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Systemic Pharm Final > Learning Objectives Focused > Flashcards

Learning Objectives Focused Flashcards

1
Q

What is the MOA of the Vitamin K Antagonist Coumadin [Warfarin]?

A

Inhibits Vitamin K dependent coagulation factor synthesis

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2
Q

What is the MOA of the Coagulation Factor Antagonist Enoxaparin [Lovenox]?

A

Irreversibly inactivates clotting factor-Xa much more-so than Factor-IIa (thrombin)
It is LMW heparin extract making it more predictable than normal heparin

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3
Q

What is the MOA of the Coagulation Factor Antagonist Rivaroxaban [Xarelto]?

A

Factor-Xa inhibitor (converts prothrombin to thrombin

Selectively blocks the active site of Factor-Xa, inhibiting blood coagulation.

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4
Q

What is the MOA of the Platelet Inhibitor Clopidogrel [Plavix]?

A

Irreversible inhibition of platelet ADP receptors which normally trigger platelet activation and aggregation via downstream activation of GIIIb/IIa

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5
Q

What is the MOA of the GPIIIa/IIb receptor antagonist Abciximab [ReoPro]?

A

Fab fragment binds to GPIIIb/IIa receptor of human platelets and inhibits platelet aggregation
Binds to vitronectin receptor on platelets and vessels wall endothelial and smooth muscle cells

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6
Q

Specify normal/abnormal total cholesterol.

A

Desirable - 200

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7
Q

Specify normal/abnormal LDL cholesterol.

A

Desirable - 130

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8
Q

Specify normal/abnormal HDL cholesterol.

A

Desirable - >60

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9
Q

Which two statins produce the greatest serum LDL cholesterol reduction?

A

Atorvastin and Rosuvastatin (50%)

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10
Q

Which statin produces the greatest triacylglycerol reduction?

A

Atorvastatin (29%)

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11
Q

Which two statins produce the greatest HDL cholesterol increase?

A

Pravastatin and Simvastatin (12%)

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12
Q

Which two statins have the ability to penetrate the CNS?

A

Lovastatin and Simvastatin

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13
Q

What is the MOA of the HMG-CoA Reductase Inhibitor Atorvstastin [Lipitor]?

A

Competitively inhibits HMG-CoA Reductase which is responsible for an early, rate limiting step in cholesterol biosynthesis
Increases hepatic LDL receptors, enhancing catabolism

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14
Q

What are the common adverse effects of Atorvstastin?

A

nasopharyngitis, myalgia, myopathy impaired function associated w/ elevated serum transaminase levels (jaundice), amnesia

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15
Q

What are the ocular adverse effects of Atorvstastin?

A

Diplopia, ptosis, pseudo-CME & blurred vision, elevated IOP, intraocular hemorrhage, cataracts

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16
Q

What happens when you take cyclosporine, erythromycin or azalea antifungals with Atorvastatin? (unique)

A

Myopathy exacerbation (a common adverse effect of Atorvastatin)

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17
Q

What is the contraindication of Atorvastatin?

A

Azole Antifungals

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18
Q

When is Fenofibrate commonly prescribed?

A

In conjunction with statins or in statin resistant patients

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19
Q

What is the MOA of the Fibrate Fenofibrate [TriCor]?

A

Stimulates nuclear receptor PPAR which modulates transcription of insulin (get’s energy into our cells) sensitive genes in live, muscle and adipose tissue (release of lipids into the bloodstream)
Enhances HDL production; inhibits triglyceride synthesis and stimulates catabolism of triglyceride-rich lipoproteins
Greatest effect on cells that reproduce the fastest

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20
Q

What are the common adverse effects of Fenofibrate?

A

headache, rhinitis, flu syndrome

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21
Q

What are the serious adverse effects of Fenofibrate?

A

SJS, TEN (toxic epidermal necrolysis), hepatitis, cirrhosis, thromboembolism, myositis, myopathy, rhabdomyolysis

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22
Q

What are the drug interactions of Fenofibrate?

A

Acyclovir, aminoglycoside, cyclosporine, gancyclovir - impaired renal elimination
Impaired metabolism of Sulfonylureas (Diabetes med)

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23
Q

What is Niacin commonly known as?

A

OTC Vitamin B3

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24
Q

What is the MOA of Niacin?

A

Inhibits lipolysis in adipose tissue, resulting in reduced hepatic VLDL synthesis and production of LDLs in plasma

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25
Q

What are the common adverse effects of Niacin?

A

headache, pseudo CME (goes away if you stop taking), flushing, pruritus, hyper pigmentation, jaundice, xeroderma, orthostatic hypotension

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26
Q

What is the unique ocular adverse effect of Niacin?

