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Intro to Pharmacology > OEQ-2023 > Flashcards

OEQ-2023 Flashcards

1
Q

Which of the following has visual side effects aggregated by dental light?

A

Gemfibrozil (Fibrate)

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2
Q

LovaSTATIN inhibits:

A

HMG-CoA reductase

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3
Q

What medications cause activation of antithrombin-III?

A

Enoxaparin & unfractioned heparin

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4
Q

Which medication is an antagonist of the protease activated receptor-1 inhibiting TRAP?

A

Vorapaxar (Zontivity)

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5
Q

Which medications can cause angioedema?

A

Sacubitril/Valsartan (Entestro)

-increased risk of angioedema when an ACE is used alongside an ARB

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6
Q

What receptor does losartan block?

A

AT1

(ARBs all block this)

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7
Q

ARB:

A

Angiotensin receptor blocker

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8
Q

What medication may increase triglycerides?

A

Colestipol

(Bile acid binding agent)

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9
Q

Which of the following would be considered a moderate intensity statin?

A

Atorvastatin 10mg

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10
Q

Riociguat can be classified in which group based on mechanism of action?

A

Soluble guanylate cyclase stimulator

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11
Q

Which of the following medication classes may cause hyperuricemia?

A

ATP-citrate lyase (ACL) inhibitor (Bempedoic acid)

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12
Q

Which of the following medications can have injection site reactions?

A

Evolcumab (PSK9 inhibitor)

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13
Q

Which of the following medications can be given intravenously?

A
  1. Bivalirudin
  2. Cangelor
  3. Unfractioned heparin

(All of the above)

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14
Q

Eplerenone works by competitively blocking action of what hormone?

What other medication does this?

A

Aldosterone

Spironolactone

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15
Q

Which medication has a high risk for hyperkalemia?

A
  1. Sacubatril/Valsartan (Entresto)
  2. Spironolactone
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16
Q

Glycoprotein IIb/IIIa is is involved in what step of thrombus formation?

A

Aggregation

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17
Q

Released by the kidneys; converts angiotensinogen to angiotensin I:

A

Renin

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18
Q

Vasoconstriction & proliferative action; bound by ANG II:

A

Angiotensin Type 1 recepto (AT1)

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19
Q

What class is Captropril?
What is an adverse reaction?

A

ACE inhibitor; cough

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20
Q

What type of drug is minoxidil? How does it work? What is an adverse reaction?

A

-Direct acting vasodilator
-Opens K+ ATP channels
-Hair growth

DOES NOT CAUSE HYPERKALEMIA

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21
Q

What is the route of administration of Apixaban?

A

Oral agent; along with edoxabam & rivaroxaban

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22
Q

What is the route of administration of Treprostinil?

A

Oral; inhalation; IV; SubQ

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23
Q

Receptor that endothelin-1 binds to; causes vaso/bronchoconstriction; increases aldosterone secretion:

A

ETA

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24
Q

According to the world health organization what group is pulmonary arterial hypertension categorized in?

A

Group 1 (also called primary pulmonary hypertension)

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25
Q

What is the mechanism of action of Nitrous Oxide?

A

Activates guanalyl cyclase & increases cGMP to cause vasodilation

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26
Q

What is the mechanism of action of Nitroprusside?

A

Increases intracellular nitric oxide concentration to cause smooth muscle relaxation

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27
Q

What is the mechanism of action of Felodipine?

A

Dihydropyridine calcium blocker; blocks L type calcium Chanels to LOWER intracellular calcium concentration & cause vasodilation; more selective in peripheral vasculature & more effective for treating hypertension

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28
Q

What is an adverse effect of spironolactone?

A

Aldosterone antagonist to decrease sodium resorption & decrease blood volume

-hyperkalemia
-man boobs
-dry mouth

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29
Q

Slidenafil mechanism of action:

A

PDE5 inhibitor; causes vasodilation & also used to treat limp noodles

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30
Q

All drugs that end in “fil” such as Slidenafil work to inhibit ____ to cause ____

A

PDE5; vasodilation

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31
Q

What is the mechanism of action of Bosentan?

A

Endothelin-1 receptor antagonist (ETA) & decreases formation of IP3 to cause smooth muscle relaxation or vasodilation

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32
Q

All drugs that end in “tan” such as Bosentan are _____ antagonist and decrease formation of ______ to cause smooth muscle____ or _____

A

ETA receptor antagonist; IP3; relaxation or vasodilation

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33
Q

What is the mechanism of action of fenofibrate?

A

Agonist of PPAR-alpha nuclear receptor; increases transcription of lipoprotein lipase; decreases VLDL and triglyceride levels

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34
Q

What is the function of PPAR-alpha nuclear receptor?

A

Increases synthesis of lipoprotein lipase

35
Q

Ezetimibe mechanism of action:

A

blocks cholesterol absorption by blocking NPC1L1 transport protein at enterocyte brush border

36
Q

What is the first step in atherosclerosis?

A
  1. Endothelial dysfunction
37
Q

Regarding the steps of atherosclerosis:

  1. ____ dysfunction
  2. ____ injury
  3. _____ deposits into vessel wall
  4. formation of ____
  5. ____ formation
  6. _____
  7. ____ formation
A
  1. ENDOTHELIAL dysfunction
  2. ENDOTHELIAL injury
  3. LDL deposits into vessel wall
  4. Formation of FOAM CELLS
  5. FATTY STREAK formation
  6. INFLAMMATION
  7. FIBROUS CAP formation
38
Q

Optimal level of LDL:

A

Less than 100 mg/dL

39
Q

ASCVD info is used to estimate:

A

10 year risk for MI or stroke

40
Q

Risk factors for atherosclerosis:

A
  1. smoking
  2. HTN
  3. hyperlipedemia
  4. diabetes
  5. age
  6. obesity
  7. physical inactivity
41
Q

What drugs have the most potent effect on LDL?

