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002 - Pathology - (02) - Inflammation > (01) Lecture 1 > Flashcards

(01) Lecture 1 Flashcards

1
Q

(Cardinal Signs of Acute Inflammation)

(Give what each of these means)

  1. rubor
  2. calor
  3. dolor
  4. tumor
  5. functio laesa
A
  1. redness
  2. heat
  3. pain
  4. swelling
  5. loss of function
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2
Q

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

5-6 Chronic Inflammation consists of what two phases?

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

1-2. What are the functions of inflammation?

A
  1. dilute, sequester, kill
  2. repair (removal of damaged tissue, wound healing factors, restrict appendages)
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4
Q

1-3. Three times when inflammation is harmful

A
  1. inflammation itself
  2. infectious disease made worse by inflammation
  3. post-inflammatory fibrosis
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5
Q

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

A
  1. tissue damage (exo and endogenous)
  2. hyperemia due to vasodilation
  3. endothelial changes (postcapillary venules) –> leakage of plasma fluid and plasma proteins
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6
Q

(Acute inflammation: endothelial cell dynamics)

(endothelial gaps widening)

1-2. caused by what two things?

(injury to endothelial cells)

  1. leads to what?

(leukocyte induced injury)

(increased transcytosis)

  1. is what?
A
  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
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7
Q

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

cytokines

inflammatory mediators and adhesion molecules

  1. transudate (ultrafiltrate of plasma)
  2. exudate (larger plasma proteins and cells (neutrophils))
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8
Q

(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?
A
  1. albumin
  2. hydrostatic pressure
  3. outflow
  4. slowed
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9
Q

(Vascular Events)

  1. Vasodilation caused by what three things?
  2. do what?
A
  1. Histamine, NO, PG
  2. increase permeability
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10
Q

(Vascular Events)

  1. What 3 compounds cause early permeability (1-2 hours)?
  2. Later (3-6)?
A
  1. histamine, bradykinin, leukotrines
  2. cytokines, hypoxia, leukotrines
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11
Q
  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?
A
  1. transudate = clear and watery

exudate = more turbid (cloudy) and more viscous

  1. increase vascular permeabilty; increased capillary hydrostatic P; decreased plasma osmotic P
  2. inflammation, congestive heart disease, protein loss or heart disease
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12
Q
  1. What is used to differentiate between modified transudate and exudate (beacuse they can look similar)?
A
  1. cytologic evaluation and protein analysis (modified transudate will gel over time due to increased protein (fibrin))
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13
Q

(Acute Inflammation: Overview)

(Fibrin)

  1. traps what?
  2. sequesters what?
  3. attracts and provides routes for what?
  4. provides framework for what?
A
  1. microorganisms
  2. injurious stimulus
  3. neutrophils
  4. initial wound healing
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14
Q

(Acute Inflammation: Overview)

(Chemotaxis)

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

(?)

A
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15
Q

(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?
A
  1. luekocyte adhesion cascade
  2. neutrophils
  3. endothelial cells
  4. intercellular gaps
  5. along
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16
Q

(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

A
  1. chemotactic gradient
  2. soluble, attract WBC
  3. bacterial products (TLR)
  4. necrotic cells
  5. complement
  6. leukotriene
  7. cytokines/chemokines
17
Q

look at this

18
Q

(Stimuli Inducing an acute inflammatory response)

  1. exogenous
  2. and endogneous (auto-reactive) - what are two possibilityes here?
A
  1. newly formed auto-antigens, hypersensitivity to existing auto-antigen
19
Q

(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?
A
  1. penetrate or break body surfaces
  2. activation of the innate immune system
20
Q

read/learn this

21
Q

(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?
A
  1. receptor on target cell
  2. can be either
  3. taret cells
  4. rapidly (short half-life)
22
Q

(Chemical Mediators: Classes)

1-6 What are they?

A
  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)
23
Q

(Chemical Mediators)

(Vasoactive Amines)

(Histamine)

  1. from what?
  2. do what?

(Serotonin)

  1. from what?

(what else?)

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

(bradykinin and tachykinin - includes substance P)

24
Q

(Chemical Mediators)

(Plasma Proteins and Proteases)

1-3. consist of what three things?

A
  1. kinin system
  2. complement system
  3. clotting and fibrinolyic systems
25
Q

(Chemical Mediators)

(Plasma Proteins and Proteases)

(Bradykinin)

  1. a vasoactive peptide - how many times more potent than histamine?
  2. Function?

(look at image)

A
  1. 10X
  2. vasodilation, perm, pain, bronchoconstriction (similar to histamine)

(look at this too)

26
Q

(Chemical Mediators)

(Complement System)

  1. which are the anaphylatoxins?
  2. What serves as a chemotaxi?
  3. What does opsonization/phagocytosis?
A
  1. C5a, C3a
  2. C5a
  3. C3b (mostly by neutrophils but some by macrophages)
27
Q

(Chemical Mediators)

28
Q

this belongs with AA stuff

29
Q

(Chemical Mediators)

(Cytokines)

  1. What are the major ones of acute inflammation?
  2. Source?
  3. Stimuli?
  4. act locally or systematically?
A
  1. IL-1 and TNFa
  2. macrophages, NK, endothelial cells
  3. LPS, Ag-Ab complexes, etc
  4. either
30
Q

(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?
A
  1. adhesion molecules and chemical mediators
  2. neutrophils
  3. fibroblasts
  4. ECM
31
Q

(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?
A
  1. lymphocytes (and many other cells)
  2. virus, parasites, neoplastic
  3. NK cells and macrophages
  4. macrophages and cells undergoing oncosis
32
Q

(Nitric Oxide: chemical mediator of inflammation)

  1. produced by what?
  2. soluble gas with how long of half-life?
  3. Synthesized by what?
  4. 1 constitutive in what?
  5. 2 induced in what?

(Function)

  1. what three?
A
  1. mo, EC, neurons
  2. short
  3. NOS
  4. 1 EC, neurons
  5. 2 mo
  6. vasodilation, decreased platelet aggregation and WBC adhesion, lipid peroxidation
33
Q

(Oxygen-Derived free radicals)

  1. produced by mo and PMS
  2. damage to EC, ECM, and increase chemotaxis
  3. what are the effects?
A
  1. lipid peroxidation, denaturaion of proteins, DNA damage, DNA adducts

002 - Pathology - (02) - Inflammation (6 decks)

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