability

Question 10

(Vascular Events)

1. What 3 compounds cause early permeability (1-2 hours)?
2. Later (3-6)?

Answer 10

1. histamine, bradykinin, leukotrines
2. cytokines, hypoxia, leukotrines

Question 11

1. What is the difference between transudate and exudate?
2. What is exudate’s mechanism for release? modified transudate? transudate?
3. What is the cause in the same order as two?

Answer 11

1. transudate = clear and watery

exudate = more turbid (cloudy) and more viscous

2. increase vascular permeabilty; increased capillary hydrostatic P; decreased plasma osmotic P
3. inflammation, congestive heart disease, protein loss or heart disease

Question 12

1. What is used to differentiate between modified transudate and exudate (beacuse they can look similar)?

Answer 12

1. cytologic evaluation and protein analysis (modified transudate will gel over time due to increased protein (fibrin))

Question 13

(Acute Inflammation: Overview)

(Fibrin)

1. traps what?
2. sequesters what?
3. attracts and provides routes for what?
4. provides framework for what?

Answer 13

1. microorganisms
2. injurious stimulus
3. neutrophils
4. initial wound healing

Question 14

(Acute Inflammation: Overview)

(Chemotaxis)

1. bacteria
2. fibrin
3. foreign material
4. neoplastic cells
5. chemotactic cytokines

(?)

Question 15

(Acute Inflammation: OVerview)

(Chemotaxis)

1. stimulate what?
2. Induction of receptors and molecules on what?
3. Movement and attachment of neutrophils to what?
4. migration between endothelial cells through what what?
5. migration within exudate along or against gradient?

Answer 15

1. luekocyte adhesion cascade
2. neutrophils
3. endothelial cells
4. intercellular gaps
5. along

Question 16

(Leukocyte Migration and Chemotaxis)

1. Movement along what gradient?
2. Chemotactic Substances have what properties?

(Exogenous)

1. what is one?

(Endogenous)

1-4 four examples

Answer 16

1. chemotactic gradient
2. soluble, attract WBC
3. bacterial products (TLR)
4. necrotic cells
5. complement
6. leukotriene
7. cytokines/chemokines

Question 17

look at this

Question 18

(Stimuli Inducing an acute inflammatory response)

1. exogenous
2. and endogneous (auto-reactive) - what are two possibilityes here?

Answer 18

2. newly formed auto-antigens, hypersensitivity to existing auto-antigen

Question 19

(Stimuli Inducing the acute inflammatory response)

1. injurious stimuli must to do what to elicit inflammatory response?
2. Acute inflammatory response occurs simultaneously with what?

Answer 19

1. penetrate or break body surfaces
2. activation of the innate immune system

Question 20

read/learn this

Answer 20

and this

Question 21

(Chemical Mediators: General Concepts)

1. act via binding to what?
2. are they in plasma or are they cell associated?
3. stimulate what?
4. how quickly inactivated?

Answer 21

1. receptor on target cell
2. can be either
3. taret cells
4. rapidly (short half-life)

Question 22

(Chemical Mediators: Classes)

1-6 What are they?

Answer 22

1. vasoactive amines
2. plasma proteins and proteases
3. arachidonic acid metabolites
4. cytokines (including chemokines)
5. nitric oxide
6. O2 derived free radicals (ROS)

Question 23

(Chemical Mediators)

(Vasoactive Amines)

(Histamine)

1. from what?
2. do what?

(Serotonin)

3. from what?

(what else?)

Answer 23

1. mast cells
2. vasodilation, perm, bronchial constriction, PGF2 release, pain/itching, tachycardia and eosinophil chemotaxis
3. platelets

(bradykinin and tachykinin - includes substance P)

Question 24

(Chemical Mediators)

(Plasma Proteins and Proteases)

1-3. consist of what three things?

Answer 24

1. kinin system
2. complement system
3. clotting and fibrinolyic systems

Question 25

(Chemical Mediators) (Plasma Proteins and Proteases) (Bradykinin) 1. a vasoactive peptide - how many times more potent than histamine? 2. Function? (look at image)

Answer 25

1. 10X 2. vasodilation, perm, pain, bronchoconstriction (similar to histamine) (look at this too)

Question 26

(Chemical Mediators) (Complement System) 1. which are the anaphylatoxins? 2. What serves as a chemotaxi? 3. What does opsonization/phagocytosis?

Answer 26

1. C5a, C3a 2. C5a 3. C3b (mostly by neutrophils but some by macrophages)

Question 27

(Chemical Mediators)

Answer 27

Question 28

this belongs with AA stuff

Question 29

(Chemical Mediators) (Cytokines) 1. What are the major ones of acute inflammation? 2. Source? 3. Stimuli? 4. act locally or systematically?

Answer 29

1. IL-1 and TNFa 2. macrophages, NK, endothelial cells 3. LPS, Ag-Ab complexes, etc 4. either

Question 30

(IL-1, TNF-a: local actions) 1. EC activation - synthesis of what two things? 2. Increase vasc perm 3. activation of what? 4. proliferation of what? 5. synthesis and degradation of what?

Answer 30

1. adhesion molecules and chemical mediators 3. neutrophils 4. fibroblasts 5. ECM

Question 31

(Other Cyotkines of the acute inflammatory response) (interferon a and y) 1. produced by what? 2. stimulus? 3. active what? (High mobility group box protein 1) 1. Pro-inflammatory cytokine that relesease from what two things?

Answer 31

1. lymphocytes (and many other cells) 2. virus, parasites, neoplastic 3. NK cells and macrophages 4. macrophages and cells undergoing oncosis

Question 32

(Nitric Oxide: chemical mediator of inflammation) 1. produced by what? 2. soluble gas with how long of half-life? 3. Synthesized by what? 3. 1 constitutive in what? 3. 2 induced in what? (Function) 1. what three?

Answer 32

1. mo, EC, neurons 2. short 3. NOS 3. 1 EC, neurons 3. 2 mo 4. vasodilation, decreased platelet aggregation and WBC adhesion, lipid peroxidation

Question 33

(Oxygen-Derived free radicals) 1. produced by mo and PMS 2. damage to EC, ECM, and increase chemotaxis 3. what are the effects?

Answer 33

3. lipid peroxidation, denaturaion of proteins, DNA damage, DNA adducts