Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Musculoskeletal System Pharmacology > Flashcards

Musculoskeletal System Pharmacology Flashcards

1
Q

NSAIDS

A

Nonsteroidal anti-inflammatory drugsare anti-inflammatory, analgesic, and antipyretic agents

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

Examples of NSAIDS

A

Ibuprofen, naprozen, indomethacin, ketorolac and aspinr

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

MOA NASIDS

A

Reversible inhibition of cox1 and cox2 which blocks prostaglandin synthesis, along withthromboxane and prostacycline synthesis

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

What can NSADS decrease

A

Inflammation, pain, fever, and platelet aggregation

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

Side effects NSAIDS

A

Renal ischemia, interstitial nephritis, and gastric ulcers

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

Indications for NSAIDS

A

Anti-inflammatory
Analgesic
Fever
Closure of PDA

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

Anti-inflammatory NSADIS

A

Inhibit cox2

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

Analgesic NSAIDS

A

Inhibition COX 1 and 22

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

NSAIDs fever

A

Block PGE2 via COZ inhibition

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

NSAIDS closure of PDA

A

PGE1 is responsible for the potency of ductus arteriosus NSAID block PGE1 and close PDA

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

MOA NSAIDS

A

Reversible inhibit COX1 and 2 which results in inhibition of production of prostagladins and thromboxanes

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

If COX is inhibited, ___ cannot turn into prostagladins

A

Endoperoxides, preventing PGs from performing their role in inflammatory responses, pain processing and fever production

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

Side effects NSAIDS

A

Interstitial nephritis
Gastric ulcer
Renal ischemia

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

Interstitial nephritis from NSAID

A

Fever, rash, hematuria, CVA tenderness

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

Gastric ulcer nsaids

A

COX1 make PGs that help maintain the protective GI mucosal barrier in the stomach and intestines.

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

Renal ischemia NSAIDS

A

Decrease renal blood flow and renal damage from the vasodilator PGs

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

Aspirin /acetylsalic acid

A

Anti inflammatory, antipyretic, analgesic and antiplatlet drug
It is an NSAID

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

Asprin is an NSAID, but its MOA differs.

A

Irreversibly inhibits COx1 and 2 others do irreversibly

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

Indications for asprin

A

Fever, pain and headache, CVD

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

Fever asprin

A

Blocks PGE2

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

Asprin pain and headache

A

Inhibits COX1 and 2

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

Asprin CVD

A

Prevent MI and ischemic stroke

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

MOA asprin

A

Irreversible inhibition of COx1 and 2 inhibiting production of PG and TX

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

Cell membrane phospholipids are turned into arachidonic acid by _____

A

Phospholipase a2

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

Arachidonic acid is turned into COX 1 and 2 by what

A

Cyclooxygenase pathway

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

Arachidonic acis is turned into leukotrienes by what

A

Lipooxygenase pathway

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

COX1 (physiologic)

A

Prostagladins, thromboxane (stomach, intestine, kidney, platelets) mucosal protection, renal blood flow and haemostasis

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

COX2 (inducible)

A

Prostagladins

(Inflammatory sites, macrophages, synovocytes) inflammation pain and fever

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

Leukotrienes (inflammatory sites) inflammation

A

Inflammation

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

Side effects asprin

A 
Reye’s syndrome
Tinnitus
Peptic ulceration
Mixed acidosis/alkalosis
Nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Reye’s syndrome asprin

A

In kids with viral infection -cause microvesicular stratosphere of hepatocytes, hepatoencephalopathy and potentially death

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

Tinnitus asprin

A

3g or more a day may cause ruining possibly due to activation of cochlear NMDA receptors

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

Peptic ulcer asprin

A

PG by COX1 help maintain the protective GI mucosal barrier in the stomach and intestines. Block can get ulcer

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

Asprin and mixed acidosis/alkalosis

A

Initial respiratory alkalosis due to hyperventilation and then metabolic acidosis
Presents as a mixed respiratory alkalosis and metabolic acidosis

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

Nephropathy asprin

A

Renal ischemia due to decreased renal blood flow, renal papillary necrosis or intestinal nephritis

