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PHRM 845: Therapeutics III > ISHD > Flashcards

ISHD Flashcards

1
Q

What is the pathophysiology of Stable Angina?

A
  • Ischemia: the imbalance between oxygen supply and demand
  • Angina: the symptoms from the imbalance
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2
Q

What is Stable Angina?

A

Discomfort in the substernal part of the chest that can radiate down the left arm
- NO miocardial nercrosis
- NO change over the last 2 months

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3
Q

Explain how the PQRST relates toward the clincial presentations?

A

P: Precipitative factor & Palliative measures [what causes it and what helps it]
Q: Quality & Quantity of pain [tightness, pressure, etc…]
R: Region & Radiation [Where? - substernal]
S: Severity of pain [scale of 1 to 10]
T: Timing [How long does it last? - <20mins?]

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4
Q

What are some of the clinical presentations that are associated with Stable Angina?

A
  • Pain that occurs behind the sternum that then radiates up to the jaw and/or down the left arm
  • SOB, Massive pressure, tightness, crushing…
  • Caused by weather [HOT or COLD], physical activity, large meals, emotional stress, sexual activity…
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5
Q

How does the ECG appear with a patient with Stable Angina?

A

Typically the ECG will appear normal but DURING AN EVENT the ECG will have ST DEPRESSION

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6
Q

What are some of the diagnostic procedures used to determine IHD [Ischemic Heart Disease]?

A
  • Can use a ECG, will show whether the patient has ST Elevation [more CAS - Variant] or ST Depression [during an event or NSTEMI]
  • Exercise testing: will help with looking at the ECG to see and abnormalities
  • Heart Cath to see what is really happening within the arteries
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7
Q

For the treatment of SIHD, what are some way that we prevent ACS and Death?

A
  • Lifestyle and rick factors modifications
  • Vaccines
  • Comorbidities: check BP and DM
  • Antiplatelets: Aspirin 81mg or Clopidegrel 75mg
  • ACEi: when they have HTN, LVEF <40% or CKD
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8
Q

For the treatment of SIHD, what are some of the ways that we help manage anginal episodes?

A
  • NTG: Acute attacks
  • Vasospastic?: high BP - Nitrate; low BP - CCB
  • HR > 60bpm: Beta-Blocker then NON DHP
  • Controlled?: monitor
    -Not controlled & BP still high: Ranolazine or LA
    Nitrate OR DHP CCB
  • Still angina: PCI or CABG
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9
Q

What is the role of atherosclerotic plaque, platelets and coagulation systems in CAD?

A
  • Atherosclerotic plaques are a build up of fat due to monocytes becoming macrophages within the cell, eating up all the cholesterol.
  • They then rupture, activating the clotting cascade making a thrombus - narrowing & blocking the arteries
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10
Q

What are some of the variables that influence myocardial oxygen supply and demand?

A
  • Increase heart rate, contractility, preload, afterload [increase demand while decrease supply]
  • Any sort of blockage in the arteries [decrease supply]
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11
Q

List the pharmacological ways to prevent ACS and Death?

A

Antiplatelet, Statins, ACEi/ARBs, Beta-Blockers

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12
Q

What is the drugs used in Antiplatelet therapies?

A

Aspirin & P2Y12 Inhibitors

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13
Q

What is the mechanism of Aspirin?

A
  • At low doses, it inhibits COX-1 = blocking the formation of TXA2 [platelet aggregant and vasoconstrictor]
  • At high doses, it inhibits COX-2 = blocking PGI2 [allowing platelets to aggregate]
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14
Q

What are the P2Y12’s and what is there mechanism?

A
  • Clopidigrel, Ticagrelor, Cangrelor
  • They inhibit adenosine diphosphate induced platelet aggregation
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15
Q

What are some of the adverse affects for Aspirin?

A
  • Main one is INCREASED BLEEDING
  • also have patients chew and swallow any aspirin during chest pain
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16
Q

What are some of the adverse affects for the P2Y12 Inhibitors?

A

Mainly all cause bleeding [a little bit higher than Aspirin], Diarrhea, Rash, Bradycardia [Most Ticagrelor]

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17
Q

What are the three clinical scenarios for Chronic CAD?

A

No Stent, PCI + Stent, CABG

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18
Q

Describe what NO STENT is in terms of a clinical scenario?

A
  • Basically they do not put a stent in just yet, they just use ASPIRIN as a secondary prevention [could also use Clopidigrel if aspirin allergy]
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19
Q

Describe what PCI + STENT is in terms of a clinical scenario?

A
  • They do a HEART CATH [PCI] on the patient seeing if they are in need of a STENT or NOT [Before; they give the patient 325mg of Aspirin and 300-600mg of Clopidigrel]
20
Q

What are the two different types of STENTS?

