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Systems Screening III > Ruggles Lecture 2 > Flashcards

Ruggles Lecture 2 Flashcards

1
Q

What drugs end in -pril?

A

ACE inhibitors

- block angiotensin converting enzyme

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2
Q

What do ARBs do?

A

Arbs block angiotensin II from binding to receptors that cause vasoconstriction
- end in -sartan

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3
Q

What is the vicious cycle of CHF?

A
  1. Decreased cardiac performance - impaired pumping ability due to MI, HTN, valve dysfunction, etc.
  2. Neurohoumoral compensation - incr. symp activity, incr. renin-angiotensin II, incr. aldosterone
  3. Increased cardiac workload - incr. vascular resistance, incr. fluid volume
  4. changes in myocardial cell function - structural damage, altered Ca+ transport
    - -repeat–
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4
Q

What drugs increase myocardial contraction force?

A
  1. Digoxin
  2. Phosphodiesterase inhibitors
  3. Dopamine
  4. dobutamine
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5
Q

What drugs decrease cardiac workload?

A
  1. ACE-Inhibitors
  2. Beta blockers
  3. Diuretics
  4. Vasodilators
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6
Q

Improves cardiac pumping ability by elevating intracellular calcium levels and facilitating actin-myosin interaction in cardiac cells; Inhibits the sodium-potassium pump on the myocardial cell membrane. This transport system usually transports sodium out of the cell and transports potassium into it. Inhibition of this pump causes sodium to accumulate within the cell; Increased intracellular sodium leads to increased intracellular calcium; Because more calcium is stored in the cardiac cell, the sarcoplasmic reticulum releases more calcium during each action potential, thereby initiating greater actin-myosin interaction and a stronger cardiac contraction

A

Digitalis (Digoxin)

  • improves symptoms of CHF
  • makes pt feel better, but questionable evidence of actually increasing lifespan
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7
Q

What are the symptoms of digoxin toxicity?

A
  1. GI distress (nausea, vomiting, diarrhea)
  2. CNS disturbances (drowsiness, fatigue, confusion, visual disturbances)
  3. Arrhythmias
    - digibind is used to treat toxicity, binds with the drugs and decreases toxic effects
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8
Q

Inhibit the phosphodiesterase enzyme that breaks down cyclic adenosine monophosphate (cAMP) in cardiac cells which enhances myocardial contractility; cAMP acts on membrane calcium channels to allow more calcium to enter the cell

A

Phosphodiesterase inhibitors

- IV for short term treatment

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9
Q

What are the types of phosphodiesterase inhibitors?

A
  1. Inamrinone

2. Milrinone

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10
Q

Decrease morbidity and mortality in patients with CHF; Reduces peripheral vascular resistance by preventing angiotensin II induced vasoconstriction and vascular hypertrophy/remodeling; Limits aldosterone secretion which prevents sodium and water retention; Promotes vasodilation by prolonging the effects of bradykinin

A

ACE inhibitors

- end in -pril

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11
Q

Stimulate cardiac beta-1 adrenergic receptors, which selectively increases myocardial contraction force; Reserved for patients who do not respond to other positive inotropic agents such as digoxin; May be associated with increased mortality

A

Dopamine and Dobutamine

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12
Q

Just as effective as ACE-Inhibitors in treating heart failure and preventing mortality; Reduce angiotensin II induced peripheral vascular resistance and cardiovascular hypertrophy/ remodeling by blocking angiotensin II receptors on the heart and vasculature

A

Angiotensin II Receptor Blocker (ARBs)

  • end in -sartan
  • as effective as ACE in decreasing mortality
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13
Q

block the effects of norepinephrine and epinephrine on the myocardium to normalize sympathetic stimulation and decrease heart rate

A

Beta blocker

  • non selective are more helpful in CHF than selective
  • Newer beta blockers such as carvedilol and nebivolol are especially useful because they also block alpha-1 receptors on the vasculature causing peripheral vasodilation
  • end in -olol
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14
Q

What are the ADRs of beta blockers?

