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Pharmacotherapeutics Exam 5 Part 1 OA/RA

Total questions: 83

Worksheet time: 42mins

Name
Class
Date
1.

NSAIDs affect 3 stages of disease. What are they?

a)

Pain

b)

Inflammation

c)

Fever

2.

What is the max dose of NSAIDs daily?

a)

3200mg/day

b)

4500mg/day

3.

NSAID example medications?

a)

Aspirin, Celecoxib

b)

Diclofenac, Indomethacin

c)

Ketorolac, Piroxicam

d)

Meloxicam

4.

NSAID Mechanism of action?

a)

Inhibit Cyclooxygenase Enzyme

b)

Degranulation of mast cells

5.

Drug specific to COX-2 receptor?

a)

Celecoxib (Celebrex)

b)

Pregabalin (Lyrica)

6.

COX-1 is mostly found ___ and COX-2 is found in ____.

a)

GI mucosa and other tissues ; Injury site

b)

Injury site ; GI mucosa and other tissues

7.

NSAID absorption, metabolism and excretion?

a)

Absorbed rapidly from GIT

b)

90% bound and carried to inflammation site by albumin

c)

Metabolized by liver

d)

99% excreted in urine

8.

Adverse drug reactions of NSAIDs?

a)

Fluid retention = (remember the afferent arteriole is constricted)

b)

Abd pain/Cramps (decreased prostaglandin synthesis leads to risk of injury)

9.

NSAIDs block?

a)

COX-1 and COX-2

b)

COX-1 Only

c)

COX-2 Only

10.

Half life of NSAIDs?

a)

2-4 hours, but variable

b)

88 hours exactly

11.

NSAID drug interactions?

a)

Antihypertensives (inhibited by NSAIDs, we'll review this when we do clin med Nephro)

b)

Decreased Platelet aggregation occurs with anticoagulants leading to increased risk of GI bleed

12.

Aminoglycoside drug interaction with NSAIDs?

a)

Decreased renal clearance (why?)

b)

Increased renal clearance

13.

Corticosteroid use with NSAID drug interaction?

a)

Increased risk of GI bleed

b)

Decreased risk of GI Bleed

14.

Contraindications to NSAID?

a)

Peptic Ulcer Disease (PUD)

b)

Chronic GI Inflammation

15.

Aspirin is considered? (2 are right, Possesses analgesic, antipyretic, and antiplatelet properties)

a)

Prototype drug for Non-Narcotic Analgesics

b)

Considered an NSAID

c)

Considered an antcoagulant

16.

Aspirin mechanism of action? (2 are right)

a)

Inhibits prostaglandin and thromboxane synthesis, providing its NSAID and Antiplatelet effect

b)

Acetylates Serine at platelet Cyclooxygenase preventing Thromboxane A and decreasing platelet Aggregation

c)

Destroys platelets

17.

Aspirin inhibiting effect lasts?

a)

Until new platelets are formed (8 days)

b)

Until Plasmapheresis is done

c)

Until new WBC are formed

18.

Aspirin absorption, metabolism and excretion?

a)

Salicylates (Aspirin) is rapidly absorbed with 1-2 hour peak

b)

Metabolized by liver

c)

Excreted in urine

d)

3-6 hours half life of small doses // high doses is 15-30 hours

19.

Aspirin adverse effects?

a)

GI intolerance due to decreased prostaglandin synthesis = decreased

b)

Hematology: Antiplatelet effect

c)

Metabolism: Acid-Base Imbalance

d)

Neuro: Toxic doses may cause convulsions and depression

20.

Renal ADR of ASA?

a)

low doses such as 2 grams or less decrease urate excretion which is needed for uric acid excretion

b)

low doses such as 2 grams or less Increase urate excretion which is needed for uric acid excretion leading to more uric acid pumped out

21.

Acetaminophen DOES NOT have what compared to ASA?

a)

Gastritis, Ulceration

b)

Inhibition of platelets effect caused by ASA effect

22.