A

Toxic Amblyopia (the only one that does this)

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27
Q

What are the serious adverse effects of Niacin?

A

Hepatotoxicity, arrythmias

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28
Q

What are the drug interactions of Niacin?

A

Alpha and Beta Blockers - additive effect

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29
Q

What are the cautions to consider when thinking of using Niacin?

A

Diabetes (elevated blood sugar), sugar (anti-platelet effect)

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30
Q

What is the MOA of the Cholesterol Absorption Inhibitor Ezetimibe [Zetia]?

A

Inhibits dietary and biliary cholesterol absorption at small intestinal brush border
Used in conjunction with statins (inhibit cholesterol function, while these inhibit absorption)

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31
Q

What are the common adverse effects of Ezetimibe?

A

sinusitis, influenza, diarrhea

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32
Q

What are the serious adverse effects of Ezetimibe?

A

angioedema, anaphylaxis, hepatitis (need a healthy liver to lower lipid levels), thrombocytopenia

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33
Q

What is the effect of taking Cyclosporine and Ezetimibe?

A

May increase levels of both drugs as they are both processed through the liver

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34
Q

What are the cautions when taking Ezetimibe?

A

Hepatic Impairment

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35
Q

By what factor can you multiply A1C by to get your eAG?

A

Between 21 and 24
Ex. 6 * 21 = 126
Ex. 10 * 24 = 240
These values correspond to the table provided

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36
Q

Why is Metformin the first line drug for DM-2 treatment?

A

High efficacy, low hypoglycemia risk, has neutral/loss of weight, low cost

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37
Q

What are the main second line DM-2 drugs and why?

A

DPP-4 Inhibitors and GLP-1 Receptor Agonists

Because they have similar effects (most importantly weight effects) to Metformin although they are more expensive

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38
Q

For DM-2 when do we decide to use Insulin?

A

When Metformin does not work by itself, in a 2 drug combo or a 3 drug combo. This is the most complex of insulin strategies.

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39
Q

What is the average age of onset/diagnosis for DM-1?

A

Childhood or puberty

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40
Q

What is the average age of onset/diagnosis for LADA?

A

Adults

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41
Q

What is the average age of onset/diagnosis for DM-2?

A

Commonly >35 years of age

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42
Q

What is the average age of onset/diagnosis for MODY?

A

20 - 60 years of age

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43
Q

What is the MOA of the Biguanide Metformin [Glucophage]?

A

Biguanide based; activates AMP-activated protein kinase (AMPK) which in turn suppresses hepatic gluconeogenesis & intestinal glucose absorption; increases insulin sensitivity
Essentially is helps cells respond better to insulin

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44
Q

What are the common adverse effects of Metformin?

A

Headache, metallic taste, rash

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45
Q

What are the serious adverse effects of Metformin?

A

Lactic Acidosis (CO in bloodstream = toxic), Megaloblastic anemia (reduced oxygen transport to eye)

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46
Q

What are the main drug interactions of all Diabetes drugs?

A

Fish Oils, Decongestants, Steroids - antagonistic (increase blood sugar)
Flaxseed Oil - Additive
Beta-Blockers - Mask Hypoglycemia
NSAIDs - prolonged effect

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47
Q

Which drugs when taken with Metformin cause induced lactic acidosis?

A

Aminoglycosides, amphotericin, ganciclovir, acyclovir due to nephrotoxicity

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48
Q

What is the MOA of the Sulfonylurea Glipizide [Glucotrol]?

A

It is a Sulfonylurea which stimulates pancreatic islet beta cell insulin release through a Ca++ dependent pathway

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49
Q

What are the common adverse effects of Glipizide?

A

headache, photosensitivity, hypoglycemia

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50
Q

What are the serious adverse effects of Glipizide?

A

Death due to cardiovascular complications

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51
Q

What is the MOA of Thiazolidinedione/TZD/Glitazone Pioglitazone [Actos]?

A

Insulin sensitizer selectivity stimulates nuclear receptor PPAR which increases insulin sensitivity in the liver, skeletal muscle and adipose tissue

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52
Q

What are some additional effects that can happen when messing with the PPAR pathway?

A

Increasing sensitization of insulin, creation of ROS, and creation of substances integral in inflammation

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53
Q

What are the common adverse effects of Pioglitazones?

A

Fluid retention, weight gain (due to pulling lipids out of the bloodstream), headache, sinusitis, pharyngitis, dyspnea

54
Q

What are the serious adverse effects of Pioglitazone?

