Aa

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Efalizumab

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- binds the CD11a adhesion molecule

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Orally active TNF-α inhibitor

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thalidomide

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extracellulardomain of the human TNF receptor fusedto the Fc region of human IgG1.

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Etanercept

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monoclonal antibodies against the IL-2 receptor

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basiliximab

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metabolised to give mercaptopurine, apurine analogue that interferes with purinesynthesis and therefore inhibits DNA synthesis

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azathioprine

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contraction of bronchial andgastrointestinal tract (GIT) smooth muscle

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ep1

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relaxation of bronchial, vascular andGIT smooth muscle

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ep2

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if the ligand is LTB4

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blt

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if the cysteinyl-leukotrienes.

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Cys LT

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if the cysteinyl-leukotrienes.

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Cys LT

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The CysLT-receptor antagonists

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zafirlukast

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5-lox inhibitor

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zileuton

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PAF is released from activated inflammatorycells by

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PLa-2

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h1 antagonist

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mepyramine

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h2 antagonist

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cimetidine

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COX-2 knockout mice are ________

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severe kidney development problems

serious problems with kidneys(anomalous development) and reproductive system

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non-sedating h1 antagonist

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terfenadine

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h1-antagonist for sedation

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promethazine

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t prevents migration of neutrophils into the joint,by binding to tubulin, resulting in thedepolymerisation of the microtubules and reducedcell motility

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colchicine

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metal chelator

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penicillamine

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can be given to preggo

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chloroquine

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Binds FKBP to inactivate calcineurin in order to prevent it from dephosphorylating NFAT

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Tacrolimus

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Binds ciclophilin to inactivate calcineurin prevent it from dephosphorylating NFAt

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active in gfj

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furanocoumarins decrease first pass metabolism more drug hits you

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alkylates DNA

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cyclophosphamide

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PROPHYLACIS NEVER ACUTE ATTACK!

primarily to treat hyperuricemia (excess uric acid in blood plasma) and its complications, including chronic gout.[1] It is a xanthine oxidase inhibitor which is administered orally.

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ALLOPURINOL

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may act by increasing levels of adenosine, whichis an endogenous anti-inflammatory mediator– inhibits neutrophil adhesion, phagocytosis, and superoxidegeneration.• cause apoptosis of activated CD4+ and CD8+ Tcells, but not of resting cells.

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METHOTREXATE

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most cox-2 selective --cardiac problems

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rofelcoxib

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NSAID - reduce the requirement for narcotic analgesics

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ketorolac

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non drowsy anti H1

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terfenadine

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terfenadine

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Knwo this

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zafirlukast

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CysLT antagonist

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Zileutin

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5-LOX inhibitor

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chimeric mouse-human monoclonal antibody to the α chain (CD25) of the IL-2 receptor of T cells.

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Basiliximab

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Ab to Il-2

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basiliximab

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mAb to CD28

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TGN 1412

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Tricyclic antidepressants

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imipramine

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SSRI

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Fluoxetine

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Fluoxetine

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SSRI

Front 40

Moclobemide & moclobemide are?

Which 1 is irreversible ?

Which 1 is reversible ?

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moclobemide = reversible

MAOI inhibitors

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PROZAC SSRI name?

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fluoxetine

Front 42

Neuroplasticity hypothesis

Too much _________

Loss of spines

excitotoxicity

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Glutamate

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4 hypothesis

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1_ mono amine hypothesis

2- receptor downregulation hypothesis

3- neuroplasticity hypothesis

4- Neurotransmitter receptor hypothesis

Front 44

most commonly prescribed DEPP> treatment

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SSRI

Front 45

binds the CD11a adhesion molecule,approved in some countries for psoriasis

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efalizumab

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BINDS VERY LATE ANTIGEN 4

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NATALIZUMAB

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–Increasein size of organs and cells due to protein accretion–Responseto increased work load (cardiac, skeletal muscle) or hormonal stimulation(uterine muscle)–Permanentlydifferentiated cells cannot resume cell cycle to increase their number

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Hypertrophy

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–Increasein cell number and organ size–Responseto hormonal stimulation or compensatory to damage–Cellsthat normally turn over or issue-specific stem cells resume cell cycle toincrease in number—liver, endocrine glands, glandular epithelium, lymph nodes

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hyperplasia

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–Changein cellular organization, size and organ architecture –almost always used todescribe changes in epithelium–Responseto irritation and damage (classic example is Pap smear)

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dysplasia

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–Substitutionof one cell type for another within an organ–Responseto different concentration or assortment of growth factors or extracellularmatrix components, which is a response to irritation or injury_back_html[]&card_hint_html[]

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metaplasia

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–Decreasein cell size and number –Responseto decreased work load (use), hormonal or neuronal stimulation, blood supply,nutrition, or aging; in adults (atrophy) or during development (hypoplasia)

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atrophy/hypoplasia

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–Developmentaldefects; result of genetic defect or in uterodeficiency (i.e. folate)_back_html[]&card_hint_html[]

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aplasia / agenesis

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–theseallow the cell to enter the cell cycle

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mitogens

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increase in cell mass

suppress apoptosis

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–Growth factors -

–Survival factors

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Ligation of death receptors (extrinsicpathway) leads to the activation of caspase ?, which in turn activates theexecutioner caspase, caspase ??.