Aspirin drug interactions? (discuss why! Important for nephro)

a)

ACEi

b)

Beta Blockers

c)

Loop Diuretic

d)

Thiazide Diuretic

23.

APAP acute overdose may cause?

a)

Hepatic Necrosis

b)

Creudzfeldt Jakob Disease

24.

APAP max dose?

a)

4 grams (4000 mg)

b)

6000mg

25.

APAP clinical uses?

a)

Analgesic

b)

Antipyretic

c)

MILD forms of arthritis

26.

APAP Mechanism of action?

a)

Raise pain threshold by inhibiting nitric oxide pathway that would act on substance P and NMDA receptors

b)

Narrow pain threshold by inhibiting nitric oxide pathway that would act on substance P and NMDA receptors

c)

Blocks production of prostaglandin release into CNS = no effect on anterior hypothalamus = prevents increase in body heat and preventing retention of heat

27.

Why would you choose APAP vs NSAIDs?

a)

Patient on anticoagulation

b)

Allergy to ASA

c)

Children preferred because it is not associated with Reye Syndrome

28.

Absorption, metabolism, half life and excretion of APAP?

a)

85-98 % absorbed

b)

Does not enter fat tissue and metabolized by liver

c)

Excreted in urine

d)

Half life of 1-4 hours

29.

What can alter absorption of APAP?

a)

Diseased states or meds that delay gastric emptying

b)

xx

30.

GU/GI APAP adverse effects?

a)

Hepatic Failure with high doses

b)

Renal Failure with high doses

31.

APAP drug interactions?

a)

Warfarin effect increased with 2 grams or more

b)

Alcohol increases hepatic toxicity

c)

Carbamazepine, Isoniazid and Rifampin decrease APAP effect

d)

Cholestyramine decrease absorption of APAP

32.

Is APAP safe in pregnancy?

a)

Yes, it also crosses placenta and little bits into breast milk

b)

xx

33.

Contraindications to APAP?

a)

Liver disease

b)

Restless leg syndrome

34.

Synthetic prostaglandin analogue can be used for? What is the name of the drug?

a)

Prevention of gastric mucosa damage by NSAIDs

b)

Misoprostol

c)

Carbamazepine

d)

Phenytoin

35.

MOA for Misoprostol and ADR of Misoprostol?

a)

Affect basal and nocturnal acid secretion to prevent ulceration

b)

Miscarriage and menstrual disorder

c)

Increase gastric acid secretion

d)

Increases T3 and T4

36.

Misoprostol Drug Interactions?

a)

Increased toxicity of methotrexate, digoxin, cyclosporine and lithium

b)

Hyperkalemia with K+ sparing diuretics

37.

Ibuprofen MOA and when does it have an antiplatelet effect?

a)

Only when in the blood

b)

Inhibits COX, blocking prostaglandin synthesis

c)

Proton Pump Inhibitor

d)

In the urine

38.

Ibuprofen absorption, metabolism, excretion and half life? ADR?

a)

Absorbed rapidly and readily in GIT, bound to albumin

b)

Hepatic Metabolism, Renal Excretion, Half Life of 2-4 hours

c)

Prolonged bleeding time and thrombocytopenia, GI Bleed and Drowsiness

39.

Ibuprofen drug interactions? Ibuprofen increases the risk of bleeding with which drugs?

a)

Limits cardioprotective effect of ASA

b)

Increased Hypoglycemia effect and increased effect with NSAID, ASA, and Corticosteroid

c)

Cefotetan, Valproate and Anticoags increase bleeding risk

40.

CI to ibuprofen + Chewable ibuprofen is contraindicated in ___ because ____.

a)

CI to Ibuprofen are Cardiovascular Dz, Hepatic Dz

b)

Pheynketonuria ; it contains Aspartame

41.

