chd Flashcards

1
Q

Cardiovascular disease

A

a very broad term that encompasses many different diseases of the heart and blood vessels.

-We will focus on:
•	Atherosclerosis
•	Hypertension
•	Coronary Heart Disease (CHD)
•	Metabolic Syndrome
•	Congestive Heart Failure
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2
Q

Coronary Heart Disease (CHD)

The major underlying cause of CHD

can result in

A

–Also called coronary artery disease (CAD) or ischemic heart disease (IHD).

  • Definition: Heart disease resulting from a lack of adequate blood flow in the blood vessels serving the heart or myocardium (coronary arteries).
  • The major underlying cause of CHD is atherosclerosis: Structural and compositional changes in the innermost or intimal layer of the arteries producing impaired blood flow.

Atherosclerosis in the coronary arteries can result in:

  • angina
  • myocardial infarction: Ischemia in the coronary arteries resulting in necrosis, tissue damage, and sometimes sudden death.

Atherosclerosis in the cerebral arteries can result in stroke.

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3
Q

Major risk factors for CHD (Risk is additive)
(Nonmodifiable)
modifiable

A
(Nonmodifiable)
-	increasing age
-	male sex
-	family history of CHD, especially premature CHD (younger than 60 yr of age)
-	diabetes mellitus
-	 
(Modifiable)
-	tobacco smoke
-	high blood pressure (hypertension)
-	dyslipidemia:  e.g.  total serum cholesterol and LDL-C;  HDL-C
-	physical inactivity
-	overweight and obesity
-	prediabetes (Remember this term from our diabetes classification)
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4
Q

Hypertension

CATEGORY

A

High Normal systolic: 130-139 +/or diastolic 85-89

Hypertension systolic > 140 +/or diastolic > 90

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5
Q

Hypertension

CATEGORY

A

High Normal systolic: 130-139 +/or diastolic 85-89
Hypertension systolic > 140 +/or diastolic > 90

Physician will use a lower cutoff if patients present with multiple risk factors e.g. diabetes

Systolic: BP during contraction
Diastolic: BP during relaxation

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6
Q

•What are myocardial infarction (heart attack) warning signs that should prompt a person to CALL 9-1-1 ? (Heart and Stroke)

A
  • Chest discomfort (uncomfortable chest pressure, squeezing, fullness or pain, burning or heaviness)
  • Discomfort in other areas of the upper body (neck, jaw, shoulder, arms, back)
  • Shortness of breath
  • Sweating
  • Nausea
  • Light headedness
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7
Q

What are signs of stroke that should prompt a person to CALL 9-1-1? (Heart and Stroke)? FAST

A

Face: is it drooping?
Arms: can you raise both?
Speech: is it slurred or jumbled
Time: call 911 right away

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8
Q

TREATMENT AND PREVENTION OF CHD

A
  • Medical procedures e.g. angioplasty, stents, bypass surgery - in Lab
    • Drug therapy
    • Nutritional and other lifestyle
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9
Q

I. DRUG CLASSES OF LIPID ALTERING MEDICATIONS

A
  1. statins
  2. ) PCSK9 Inhibitor
    3) Fibrates
  3. Bile Acid Resins (sequestrants)
    5) Cholesterol absorption inhibitors
    6) Nicotinic acid
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10
Q

II. DRUG CLASSES OF ANTIHYPERTENIVE AGENTS

-there are many different agents that decrease BP by different mechanisms, and more than one agent is often used.