A

Diabetic macular edema (due to fluid retention), bladder cancer (lawsuits)

55
Q

What is the MOA of the DDP-4 Inhibitor Sitagliptin [Januvia]?

A

Inhibits DDP-4, slowing incretin (GI hormone secreted while eating) breakdown, insulin synthesis/release, decreasing glucagon levels

56
Q

What are the common and adverse effects of Sitagliptin?

A

Common - headache

Serious - renal failure, SJS

57
Q

What is the MOA of the SGLT-2 Inhibitor/Gliflozin Canaglifozin [Invokana]?

A

Inhibits sodium-glucose cotransporter 2, reducing glucose reabsorption & increasing urinary glucose secretion
The kidney eliminates sugar from the bloodstream resulting in more urination, thirst and dehydration

58
Q

What are the common adverse effects of Canaglifozin?

A

Increased urination, thirst and dehydration

59
Q

What are the serious adverse effects of Canaglifozin?

A

Orthostatic hypotension, fractures, bone density loss (loss of electrolytes like Ca due to increased urination)

60
Q

What additive effect can Ophthalmic Beta Blockers have when taken with Canaglifozin?

A

Additive risk of hypotension

61
Q

What is the MOA of the GLP-1 Agonist Dulaglutide [Trulicity]?

A

Activates glucagon-like-peptide-1 receptor on beta cells, increasing insulin secretion, decreasing glucagon secretion and delaying gastric emptying (incretin mimetic)

62
Q

What are the common and serious adverse effects of Dulaglutide?

A

Common - tachycardia

Serious - hypersensitivity, thyroid carcinoma

63
Q

What is the MOA of Insulin Glargine [Lantus, Youjeo]?

A

Slow release, micro-crystalized rDNA insulin analog for stable day long blood sugar regulation to be used in post-prandial combination with fast acting insulin
Insulin stimulates peripheral glucose uptake and inhibits gluconeogenesis, lipolysis and proteolysis

64
Q

What are the common adverse effects of Insulin Glargine?

A

Hypoglycemia, local lipodystrophy, pruritus (due to crystals?), weight gain, edema

65
Q

Should insulin be taken after its expiration?

A

No, it is one of the few drugs that is not recommended to be taken after its expiration date

66
Q

What is the biggest caution to consider when taking Insulin Glargine?

A

Infection b/c it causes your body to go into fight or flight which dumps glucose into the bloodstream. If the pt has poor glucose regulation, they will have an augmented reaction to any infection

67
Q

When Beta 2 is stimulated how does it affect the liver and kidneys?

A

Hepatic - causes glycogenolysis and gluconeogenesis

Pancreatic - causes increased insulin released

68
Q

When Alpha 2 is stimulated how does it affect the kidneys?

A

Decreased insulin release

69
Q

What is the MOA of the Proton Pump Inhibitor Esomeprazole [Nexium]?

A

Irreversibly inhibits gastric parietal cell H+-K+-ATPase inhibiting gastric acid secretion
Histamine, ACh, PG’s and gastrin all cause activation of the the proton pump, esomeprazole blocks all of these

70
Q

What are the common adverse effects of Esomemeprazole?

A

Headache, constipation or diarrhea, xerostomia, flatulence

71
Q

What at the serious adverse effects of Esomeprazole?

72
Q

What are the drug interactions to consider when prescribing Esomeprazole?

A

Impaired absorption of Azole Antifungals and Certain Antiviral Agents (take with acidic drink to enhance absorption)
Azole Antifungals - impaired metabolism
CAIs: exacerbation of hypomagnesemia

73
Q

What is the MOA of the H2 Receptor Blocker Cimetidine [Tagamet]?

A

Selective antagonism of gastric parietal cell H2 receptors

74
Q

What was the first H2 receptor blocker found?

A

Cimetidine

75
Q

What are the common adverse effects of Cimetidine?

A

Headache, dizziness

76
Q

What are the serious adverse effects of Cimetidine?

A

Food and drug allergies (GI not used to undigested food, similar to trying to breath water), blood dycrasias, psychosis, depression, reversible impotence, gynecomastia

77
Q

What are the drug interactions to consider when prescribing Cimetidine?

A

Impaired absorption of azalea antifungals/certain antivirals
Impaired metabolism of caffeine (NSAID + Caffeine)
Impaired metabolism of cyclosporine

78
Q

What are the common causes of Gatric/Peptic Ulcers?

A

Excessive hydrochloric acid secretion
Helicobacter pylori infection
NSAID toxicity
Inadequate mucosal defense against gastric acid

79
Q

What is the cause of Gastric-Esophageal Reflux Disease (GERD)?