A
  • BMS [Bare Metal Stent]: Just what is sounds like, a metal stent that helps open the arteries [no meds released; clopidigrel for only 1 MONTH]
  • DES [Drug Eluting Stent]: Stent that releases Anti-anginals so cells cant grow in that section [Clopidigrel for 6 MONTHS]
21
Q

What do ACEi/ARBs do for ACS prevention?

A
  • Reduce the cholesterol build up, which helps with reducing the plaques [doesn’t help with ischemia but helps with the cardiovascular events]
  • Use ARBs when there is a dry cough
22
Q

What are some way that we are able to decrease myocardial demand?

A
  • Beta Blockers and NON DHP: decrease HR and Contractility
  • Nitrates: Preload
  • DHP: Afterload
23
Q

What are some ways that we are able to increase myocardial supply?

A
  • Dilation of the arteries and increase blood flow: Nitrates
24
Q

What medicaitons do we use for the acute treatment of angina?

A

Nitroglycerin

25
Q

What are the effects that NTG has on myocardial oxygen?

A
  • Increase supply: Dilation of the arteries
  • Decrease Demand: Because of the decrease in preload; the heart isn’t stretching as much
26
Q

How to properly take NTG?

A
  • Can take up to 3 tabs; taking one every 5 minutes – call 911 if the first tab doesn’t work
27
Q

What are some side effects for NTG?

A
  • Headache [most common], Hypotension, dizziness, lightheadedness…
  • DO NOT take with NSAIDs
  • DO NOT take with PDE5i [Cause massive dilation]
28
Q

What are some of the drugs used in the PREVENTION of ischemia and angina sypmtoms?

A

Beta-Blockers, CCBs, Nitrates

29
Q

What effects do the Beta-Blockers have on the myocardial?

A
  • It will block Norepi and Epi from binding to the Beta Receptors [will decrease the HR, Contractility, Afterload - ALL will decrease DEMAND]
30
Q

Describe the cardioselectivity of the Beta-Blockers?

A

B1: Metoprolol, Atenolol, Bisoprolol, Nebivolol
[Heart]
B2: Propranolol, Nadolol Sotaolol, Pindolol
[Lungs]
Mixed: Carvedilol, Labetolol
[B1, B2, a]

31
Q

What might happen if given a higher does of a B1 selective beta-blocker?

A

It could cause some B2 blockage

32
Q

What are some of the side effects of teh Beta-Blockers?

A
  • Bradycardia [Decreased HR], Sinus Arrest [NO HR], AV blockage
33
Q

What are the monitoring parameters that we should pay attention toward when giving a Beta-Blockers?

A
  • Goal HR: 50 - 60BPM at rest; <100BPM during exercise
  • Amount of NTG tabs used
34
Q

What is the mechanism of action for the Calcium Channel Blockers?

A
  • Block the passage of external Ca2+ from entering into the cell; this I’ll not all the binding of Ca2+ to Calmodulin - decreasing the producing of MLCK, which will DECREASE contraction
35
Q

What are the two classes of CCBs?

A

DHP: “-pines” [will have more of an effect on ARTERIES]
NON DHP: “Verapamil & Diltiazem [will have more of an effect on the HEART - mainly the SA and AV node]

36
Q

What are the side effects for the CCBs?

A
  • DHP: Hypotension, Dizziness, Lightheadness [Similar to Nitrates], Edema
  • NON DHP: Decrease contractility, Bradycardia, AV Block, Constipation [V>D]
37
Q

How should we monitor someone on a CCB?

A
  • Amount of NTG usage
  • Goal HR: 50 - 60BPM at rest; <100BPM during exercise
38
Q

How do Nitrates help with Prevention of anginial symptoms?

A
  • They will dilate the veins causing an increase in blood flow [increasing the supply while reducing the demand]
  • Will decrease preload
39
Q

What causes Nitrate Tolerance?

A
  • It occurs with high does or frequent usage of nitrate = decreasing the response of them
40
Q

How to prevent Nitrate Tolerance?

A
  • Need to have a Nitrate FREE period of at least 10 - 12 hours
41
Q

What should you monitor for when taking Nitrates?

A
  • Amount of NTG tabs taken
  • SE: headache, hypotension
42
Q

What is the mechanism of Ranolazine?

A
  • Inhinbition of late inward Na+ current in ishcemic myocytes, Decreases Na+ causing decrease Ca2+ influx
43
Q

When should Ranolazine be used?

A
  • Combo with Beta-Blockers, CCBs or Nitrates when they aren’t working well
  • Monotherapy: When BP and HR are too low for the first line agents [DOES NOT effect BP, HR, Inotropy or Perfusion]
44
Q

What are the adverse side effects of Ranolazine?

A
  • Constipation, Nausea, Dizziness, Headache
  • QT interval Increase
45
Q

What are the selection of drug therapy for chronic stable angina?

A

Beta-Blockers, Nitrates, CCBs

46
Q

When should Beta-Blockers be used in therapy?

A
  • 1st line therapy without contraindications [Bradycardia, AV block, sinus syndrome]

PHRM 845: Therapeutics III (25 decks)

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