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002 - Pathology - (02) - Inflammation > (03) Lecture 3 > Flashcards

(03) Lecture 3 Flashcards

1
Q

(Cellular Players: Monocytes/Macrophages)

  1. Born in what?
  2. what are they called in blood?
  3. in tissues?
A
  1. bone marrow
  2. monocytes
  3. macrophages
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2
Q

(Monocytes/Macrophages)

  1. what is circulation half life?
  2. in tissues?
  3. can they divide?
A
  1. 1-3 days
  2. weeks to months (maybe years?)
  3. yes
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3
Q

(Macrophages)

1-2. What are the two macrophage systems?

A
  1. monocyte-macrophage system (MPS)
  2. Dendritic Cell system )DCS)
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4
Q

(Macrophages)

(Monocytes-Macrophage System)

  1. describe it

(Dendritic Cell System)

  1. where located?
  2. function?
A
  1. monocytes in blood recruited to tissues recruited to site of inflammation

there they become tissue macrophages and may be free or fixed

  1. skin (Langerhans cell), mucous membranes, connective tissue and lymphoid tissue
  2. phagocytize/process antigen - home to local lymph node and present antigen to lymphocytes (stimulation of adaptive)
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5
Q

(Macrophages)

  1. what are connective tissue macrophages with round to spindle shaped cells with reniform nuclei?
  2. What have extensive surface projections, are antigen presenting cells, and exist in several types…
A
  1. histiocytes
  2. dendritic cells
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6
Q

(Monocytes in CBC)

  1. monocytosis = ?
  2. Any time what occurs?
  3. observed in what type of inflammation?
  4. in dogs common in what?
A
  1. increase in monocytes
  2. neutrophilia
  3. acute and chronic
  4. “stress leukogram”
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7
Q

(Macrophage Functions)

(Phagocytosis)

  1. Rc for what?
  2. general scavengers
  3. destroy ingested material - O2 dependent uses what? O2 independent uses what?
A
  1. C3b and Ig Fc
  2. NO, lysosomal enzymes
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8
Q

(Macrophage Functions)

(Secretion)

  1. powerful mediators of inflammation
  2. cytokines, GF, AA metab, TNF
  3. most effiecient after stimulation by what two things?
  4. stimulate what two processes

(ALSO PRESENT ANTIGENS)

A
  1. LPS, IFN-y
  2. healing and repair
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9
Q

(Formation of a classic granuloma - a type of delayed hypersensitivity reaction)

1-2 Usually due to what two things?

(note that the horseshoe look is langhans type and that the other spread out one is foreign body type)

A
  1. persistent intracellular pathogens (mycobacterium)
  2. (sterile) particles such as silica or talcum powder that are difficult to destroy
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10
Q

just read this

A

and this

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11
Q

(Lymphocytes and Plasma Cells)

  1. of lymphoid origin
  2. born in what?
  3. Ag dependent or independent maturation?
  4. can they divide?
  5. functionally diverse
  6. life span short if they are what? long if what?
A
  1. bone marrow
  2. can be either
  3. yes
  4. effector cells; memory cells
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12
Q

(Lymphocytes)

  1. how motile?
  2. majority are what in circuation?

(Functions)

  1. T cells - regulate what?
  2. B cells - what kind of immunity?
  3. NK cells - killing of what?
A
  1. motility is limited
  2. T-cells
  3. immunity, inflammation, hematopoesis and lymphopoesis
  4. humoral (ag presenting)
  5. virus-infected and tumor cells
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13
Q

(Lymphoplasmacytic Inflammation)

  1. consists of what?
  2. sequela to what?
  3. Viral infection (termed “mononuclear” inflammation, if macrophages are also among infiltrate)???
  4. immune-mediated process
  5. idiopathic
  6. subacute or chronic process?
A
  1. lymphocytes and plasma cells
  2. acute inflammation
  3. can be either
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14
Q

(Systemic Effects of acute inflammation)

1-2. What are the two main mediators?

(IL-1)

  1. released from what?
  2. does what?

(TNF-a)

  1. released from what?
  2. do what?
A
  1. IL-1 and TNF-a
  2. macrophages, endothelial cells
  3. vasodilates, perm, chemotactic
  4. T lymphocytes and macrophages
  5. vasodilate, perm, chemotactic - Activate a wide variety of cell types
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15
Q

learn these

A

learn these

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16
Q

(Acute Phase Response)

(Fever)

from the picture

–> ? —> ? —->?

A

PGE2 (hypothalamus) –> neutrotransmitters –> reset temp

17
Q

(Acute Phase Response)

(Acute Phase Proteins)

  1. synthesized by what?
  2. stimulated by what?
  3. Increased concentration in blood during what?
  4. Are they inhibitors or mediators of inflammation?
A
  1. liver
  2. IL-1, IL-6, TNF-a
  3. severe inflammation
  4. can be either
18
Q

(Acute Phase Proteins)

(Bind to Microbial Wall)

1-2. and then do what two things?