Meloxicam Clinical Use and MOA?

a)

OA, RA, Juvenile Arthritis

b)

Increased inhibition of COX, leading to decreased prostaglandin synthesis

c)

Decreased inhibition of COX, leading to decreased prostaglandin synthesis

42.

Meloxicam absorption, metabolism, and excretion? ADR?

a)

Levels Prak in 4-5 hours; Metabolized by liver; Excreted in urine; Halflife of 15-20 hours

b)

ADR: SJS, TEN, Abnormal LFT's, Anemia, Leukopenia and Thrombocytopenia

c)

ADR: Priapism

43.

Nephrotoxicity by COX2 inhibitors is worse why? Meloxicam drug interactions?

a)

Nephrotoxicity because: Kidney expresses COX2

b)

Decreases antihypertensive effect of ACEi

c)

Reduce diuretic effect of thiazides and loop diuretics

44.

Example of a COX-2 inhibitor? Clinical use of COX-2 inhibitor?

a)

Celecoxib

b)

RA, OA, Dysmenorrhea

c)

Malaria

d)

Aspirin

45.

MOA for COX-2 inhibitors? COX-2 absorption, metabolism, excretion and half life?

a)

Inhibits prostaglandin synthesis by blocking COX-2 with little to no effect on COX-1 and no antiplatelet activity

b)

Well absorbed orally, Metabolized by liver, Excreted in urine and feces, Half life of 11 hours

c)

Enhances prostaglandin synthesis by blocking COX-2 with little to no effect on COX-1 and no antiplatelet activity

46.

COX-2 inhibitors ADR? Drug interactions?

a)

Increased risk of MI/CVA, Swelling of extremities, Black tarry stools, Vomit, Wt gain

b)

Renal Toxicity, Tiredness and Flulike symptoms

c)

Increases effect of Warfarin

d)

Other drugs that have bad interactions are Diazepam, Glyburide, Estradiol, Omeprazole and ASA

47.

Contraindication to Celecoxib? Step up therapy for Hip OA?

a)

Renal failure and CVD are contraindications

b)

Step up therapy: Lifestyle Mod, APAP, NSAID, Glucosamine/Chondroitin, Opiod, CCS, Hyaluronic Acid, Hip Arthroplasty

48.

Drugs such as methotrexate produce only 18-20% reduction in symptoms after? AND Methotrexate is issued as a?

a)

1 year

b)

3 years

c)

Administered as a weekly schedule

d)

Administered as a yearly schedule

49.

Examples of DMARDs? (Disease Modifying Anti Rheumatic Disease) (Enbrels Ritual to Orencia was HUM, RAP and REM)

a)

Enbrel, Humira

b)

Orencia, Raptiva

c)

Remicade, Rituxan

50.

Methotrexate is a ____. What drug can be used to reduce methotrexate toxicity?

a)

Methotrexate is : Antimetabolite, antineoplastic, and immunosuppressant and a DMARD

b)

Leucovorin can be used to decrease toxicity but reduces effect and does not reverse neurotoxin

c)

Methotrexate is : An antacid

51.

Methotrexate clinical use? Methotrexate MOA?

a)

Can be used for: Psoriasis, SLE, Sarcoidosis, Rheumatoid Arthrits

b)

Can be used for: Antifolate property for lung, head/neck, breast cancer and leukemia

c)

MOA: Folate Antimetabolite that inhibits DNA Synthesis, Unknown Mech in Arthritis but thought to work by Cel ANTIPROLIFERATION

52.

Methotrexate absorption, metabolism, excretion and half life?

a)

Absorbed readily in GIT in small doses, large doses incompletely absorbed

b)

Slow delivery to tissues, Hepatic Enzymes convert to inactive metabolite, 90% unchanged dose and metabolite is excreted in URINE

53.

Methotrexate ADR? Hematologic Toxicity when taking methotrexate is increased when? READ WELL!!!

a)

ADR: Transient blindness, Mucosal Ulcer, Hep Toxicity, Anorexia, Infertility

b)

ADR: Blood Problems, Nephropathy, Soft Tissue Necrosis, Pulm Fibrosis

c)

Hema Tox Worse When: given with high dose ASA, NSAID, Oral Hypoglycemics, Tetracyclines and Sulfonamides

54.

