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Pathoma Ch2

Terms in this set (95)

on macrophages and dendritic cells; activated by PAMPs on microbes
Toll Like Receptors
TLR on macrophages that recognizes LPS on gram negative bacteria
CD14
Activation results in upregulation of NF-kB, resulting in cytokine production
TLR
Mediate vasodilation and increased vascular permeability
PGI2, PGD2, PGE2
Mediates FEver and pain
PGE2
4 major neutrophil attractants
1. LTB4
2. C5a
3. IL-8
4. bacterial products
slow reacting substances of anaphylaxis - cause vasoconstriction, bronchospasm, and increased vascular permeability
LTC4, LTD4, LTE4
activated by tissue trauma, anaphylatoxins, and IgE cross-linking
Mast cells
mast cell immediate response
histamine release from preformed granules -> vasodilation, increased vascular permeability
delayed mast cell response
arachidonic acid metabolites, mainly leukotrienes
mechanism for DIC in gram negative sepsis
microbes directly activate factor XII (Hageman factor)
activation of classical complement pathway
IgG/IgM-antigen complex binds C1
alternative pathway of complement activation
microbial products directly activate complement
MBL pathway of complement activation
MBL binds mannose on microbes, activating complement
opsonins for phagocytosis (2)
C3b, IgG
what MAC does
creates hole in microbe cell membrane, inducing lysis
Things Hageman Factor (XII) does
1. coagulation/fibrinolytic system activation
2. complement activation
3. kinin system activation
actions of bradykinin
vasodilation
increased vascular permeability
pain
mediators of the pain of acute inflammation (Dolor)
PGE2
bradykinin
mediators of Rubor and Calor (warmth)
histamine, prostaglandins, bradykinin
mediators of Tumor
histamine
tissue damage
fever mechanism
pyrogens cause macrophages to release IL-1 and TNF
These increase COX activity in perivascular cells of hypothalamus, resulting in increased PGE2
This raises temperature set point
Steps in neutrophil arrival and function
1. margination
2. rolling
3. adhesion
4. transmigration and chemotaxis
5. phagocytosis
6. destruction of phagocytosed material
7. resolution
molecules responsible for rolling of neutrophils
selectin "speed bumps" on endothelial cells
P-selectin is released from _ by _
from Weibel-Palade bodies
Released by histamine
E-selectin is induced by _
TNF, IL-1 (same things as cause fever!)
what selectins on endothelial cells bind to on leukocytes
sialyl Lewis X
upregulate ICAM and VCAM expression on endothelium
TNF, IL-1
upregulate integrins on leukocytes
C5a
LTB4
autosomal recessive defect of integrins
Leukocyte adhesion deficiency
subunit of integrin involved in leukocyte adhesion deficiency
CD18
delayed umbilical cord separation
increased circulating PMNs
recurrent non-pyogenic infections
leukocyte adhesion deficiency
recurrent pyogenic infections
neutropenia
defective primary hemostasis
albinism
peripheral neuropathy
Chediak-Higashi syndrome
giant granules in leukocytes, neutropenia, peripheral neuropathy
Chediak-Higashi syndrome
defect in Chediak-Higashi syndrome
autosomal recessive - microtubule/protein trafficking defect with impaired phagolysosome formation
main killer in O2-dependent killing
HOCl
converts H2O2 to HOCl
myeloperoxidase
recurrent infection and granuloma formation with Staph, Pseudomonas, Serratia, Nocardia, Aspergillus
chronic granulomatous disease - defect in NADPH oxidase leads to impaired respiratory burst
nitroblue tetrazolium test in myeloperoxidase deficiency
blue/normal
increased risk for _ infections in MPO deficiency
Candida
timing of macrophage peak in acute inflammation
2-3 days post insult
macrophage cytokines that promote resolution and healing
IL-10, TGF-beta
what macrophages secrete when they need more neutrophils
IL-8
how macrophages initiate chronic inflammation
present antigen to CD4 helper T cells, which secrete cytokines that promote chronic inflammation
components of TCR complex
T cell receptor
CD3
2nd signal for CD4 T cell activaton
B7 on APC binds CD28 on CD4 helper T cell
Th1 helper T cells secrete _ which do _
IL2 and IFN-gamma
