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)
2
Q
What is the primary positive inotrope?
A
digitalis
3
Q
What is Digitalis group of agents?
A
digitalis glycosides
4
Q
What is Digitalis originally derived from?
A
foxglove plant
5
Q
What is the primary indication for digitalis?
A
Congestive heart failure
6
Q
The mechanism of Digitalis has what 2 effects?
A
- Mechanical effects
- Autonomic effects
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
8
Q
What is the autonomic effect of Digitalis?
A
Decrease HR
9
Q
How does Digitalis decrease HR?
A
- Stimulating vagus
- Inhibiting sympathetic to heart
10
Q
What is the primary problem with Digitalis?
A
Digitalis toxicity
11
Q
What are some common symptoms of Digitalis toxicity?
A
- GI distress
- Fatigue
- Confusion
- Depression
- Blurred vision
- Arrhythmias
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
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
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
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
16
Q
T/F: Digitalis can produce toxic effects, including potentially severe arrhythmias
A
True
17
Q
Inadequate clotting is?
A
hemorrhage
18
Q
Excessive clotting is?
A
thrombogenesis
19
Q
Clotting mechanisms maintain balance between?
A
Clot formation and clot breakdown
20
Q
What are the drugs used for overactive clotting?
A
- Anticoagulants
- Antithrombotics
- Thrombolytics
21
Q
When are anticoagulants used primarily?
A
Venous thrombosis
22
Q
What are the 2 primary types of anticoagulants?
A
- heparin
- Oral anticoagulants
23
Q
What is the mechanism of heparin?
A
Increases the effects of antithrombin III
24
Q
Heparin has (BLANK) effects
A
Rapid
25
How is heparin administered?
Parenterally
26
How is unfractionated heparin administered? Are the effects predictable?
- Admin: IV admin (heparin lock), several injection per day
- No, unpredictable effects
27
How is Low molecular weight heparin (LMWHs) administered? Are the effects predictable?
- Admin: Subcutaneously, usually once a day
- Yes, more predictable, safer response
28
Why are low molecular weight heparins (LMWHs) more predictable?
preferentially inhibit factor Xa
29
Why does Heparin- induced thrombocytopenia (HIT) occur?
Heparins can decrease platelets (thrombocytopenia)
30
What is the difference between Type I HIT & Type II HIT?
Type I HIT: asymptomatic, resolves spontaneously
Type II HIT: immune reaction, causes serious thrombosis, life/limb threatening
31
Why are low molecular weight heparins are often preferred to more conventional (unfractionated) heparin?
LMWH:
- Can be administered subcutaneously
- usually do not need to be administered as frequently as traditional heparin
- Provide more predictable anticoagulant effects
32
What is the mechanism of oral anticoagulants (Warfarin)?
Inhibit Vitamin K function in liver, decreasing synthesis of certain clotting factors
33
Oral anticoagulants are easy and convenient but typically have a time lag of (BLANK) before effect
3-4 days
34
T/F: Oral anticoagulants are typically used before Heparin
False (typically used after)
- Begin treatment with heparin
- switch over to oral anticoagulant
- continue oral anticoagulant as needed
35
Several newer option of anticoagulants are currently available or in development. When would these be used?
- Used as primary anticoagulants
- If other anticoagulants are not tolerated or contraindicated (patient with HIT)
36
Aspirin is an (BLANK) drug; typically used to prevent what?
- Aspirin is an antiplatelet drug
- Typically used to prevent arterial clots in MI, stroke
37
Recent evidence shows that aspirin can prevent what post total hip and knee replacement?
DVT
38
What is the typical dose of aspirin?
1 tablet, twice each day for 6 weeks
39
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?
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
How do newer oral anticoagulants reduce clotting?
Either:
- inhibiting thrombin
- Inhibiting clotting factor X
41
What is the mechanism of antithrombotics?
Inhibit platelet activity, decreasing platelet induced clots
42
What are the primary agents of antithrombotics?
-Aspirin
- Newer anti platelet drugs
43
What are the anti clotting effects of aspirin?
- Aspirin inhibits PG and thromboxane (TX) biosynthesis
- Decreased TXs = less platelet induced clots
44
Since aspirin inhibits platelet function what can this prevent in MI & ischemic stroke?