A

Excessive hydrochloric acid secretion

80
Q

What is the MOA of the thyroid therapy Levothyroxine Sodium?

A

Synthetic T4 (tetra-iodothryonine)

81
Q

What are the common adverse effects of Levothyroxine Sodium?

A

Basically it would induce hyperthyroidism
Weight loss, diaphoresis, headache, alopecia, hypertension, pseudo tumor cerebra in children (swelling of the optic nerve due to ICP), hallucination

82
Q

What are the ocular adverse effects of Levothyroxine Sodium?

A

Myasthenia graves like symptoms - diplopia, ptosis, EOM paresis

83
Q

What are the drug interactions to consider when prescribing Levothyroxine?

A

Sympathomimetics (phenylephrine) - additive

Sympatholytics - antagonistic

84
Q

What is the MOA of the Menopausal Therapy Estrone [Menest]?

A

Binds to estrogen receptors, developing and maintaining female sex characteristics and reproductive systems

85
Q

What are the common adverse effects of Estrone?

A

Headache, migraine, elevated BP, weight changes, fluid retention, contact lens intolerance (eyes to dry), vision changes.

86
Q

What are the Black Box Warnings for Estrone?

A

Endometrial cancer, stroke, DVT, MI and Invasive Breast Cancer

87
Q

What are the drug interactions to consider when prescribing Estrone?

A

Azole Antigungals - impaired metabolism
Adverse effects of steroids may be increased
Anti-hyperlipidemic effects of Omega-3FA’s may be antagonized

88
Q

What are the contraindications of Estrone and Yaz?

A

Hypertension, Smoking, Migraine (with aura > without aura)

89
Q

What is the MOA of the contraceptive drug Drospirenon/Ethinyl Estradiol [Yaz]?

A

Suppresses LH & FSH, inhibiting ovulation; alters cervical mucous and endometrium

90
Q

What is the dosing schedule of Yaz?

A

It is monophasic meaning you take it as one constant dose throughout the entire cycle

91
Q

What are the common adverse effects of Yaz?

A

Headache, weight changes, BP elevated, increased cholesterol, contact lens intolerance

92
Q

What are the severe adverse effects of Yaz?

A

MI, stroke, ocular lesions

93
Q

What are the Black Box warnings associated with Yaz?

A

Smoking and CV events

94
Q

What are the drug interactions associated with Yaz?

A

Impaired metabolism of Cyclosporine
NSAIDs - additive hyperkalemia
Tetracyclines, penicillins, cephalosporins, macrolides, quinolones - decreased efficacy
Ascorbic acid - decreased metabolism

95
Q

What are the MOA of the Selective Estrogen Receptor Modulator (SERM) Tamoxifen [Soltamox]?

A

Binds to estrogen receptors, producing estrogenic and anti-estrogeni effects

96
Q

What are the common adverse effects of Tamoxifen?

A

Dizziness, headache, VA changes

97
Q

What are the severe adverse effects of Tamoxifen?

A

Thromboembolism, stroke, pancytopenia, retinopathy, cataracts

98
Q

What are the drug interactions to consider when prescribing Tamoxifen?

A

May increase cyclosporine, systemic steroid, oxycodone levels
Chlorpheniramine, macrolides - inhibit hepatic production of active metabolites

99
Q

What is the dosing for each indication for the osteoporosis drug Alendronate [Fosamax]?

A

Osteoporosis - 35 - 70mg awk

Paget’s Bone Disease - 40 mg qd x 6 months

100
Q

What are the adverse effects of Alendronate?

A

Common - photosensitivity

Serious - angioedema, uveitis (risk in new users/women), scleritis

101
Q

What are the drug interactions to consider when prescribing Alendronate?

A

NSAIDs - additive GI irritation

102
Q

Describe the pathology and relative incidence of Osteoporosis.

A

Characterized by a reduction in bone density and structure, increasing the risk of fracture.
Commonly seen in post-menopausal women vs age-related senile causes; both effect females 2X more than males
Iatrogenic causes include steroids, some anti-epileptic agents, anticoagulants, PPI’s, thiazolidinediones and lithium

103
Q

What are the most common cancers responsible for cancer-related deaths?

A

Males - 28% lung and bronchus, 10% prostate

Females - 26% lung and bronchus, 14% breast

104
Q

What are the most common causes of newly diagnosed cancer cases?

A

Men - 28% prostate, 14% lung and bronchus

Female - 29% breast, 14% lung and bronchus

105
Q

What are the indications of Methotrexate [Trexall]?