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

Functions of asprin

A

Inhibiting platelet aggregation and as NSAID

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

Indication for asprin

A

Fever, pain, inflammatory conditions, prevention of thrombotic events

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

Side effects asprin

A

GI ulcer, bleeding, pancytopenia

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

Who should not be given asprin. Why

A

7-10 days after surgery or kids under 12

Reye’s syndrome

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

How does asprin inhibit platelet aggregation

A

Irreversible and by inhibiting cyclooxygenase

Effects will last as long as lifespan of the platelet (8 days)

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

NSAID asprin

A

Inhibit COX

Low dose-pain
High does-anti inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Indications for asprin

A

Thrombotic event prevention
General pain
Inflammatory conditions
Fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Asprin thrombotic event prevention

A

Stroke, MI, also colorectal cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Inflammatory conditions that asprin can help

A

Arthritis, RA, osteoarthritis, rheumatic fever, tendinitis, bursitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Side effects asprin

A

Pancytopenia
GI ulcers
Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Pancytopenia and asprin

A

Aplastic anemia, agranulocytosis, thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why not give asprin 7-10 days after surgery

A

It inhibits platelet aggregation for the entire lifespan of the platelet around 8 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is patient is on asprin before surgery

A

Increased risk of hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Reye’s syndrome

A

Kids under 12 taking asprin
usually when taking when recovering from chickenpox or other viral

Never give kids asprin when recovering from an illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Asprin poisoning is called what

A

Salicylism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Early symptoms of salicylism

A

Nausea vomiting (pH)
Tinnitus
Confusion (pH affect brain caused by hyperventilation or metabolic acidosis)
Hyperventilation (compensatory response—>respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Late symptoms of asprin poisoning

A 
Metabolic acidosis (compensatory)
Coma (pH changes )
Hyperthermia (may result in seizure or diaphoretic state)
53
Q

Reye’s syndrome

A

Asprin in kids with viral illness such as chicken pox or flu

54
Q

What can we use in kids recovering from illness instead of asprin

A

Acetaminophen

55
Q

What is Reyes

A

Affects various organs throughout the body including fatty changes int he liver. As the child s liver begins to fail, lab results may show increased liver enzymes, such as ast, ALT and increased ammonia levels.

56
Q

Characterization of Reyes

A

Acute encephalopathy

57
Q

Early detection and treatment of Reyes is essential as death may result within hours if left untreated

A

Oh god

58
Q

Assessment for Reyes

A

Cerebral edema-seizures/decreased consciousness

Lethargy-tired weak
Vomiting-common

Liver failure-fatty changes should check AST ALT and ammonia

59
Q

Treat reyes

A

Early detection
Monitor OCP, respiratory rate, and bp

Give mannitor

60
Q

Increased ICp

A

Cerebral edema

Changes in consciousness, headache, vomiting, abnormal/asymmetrical pupils and posturing

61
Q

Mannitor

A

Osmotic diuretic treats ICP. Works by creating an osmotic gradient that pulls fluid from the brain into the vasculature and provides an immediate plasma expanding effect that reduces hematocrit and blood viscosity and leads to diuresis

62
Q

No asprin for kids

A

Use acetaminophen

63
Q

Ibuprofen (Advil Motrin)

A

NSAID that functions by inhibiting COX

64
Q

Indication ibuprofen

A

General pain, fever, inflammatory conditions

65
Q

Side effects ibuprofen

A

GI ulcers, nephrotoxicity, rash

66
Q

Why no take ibuprofen with alcohol

A

Increase risk of GI irritation and bleeding, decreases platelet aggregation which is further produced with alcohol use

67
Q

Risk of thrombotic event with ibuprofen

A

Selective COX2 inhibitor

68
Q

Why do we not get risk of thrombotic event when COX1 and 2 are inhibitred

A

COX1 decreases platelet aggregation which does not occur with selective COX2 inhibitors

69
Q

Acetaminophen(Tylenol)

A

Anti-pyretic and analgesic drug that lacks the anti-inflammatory or anti platelet effects seen with asprin and NSAIDS

70
Q

Acetaminophen reversible or irreversible

A

Reversible inhibiting COX and having centrally activity

71
Q

Indications acetaminophen

A

Fever

Pain

72
Q

MOA acetaminophen

A

Reversible inhibit COX

Acts in CNS -useful for fever and headache

73
Q

Side effects acetaminophen

A

Hepatic necrosis

N-acetylcysteine antidote

74
Q

Hepatic necrosis acetaminophen

A

5% metabolized by CYP enzymes to NAPQI, which is conjugated with glutathione

75
Q

What happen with high doses of acetaminophen

A

NAPQI accumulate and cause centrilobular hepatic necrosis due to biding and damage to hepatic proteins and increased susceptibility to reactive oxygen species

76
Q

N-acetylcysteine

A

Antidote to acetaminophen toxicity.

