Pharmacology Nov 13Th

Front 1

rheumatism
rheumatic arthritis

Back 1

Any of several pathological conditions of the muscles, tendons, joints, bones, or nerves, characterized by discomfort and disability.

Front 2

Analgesia

Back 2

loss of sensibility to pain.
Oh: hey your prbolem is anelgesia you have no sense of pain and suffering;

Front 3

pyretic
pyrogenic

Back 3

causing fever

Front 4

Dampen

Back 4

depress

Front 5

modulate

Back 5

to adjust

Front 6

what is the function of glucocorticoids; cortisol and corticosterones?

Back 6

1. they help regulate carbohydrate, fat and protein metabolism
2. endow organism with the ability ot resist stressful stimuli
3. modulate imuune response 4. diminishes response to catecholamines(neurotansmitters and hormones)

Front 7

what happens if you give too much glucocorticoids?

Back 7

it functions as negative feedback and if given too much it would shut down its production

Front 8

prostaglandins

Back 8

any of a group of hormonelikne substances mediate a wide range of physiological funtions, such as control of blood pressure, contraction of smooth muscle and modulation of inflammation.

Front 9

arachidonic acid

Back 9

An essential fatty acid that is a component of lecithin and a basic material for the biosynthesis of some prostaglandins.
so
arachidonic + arachidonic= lecithin
lecithin + lecithin= postaglandinds

Front 10

what are the two antiinflammatory effects of glucocorticoids?

Back 10

1. Lowering immune cells
wbc, cytokine production, antibody production, migration

2. lowering arachidonic cascades.
phospholipase A2. COX 2 induction

Front 11

intracellular mechanism of glucocorticoid?

Back 11

the steroid recepotr in cell is CBG. it enters the nucleus, binds to Gluc response element and then rgulates transcription. the resluting mRNA is sent to cytoplasm to make antiinflammatory poroteins. Annex 1
MapK phosphatase
Note that this takes sometime to take effect and for the effect to go away.
2. there is another method:
where it blocks the production of pro-inflammatory proteins. proteins such as cytokines, chemoattractant protiens, adhesion molecules, collagenase, matrix metallloproteins.

s9

Front 12

what is the glucocorticoid's effects on arachidonic cascade? what do they inhibit?

Back 12

INHIBITS ACTIVATION OF:
1.phospholipase A2
2.COX2

Front 13

List the short to medium-acting synthetic glucocorticoids.

Back 13

1. Hydrocortisone(cotisol)
2. Cortisone
3. Prednisone
4.predinsolone
5.Methylprednisolone
oh: Heydar Parid to Solon Fast

Front 14

List intermediate-acting glucocorticsole:

Back 14

Triamocinolone.
Oh: TRI to find AMO CINO who is very intermediate acting ALONE.

Front 15

Long-acting glucocorticoids

Back 15

1.Betamethasone
2.Dexamethasone

Oh: Betty Delays

Front 16

what are the Contraindicated symptoms of glucocorticoids

Back 16

Peptic ulcer disease
Hypertension with heart disease
Certain infections
Varicella
TB
Psychoses: glucco effects cns and psych
Diabetes
Osteoporosis
Glaucoma: Glaucoma is a group of eye diseases characterized by damage to the optic nerve usually due to excessively high intraocular pressure (IOP).

Front 17

most widley used drugs in the world?

Back 17

NSAIDS

Front 18

How does aspirin affect cox1 and cox2?

Back 18

it is nonspesific irreversible
inhibitor of cox 1 and cox2

Front 19

how do traditional NSAIDS effect cox 1 and 2

Back 19

nonspecific reversible inhibitor of cox 1 and cox2

Front 20

How do coxib effect cox 1 and cox2

Back 20

selective and reversible inhibor of cox 2

Front 21

cox 1
function? is it on all the time

Back 21

housekeeping: GI mucosal integrity
Platelet aggregation
Renal Function

on all the time

Front 22

COX II
function? is it on all the time

Back 22

mediates inflammation,

it is induceable

Front 23

Aspirin is used to...... TXA2

Back 23

Inhibit

Front 24

nociceptive

Back 24

causing pain

Front 25

..... amplify nocioceptive signals

Back 25

eicosanoids

Front 26

clinical effects of glucocorticoids.
objective

Back 26

desired therapeutic effects
1. immunosupression
2. antiinflammatory
3. antiallergic
4. pain relief ( secondary)
5. lowering permeablity

Front 27

adverse effects with long-term use of glucocortisoids.
objective

Back 27

1. infection
2. muscle: mayopathia
3.bone: osteoprosis,osteonecrosis
4. cns, HPA axis: neuropshchiatric, HPA axis
5. Metabolism: wieght gain/ obesity, fluid retntion/ adema, cushingoid appearance, impaired glucose metablism
6. skin: skin thinning ecchymoses
7. eyes: catract, glaucoma
8. cardiovascular

Front 28

anti inflammatory effects of aspirint.
objective

Back 28

inflammatory joint conditions
rheumatoid arthritis
rheumatic fever
Osteoarthritis
Gout: Gout is a form of acute arthritis that causes severe pain and swelling in the joints
Psoriatic arthritis
Arthritis associated with inflammatory bowel disease
inflammation associated with mild bone and muscle trauma

Front 29

mechanism for pain inhibtion of aspirin

Back 29

Mechanism for pain inhibition
reduction of inflammation
inhibition of pain stimuli in neurons

Front 30

interleukins:
function?
produced by?

Back 30

produced by macrophages and activate leukocytes.

Front 31

what is a theraputic uniquness of DMARDs, when compared with steroids and NSAIDS?

Back 31

stops disease progression

Front 32

can steroids be helpful in slowing the new bone erosion?

Back 32

Slows the appearance of new bone erosion. Can be used initially while waiting for effects of DMARD therapy—”Bridge therapy

Front 33

Drug modifying antirheumatic drugs. DMARDs are called......
?

Back 33

immunosupressive drugs

Front 34

what are the DMARD's use?

Back 34

a. inhibit junction and division of immune cells
b. started soon after Rehumatic arthriitis diagnosed
c.it is slow-acting and may take several months to show effects
efficacy of mehotrexate, sulfasalazine, IM gold, and pnicillamine is similar
d. antimalrials are less effective

Front 35

As an anticancer drug that is used to treat RA:
*Methotrexate
MOA, Kinetic and toxicity.
objective. he highlighted

Back 35

Folic acid analogue inhibits dihydrofolate reductase, which is required for new DNA synthesis

Oral or intrathecal

inhibits all fast growing cells (gut epithelium, bone marrow blood progenitor cells, teratogen—Cat X), hepatotoxicity

Front 36

Gout?

Back 36

Familial metabolic disease
recurrent episodes of acute arthritis due to monosodium urate deposits in joints and cartilage
high serum uric acid levels
an end product of purine metabolism