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Clinical Med (Year 2) > Last Pharm (Exam 2) > Flashcards

Last Pharm (Exam 2) Flashcards

1
Q

A positive inotropic drug can help (BLANK) cardiac output and reduces symptoms, especially in (BLANK)

A

A positive inotropic drug can help (increase) cardiac output and reduce symptoms, especially in (systolic HF)

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2
Q

What is the primary positive inotrope?

A

digitalis

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3
Q

What is Digitalis group of agents?

A

digitalis glycosides

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4
Q

What is Digitalis originally derived from?

A

foxglove plant

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5
Q

What is the primary indication for digitalis?

A

Congestive heart failure

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6
Q

The mechanism of Digitalis has what 2 effects?

A
  • Mechanical effects
  • Autonomic effects
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7
Q

What is the mechanical effect of Digitalis? In regards to the:
- Sodium - Potassium pump?
- Intracellular Na+ ?
- Intracellular Ca++?
- Actin-myosin binding?
- Cardiac Contraction?

A
  • Digitalis inhibits the Na+ - K+ (sodium - potassium) pump in cardiac cells so Na+ accumulates in cell
  • As intracellular Na+ increases, less calcium is extruded from cell by Na+ - Ca++ (sodium - calcium) exchanger thus intracellular calcium increases
  • Increasing intracellular calcium causes increased actin-myosin binding causing stronger cardiac contraction
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8
Q

What is the autonomic effect of Digitalis?

A

Decrease HR

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9
Q

How does Digitalis decrease HR?

A
  • Stimulating vagus
  • Inhibiting sympathetic to heart
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10
Q

What is the primary problem with Digitalis?

A

Digitalis toxicity

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11
Q

What are some common symptoms of Digitalis toxicity?

A
  • GI distress
  • Fatigue
  • Confusion
  • Depression
  • Blurred vision
  • Arrhythmias
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12
Q

Why should patients on Digitalis be monitored carefully?

A
  • Can cause severe cardiac arrhythmias
  • Toxic effects can occur even when blood levels are in therapeutic range
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13
Q

Another positive inotrope used in acute or severe heart failure is Phosphodiesterase inhibitors, what is the mechanism of this drug?

A

Increase myocardial Ca++ by preventing cAMP breakdown

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14
Q

Another positive inotrope used in acute or severe heart failure is Dopamine, dobutamine (Dobutrex), what is the mechanism of this drug?

A

Stimulate beta-1 receptors

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15
Q

What are some limitations of other positive inotropes (Dobutamine & Phosphodiesterase inhibitors)?

A
  • Parenteral administration (IV drip)
  • Not more effective than digitalis
  • Typically used in acute or severe heart failure
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16
Q

T/F: Digitalis can produce toxic effects, including potentially severe arrhythmias

A

True

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17
Q

Inadequate clotting is?

A

hemorrhage

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18
Q

Excessive clotting is?

A

thrombogenesis

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19
Q

Clotting mechanisms maintain balance between?

A

Clot formation and clot breakdown

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20
Q

What are the drugs used for overactive clotting?

A
  • Anticoagulants
  • Antithrombotics
  • Thrombolytics
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21
Q

When are anticoagulants used primarily?

A

Venous thrombosis

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22
Q

What are the 2 primary types of anticoagulants?

A
  1. heparin
  2. Oral anticoagulants
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23
Q

What is the mechanism of heparin?

A

Increases the effects of antithrombin III

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24
Q

Heparin has (BLANK) effects

A

Rapid

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25
Q

How is heparin administered?

A

Parenterally

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26
Q

How is unfractionated heparin administered? Are the effects predictable?

A
  • Admin: IV admin (heparin lock), several injection per day
  • No, unpredictable effects
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27
Q

How is Low molecular weight heparin (LMWHs) administered? Are the effects predictable?

A
  • Admin: Subcutaneously, usually once a day
  • Yes, more predictable, safer response
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28
Q

Why are low molecular weight heparins (LMWHs) more predictable?

A

preferentially inhibit factor Xa

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29
Q

Why does Heparin- induced thrombocytopenia (HIT) occur?

A

Heparins can decrease platelets (thrombocytopenia)

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30
Q

What is the difference between Type I HIT & Type II HIT?

A

Type I HIT: asymptomatic, resolves spontaneously
Type II HIT: immune reaction, causes serious thrombosis, life/limb threatening

31
Q

Why are low molecular weight heparins are often preferred to more conventional (unfractionated) heparin?

A

LMWH:
- Can be administered subcutaneously
- usually do not need to be administered as frequently as traditional heparin
- Provide more predictable anticoagulant effects

32
Q

What is the mechanism of oral anticoagulants (Warfarin)?

A

Inhibit Vitamin K function in liver, decreasing synthesis of certain clotting factors

33
Q

Oral anticoagulants are easy and convenient but typically have a time lag of (BLANK) before effect

A

3-4 days

34
Q

T/F: Oral anticoagulants are typically used before Heparin

A

False (typically used after)
- Begin treatment with heparin
- switch over to oral anticoagulant
- continue oral anticoagulant as needed

35
Q

Several newer option of anticoagulants are currently available or in development. When would these be used?

A
  • Used as primary anticoagulants
  • If other anticoagulants are not tolerated or contraindicated (patient with HIT)
36
Q

Aspirin is an (BLANK) drug; typically used to prevent what?

A
  • Aspirin is an antiplatelet drug
  • Typically used to prevent arterial clots in MI, stroke
37
Q

Recent evidence shows that aspirin can prevent what post total hip and knee replacement?

A

DVT

38
Q

What is the typical dose of aspirin?