Any drug that competes with methotrexate for excretion can lead to? AND What stimulant will lower effect of methotrexate?

a)

Kidney/Liver Disease can result

b)

Caffeine will lower the effect

c)

Water will lower the effect

d)

Tourette can result

55.

What herbs can interfere with immune suppression effect of methotrexate? Methotrexate is CI in? (3 are right)

a)

Herbs: Echinacea, Melatonin

b)

Herbs: Albaca, Romero

c)

CI: Women AND MEN attempting pregnancy

d)

Men should wait 3 months before attempting because of teratogenic effects

56.

Leflunamide is an immunomodulator and what should you check when using this drug? Leflunomide MOA? (READ CAREFULLY)

a)

MOA PART 1: Ibhibits de novo ribonucleotide synthesis, arrests cell in G1 Phase= inhibition of Enzyme Required for Pyrimidine Synthesis

b)

MOA PART 2: Alleviates pain and inflammation = slow progression of dz and improves joint function

c)

Check ROM, Swelling and Pain

d)

Check Bilirubin and Alk Phosphate

57.

Leflunomide absorption, distribution, and excretion? Drug Interactions? (half life is 4-18 days)

a)

80% absorbed, rapidly converted to active metabolite

b)

99% Protein Bound, Half Excreted in feces and Half in urine

c)

Interactions: Any hepatotoxic drugs

d)

Interactions Water

58.

Adverese effects of leflunomide? Leflunomide Contraindications?

a)

ADR: Alopecia, Rhinitis, Cell turnover of B&T cells is increased leading to increased bilirubin, Abn LFTs, Synovitis

b)

Contraindiated in Pregnancy and Liver Disease

59.

Hydroxychloroquine requires frequent eye exams because?

a)

Causes irreversible retinopathy leading to blindness

b)

It causes Drussen spots to appear

60.

Hydroxychloroquine is a ___ drug, and is used for?

a)

Last resort ; Antirheumatic, SLE, Suppress Malaria

b)

1st line ; Antirheumatic, SLE, Suppress Malaria

c)

Last resort ; Antiarrhythmic

61.

MOA for Hydroxychloroquine and ADR?

a)

MOA: suppress T cell response to mitogens to treat RA

b)

ADR: Bleaching of hair, Ototoxicity, Cramps, Agranulocytosis, Psychosis

c)

MOA: Increase T cell response to mitogens to treat RA

d)

ADR: Priapism

62.

Hydroxychloroquine absorption, distribution, metabolism, excretion and half life? CI to Hydroxychloroquine?

a)

Safer Orally and rapidly aborbed from GIT, Slow distribution, Metabolized by liver, Excreted by urine, Half life 30-60 days

b)

Contraindications: Liver Disease, Renal Disease, Alcohol Use

63.

Hydroxychloroquine drug interactions?

a)

Drugs requiring biliary excretion result in increased hepatotoxicty

b)

Drugs requiring biliary excretion result in decreased hepatotoxicty

64.

Penicillamine chelates Copper, Iron, Mercury, and lead to form complexes to excrete?? Indication?

a)

to excrete Copper and also helps with chelating Cysine Complexes to decrease Cystine Stones

b)

Indicated for: RA Juvenile Arthritis

c)

Indicated for Restless leg syndrome

d)

to excrete water

65.

Penicillamine absorption, metabolism, excretion and half life? Penicillamine MOA?

a)

Only 50% absorbed, liver metabolism, found in urine and feces unchanged or as metabolite, 1.7-3.2 hours is the half life

b)

MOA: Decrease cell mediated immune response, inhibits collagen formaation= anti inflammatory

c)

MOA: Increase cell mediated immune response, inhibits collagen formaation= anti inflammatory

66.