A

1) Thiazide diuretics
2) -Adrenergic blockers
3) Angiotensin-converting enzyme (ACE) inhibitors
4) Angiotensin II Receptor Blockers
5) Ca channel blockers

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11
Q

1) Statins

A
  • ***This is the major category of lipid-lowering drugs used.
  • Major examples are: rosuvastatin, atorvastatin (newer one), pravastatin, simvastatin, lovastatin, fluvastatin
  • Block HMG-CoA reductase, the rate-limiting step in de novo cholesterol synthesis.
  • This is the major category of drugs used for LDL-C lowering (~90% of the market) …but note that they can have some weak effects on HDL-C and TG as well.
  • Remember that the grapefruit-drug interaction is significant for some of the statins (lovastatin, simvastatin, atorvastatin).
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12
Q

2) PCSK9 Inhibitor

A
  • New class of drug recently approved by Health Canada. (hugey expensive and not covered)
  • alirocumab and evolocumab
  • Monoclonal antibodies that inactivate proprotein convertase subtilisin–kexin type 9 (PCSK9)—This causes decreased LDL-receptor degradation, increased recirculation of the receptor to the surface of hepatocytes, and consequent lowering of LDL cholesterol levels in the bloodstream.
  • They have an even greater effect on LDL-C lowering than statins.
  • injected, expensive.
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13
Q

3) Fibrates

A
  • Major examples are: bezafibrate, gemfibrozil, fenofibrate
  • These drugs are peroxisome proliferator-activated receptor  (PPAR) ligands.
  • They are the major drugs used for treating elevated triglycerides, although there can also be effects on LDL-C and HDL-C too.
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14
Q

4) Bile Acid Resins

A

4) Bile Acid Resins (sequestrants) RARELY USED ANY MORE because of fat malabsorption symptom
e. g cholestyramine
- this drug binds bile acids, which are then excreted in the GIT (instead of returning to the liver via enterohepatic circulation)  increases demand by liver for cholesterol (to make more bile acids)  upregulation to increase transcription of LDL receptor gene to bring in more cholesterol  plasma LDL-C decreases.

-Intended use is to decrease LDL-C, but these drugs are little used any more due to the severe GI side effects. Also, they are formulated as a powder that has to be made into a (rather disgusting) drink.

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15
Q

5) Cholesterol absorption inhibitors

A

5) Cholesterol absorption inhibitors never used on its own
e. g. ezetimibe
- Better tolerated than cholestyramine.
- On its own has weak effects on serum LDL-C lowering—more likely to be used in combination with statins.

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16
Q

6) Nicotinic acid

A
  • would be the most effective agent for increasing HDL-C, but very little used because of the severe side effect of flushing.
  • One product, Niaspan®, is better tolerated, but very expensive.
  • Note: Over the counter niacin products marketed to not have this flushing side effect have been modified (often niacinamide), and thus they have lost their ability to alter dyslipidemia.
17
Q

1) Thiazide diuretics

A

-It is mainly this type of diuretic used to treat hypertension.

e. g. hydrochlorothiazide
- acts by: 1) increasing kidney excretion of Na and water, decreasing blood volume, and
2) causing blood vessels to dilate.
- Note potential to cause hypokalemia

18
Q

2) -Adrenergic blockers

A

– blocks -receptors in the heart (sympathetic nervous system) to decrease heart rate and cardiac output.
-However, note that they have another effect, which is to inhibit renin release, so they are rather like the ACE inhibitors below.
e.g. atenolol
Note potential for hyperkalemia.

19
Q

3) Angiotensin-converting enzyme (ACE) inhibitors

A
  • lower blood pressure by increasing dilatation of arterioles (thus decreasing peripheral vascular resistance) by blocking the angiotensin-converting-enzyme (ACE), thus decreasing production of angiotensin II.
    e.g. captopril, benazepril, enalapril, lisinopril, ramipril.
    Note potential for hyperkalemia.
20
Q

4) Angiotensin II Receptor Blockers

A

-Lower blood pressure by interfering with renin-angiotensin system (i.e. blocks the angiotensin II receptor). Has a very similar target as ACE inhibitors (above), so these drugs are highly similar and should rarely (if ever) be used together.
e.g. candesartan, valsartan, losartan, telmisartan, olmesartan.
Note potential for hyperkalemia.

21
Q

5) Ca channel blockers

A

e. g. verapamil, diltiazem, felodipine, nifedipine, amlodipine
- cause arterioles to dilate by altering the movement of Ca.
- Verapamil and diltiazem are in a subclass of Ca channel blockers that primarily reduce heart rate and strength of contraction.
- Remember that the grapefruit-drug interaction is significant for some drugs in this category: felodipine, nifedipine, amlodipine.