A

1 tablet, twice each day for 6 weeks

39
Q

Your patient develops DVT following a total hip arthroplasty performed 2 days ago. She is currently asymptomatic and was started on LMWH yesterday. There is no other relevant comorbidities or other risk factors. Can you continue to ambulant this patient?

A

Yes b/c
- she has been on anticoagulant therapy for at least 5 hours
- no other risk factors appear to be present
- she does not have signs of an active pulmonary embolism

40
Q

How do newer oral anticoagulants reduce clotting?

A

Either:
- inhibiting thrombin
- Inhibiting clotting factor X

41
Q

What is the mechanism of antithrombotics?

A

Inhibit platelet activity, decreasing platelet induced clots

42
Q

What are the primary agents of antithrombotics?

A

-Aspirin
- Newer anti platelet drugs

43
Q

What are the anti clotting effects of aspirin?

A
  • Aspirin inhibits PG and thromboxane (TX) biosynthesis
  • Decreased TXs = less platelet induced clots
44
Q

Since aspirin inhibits platelet function what can this prevent in MI & ischemic stroke?

A

Prevents arterial thrombogenesis

45
Q

Aspirin is better at preventing:
MI (Men or Women?)
Stroke (Men or Women?)

A

Better at preventing:
MI in men
Stroke in women

46
Q

Therapeutic effects of aspirin occur at (BLANK) doses

A

extremely low doses

47
Q

What is the mechanism of another antiplatelet drug, ADP inhibitors?

A

Block effects of ADP on platelet (PDY12 receptor inhibitors)

48
Q

What is the mechanism of another antiplatelet drug Glyciprotein (GP) IIb-IIIa inhibitors?

A

Block effects of fibrinogen, other activators on platelet

49
Q

What is the mechanism of Thrombolytics?

A
  • Initiate clot breakdown by activating plasmin (fibrinolysin)
50
Q

Thrombolytics help dissolve clots in (BLANK & BLANK) arteries. This can restore blood flow and prevent/restore damage during what?

A
  • Dissolve blood clots in coronary, carotid arteries
  • Restore/Precent damage during MI, ischemic stroke
51
Q

T/F: There is an agent of Thrombolytics is clearly superior to another when treating MI

A

False
- There is no one agent that is superior

52
Q

Thrombolytics can decrease mortality by 50% if given within (BLANK) after symptom onset. But may still be helpful within (BLANK) after onset

A
  • Decrease mortality by 50% if given within 1 hour after symptoms onset
  • May still be helpful if administered within 3-12 hours after onset
53
Q

What must first be ruled out if using Thrombolytics in an ischemic stroke? What drug may be preferred?

A
  • First rule out hemorrhage
  • Activase (r-tPA) may be preferred
54
Q

Thrombolytics used in treating an ischemic stroke are typically administered (BLANK) after symptom onset.

A

2 hours

55
Q

T/F: Benefits of thrombolytics in an ischemic stroke must be balanced against risk of intracranial hemorrhage

A

True

56
Q

What is the primary rehab concern when a patient is using anticlotting drugs?

A

Risk of hemorrhage

57
Q

If a patient is on anti clotting drugs use care when administering?

A
  • Dressing changes
  • Debridement
  • agressive manual techniques
58
Q

What is the treatment of clotting deficiency, hemophilia?

A

Clotting factor replacement
(Hemophilia type A: factor VIII or Hemophilia type B: factor IX)

59
Q

How are clotting factors usually obtained when treating hemophilia?

A

From rDNA techniques, safe but expensive

60
Q

What treatment should be done if patient with hemophilia develop alloantibodies to synthetic clot factors?

A

treat with rituximab

61
Q

When can fibrinolysis inhibitors be used?

A

Hemophilia and hyperfibrinolysis syndromes

62
Q

When is vitamin K supplement administered?

A
  • To newborns or in severe vitamin K deficiency
  • Can help treat excessive warfarin
63
Q

What are the treatment options of hyperlipidemia?

A
  • Statins
  • Fibric acids
  • others
64
Q

What is the mechanism of statins?

A
  • Inhibit HMG-Co A reductase enzyme which:
  • decreases cholesterol biosynthesis
  • increase hepatic LDL breakdown
65
Q

What are the primary effects of statins?

A
  • Decrease LDL, VLDL cholesterol
  • May also decrease triglycerides, and increase HDL
66
Q

What are some additional beneficial effects of Statins?

A
  • Enhance vasodilation by nitric oxide
  • Anti inflammatory effects
  • Anti oxidant effects
67
Q

Patients who are taking Statins and spontaneously develop muscle pain and weakness might have?

A

Statin induced myopathy
(they should be referred for blood tests)

68
Q

What is the mechanism of Fibric acids?

A

Activate nuclear receptors that affects genes controlling lipid metabolism

69
Q

What is the primary effect of Fibric acids?

A
  • Decrease triglycerides
  • Increase VLDL breakdown
70
Q

Other anti lipid agents:
What is the mechanism of Niacin?

A
  • Decrease VLDL & LDL synthesis
  • Decrease triglyceride levels
71
Q

Other anti lipid agents:
What is the mechanism for Ezetimibe?

A

Inhibits cholesterol absorption from GI tract
(also can be combined with statin)

72
Q

Other anti lipid agents:
What is the mechanism for Bile acid binding drugs?

A
  • Increase GI excretion of bile acids
  • Decrease plasma cholesterol
73
Q

What are anti lipid agents adverse effects & rehab concerns in regards to:
- GI
- Others
- And what should you watch for signs of?

A
  • GI: nausea, diarrhea, bloating
  • Others: Liver toxicity, pancreatitis, blood dycrasias, arrhythmias
  • Watch for signs of myopathy (muscle pain, weakness)
74
Q

What do Thromboxanes (TX) do?

A

Increase platelet activity/ aggregation

Clinical Med (Year 2) (17 decks)

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