MSK Personal > Second Half Pharm > Flashcards

Second Half Pharm Flashcards

(56 cards)

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1
Q

COX-1

A

Constitutive
Generally Protective
Vasodilator; kidney blood flow; blood clotting, uterine contraction, muscle growth, synaptic transmission

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2
Q

COX-2

A

Inducible form
Makes High concentrations of PG and TXA
Generates prostacyclin (vasodilation, counter platelet agg)
PGE2 is major inflammatory mediator

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3
Q

NF-kB

A

Induces expression of cytokines
IL1, IL6,INFB
Enhances inflammatory response

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4
Q

Aspirin

A

Irreversible, Nonselective COX inhibitor
New enzyme required for recovery of fx
Inactivates enzyme by acetylation

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5
Q

Ibuprofen, Naproxen, Diclofenac, Indomethacin etc…

A 
Older NSAIDs
Reversible Non-specific COX inhibitors
Salicylate inhibits NFkB
Effects determined by plasma half-life
Impaired Kidneys, Gastric Ulcers, Bleeding
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6
Q

Celecoxib

A 
Specific Reversible COX2 Inhibitor
"Celebrex"
Good for treatment of OA, Dental Pain, and patients with Ulcers
Platelet agg not impaired (no P-cyclin)
Long term use hurts heart function
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7
Q

Acetaminophen

A

Weak COX inhibitor
Effective analgesic and antipyretic
Less effective anti-inflammatory

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8
Q

Glucocorticoids

A

Effective antiinflammatory; significant side effects (avascular necrosis)
Inhibition of PLA2 and COX2
Inhibition of inflammatory cytokines
Inhibition of NFkB

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9
Q

NSAIDs with short half lives

A

aspirin, ibuprofen, indomethacin

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10
Q

NSAIDS with long half lives

A

naproxen, phenybutazone, salicylate

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11
Q

Why is acetaminophen toxic

A

Induction of Cyp2E1 by chronic ethanol use (3 drinks/day) leads to metabolism to NAPQI, a hepatotoxin that impairs calcium handling causing necrosis

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12
Q

How is Aspirin eliminated

A

10% in the kidney as salicylic acid
75% conjugated with glycine as salicyluric acid
15% as gluconurides

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13
Q

GI problems from NSAIDs

A 
Dyspepsia
Peptic Ulcer 
GI Inflammation
Gastric Erosion
Major Upper GI Hemorrhage
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14
Q

Treatment of NSAID GI Problems

A

PPI (Omeprazole)
Misoprostol (Prostaglandin analog)
Mucosal protectants (sucralfate)

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15
Q

Renal effects of NSAIDs

A

Reversible reduction of glomerular filtratrion
Edema
Papillary Necrosis
Inhibition of Loop diuretics (require Pgs)
Acute renal failure
Insterstitial Nepritis
Hyperkalemia

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16
Q

How does sensitivity to Aspirin induce bronchospasm

A

Blocking of COX pathways shunts Arachidonic acid metabolism to the Lipoxegenase pathway leading to increased production of leukotrienes and consequently bronchospasms

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17
Q

Other side effects of COX inhibitors

A

Erythema multiforme, urticaria
Drowsiness and headache
Rare severe reactions (pneumonitis, hepatitis)

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18
Q

Absolute contraindications of NSAIDS

A

Pregnancy
Hypersensitivity to NSAIDs
Bleeding disorders

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19
Q

Reyes Syndrome

A

Can be caused by Ibuprofen in children with certain viral infections. When children have fever of unknown origin use acetaminophen

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20
Q

Salicylism

A

Salicylate toxicity

Nausea, vomiting, tinnitus

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21
Q

GI bleeding

A

Increased blood loss with a single aspirin tablet

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22
Q

Hemostasis

A

decreased platelet aggregation

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23
Q

Respiratory alkalosis

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A

Stimulation of respiratory center causes kidney compensation and release of bicarb, sodium, potassium, and water; metabolic acidosis is superimposed to compensate