22
Q

III. DRUG CLASSES OF DIURETICS

A
  • increase urinary excretion of Na and water to treat problems such as hypertension (as above) and heart failure.
  • see your drug-nutrient interactions notes for the 3 classes of diuretics available.
  • Remember previously discussed variable effects on serum [K], depending on the type of diuretic.
23
Q

VI. DRUG CLASSES OF ANTICOAGULANTS

A
  • These inhibit production of clotting factors.
    1) Warfarin
  • reduces ability of blood to clot by antagonizing vitamin K-dependent production of clotting factors (7 clotting factors). (We will discuss the interaction and recommendations more below).
  • used to reduce risk for stroke and myocardial infarction.

2) A newer group of anticoagulant medications
- Have major advantages over warfarin in: 1) the lack of requirement for regular blood monitoring (don’t have to do as many blood tests). 2) There is no need to monitor vitamin K.
- Those that inhibit clotting factor Xa: 1) Apixaban (Eliquis®), 2) Rivaroxaban (Xarelto®)
- A third one inhibits Thrombin (Factor IIa) - dabigatran (Pradax®).
- These are very expensive, so the warfarin-Vitamin K interaction will remain relevant for patients, at least for some time.

24
Q

Warfarin-Vitamin K interaction:

a) In a patient taking warfarin, what is the current recommendation for amount of vitamin K intake? Why?

– %TTR

A

a) In a patient taking warfarin, what is the current recommendation for amount of vitamin K intake? Why?
The current recommended practice is CONSISTENT vitamin K intake that meets the AI (the recommendation is NOT low vitamin K.). AI: 120 mg for males
90mg for females
Too much warfarin activity can lead to bleeding
Too little warfarin activity can lead to too much clotting- high risk for heart attack and stroke
This takes a lot of blood testing to see if its at the right level

  • Warfarin has a narrow therapeutic window.
  • This is assessed by measuring prothrombin time expressed as the internationalized ratio (INR).

• “Subtherapeutic INR” means too much clotting (not enough warfarin action).

• Unfortunately, despite a high level of monitoring, patients are often not in the therapeutic range if you study this over time.
– %TTR = percentage of time in the therapeutic range.

25
Q

b) Which are the major food sources of vitamin K?
d) What do you think would be your best strategy for confirming in a patient a suspected dietary vitamin K interaction with warfarin?

A

leafy greens, plant oils: soybean, canola, olive and cottonseed oil. Any kind of fermented soybean, natto. Saladdressing, mayonnaise, multivitamin

FFQ, food diary

26
Q

Is the dietary recommendation being followed (consistent vit K intake)?

A
  • -no, did a study of 317 warafarin users- what advice were they given and by who- found that
  • 10% consistent vit k
  • 22% no advice
  • 6% talked to a deititan
  • Theses patientst were not aware of sources of vit k other than green veg

……some newer research…..
• Even if our current recommendation optimal (CONSISTENT vit K) gets followed, would high vit K intake (>AI) be an even better recommendation?

  • Several studies have now shown that those people who usually take low amounts of vitamin K have an increased risk (~3x) of having a subtherapeutic INR(not enough warfarin action) if they increase their vitamin K intake above 100 μg/d on a given day in comparison to when their vitamin K intake stays below 100 μg/d.
  • This increase in risk is not present in individuals with a normal or high usual vitamin K intake.
  • That is, high dietary vitamin K intake is more and more being associated with more stable anticoagulant therapy.

A more recent study (Dr. Ferland) investigated the association between usual vitamin K intake and %TTR in warfarin-treated older adults (Leblanc et al Thrombosis Res 134: 210, 2014). Findings:

  • Higher vitamin K intake was significantly associated with higher %TTR.
  • Higher vitamin K intake was associated with fewer INR tests.
27
Q

Metabolic syndrome:

A

Metabolic syndrome: cluster if factors that increase risk for coronary heart disease and diabetes.
Examples: hypertension, insulin resistance, dyslipedimia, and others