Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Musculoskeletal > Pharm > Flashcards

Pharm Flashcards

1
Q

what mediators does cyclooxygenase produce?

A

prostacyclin (anti-platelet)
prostaglandin E (pain, erythema, edmea)
prostaglandin F (uterine contraction)
thromboxane (platelet aggregation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what mediators does the lipoxygenase pathway produce?

A

leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what part of the arachadonic pathway do glucocorticosteroids inhibit?

A

phospholipase A making arachadonic acid from phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what part of the arachadonic pathway do NSAIDs inhibit?

A

cyclooxygenase 1 and 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

info for COX1

A

expressed in most tissues generating low levels of prostaglandins
responsible for protective measures (gastric mucosa), vasodilation (restricting kidney flow), blood clotting, uterine contraction, muscle growth, and synaptic transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

info for COX2

A

inducible form of enzyme that is expressed in high concentrations after induced by inflammatory mediators producing high concentrations of prostaglandins and thromboxanes leading to inflammation
constitutively on in kidneys and some parts of brain (local inflammation, wound healing, resistance to infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what compound do cyclooxygenases require?

A

molecular oxygen!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what other mediator is critical for inflammatory conditions?

A

NFkB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

info on NFkB

A

activated by many signals and induces expression of cytokines (IL-1,6), INFB, cell adhesion molecules, enhancing inflammatory process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what signals activate NFkB

A

infection (LPS, dsDNA)
antigen receptors (TCR, BCR)
cytokines (TNFalpha, IL-1)
genotoxic stress (UV, gamma-radiation, ROS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

COX1 predominant..?

A

platelets to make thromboxane causing vasoconstriction and platelet aggregation
gastric mucosa to provide protection via prostaglandins E and I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

COX2 predominant…?

A

joints - where prostaglandins E and I produce pain and inflammation
endothelial cells - where prostacyclins decrease platelet aggregation and increase vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is aspirin?

A

acetyl salicylic acid which is an irreversible, non-selective cox inhibitor via acetylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the reversible, non-selective COX inhibitors?

A

ibuprofen, naproxen, indomethacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is salicylate

A

also a non-selective, reversible COX inhibitor but it is a weak one that may be more important in NFkB inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is acetaminophen?

A

an analgesic and antipyretic and weak anti-inflammatory; it is a weak inhibitor of COX
often used in babies for headache and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do glucocorticoids block?

A

phospholipase A (block arachadonic acid production), inhibit NFkB, COX2, inflammatory cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are some things we treat with COX inhibitors?

A

headache, dental pain, muscle pain, menstrual cramps, osteoarthritis, ankylosing spondylytis, RA, gout, tendonitis, bursitis - provide symptomatic relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

problem with aspirin?

A

patients can sometimes not tolerate its gi toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

NSAID toxicity?

A

gi ulcers, inflammation, gastric erosion
decreased GFR, renal edema, necrosis, nephritis
hypertension, allergic hypersensitivity reaction, CNS toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what should you give kids?

A

acetaminophen, not aspirin which can cause Reye’s syndrome (liver and brain swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why take daily does of aspiring?

A

decreases risk of MI and ischemic stroke; long term use can decrease cancer incidence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

why take other NSAIDs with daily dose of aspirin?

A

to attenuate the anti-platelet affects of aspirin (i.e. make them less effective)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is bartter’s syndrome and what do we use for it?

A

renal problems - NSAIDs reverse symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is patent ductus arteriosus? and what is used for it?

A

improper duct closure - NSAIDs allow ducts to close in premature babies without surgical intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is aspirin metabolized to?

A

salicylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the NSAIDS with short half-lives?

A

aspirin, ibuprofen, indomethacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the NSAIDs with long half-lives?

A

naproxen, salicylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why are acetaminophen and chronic alcohol use a problem?

A

because ethanol induces CYP2E1 which causes acetaminophen to turn into NAPQI which normally combines with glutathione, but once that is used up it reacts with liver proteins and becomes heptatoxic and necrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

where are most NSAIDs normally located?

A

albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

which COX is needed for normal renal development and function?

A

COX2 - prostaglandin synthesis is important for autoregulation of renal blood flow - so non-selective and selective COX2 inhibitors may affect renal efficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

which mediator modulates vascular tone?

A

prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

which NSAID can cause asthma?

A

aspirin in sensitive people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

drug interactions with NSAIDs?