  1. (Bind to what else?)
  2. (serve as substrate for production of what?)
A
  1. –> opsonization –> phagocytosis
  2. –> activate complement system
  3. nuclear chromatin
  4. fibrin (hemostasis/coagulation/inflammation)
19
Q

(Acute Phase Proteins)

  1. What is a sustained increase in SAA (serum amyloid A) called?
  2. An increase in acute phase proteins leads to what?
  3. Seen how soon after onset of inflammation?
A
  1. amyloidosis
  2. hyperproteinemia
  3. by day 2
20
Q

Leukocytosis (CBC)

  1. Leukocytosis = ?
  2. neutrophilia = ?
  3. Immediate release of what?
  4. Increase proliferation of what in BM?
  5. left shit (immature forms)
A
  1. increase in WBC
  2. increase in neutrophils
  3. BM storage pool (by IL-1, TNF-a)
  4. myeloid precursors (delayed response (2-4 days) - GM-CSF, G-CSF, M-CSF)
21
Q

(Anemia of Inflammatory Disease)

  1. Anemia = ?
  2. occurs how many days after insult?

(Mediated by IL-1, TNF-a, IFN-y)

say if increase or decrease

  1. BM response to erythropoietin
  2. erythropoietin release
  3. availability of Fe
  4. RBC life span
A
  1. low RBC
  2. 3-10 days

3-6. all decrease

22
Q
  1. What is an increase in platelets called?
  2. What is the mechanism?
A
  1. thrombocytosis
  2. IL-6 –> increased platelet production
23
Q

look at picture first…

  1. mediated by what and what?
  2. redirection of blood flow away from what?
A
  1. TNF-a and IL-1
  2. cutaneous vascular beds
24
Q

(System Inflammatory Response Syndrome - SIRS)

inflammatory state of the whole body

1-5. What are the five clinical features?

A
  1. tachycardia
  2. tachypnea
  3. hypotension
  4. fever or decreased body temp
  5. low or high WBC
25
Q

(Septicemia - pathogens in bloodstream)

(Necropsy “gross findings”)

  1. sometimes none
  2. “portal of entry” (inflamed wound, etc)
  3. enlarged red soft what?
  4. sero-fibrinous polyserositis
A
  1. speen (red pulp hyperplasia)
26
Q

(Septicemia)

(Histological Findings)

  1. bacteria are where?
  2. with or without thrombosis? hemorrhage? inflammatory response?
  3. Acute necrosis of renal tubular epithelial cells, cardiomyocytes, etc.)

(Microbiology Findings)

  1. isolation of bacteria from mutliple organs in large number and in pure culture
A
  1. capiallaries and sinusoids of mutliple organs
  2. all either
27
Q

(Septicemia)

  1. Multiplication of bacteria in what?
  2. generalized production and release of what?
  3. generalized vascular leakage (eg effusions)
  4. disseminated intravascular coagulation with depletion of proteins (eg fibrinogen, completment) and thrombocytopenia
  5. hemorrhages –> ?
  6. –> clinical syndrom of sepsis/shock
A
  1. vasculature
  2. inflammatory mediators (eg IL-1 and TNF-a)
  3. hypovalemic shock
28
Q

(System Inflammatory Response Syndrome - SIRS - due to septicemia)

  1. large amounts of what?
  2. MAssive production of what?
  3. look at pic - figure out what some of those abbraviations are…
A
  1. LPS (endotoxin)
  2. IL-1 and TNF-a
29
Q

(Acute Inflammation: Resoluation)

(Prerequisites for resolution)

  1. what is completed in correct sequence?
  2. what completely removed by macrophages?
  3. complete removal of what?
  4. damage that left stroma inctact allowing for what?
  5. ability to form new what?
A
  1. acute inflammation
  2. exudate
  3. inciting cause
  4. scaffold for regeneration
  5. blood vessels (angiogenesis)
30
Q

(Chronic Inflammation)

  1. Simultaneous tissue destruction/repair
  2. Are vascular changes and fluid accumulation features?

3-5. What are the cellular components?

A
  1. NO!
  2. mononuclear cells (mo, dc, lymphos, plasma cells) and eos, mast cells
  3. endothelial cells (–> angiogensis)
  4. fibroblasts (–> fibroplasia)
31
Q

learn these

A

learn these

32
Q

(Chronic Inflammation)

  1. What are the hallmark inflammatory cells of chronic inflammation?
A
  1. Macrophages
33
Q

this is a handy guide!

A
34
Q
A

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

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