Prevents arterial thrombogenesis
45
Aspirin is better at preventing:
MI (Men or Women?)
Stroke (Men or Women?)
Better at preventing:
MI in men
Stroke in women
46
Therapeutic effects of aspirin occur at (BLANK) doses
extremely low doses
47
What is the mechanism of another antiplatelet drug, ADP inhibitors?
Block effects of ADP on platelet (PDY12 receptor inhibitors)
48
What is the mechanism of another antiplatelet drug Glyciprotein (GP) IIb-IIIa inhibitors?
Block effects of fibrinogen, other activators on platelet
49
What is the mechanism of Thrombolytics?
- Initiate clot breakdown by activating plasmin (fibrinolysin)
50
Thrombolytics help dissolve clots in (BLANK & BLANK) arteries. This can restore blood flow and prevent/restore damage during what?
- Dissolve blood clots in coronary, carotid arteries
- Restore/Precent damage during MI, ischemic stroke
51
T/F: There is an agent of Thrombolytics is clearly superior to another when treating MI
False
- There is no one agent that is superior
52
Thrombolytics can decrease mortality by 50% if given within (BLANK) after symptom onset. But may still be helpful within (BLANK) after onset
- 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
What must first be ruled out if using Thrombolytics in an ischemic stroke? What drug may be preferred?
- First rule out hemorrhage
- Activase (r-tPA) may be preferred
54
Thrombolytics used in treating an ischemic stroke are typically administered (BLANK) after symptom onset.
2 hours
55
T/F: Benefits of thrombolytics in an ischemic stroke must be balanced against risk of intracranial hemorrhage
True
56
What is the primary rehab concern when a patient is using anticlotting drugs?
Risk of hemorrhage
57
If a patient is on anti clotting drugs use care when administering?
- Dressing changes
- Debridement
- agressive manual techniques
58
What is the treatment of clotting deficiency, hemophilia?
Clotting factor replacement
(Hemophilia type A: factor VIII or Hemophilia type B: factor IX)
59
How are clotting factors usually obtained when treating hemophilia?
From rDNA techniques, safe but expensive
60
What treatment should be done if patient with hemophilia develop alloantibodies to synthetic clot factors?
treat with rituximab
61
When can fibrinolysis inhibitors be used?
Hemophilia and hyperfibrinolysis syndromes
62
When is vitamin K supplement administered?
- To newborns or in severe vitamin K deficiency
- Can help treat excessive warfarin
63
What are the treatment options of hyperlipidemia?
- Statins
- Fibric acids
- others
64
What is the mechanism of statins?
- Inhibit HMG-Co A reductase enzyme which:
- decreases cholesterol biosynthesis
- increase hepatic LDL breakdown
65
What are the primary effects of statins?
- Decrease LDL, VLDL cholesterol
- May also decrease triglycerides, and increase HDL
66
What are some additional beneficial effects of Statins?
- Enhance vasodilation by nitric oxide
- Anti inflammatory effects
- Anti oxidant effects
67
Patients who are taking Statins and spontaneously develop muscle pain and weakness might have?
Statin induced myopathy
(they should be referred for blood tests)
68
What is the mechanism of Fibric acids?
Activate nuclear receptors that affects genes controlling lipid metabolism
69
What is the primary effect of Fibric acids?
- Decrease triglycerides
- Increase VLDL breakdown
70
Other anti lipid agents:
What is the mechanism of Niacin?
- Decrease VLDL & LDL synthesis
- Decrease triglyceride levels
71
Other anti lipid agents:
What is the mechanism for Ezetimibe?
Inhibits cholesterol absorption from GI tract
(also can be combined with statin)
72
Other anti lipid agents:
What is the mechanism for Bile acid binding drugs?
- Increase GI excretion of bile acids
- Decrease plasma cholesterol
73
What are anti lipid agents adverse effects & rehab concerns in regards to:
- GI
- Others
- And what should you watch for signs of?
- GI: nausea, diarrhea, bloating
- Others: Liver toxicity, pancreatitis, blood dycrasias, arrhythmias
- Watch for signs of myopathy (muscle pain, weakness)
74
What do Thromboxanes (TX) do?
Increase platelet activity/ aggregation