A

Rheumatoid arthritis, psoriasis, choriocarcinoma

106
Q

What is the dosing schedule for Methotrexate?

A

RA, Psoriasis - 7.5 - 25mg PO qwk

Choriocarcinoma - 15 - 30 mg PO qd x 5d

107
Q

What is the MOA of Methotrexate?

A

Acts on folic acid analogue, inhibits DHFR, thus preventing formation of FH4 (sulfas & trimethoprim follow this pathway)
Inhibits lymphocyte proliferation
Anti-inflammatory effects mediated by adenosine pathways

108
Q

What are the common and severe adverse effects of Methotrexate?

A

Common - photosensitivity, pruritus, anemia, dizziness

Serious - nephrotoxicity

109
Q

What are the Black Box warnings associated with Methotrexate?

A

Deaths reported; monitor bone marrow (reduction of immune cells opening up to infection), liver, lung & kidneys; opportunistic infections, potentially fatal myelosuppression w/ NSAIDs (two drugs put together put too much stress on the kidneys)

110
Q

What are the drug interactions to consider when prescribing Methotrexate?

A

NSAIDs, Sulfa, Cipro, Penicillins - reduced renal elimination
Tetracyclines - elevated levels
Cyclosporine - reduced hepatic metabolism
Ganciclovir - additive myelosuppression
Systemic Corticosteroids - additive immunosuppression

111
Q

Describe the underlying pathological process responsible for Emesis.

A

A protective mechanism that eliminates harmful substances from the GIT.
There are two brainstem sites: the chemoreceptor trigger zone (outside BBB), the emetic center (protected by BBB)

112
Q

What kind of drugs will be anti-emetics?

A

Drugs that induce fight or flight like steroids, anticholinergics, antihistamines.
Benzodiazepines stimulate GABA creating an overall inhibitory effect making it a low anti-emetic

113
Q

What is the emetic potential of Methotrexate?

114
Q

Why is Promethazine prescribed?

A

It is an antihistamine by design, used as an antipsychotic previously
Since antihistamines have anticholinergic effects it is an effective anti-emetic

115
Q

Why is Ondanestrone prescribed?

A

Made specifically for X-ray & chemotherapy related N & V making it the most likely anti-emetic patients on chemo will be on

116
Q

What is the MOA of the H1 Antagonist Promethazine [Phernergan]?

A

Non selective central and peripheral H1 antagonist

Some D2 antagonism exists

117
Q

What is the MOA of the D2 Antagonist Chlorpromazine [Thorazine]?

A

Selective D2 Antagonist

118
Q

What is the MOA of the 5-HT3 Antagonist Ondanestron [Zofran, Zuplenz]?

A

Selectively antagonizes 5-HT3 receptors

119
Q

What are the common adverse effects of Promethazine?

A

Drowsiness, blurred vision, confusion, dermatitis, photosensitivity

120
Q

What are the serious adverse effects of Promethazine?

A

Thrombocytopenia, agranulocytosis

121
Q

What are the Black Box Warnings associated with Promethazine?

A

Respiratory depression, severe tissue injury (gangrene)

122
Q

What are the drug interactions commonly associated with Promethazine and Chlorpromazine?

A

Macrolide’s, Azoles, CAIs - prolonged Qt segment
Pilocarpine - antagonistic
Impaired metabolism of Beta-Blocker (liver)
Anticholinergics, sedating antihistaminic, olopatadine nasal - additive
Seizure risk w/ Omega-6FA (no explanation) > only for Promethazine

123
Q

What does dosing look like for Chlorpromazine?

A

Takes 10 - 20 times more to treat psychosis which is why they look like zombies

124
Q

What are the common adverse effects of Chlorpromazine?

A

Drowsiness, blurred vision, ocular pigmentation, photosensitivity

125
Q

What other drugs do you see ocular pigmentation as a side effect in?

A

Prostaglandin Analogs

Phenylephrine (adenochrome deposits from phenylephrine)

126
Q

What are the serious adverse effects of Chlorpromazine?

A

Blood dycrasias

127
Q

What are the common adverse effects of Ondanestrone?

A

Headache, urinary retention, constipation

128
Q

What are the serious adverse effects of Ondanestrone?

A

SJS, TEN, Serotonin Syndrome

129
Q

What are the very unique ocular adverse effects of Ondanestrone?

A

Transient Blindness, Oculogyric Crisis (bilateral upward deviation)

130
Q

What are the drug interactions considered when prescribing Ondanestrone?

A

Macrolide’s, steroids, opioids, fluoroquinolone - prolonged QT

Systemic Pharm Final (1 decks)

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