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MSK Personal > Second Half Pharm > Flashcards

Second Half Pharm Flashcards

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

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

A

Hepatotoxicity
Hypoglycemic coma
Renal tubular necrosis
hypersensitivity

25
Q

DMARDS

A

Reduce the disease process slowly
No initial analgesic effects
Typically taken with NSAIDs

26
Q

When should DMARDS be started

A

Early the disease process because NSAIDS to not stop destruction of the joint

27
Q

Methotrexate

A

Single weekly oral dose
Works in 4-6 weeks
Usually combined with cyclosporine or infliximab to improve efficacy

28
Q

Leflunamide

A

Oral
Inhibits lymphocyte proliferation (immunosuppressant)
Can be given with Methotrexate

29
Q

Etanercept

A

TNF-a trap
Subq injection 2x/week
Fc region bound to p75 TNF receptor
Effective in 2 weeks to 3 months

30
Q

Infliximab

A

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
Q

Abatacept

A

Selectively modulates costimulatory signal for T cell activation
Reduces TNF-a production
CTLA-4 bound to human IgG fc domain

32
Q

Rituximab

A

Anti CD20 monoclonal ab
Causes elimination of CD20 B lymphocytes
Useful in TNF-a inhibitor resistant RA

33
Q

Anakinra

A

Naturally occurring IL-1 receptor antagonist
Inhibits IL-1 action
Should not be given with TNF-a antagonist

34
Q

Tocilizumab

A

AB that binds IL6 receptor blocking IL6 action

35
Q

Tofacitinib

A

JAK kinase inhibitor

Blocks activation of lymphocytes and secretion of cytokines

36
Q

Side effects of DMARDs

A

Increased incidence of serious infections
Allergic reactions
Possible malignancies

37
Q

How does Estrogen maintain bone homeostasis

A

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
Q

How does estrogen deficiency cause bone loss

A

Estrogen deficiency leads to increased IL1B and TNF-a which lead to increased levels of RANKL and increased differentiation of Osteoclasts

39
Q

How to aromatase inhibitors lead to bone loss

A

They prevent the conversion of androgens to estrogens in peripheral tissues

40
Q

Antiresorptive drugs

A

Denosumab, Calcitonin, SERMs, and Bisphosphonates

41
Q

Osteoanabolic drugs

A

Teriparatide

42
Q

Bisphosphonates

A

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
Q

SERMs

A

Reloxifene
Estrogen derivates that act as agonists in some tissues and antagonists in others
Inhibit bone resorption without increasing risk of breast cancer

44
Q

Denosumib

A

Anti-RANKL antibody
Acts like OPG to prevent binding of RANKL to RANK
Given by injection once/3-6months
Not recommended in hypocalcemia

45
Q

Calcitonin

A

Reduces osteoclast activity and lowers serum Ca2+

Usually a synthetic salmon calcitonin is used

46
Q

How does PTH affect bones?

A

Increased plasma Ca2+ concentration by increasing osteoclast activity
Increases Vitamin D synthesis in the kidney
Increases kidney absorption of Ca2+

47
Q

How does Vitamin D affect bones?

A

Increases synthesis of Ca2+ binding protein for transport of Calcium out of the gut

48
Q

How does calcitonin affect bones?

A

Decreases bone reabsorption and decreases kidney reabsorption of Ca2+

49
Q

What are common clinical uses for skeletal muscles relaxants

A

Surgical relaxation
Orthopedic Procedures
Intubation with endotracheal tube
Control of ventilation

50
Q

What are the non-depolarizing blockers of nAchR

A 
D-turbocurarine 
Pancuronium
Vecuronium
Atracuronium
Rocuronium
Mivacurionium
51
Q

What is the mechanism of non-depolarizing blockers

A

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
Q

What is the prototype depolarizing blocker?

A

Succinylcholine

53
Q

How do depolarizing blockers work?

A

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
Q

What problems are associated with succinylcholine?

A

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
Q

How are non-depolarizing blocks reversed?

A

Edrophonium or neostigmine in addition to a muscarinic receptor antagonist like atropine to prevent bradycardia.

56
Q

What are the drug interactions of skeletal muscle relaxants

A

Inhaled anesthestics
Local anesthetics
Ca2+ channel blockers
AchE Inhibitors and Neuromuscular blockers
Antibiotics: aminoglycosides and tetracyclines

MSK Personal (12 decks)

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