A

Statins

(cannot use when pregnant)

42
Q

PCSK-9 enzyme functions to:

A

promote the degradation of LDL receptors

(makes LDL levels higher so we have meds that inhibit this enzyme)

43
Q

Warfarin coagulation parameter:

A

Monitored using INR/PT

44
Q

The 4 G’s:

A
  1. decreased platelet activation & aggregation
  2. GP IIb/IIIa receptor inhibitors (prevent platelet aggregation)
  3. Eptifibatide & Tirofiban
45
Q

Virchows triad:

A
  1. stasis
  2. vessel wall injury
  3. hypercoaguability
46
Q

Intrinsic pathways information:

A

all components are present in the blood

47
Q

Intrinsic pathway is monitored by:

A

aPTT

48
Q

Which are the vitamin K dependent clotting factors?

A

2,7,9,10

49
Q

Aspirin mechanism of action:

A

COX 1 inhibitor

50
Q

Heparin mechanism of action:

A

Activates antithrombin III to bind to both factor Xa and thrombin; measured with aPTT

51
Q

Aminocaproic acid mechanism of action:

A

Blocks conversion of plasminogen to plasmin by tissue plasminogen activator (TPA)

52
Q

P2Y12 inhibitor:

A

Prasurgal

53
Q

Tadalafil mechanism of action:

A

PDE5 inhibitor

(also Slidenafil)

54
Q

Bempedoic acid mechanism of action:

A

ATP-citrate lyase (ACL) inhibitor

55
Q

Anything that ends in “fil” is a:

A

PDE5 inhibitor

(vascular smooth muscle reaction due to lowering intracellular calcium)

56
Q

Drug class thats ends in “entan” works by:

A

Endothelian-1 receptor agonist

57
Q

What is the reason behind ACE inhibitors causing cough?

A

Bradykinin buildup

58
Q

What is responsible for platelet adhesion?

A

Vonwillebrand factor responsible for platelet adhesion

59
Q

What are the three steps in thrombus formation?

A
  1. platelet adhesion (VWF)
  2. platelet activation (ADP, TXA2, Thrombin)
  3. platelet aggregation (gp IIb/IIIa)
60
Q

Left sided heart failure resulting in pulmonary hypertension puts a patient in the category:

A

Group 2

61
Q

pulmonary arterial HTN (PAH)- PRIMARY pulmonary HTN, is categorized as:

A

Group 1

62
Q

Pulmonary HTN due to LUNG DISEASE is categorized as:

A

Group 3

63
Q

Chronic thromboembolic pulmonary HTN (CETPH) is categorized as:

A

Group 4

64
Q

Pulmonary HTN with UNCLEAR MECHANISM is categorized as:

A

Group 5

65
Q

Primary = group 1
Hefty lefty = group 2
Diseased girlies= group 3
Chronic girlies = group 4
Unclear girlies = group 5

A
66
Q

Apixaban/Edoxaban mechanism of action:

A

Bind factor Xa and precent conversion of prothrombin to thrombin

67
Q

Warfarin/Coumadin adverse effects include:

A
  1. taste disturbances
  2. purple toes
68
Q

Spironolactone mechanism of action:

A

Aldosterone antagonist

69
Q

Prasugrel mechanism of action:

A

P2Y12 inhibitor- antiPlatelet medication

70
Q

Medications that end/include “grel” are ____ medications that inhibit ____

A

antiplatelet medication; P2Y12 inhibitor

71
Q

Tadalafil mechanism of action:

A

Phosphodiesterase 5 inhibitor (PDE5)

72
Q

Medications that end in “fil” work by:

A

inhibiting phosphodiesterase 5 (PDE5)

73
Q

Bile acid binding agents effect on triglyceride levels:

A

Increase triglyceride levels while decreasing LDL levels

74
Q

Apixaban and Edoxaban mechanism of action:

A

Factor Xa inhibitors

(precent conversion of prothrombin to thrombin)

75
Q

Adverse effect of statins:

A

Myopathy

(also hepatotoxicity and this drug class is contraindicated in pregnancy)

76
Q

What is the mechanism of action of aninocaproic acid? How is it administered?

A

Binds to plasminogen to inhibit plasmin activation; used as a mouthwash following dental surgery to prevent hemorrhage in patients taking oral anticoagulants; hemostatic agent

77
Q

Amount of triglycerides in different molecules:

A

Chylomicrons have the highest, then VLDL, then LDL, then HDL

78
Q

What is the mechanism of action of Slidenafil?

A

PDE5 inhibitor (as are other drugs that end in fil)

79
Q

Treprostinil route of administration:

A

Oral, inhalation, IV, subQ

80
Q

Virchow’s triad includes:

A
  1. Stasis
  2. Vessel wall injury
  3. Hypercoagulability
81
Q

Vitamin K dependent clotting factors:

A

2, 7, 9, 10

82
Q

How do we evaluate Warfarin?

A

INR/PT

83
Q

Edoxaban mechanism of action:

A

Inhibits conversion of prothrombin to thrombin

84
Q
A

Intro to Pharmacology (16 decks)

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