24
Q

Acetaminophen toxicity

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A

Hepatotoxicity
Hypoglycemic coma
Renal tubular necrosis
hypersensitivity

25
DMARDS
Reduce the disease process slowly No initial analgesic effects Typically taken with NSAIDs
26
When should DMARDS be started
Early the disease process because NSAIDS to not stop destruction of the joint
27
Methotrexate
Single weekly oral dose Works in 4-6 weeks Usually combined with cyclosporine or infliximab to improve efficacy
28
Leflunamide
Oral Inhibits lymphocyte proliferation (immunosuppressant) Can be given with Methotrexate
29
Etanercept
TNF-a trap Subq injection 2x/week Fc region bound to p75 TNF receptor Effective in 2 weeks to 3 months
30
Infliximab
TNF-a chimeric monoclonal antibody (Human FC, Mouse TNF-a receptor) Given I.V. Adalimumab, golimumab, certolizumab pegol are slightly different but also MCAB
31
Abatacept
Selectively modulates costimulatory signal for T cell activation Reduces TNF-a production CTLA-4 bound to human IgG fc domain
32
Rituximab
Anti CD20 monoclonal ab Causes elimination of CD20 B lymphocytes Useful in TNF-a inhibitor resistant RA
33
Anakinra
Naturally occurring IL-1 receptor antagonist Inhibits IL-1 action Should not be given with TNF-a antagonist
34
Tocilizumab
AB that binds IL6 receptor blocking IL6 action
35
Tofacitinib
JAK kinase inhibitor | Blocks activation of lymphocytes and secretion of cytokines
36
Side effects of DMARDs
Increased incidence of serious infections Allergic reactions Possible malignancies
37
How does Estrogen maintain bone homeostasis
Estrogen binds to ER-a to promote apoptosis of osteoclasts and to lower rate of apoptosis of osteoblasts and osteocytes It also lowers secretion of pro-inflammatory cytokines IL1 and TNFa
38
How does estrogen deficiency cause bone loss
Estrogen deficiency leads to increased IL1B and TNF-a which lead to increased levels of RANKL and increased differentiation of Osteoclasts
39
How to aromatase inhibitors lead to bone loss
They prevent the conversion of androgens to estrogens in peripheral tissues
40
Antiresorptive drugs
Denosumab, Calcitonin, SERMs, and Bisphosphonates
41
Osteoanabolic drugs
Teriparatide
42
Bisphosphonates
Mimic pyrophosphate and bind hydroxyapetite when it is deposited in bone When released inhibit osteoclast activity and promote apoptosis Can be used for 5 years before risk of non-traumatic femoral neck fracture Zoledronic Acid given by IV once a year
43
SERMs
Reloxifene Estrogen derivates that act as agonists in some tissues and antagonists in others Inhibit bone resorption without increasing risk of breast cancer
44
Denosumib
Anti-RANKL antibody Acts like OPG to prevent binding of RANKL to RANK Given by injection once/3-6months Not recommended in hypocalcemia
45
Calcitonin
Reduces osteoclast activity and lowers serum Ca2+ | Usually a synthetic salmon calcitonin is used
46
How does PTH affect bones?
Increased plasma Ca2+ concentration by increasing osteoclast activity Increases Vitamin D synthesis in the kidney Increases kidney absorption of Ca2+
47
How does Vitamin D affect bones?
Increases synthesis of Ca2+ binding protein for transport of Calcium out of the gut
48
How does calcitonin affect bones?
Decreases bone reabsorption and decreases kidney reabsorption of Ca2+
49
What are common clinical uses for skeletal muscles relaxants
Surgical relaxation Orthopedic Procedures Intubation with endotracheal tube Control of ventilation
50
What are the non-depolarizing blockers of nAchR
``` D-turbocurarine Pancuronium Vecuronium Atracuronium Rocuronium Mivacurionium ```
51
What is the mechanism of non-depolarizing blockers
Competitive antagonist of ach binding to receptor Can be outcompeted and therefore made ineffective by AchE inhibitors Muscle contraction still elicited by direct stimulation
52
What is the prototype depolarizing blocker?
Succinylcholine
53
How do depolarizing blockers work?
Activate, open, and desensitize the channel Resistant to AchE Phase 1: Brief blockage leads to fasciculations and flaccid paralysis. Muscle contraction cannot be stimulated Phase 2: End plate depolarization decreases and muscle repolarizes.
54
What problems are associated with succinylcholine?
Hyperkalemia due to prolonged K efflux Prolonged Apnea resulting from decreased plasma cholinesterase activity Malignant hyperthermia caused by autosomal dominant defect in ryanodine receptor of CA2= channel. (Treat with dantrolene and keep cool and monitor acidosis)
55
How are non-depolarizing blocks reversed?
Edrophonium or neostigmine in addition to a muscarinic receptor antagonist like atropine to prevent bradycardia.
56
What are the drug interactions of skeletal muscle relaxants
Inhaled anesthestics Local anesthetics Ca2+ channel blockers AchE Inhibitors and Neuromuscular blockers Antibiotics: aminoglycosides and tetracyclines
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