A

drugs bound to albumin (warfarin, phenytoin, sulfonylureas, methotrexate) - makes them more potent
inhibition of drug metabolism of phenylbutazone
inhibits acids transport in kidneys - probenecid
increased GI bleeding after alcohol
hypotensive effects reduced for beta-adrenergics, ARBs, ACEi, diruetics
lithium clearance inhibition (increases toxicity)
postassium-sparing diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

RA and phospholipids?

A

the phospholipids get released and are converted to the endoperoxidase precursors and then into prostacyclin, prostaglandin, and thromboxanes - make inflammatory process worse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are DMARDs?

A

disease-modifying anti-rheumatic drugs

do not immediately decrease symptoms, take a long time to decrease symptoms becuase they delay they disaease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

DMARDs are often taken with…?

A

NSAIDs - they provide rapid relief for symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are the DMARDs that are immunosuppressive agents?

A

glucocorticoids, gold sodium, methotrexate, leflunomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the DMARDs that are TNFalpha blockers?

A

enteracept, infliximab, adalimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are other DMARDs?

A

anakinra (IL-1 receptor antagonist)

tocilizumab (IL-6 mAB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are some side effects of methotrexate?

A

anorexia, vomiting, abdominal cramps, infection, lymphomas, mucosal ulcers, leukopenia

42
Q

how do methotrexate and leflunomide work?

A

they prevent B cell proliferation/maturation (maybe?) and block IgM/Rheumatoid factor release

43
Q

what does leflunomide specifically inhibit?

A

dyhydroorate dehydrogenase which is important in lymphocyte proliferation

44
Q

what is entercept?

A

a TNF alpha-trap; it binds to TNF alpha preventing it from stimulating TNF-alpha receptors

45
Q

what is infliximab?

A

a TNF-alpha mAB that binds to free TNF-alpha

46
Q

what is anakinra?

A

naturally occurring IL-1 receptor antagonist completely inhibiting inflmmatory actions of IL-1

47
Q

side effects of TNF-alpha inhibitors?

A

increased incidence of serious infections, allergic reactions

48
Q

what is rilanocept?

A

an IL-1 Receptor trap

49
Q

what does estrogen do in bone?

A

it stimulates osteoclast apoptosis, suppresses osteoblast apoptosis

50
Q

what does reduced estrogen levels post-menopause lead to?

A

decrease in bone mass because you lose the blockage of osteoclasts by estrogen

51
Q

what is the relationship between OPG and estrogen?

A

as you decrease estrogen, you decrease OPG, and so more RANKL binds to RANK, more osteoclast activity

52
Q

what are anti-resorptive/anticatabolic drugs?

A

they block maturation of osteoclasts or induce apoptosis in osteoclasts, inhibiting bone reporption

53
Q

what are some antiresorptive/anticatabolic drugs?

A

bisphosphonates, SERMs, denosumab, calcitonin

54
Q

what do bisphosphonates do?

A

they bind to hydroxyapatite crystal during bone remodelling and then when osteoclasts go to resorb bone, they are released, bind to osteoclasts and induce apoptosis - have long term effects because deposited in bone

55
Q

what can you use bisphosphonates for?

A

osteoporosis, paget’s disease, metastatic bone disease

56
Q

what are some bisphosphonates?

A

alendronate and zoledronic acid

57
Q

what are side effects of bisphosphonates?

A

GI side effects, osteonecrosis of jaw rare, after 5 year small increased risk in femur fractures???not clear

58
Q

why don’t we use estrogen replacement therapy?

A

because it is linked to increased risk of breast cancer

59
Q

what are SERMS?

A

selective estrogen receptor modulators - they act beneficially in some tissue (bone, brain, liver) and antagonistically in others - they decrease ER in breast cancer, agonists in bone, this is due to the different availability of TxFs in different tissues

60
Q

what is an example of a SERM?

A

raloxifene, bazedoxifene, iasofoxifene

61
Q

what are TSECs?

A

tissue selective estrogen complexes - combine SERM with estrogen - to give a little estrogen back but blocking its negative effects

62
Q

what does denosumab do?

A

binds to RANKL, its a mAB, prevents osteoclast maturation

63
Q

bad thing about anti-resportion drugs?

A

there is no buildup of bone either

64
Q

what are osteoanabolic drugs?

A

they induce osteoblast maturation and decrease osteoblast apoptosis

65
Q

what are the osteoanabolic drugs?

A

PTH (terapatide) and strontium ranelate (not in use)

66
Q

bad thing about osteoanabolics?

A

as you increase OBs, you increase RANKL which increases OCs

67
Q

what does teriparatide do?

A

it is the active portion of PTH and it stimulates osteoblasts and increases bone mass, but may lead to osteosarcoma

68
Q

what do bone morphogenetic proteins do?