It is a glutathione precursor that when given can help result in conjugation and NAPQI.

77
Q

What is rumack Matthew normogram

A

Used to determine whether treatment with N-AC is required and N-AC can be given within 8 hours of acetaminophen ingestion

78
Q

Celecoxib

A

COX2 selective NSAID that lacks many of the toxic GI effects of other NSAIDS that have COX1 inhibitory effects in addition to COX2

79
Q

Indications for celecobix

A

RA, osteoarthritis, pain

80
Q

MOA celecobix

A

NSAID but selectively blocks COX2 little effect on 1

SO NO GI effects

81
Q

Side effects celecoxib

A

It is a sulfonamide-sulfa allergy increased risk of thrombosis (COX2 on vascular endothelial cells get decreased prostacyclin production and platelet aggregation)
GI bleed-spares COX1, but patients with history still occur

82
Q

Who should not take celecoxib

A

Pregnan tover 30 weeks

Category D drug

83
Q

Describe passage of acetaminophen

A

Rapidly absorbed from the stomach and AI and primarily metabolized by conjugation in the liver to nontoxic water soluble compounds that are eliminated in the urine,

84
Q

Overdose acetaminophen

A

Metabolism by conjugation becomes saturated and excess acetaminophen is oxidatively metabolized by CYP enzymes to the reactive metabolite NAPQI

85
Q

NAPQI

A

Extremely short half life and is rapidly conjugated with glutathione stores and really excreted

86
Q

Excess NAPQI

A

From increased formation or decreased glutathione
Covalently binds to cysteinyl sulfhydryl groups of hepatocellular proteins causing a cascade of oxidative damage and mitochondrial dysfunction

This inflammatory response propagates hepatocellular injury, death, and centrilobular (zone III) liver necrosis

87
Q

Antidote to acetaminophen poisoning

A

N-acetylcysteine which is.a precursor of glutathione among other mechanisms

88
Q

Prednisone

A

Ok

89
Q

Alendronate (fosamax)

A

Bisphosphonate that suppresses bone resorption and inhibits bone breakdown in individuals with pages disease or those experiencing post menopausal or corticosteroid induced osteoporosis

90
Q

Side effects alendronate (fosamax)

A

Esophageal ulcers, musculoskeletal pain, changes in vision, atrial fib, osteonecrosis of jaw with IV solendronate

91
Q

Why should we take alendronate on empty stomach and upright for 30 min

A

Idk but they must do that to prevent inflammation or irritation of the throat

92
Q

MOA alendronate

A

Inhibits osteoclasts

It incorporates into bone and this inhibits bone resorption which decreases the activity of osteoclasts

93
Q

Indications for alendronate

A

Osteoporosis

Pager

94
Q

Osteoporosis and alendronate

A 
Estrogen inhibits osteoclast 
During menopause we lose
And osteoclast activity
Can lead to increased risk of bone loss 
In men aldonrate works to increase bone mineral density, prevent fractures, and reduce loss of height related to osteoporosis
95
Q

Pa gets disease and alendronate

A

Cause by excessive bone breakdown and abnormal remodeling of the bone

Can prevent further breakdown
Given ca while on it to prevent secondary hyperparathyroidism caused by decrease Ca related to inhibition of bone resorption

Calcitonin may be prescribed for pain relief that occurs with paget

96
Q

Side effects alendronate

A

Esophageal ulcers, MSK pain, vision changes, a fib, osteonecrosis of jaw

97
Q

BRONJ

A

Bisphosphonate related osteonecrosis of the jaw associated with intravenous infusion of zolendronate

98
Q

What is gout

A

Acute inflammatory mono arthritis related to uric acid content which is painful, debilitating, and deforming

99
Q

Treatment of gout

A
  1. Drugs which are give for acute attacks

2. Drugs given for chronic maintence and prevention

100
Q

Chronic drugs for gout

A

Inhibitors of da thing oxidase such as allopurinol and febuxostat,

Inhibitors of uric acid reabsorption in the proximal tubule of the kidney like probencid