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? - 8 ??=3

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proapoptoticBcl-2 proteins card_hint_html[]

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Bak/bax

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Acentral feature of necrotic cell death is

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the rapid loss of mitochondrial membrane potential (Δψm)

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PPAR HETERDOIMERS WITH?

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RXR RETINOID X RECEPTOR

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ppar

ADIPOCYTE DIFFERENTIATION / MACROPHAGE FUNCTION

FA CATABOLISM

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ADIPOCYTE DIFFERENTIATION - GAMMA

FA CATABOLISM - ALPHA

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•ismainly expressed in adipose tissues but is also detected in the colon, spleen,retina, hematopoeiticcells, and skeletal muscle. PPARγ2 has been found mainly in the brown and whiteadipose tissue.

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PPAR-GAMMA

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PPARs bind to DNA as heterodimerswith ---, on ------ comprising direct repeats of two hexamersclosely related to the sequence ------and separated by ----nucleotide (DR-1sequence).

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PPARs bind to DNA as heterodimerswith RXR, on PPAR response elements (PPRE) comprising direct repeats of two hexamersclosely related to the sequence AGGTCA and separated by one nucleotide (DR-1sequence). []&card_front_html[]&card_back_html[]&card_hint_html[A

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cIMETIDINE & RANITIDINE ARE?

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H2 ANTAGONISTS - USED IN GASTRIC ACID SUPPRESSION

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MYLANTA II AND MYLOX ARE?

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ANTAcids

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carafate is

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gel in throat

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makes gel in throat?

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carafate

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mainLipid Digestionenzyme to hydrolyzelipids in neonat

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lingual lipase

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30%of lipid hydrolysis inadults.

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gastric lipase

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protein co-enzyme –makes pancreaticlipase more efficient

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colipase

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digests triglycerides intodiglycerides, and then 2-monoglycerides and fattyacids

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pancreatic lipase

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Keeps fatty acids from the Keeps fatty acids from thecytosol• These have a “b-clam”structure

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Fatty acid binding protein

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A fatty acyl-CoA and a MAGmolecule are covalentlyj i dt f joined to form DG;catalyzed by:

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MGAT

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catalyzethe formation of an esterli k b t f tt l linkage between a fatty acylCoA and the free hydroxylg p rou of DG to form TG.

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DGAT

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Intestinal cholesterol absorbed into enterocyte by:

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NPC1L1

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Free cholest, can be“pumped” back via

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ATP- Binding Casette

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Ezetimibe does what?

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inhibits NPC1L1

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Mammals lack the enzymes to introduce Double bonds beyond C_

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C9

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2 essential fatty acids in mammals

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linolate linoleate

linoleic acid linolenic acid

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Arachidonic Acid

#n# d #####

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20n4 5,8,11,14

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linoleate

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18:2 d9,12

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linolenate

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18:3 9,12,15 - alpha

13:3 6,12,15 - gamma

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maturation of SREPBP-1 requires the activation of ---- a chaperone protein

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SCAP - SREBP CLEAVAGE PROTEIN

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When does SCAP bind the SREBP-1 to cleave it?

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When low intracellular cholestrol concentration gotta make more

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regulatory protein that is required for the proteolytic cleavage of the sterol regulatory element-binding protein (SREBP)

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SCAP

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Deletion of what SREBP doesn't do anything

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SREBP-1c

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Deletion of what 2 isoforms of srebp-1 wreck development

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srebp-1a & srebp-2

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srebp isoform that stims. cholestrol syn

srebp isoform that stimes triglyceride syn

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cholesterol-2

triacylglyceride- 1c

Front 88

also a major anti-apoptopic factor –aberrantactivation of?????= one of the primary causes of a widerange of human diseases like in Inflammatory diseases, Rheumatoid arthritis,Asthma, Atherosclerosis, Alzheimer–Persistentactivated in many cancers - help keeping them alive@�

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NF-KB

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a drug againt nfkb would be a promising anti what drug?

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ANTI cancer

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i

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i