A

they promote osteoblast maturation specifically by causing recruitement of mesenchymal stem cells to promote bone healing - often used in surgery

69
Q

what increases serum calcium?

A

PTH, vit D

70
Q

what decreases serum calcium?

A

calcitonin

71
Q

what does PTH do?

A

increases skeletal resorption and deposition depending on situation, decreases calcium excretion, increases vit D synthesis

72
Q

how can PTH stimulate resorption AND deposition?

A

at low concentrations it stimulates bone growth, at high concentrations (which occurs when Ca levels are low) it stimulates bone resorption

73
Q

what does PTH stimulate in the kdiney?

A

1alpha-hydroxylase which hydroxylates Vit D

74
Q

what does vit d do?

A

1,2dihydroxycholecalciferol (aka calciferol) stimulates synthesis of calcium-binding transport proteins in mucosal cells of gut - which increases absorption of calcium

75
Q

what is calcitonin

A

it is made by C cells of thyroid and it inhibits osteoclast activity and decreases calcium resorption in the kidney

76
Q

how do you treat paget’s disease?

A

calcitonin - it inhibits osteoclasts, or bisphosphates

77
Q

what is the nicotinic ACH receptor composed of?

A

5 subunits, 2 alphas which are where the ACh binds - so need 2 molecules to activate receptor

78
Q

NMJ blockers and brain?

A

cannot pass thru BBB - so no affect

79
Q

when ach binds to receptors what happens?

A

get influx of Na, efflux of K (more Na than K), but it then gets densitized quickly after opening

80
Q

what are the two types of NMJ blocking agents?

A

non-depolarizing and depolarizing NMJ blockers

81
Q

what is a non-depolarizing NMJ blocker?

A

an antagonist that competes with ACH for binding pocket, when it binds, it prevents depolarization; causes flaccid paralysis
**direct muscle stimulation causes muscle contraction

82
Q

what are some non-depolarizing NMJ blockers?

A

**tubocurarine

pancuronium, vacuronium, rocuronium, atracurium, mivacurium

83
Q

how do you surmount non-depolarizing NMJ blockers?

A

increase ACH (via ACE inhib)

84
Q

what is a depolarizing NMJ blocker?

A

succinylcholine

85
Q

how do depolarizing NMJ blockers work?

A

they activate, open, and desensitize the ACH receptor and then persist at NMJ because they are resistant to ACE

86
Q

what is phase I of depolarizing NMJ blocker?

A

brief disorganized muscle excitations that lead to fasciculation and then flaccid paralysis due to persistant muscle depolarization because voltage gated sodium channels get inactivated
**muscle contraction cannot be directly stimulated

87
Q

how can you enhance phase I blockde?

A

increaseing ACh by adding ACE inhibitors or neostigmine

88
Q

what ist he phase II blockade?

A

mechanism unknown but get flaccid paralysis

end-plate depolarization decreases and muscle repolarizes and becomes similar to non-depolarizing blockade

89
Q

when do you get the phase II blockade?

A

with high doses or prolonged administration

90
Q

what is a risk of succinylcholine?

A

hyperkalemia due to prolonged K efflux (especially patients with trauma, burns, nerve damage due to denervation supersensitivity)
prolonged apnea from decreased plasma cholinesterase activity
malignant hypothermia

91
Q

what is malignant hypothermia?

A

muscle rigidity and elevated body temp that can occur when give succinylcholine and halothane

92
Q

how do you treat malignant hypothermia?

A

dantrolene which acts on muscle to decrease calcium release from SR to inhibit excitation-contraction coupling

93
Q

when giving ACEs…what else can you give and what should you also give?

A

you can give edorphonium or neostigmine instead of ACEs and you should give a muscarinic AChR inhibitor to prevent bradycardia (like atropine)

94
Q

what is the train of four stimulation paradigm?

A

non-depolarizing: fade
depolarizing phase I: no fade, but diminished
depolarizing phase II: fade

95
Q

how do inhaled anesthetics interact with NMJ blockers?

A

non-depolarizing NMJ potentiation - can use less anesthetic

96
Q

how do local anethetics and calcium channel blockers interact with NMJ blockers?

A

potentiate non-depolarizing and depolarizing ones

97
Q

NMJ blockers can cause bronchospasm how?

A

affecting histamine release

98
Q

which blocker binds to nicotinic and muscarinic?

A

succinylcholine

99
Q

how do you diagnose myasthenia gravis?

A

electrophysio test

give edrophonium and see if get better (a short acting ACE)

100
Q

how do you treat myasthenia gravis?

A

pyridostigmine

Musculoskeletal (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions