(03) Lecture 3 Flashcards
(Cellular Players: Monocytes/Macrophages)
- Born in what?
- what are they called in blood?
- in tissues?
- bone marrow
- monocytes
- macrophages
(Monocytes/Macrophages)
- what is circulation half life?
- in tissues?
- can they divide?
- 1-3 days
- weeks to months (maybe years?)
- yes
(Macrophages)
1-2. What are the two macrophage systems?
- monocyte-macrophage system (MPS)
- Dendritic Cell system )DCS)
(Macrophages)
(Monocytes-Macrophage System)
- describe it
(Dendritic Cell System)
- where located?
- function?
- monocytes in blood recruited to tissues recruited to site of inflammation
there they become tissue macrophages and may be free or fixed
- skin (Langerhans cell), mucous membranes, connective tissue and lymphoid tissue
- phagocytize/process antigen - home to local lymph node and present antigen to lymphocytes (stimulation of adaptive)
(Macrophages)
- what are connective tissue macrophages with round to spindle shaped cells with reniform nuclei?
- What have extensive surface projections, are antigen presenting cells, and exist in several types…
- histiocytes
- dendritic cells
(Monocytes in CBC)
- monocytosis = ?
- Any time what occurs?
- observed in what type of inflammation?
- in dogs common in what?
- increase in monocytes
- neutrophilia
- acute and chronic
- “stress leukogram”
(Macrophage Functions)
(Phagocytosis)
- Rc for what?
- general scavengers
- destroy ingested material - O2 dependent uses what? O2 independent uses what?
- C3b and Ig Fc
- NO, lysosomal enzymes
(Macrophage Functions)
(Secretion)
- powerful mediators of inflammation
- cytokines, GF, AA metab, TNF
- most effiecient after stimulation by what two things?
- stimulate what two processes
(ALSO PRESENT ANTIGENS)
- LPS, IFN-y
- healing and repair
(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)
- persistent intracellular pathogens (mycobacterium)
- (sterile) particles such as silica or talcum powder that are difficult to destroy
just read this
and this
(Lymphocytes and Plasma Cells)
- of lymphoid origin
- born in what?
- Ag dependent or independent maturation?
- can they divide?
- functionally diverse
- life span short if they are what? long if what?
- bone marrow
- can be either
- yes
- effector cells; memory cells
(Lymphocytes)
- how motile?
- majority are what in circuation?
(Functions)
- T cells - regulate what?
- B cells - what kind of immunity?
- NK cells - killing of what?
- motility is limited
- T-cells
- immunity, inflammation, hematopoesis and lymphopoesis
- humoral (ag presenting)
- virus-infected and tumor cells
(Lymphoplasmacytic Inflammation)
- consists of what?
- sequela to what?
- Viral infection (termed “mononuclear” inflammation, if macrophages are also among infiltrate)???
- immune-mediated process
- idiopathic
- subacute or chronic process?
- lymphocytes and plasma cells
- acute inflammation
- can be either
(Systemic Effects of acute inflammation)
1-2. What are the two main mediators?
(IL-1)
- released from what?
- does what?
(TNF-a)
- released from what?
- do what?
- IL-1 and TNF-a
- macrophages, endothelial cells
- vasodilates, perm, chemotactic
- T lymphocytes and macrophages
- vasodilate, perm, chemotactic - Activate a wide variety of cell types
learn these
learn these
(Acute Phase Response)
(Fever)
from the picture
–> ? —> ? —->?
PGE2 (hypothalamus) –> neutrotransmitters –> reset temp
(Acute Phase Response)
(Acute Phase Proteins)
- synthesized by what?
- stimulated by what?
- Increased concentration in blood during what?
- Are they inhibitors or mediators of inflammation?
- liver
- IL-1, IL-6, TNF-a
- severe inflammation
- can be either
(Acute Phase Proteins)
(Bind to Microbial Wall)
1-2. and then do what two things?
- (Bind to what else?)
- (serve as substrate for production of what?)
- –> opsonization –> phagocytosis
- –> activate complement system
- nuclear chromatin
- fibrin (hemostasis/coagulation/inflammation)
(Acute Phase Proteins)
- What is a sustained increase in SAA (serum amyloid A) called?
- An increase in acute phase proteins leads to what?
- Seen how soon after onset of inflammation?
- amyloidosis
- hyperproteinemia
- by day 2
Leukocytosis (CBC)
- Leukocytosis = ?
- neutrophilia = ?
- Immediate release of what?
- Increase proliferation of what in BM?
- left shit (immature forms)
- increase in WBC
- increase in neutrophils
- BM storage pool (by IL-1, TNF-a)
- myeloid precursors (delayed response (2-4 days) - GM-CSF, G-CSF, M-CSF)
(Anemia of Inflammatory Disease)
- Anemia = ?
- occurs how many days after insult?
(Mediated by IL-1, TNF-a, IFN-y)
say if increase or decrease
- BM response to erythropoietin
- erythropoietin release
- availability of Fe
- RBC life span
- low RBC
- 3-10 days
3-6. all decrease
- What is an increase in platelets called?
- What is the mechanism?
- thrombocytosis
- IL-6 –> increased platelet production
look at picture first…
- mediated by what and what?
- redirection of blood flow away from what?
- TNF-a and IL-1
- cutaneous vascular beds
(System Inflammatory Response Syndrome - SIRS)
inflammatory state of the whole body
1-5. What are the five clinical features?
- tachycardia
- tachypnea
- hypotension
- fever or decreased body temp
- low or high WBC
(Septicemia - pathogens in bloodstream)
(Necropsy “gross findings”)
- sometimes none
- “portal of entry” (inflamed wound, etc)
- enlarged red soft what?
- sero-fibrinous polyserositis
- speen (red pulp hyperplasia)
(Septicemia)
(Histological Findings)
- bacteria are where?
- with or without thrombosis? hemorrhage? inflammatory response?
- Acute necrosis of renal tubular epithelial cells, cardiomyocytes, etc.)
(Microbiology Findings)
- isolation of bacteria from mutliple organs in large number and in pure culture
- capiallaries and sinusoids of mutliple organs
- all either
(Septicemia)
- Multiplication of bacteria in what?
- generalized production and release of what?
- generalized vascular leakage (eg effusions)
- disseminated intravascular coagulation with depletion of proteins (eg fibrinogen, completment) and thrombocytopenia
- hemorrhages –> ?
- –> clinical syndrom of sepsis/shock
- vasculature
- inflammatory mediators (eg IL-1 and TNF-a)
- hypovalemic shock
(System Inflammatory Response Syndrome - SIRS - due to septicemia)
- large amounts of what?
- MAssive production of what?
- look at pic - figure out what some of those abbraviations are…
- LPS (endotoxin)
- IL-1 and TNF-a
(Acute Inflammation: Resoluation)
(Prerequisites for resolution)
- what is completed in correct sequence?
- what completely removed by macrophages?
- complete removal of what?
- damage that left stroma inctact allowing for what?
- ability to form new what?
- acute inflammation
- exudate
- inciting cause
- scaffold for regeneration
- blood vessels (angiogenesis)
(Chronic Inflammation)
- Simultaneous tissue destruction/repair
- Are vascular changes and fluid accumulation features?
3-5. What are the cellular components?
- NO!
- mononuclear cells (mo, dc, lymphos, plasma cells) and eos, mast cells
- endothelial cells (–> angiogensis)
- fibroblasts (–> fibroplasia)
learn these
learn these
(Chronic Inflammation)
- What are the hallmark inflammatory cells of chronic inflammation?
- Macrophages
this is a handy guide!