A
  1. Abnormally slow heart rate

2. Reduced contraction force

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15
Q

What can happened that will disturb the hemostasis balance?

A
  1. Insufficient levels of blood-clotting factors = inadequate clotting (hemophilia): Resolved by replacing the missing clotting factors or facilitating the synthesis of specific clotting factors
  2. Excessive clotting occurs during prolonged bed rest or when blood flow through vessels is partially obstructed: Rectified by drugs that prevent clot formation (anticoagulants, antiplatelets) or facilitate the removal of previously formed clots (fibrinolytics)
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16
Q

What are the 3 categories of drugs used to treat overactive clotting?

A
  1. Anticoagulant
  2. Antiplatelets
  3. Fibrinolytics
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17
Q

Control the function and synthesis of specific clotting factors; Used to prevent clot formation in the venous system (venous thrombosis)

A

Anticoagulants

18
Q

Inhibit abnormal platelet activity; Used to prevent thrombus formation in the arteries that lead to myocardial infarction and ischemic stroke

A

Antiplatelets

19
Q

Facilitate the destruction of blood clots; Used to reestablish blood flow through vessels that have been occluded by thrombi

A

Fibrinolytics

20
Q

What are the primary anticoagulants?

A
  1. Heparin
  2. Warfarin (Coumadin)
  3. Direct thrombin inhibitors
  4. Factor Xa inhibitors
21
Q

Often the initial treatment of venous thrombosis; Potentiates the activity of antithrombin. Antithrombin binds to several of the active clotting factors (thrombin, IXa, Xa) and renders them inactive; Poorly absorbed from the GI tract – given IV

A

Heparin

22
Q

Preferentially inhibits factor Xa; Results in more predictable anticoagulant effect and less lab monitoring; Less risk of adverse effects such as hemorrhage and heparin-induced thrombocytopenia; Used for the treatment of acute venous thrombosis; Used for prevention of DVT’s following surgery or medical conditions

A

Low Molecular Weight Heparin (LMWH)

  • ends in -parin
  • as effective as heparin
  • given subcutaneously
23
Q

Interferes with vitamin K metabolism in the liver which impairs the hepatic synthesis of several clotting factors; In the liver, vitamin K acts as a catalyst in the final step of the synthesis of clotting factors II, VII, IX, and X. During this process vitamin K is oxidized to an altered form known as vitamin K epoxide. For the process to continue, vitamin K must be reduced to its original form; this drug blocks the conversion of vitamin K epoxide to vitamin K which impairs the synthesis of several clotting factors; A decrease in the level of circulating clotting factors results in a decrease in blood coagulation.

A

Warfarin (Coumadin)

  • oral anticoagulant
  • several days before full effect
  • monitoring needed; lots of drug/drug and drug/food interactions
  • cheap
  • requires frequent INR monitoring
24
Q

Bind directly to the active site on thrombin and inhibit thrombin’s ability to convert fibrinogen to fibrin; Approved for preventing stroke and systemic embolism in patients with Afib; May be helpful in preventing other coagulation disorders such as DVT

A 
Direct throbbing inhibitor;
Dabigatran (Pradaxa)
- oral
- Praxbind-antidote available
- May have several advantages: More effective, Improved safety, Less drug-drug interactions, Reduced risk of hemorrhagic stroke,Fewer adverse effects
25
Q

Inhibits renin’s ability to convert angiotensinogen to angiotensin I which decreases the production of angiotensin II

A

Direct Renin Inhibitor

- Only one is Aliskiren (Tekturna)

26
Q

What are the adverse effects of drugs affecting the renin-angiotensin system?

A
  1. Skin rash
  2. GI discomfort
  3. Dizziness
  4. Persistent, dry cough
27
Q

Reduce congestion in the lungs and peripheral tissues by excreting excess fluid from those tissues; Decrease the amount of fluid the heart must pump

A

Diuretics

- loop most commonly used (furosemide, tordsemide)

28
Q

What are the ADRs of diuretics?