IL-2 is a T cell growth factor/CD8 activator
IFN gamma activates macrophages
Th2 helper T cells secrete _ which do _
IL-4, IL-5, and IL-10
IL-4 facilitates B cell class switching to IgG, IgE
IL-5 recruits/activates eos, causes maturation of B cells-> plasma cells, and causes class switching to IgA
IL-10 inhibits Th1 phenotype
class switching to IgG and IgE
IL-4
Class switching to IgA
IL-5
2nd signal for CD8 T cell activation
IL-2 from CD4 Th1 cell
mechanisms of T cell killing
perforin/granzyme -> apoptosis
FasL expression, binds Fas on target cell -> apoptosis
2nd signal for B cell activation
CD40 receptor on B cell binds CD40L on helper T cell
what happens when surface IgM or IgD on a B cell binds an antigen
maturation to IgM or IgD producing plasma cell
hallmark of granulomatous inflammation
epithelioid histiocytes
how granulomas are formed
macrophages present antigen to CD4 T cells
macrophages then secrete IL-12, inducing CD4 cell differentiation into Th1 subtype
Th1 cells secrete IFN gamma, converting macrophages to epithelioid histiocytes and giant cells
failure of development of 3rd and 4th pharyngeal pouches
DiGeorge Syndrome (22q11.2 microdeletion)
Infection with viruses, fungi
Hypocalcemia
Abnormalities of heart, great vessels
Dysmorphic facies
DiGeorge Syndrome
defective cell mediated and humoral immunity
SCID
etiologies of SCID (3)
cytokine receptor defects
adenosine deaminase deficiency
MHC class II deficiency
treatment for SCID
sterile isolation
stem cell transplantation
pathophysiology of X-linked agammaglobulinemia
mutated Bruton tyrosine kinase (X-linked) -> inadequate opsonization of bacteria and impaired mucosal immunity due to lack of IgA
bacteria, enterovirus, Giardia lamblia
infections when B cells aren't working
immunodeficiency associated with celiac ds
IgA deficiency
mutated CD40L on T cells or CD 40 receptor on B cells
Hyper-IgM syndrome -> helper T cells can't be activated -> no B cell class switching
recurrent pyogenic infections at mucosal sites
hyper-IgM syndrome
thrombocytopenia, eczema, recurrent infections
Wiskott-Aldrich syndrome (X-linked)
recurrent Neisseria infection
C5-C9 deficiencies
C1 esterase inhibitor deficiency
hereditary angioedema (periorbital, skin, mucosal edema)
combined type II and type III hypersensitivity reaction
SLE
arthritis, serosal inflammation, psychosis, renal damage
SLE
Libman-Sachs endocarditis
vegetations on both sides of mitral valve
pathognomonic for SLE
ANA and anti-dsDNA
SLE
anti-histone Abs
drug-induced SLE (remits with removal of drug)
drugs that cause lupus
INH, hydralazine, procainamide
anticardiolipin and lupus anticoagulant
characteristic of antiphospholipid antibody syndrome in SLE - leads to false-positive syphilis test and falsely elevated PTT
lupus
lupus anticoagulant (antiphospholipid antibody syndrome) -> hepatic vein thrombosis
type IV HSR against lacrimal, salivary glands
Sjogren syndrome
dry eyes, dry mouth, dental caries
Sjogren syndrome
ANA and anti-ribonucleoprotein (Ro, La)
Sjogren syndrome
increased risk for B-cell lymphoma in late ds course
Sjogren syndrome -> occurs unilaterally in parotid gland
CREST syndrome components
calcinosis/anti-centromere antibodies
raynaud phenomenon
esophageal dysmotility
sclerodactyly
telangiectasias
solid liquid dysphagia
scleroderma
ANA and anti-DNA topoisomerase I antibody
scleroderma
serum antibodies against U1 ribonucleoprotein
mixed connective tissue ds (components of SLE, systemic sclerosis, and polymyositis)
difficulty combing hair and walking up stairs
proximal muscle weakness - polymyositis
labile tissues
bowels, skin, bone marrow
where stem cells reside in bowel
mucosal cryptes
marker for hematopoietic stem cells
CD34
type 1 collagen is in:
bONE
type 2 collagen is in:
cartwolage
type 3 collagen is in:
pliable tissues - granulation tissue, embryo, uterus, keloids
type 4 collagen is in:
basement membranes
role of TGF alpha in tissue repair
epithelial and fibroblast growth factor
role of TGF beta in tissue repair
fibroblast growth factor; also inhibits inflammation
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