Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

85 Cards in this Set

  • Front
  • Back
what do myeloid stem cells give rise to?
cells of the innate immne system
- neutrophils
- eosinophils
- basophils
- mast cells
- macrophages
what do lymphoid stem cells give rise to?
cells of the adaptive immune system
what are the three granulocytes?
what do basophils and mast cells bind to?
what do TH1 cells produce, and what do they affect?
IFN-g, IL-2
influence cell mediated response of CD-8 and CD 4 cells
what do TH2 cells produce, and what do they affect?
IL-4, IL-5, IL-10
enhance antibody production by B cells
which T cell subtype is more associated with autoimmunity?
where is histamine synthesized and stored?
in granules of mast cells and basophils
why is histamine called the vasoactive amine?
dilation of arterioles and postcapillary venules
constriction of veins
contraction of endothelial cells
what type of proteases make up the complement system?
serine proteases
what are the two ways in which complement can be activated?
1. antigen-antibody interaction (classical)
2. interaction with foreign surfaces (alternative pathway)
3. interaction with mannose binding lectin (lectin pathway)
what does C3b do?
what do C3a and C5a do?
mediate leukocyte chemotaxis
what are eicosanoids?
metabolites of arachadonic acid
name two cytokines from the hematopoietic lineage that are not IL-1 and TNF-a
GM-CSF (granulocyte-monocyte colony stimulating factor)
G-CSF (granulocyte colony stimulating factor)
what is a leukocyte
a white blood cell
- monocyte
- lymphocyte
- granulocyte
name two inflammatory mediators that are important for chemotaxis
leukotriene B4 (LTB4)
COX-2 selective inhibitor
TNF-a antagonist
what is arachadonic acid synthesized from?
linoleic acid, which is derived only from dietary sources
how does arachidonic acid exist in the membrane?
esterified to the membrane phopholipids:
how is arachadonic acid released from the cellular membrane?
phospholipase A2
rate determining step
what induces phospholiase A2 release?
TNF-a, CM-CSF, INF-g, EFG, MAPK-PKC cascade
what inhibits phospholipase A2 release?
induces synthesis of lipocortin- a family of phospholipase A2 inhibiting proteins
what are three proteins that act onunesterified arachidonic acid?
1. cyclooxygenase
2. lipoxygenase
3. epoxygenase
lipoxygenase pathway
cyclooxygenase pathway
cytochrome P450 epoxygenases
epoxyicosatetraenoic acids (EETS)
what is the common chemical structure shared by prostaglandins?
prostanoid: 20 carbion carboxylic acid
synthesis pathway of prostaglandins
PGG2 --> PGH2 --> PGD2,PGE2, PGF2, thromboxane A2, porstacyclin (PGI2)
why is PGE2 important?
cytoprotective roles for gastric mucosa, myocardium, and renal parenchyma
what is the chief eicosanoid product of platelets?
thromboxane A2 (TXA2)
what does TXA2 do?
promoter of platelet adhesion and aggregation
what is the chief eicosanoid product of the vascular endothelium?
PGI2 (prostaglandin I2)
what does PGI2 do?
asodilator, venodilator, and inhibiotr of platelet aggregation
what is the balance that mediates systemic blood pressure and thrombogenesis?
TxA2 (vasoconstrictor and platelet activator) vs. PGI2 (vasodilator and platelet inhibitor)
proinflammatory sequelae:
neutorphil chemotaxis
transmigration through epithelium and endothelium
upregulates free radical production for killing
what do lipoxins LXA4 and LXB4 do?
modulate the effects of leukotrienes (possibly negative regulators, and a key player in the resolution of inflammation)
what are EETs?
epoxyeicosatetraenoic acid: derivatives from oxidized arachidonic acid (via cytochorme P450 epoxygenases)
what do EETs do?
also a negative regulator of inflammation
inhibit platelet COX and inhibot expression of ICAMs
what does the cytokine cascade in asthma cause?
generation of PGD2 and leukotrienes (LTB2)
give 2 extremely potent bornchoconstrictive compounds
LTC4 and LTD4: 1000x more potent than histamine in asthma
what is found in both UC and IBD?
elevated LTB4 levels --> abnormal leukocyte infiltration into the parenchyma
what type of cancer risk is exacerbated in UC and IBD?
adenocarcinoma of the colon
what is found to be elevated in the synovial fluid of patients with RA?
COX-2 enyzme and PGE2
what will autoimmune distruction show in blood tests?
high erythrocyte sedimentation rate and low hematocrit
give the mechanism of glomerulonephritis
elevated levels of LTB4 leads to the synthesis of LTC4 and LTD4 --> facilitate neutrophil adhesion to clomerular mesangium and epithelium
what role does LTC4 and LTD4 play in glomerulonephritis?
decrease renal blood flow and GFR
what type of cancer has COX2 inhibitors been approved for?
familial adenomatous polyposis
how do glucocorticoids work?
induce a family of lipocortins, which inhibit the actin of Phospholipase A2 and thereby inhibits the release of arachadonic acid.
what are the three functions of NSAIDs?
1. anti-inflammatory
2. antipyretic
3. analgesic
what is the mechanism of NSAIDs?
reversible, competitive inhibitor of COX1 and/or COX-2
(aspirin is non-reversible)
what is a caveat associated with NSAIDs?
only suppress the signs of the underlying inflammatory disease
what can COX-1 inhibitors precipitate?
NSAID-induced gastropathy, since you've gotten rid of the protective effects of COX-1 eicosanoid products
NSAID with long elimiation half life
NSAID with long elimiation half life
NSAID with long elimiation half life
NSAID with long elimiation half life
a salicylate
irreversible inhibitor of COX1/2 by acetylating the active site serine residue
how does aspirin act as a antithrombogenic agent?
provents platelets from synthesizing TxA2
what is the difference between aspirin's action on platelets and on endothelial cells?
platelets are anuclear- cannot synthesize new TxA2
endothelial cells cna synthesize new COX1 protein and resume synthesis of PGI2
what does aspirin do to COX-2
only partially inactivates it. you get aspirin-triggere lipoxins (ATLs) that function lipoxins as anti-inflammatory agents
what are the two side effects to aspirin?
1. aspirin-induced airway hyperreactivity in asthmatics
2. Reye's syndrome`
what is Reye's syndrome?
hepatic encephalopahty and liver steatosis in young children
T cell costimulation modulator
treates RA
treats migrane headaches
a-adrenergic blocker for BPH
substance P antagonist
anti-inflammatory for IBD
INF-b used to treat MS
endothelin receptor antagonist.
used for pulmonary artery hypertension
Carbonic anhydrase inhibitor
angiotensin II receptor antagonist for treatment of HTN
antifungal against aspergillus and candida
broad spectrum antibiotic used for treatment of bacterial infections of ear, sinus, throat and skin
treatment for intermittent claudication
stimulates erythropoiesis for anemia treatment
protease inhibitor for HIV treatment
used to treat ADD (ritalin)
class III antiarrythmic
dotrecogin alfa
recombinant form of Protein C
5-alpha reductase inhibotor
used to treat BPH and male pattern baldness
used to treat psoriasis