A
  1. Electrolyte imbalances
  2. Volume depletion
  3. Fatigue, confusion, nausea - signal a disturbance
  4. Resistance develops over time
29
Q

Decrease peripheral vascular resistance = decrease the amount of blood returning to the heart (cardiac preload) and reduce the pressure the heart must pump against (cardiac afterload)

A

Vasodilators

30
Q

What are the 3 main types of vasodilators?

A
  1. Prazosin – blocks alpha-1 receptors on vascular smooth muscle
  2. Hydralazine, organic nitrates – direct inhibitory effect on vascular smooth muscle
  3. Sildenafil – prolong the effects of cGMP promoting relaxation and vasodilation
31
Q

What are the ADRs of vasodilators?

A
  1. Headache***
  2. Dizziness
  3. Hypotension
  4. Orthostatic hypotension
  5. Reflex tachycardia
32
Q

Blood coagulation (hemostasis) is necessary to prevent excessive hemorrhage from damaged blood vessels. Under normal conditions, clotting factors in the bloodstream spontaneously interact with damaged vessels to create a blood clot that plugs the leaking vessel. ________ can lead directly to vessel occlusion and tissue infarction.

A

Thrombus formation

- a piece of a thrombus may dislodge, creating an embolism (lung or brain)

33
Q

What happens to hemostasis with hyperlipidemia?

A

Can cause thrombosis development and infarction
- Hyperlipidemia – cholesterol and other lipids are progressively deposited onto arterial walls, forming plaque-like lesions; The plaques progressively occlude the arterial lumen; can suddenly rupture

34
Q

direct contact of platelets and the first clotting factor with a damaged vessel initiates the cascade

A

intrinsic pathway of clot formation

- Ultimate goal of each pathway is to convert prothrombin to thrombin

35
Q

substance called tissue factor is released from the damaged vascular cell and other circulating cells, tissue factor and factor VII form a complex which activates subsequent factors

A

Extrinsic pathway of clot formation

- Ultimate goal of each pathway is to convert prothrombin to thrombin

36
Q

an enzyme that converts fibrinogen to fibrin (Fibrin forms individual strands that bind together to form a meshlike structure, which forms the framework for the blood clot)

A

Thrombin

37
Q

Clot breakdown process: ____________ converts plasminogen to plasmin. What does plasmin do?

A

Tissue plasminogen activator

- Plasmin is an enzyme that directly breaks down the fibrin mesh

38
Q

What are the ADRs of anticoagulant drugs?

A
  1. Bleeding
  2. heparin-induced thrombocytopenia (HIT)
  3. GI distress (nausea, stomach cramps, diarrhea)
  4. Skin reactions
39
Q

anticoagulant that is really dosed (can’t co over a certain amount for kidneys, otherwise pt must go on warfarin); Directly affects the active form of Xa

A

Factor Xa Inhibitors

  • fondaparinux (Arixtra) - subQ; prevents DVT; may be more effective for DVT prevention than heparin and LMWH; lower risk of causing heparin-induced thrombocytopenia
  • apixaman (delinquis) and Rivaroxaban (Xarelto) - oral; safe, convenient, and effective way to treat venous thrombosis and other hypercoagulation
40
Q

What are the ADRs of anticoagulant drugs?

A
  1. Bleeding
  2. Heparin-induced thrombocytopenia (HIT)
  3. GI distress (nausea, stomach cramps, diarrhea)
  4. Skin reactions
41
Q

Immune mediated; Can lead to increased thrombosis in vascular tissues; Emergent situation; caused by anticoagulant drugs

A

Heparine-induced thrombocytopenia (HIT)

  • resolved by discontinuing heparin and substituting a non-heparin anticoagulant
  • ranges from asymptomatic and resolves spontaneously (type I HIT) to severe (type II HIT)

Systems Screening III (9 decks)

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