Penicillamine ADR? Drug Interactions? Contraindications?

a)

ADR: Leukopenia, White Papules on Venipuncture, Hot flashes

b)

Drug Interactions: Cross reactivity with PCN, Mg and Aluminum hydroxide Antacid block absorption

c)

Contraindicated in pregnancy, aplastic anemia, and renal failure

67.

Gold Compounds are used to treat inflammation, drawbacks? And Myochrysine is used to treat?

a)

Drawback: Very short acting and toxic, LAST RESORT as well.

b)

Myochrysine is used to treat Juvenile arthritis

c)

Myochrysine is used to treat HIV-1

68.

Any minor reaction to a gold compound warrants? Gold copound drug drug interaction?

a)

Discontinuation of gold compound is warranted with any reaction

b)

No drug-drug interactions are noted

c)

Water interaction

69.

Examples of Gold Compound? (RSM)

a)

Ridaura (Auranofin)

b)

Solganal (Aurothioglucose)

c)

Myochrysine (Gold Sodium Thiomalate)

d)

Figure it out LOL

Ridaura Solganal some Myochrysine

70.

Gold compounds mechanism of action? ADR? Contraindications?

a)

Interferes with IL-1 and TNF, inhibit phagocyte function and decrease their antiinflammatory mediators. IM Gold salts are used to treat synovitis but not curative

b)

ADR: Oral ulceration, altered taste is SUPER COMMON, Nephritic Syndrome, Blood Dyscrasias

c)

CI: Hx of Blood disorders, CHF, Dermatitis

71.

Examples of TNFinhibitors

a)

Etanercept (Enbrel)

b)

Infliximab (Remicade)

c)

Anakinra (Kineret)

d)

(AEI = Ana Etane and Inflix)

72.

Patients on TNFi require that they be monitored for? Indicated for?

a)

Monitor for: Latent or active TB

b)

Indicated for: Moderate to severe Rheumatoid Arthritis

c)

MIld RA

73.

What drug may be used concurrently with TNFi? What GI disease that is a moderate to severe can be treated with TNFi?

a)

Concurrently with: Methotrexate

b)

Other GI Dz: Crohn's

c)

Other GI Dz: Hirschsprung's

74.

Etanercept/Infliximab can be used for?

a)

Moderate to severe RA or inadequate response after DMARD

b)

Mild RA

75.

Etanercept MOA? Choose both

a)

Protein that acts as a TNFi, developed by recombinant DNA synthesis

b)

Interfere with inflammation cascade initiated by TNF= Lowering Cytokines, by inactivating them and unable to drive inflammation response of cell surface receptors found in synovial fluid in those with RA

76.

Infliximab MOA?

a)

Chimeric monoclonal AB

b)

Neutralizes and prevents TNF-alpha = anti-inflammatory and anti-proliferative activity

77.

Anakinra Mechanism of action?

a)

Blocks action of IL-1 and is an immunomodulator

b)

Increases action of IL-1 and is an immunomodulator

78.

Absorption of Anakinra? Etanercept? Infliximab?

a)

Anakinra is not stored or accumulated in tissue after daily SC doses

b)

Etanercept is well absorbed post SC dose

c)

infliximab is well absorbed due to IV administration

79.

Excretion of TNFi?

a)

Anakinra excreted in urine

b)

Others are unknown

80.

Distribution and metabolism of of TNFi?

a)

Unknown

b)

Liver

c)

Lung

81.

Half Lives of TNFi?

a)

Infliximab has longest

b)

Anakinra is lowest half life

c)

Etanercept is in between the others

82.

ADR of TNFi? Drug Interactions?

a)

ADR: Oral and Tooth Pain, Involuntary muscle spasm, Increased URI

b)

Drug Interactions: None

c)

Drug interactions: Metformin

d)

ADR: Priapism

83.

CI to TNFi?

a)

Patients with serious infections

b)

People with infectious TB or latent TB

c)

People with leg pain

d)

People with finger pain