101
Q

Acute gout meds

A

NSAIDS, glucocorticoids, colchicine

102
Q

Colchine

A

Impaired leukocyte chemotaxis
It inhibits microtubule polymerizationby binding to tubules. As tubules is important for mitotic function, it works as a mitotic poison . This inhibits cytoskeleton recruitment, impairing leukocyte chemotazis and degranulation

103
Q

Allopurinol and febuxostat

A

Inhibit xanthine oxidase

104
Q

Probenecid

A

Inhibits reabsorption or uric acid in proximal tubule of kidney so excrete more

105
Q

MOA probenecid

A

Interfering with kidneys organis anion transporter, which reclaims uric acid from the urine and returns it to the plasma. Preventing reabsorption or uric acid so it is in pee
For chronic gout

106
Q

TNF-alpha inhibitors

A

Work to block tumor necrosis factor

107
Q

TNFa

A

Released by macrophages and is the master regulator of the inflammatory response in many organ systems and directs other cytokines and lymphocytes to cause cell destruction and inflammation

108
Q

What causes autoimmune disease

A

Overactive immuneresponse

109
Q

What drugs inhibit TNFa

A

Etanercept and infliximab

110
Q

MOA tnfa inhibitors

A

Prevent activation of macrophages and destruction of phagocytosis material helping to treat autoimmune disorders

111
Q

MOA TNFa inhibitors

A

Downregulates proinflammatory cytokines
Decreased lymphocyte activation and migration (fever and hypotension by leukocyte recruitment so this is blocked)
Granuloma breakdown (tnfa needed to induce and maintain granuloma)

112
Q

Indication for TNFa inhibitor

A 
Crowns disease 
RA
Juvenile RA
Psoriasis
Ankylosis spondylitis
113
Q

Crowns

A

Characterized by noncaseating granuloma and lymphoid aggregates leading to transmural bowel wall inflammation

114
Q

RA TNFA inhibitors

A

Cytokines and type III and IV hypersensitivity mediated destruction of synovial joints

115
Q

Juvenile RA and TNFA inhibitors

A

Seronegative arthritis and inflammation of synovial joints, without cause. Treated with newer TNFa inhibiting drugs

116
Q

Ankylosis spondylitis

A

Chronic inflammatory arthritis associated with bamboo spine on x ray and HLAB27 serum protein can be treated with TNFa inhibitor

117
Q

TNFa does what

A

Inflammatory. Process and leads to cachexia and is a potent pyrogen and plays a large role indiseases such as ankylosing spondylitis, RA, crohns and other.

118
Q

Complications of TNFA inhibitors

A

Infection, TB reactivation or dissemination

119
Q

Etanercept

A

TNF decoy receptor which binds to TNF and blunts the immune response

120
Q

Etanercept works as a __ protein, which acts as a TNF decoy receptor

A

Fusion

121
Q

What does etanercept do

A

Mimics the inhibitory effects of naturally occurring TNF receptors but has a longer half life and more profound long standing inhibitory effect

122
Q

Anti TNF a antibody neutralizes the actions of TNFa by working as an anti TNFa antibody. It binds with high affinity to TNF, blunting the inflammatory response by autoantibodies in various disorders

A

Ok

123
Q

Adalimumab

A

Monoclonal antibody and has a high specificity and affinity for TNF a . It has the capability to lyse cells involved in the inflammatory process helping to alleviate symptoms

124
Q

Infliximab

A

Monoclonal antibody and has a high specificity and affinity for TNFa . It has the capability to lyse cells involved int he inflammatory process, helping to alleviate symptoms

125
Q

Complications of TNFa inhibitors infection

Predispose to TB reactivation

A

Ok

126
Q

Why do TNFa inhibitors increase risk of infection

A

Blunting recruitment of other cytokines and lymphocytes preventing activation of macrophages and inflammation leads to an increased risk of infection and patients should be considered immunocompromised

127
Q

Why do TNFa inhibitors predispose to TB reactivation

A

Latendresse TB deactivated as macrophages are inhibited. Granuloma are effectively broken down with these medications, which release and disseminate TB which was encapsulated and isolated

128
Q

What do before put on TNFa inhibitor

A

PPD skin test

Quantiferon gold in tubeorder heat x ray

129
Q

QFT

A

Interferon y release assay used in TB diagnosis . The QFT-GIT assay in Elisa based, whole blood test that uses peptides from there TB antigens in an in tube format. This test has 99% specificity and sensitivities 92

Pharmacology (52 decks)

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