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Year 1: Patho/Pharm > CAD and ACS PHARM > Flashcards

CAD and ACS PHARM Flashcards

1
Q

Treatment Pathway
Primary prevention ASCVD

A
  1. +/- ASCVD Risk factors
  2. Framingham Risk Score (10 year risk CVE)

Classify patient based on
1. High 2. moderate 3. low risk

Determines Treatment
1. Pharmacological and/or Non pharmacological
2. Treatment Goal (LDL reduction goal)

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2
Q

ASCVD Risk Factors

A
  • Age
  • Black
  • HTN
  • HDL
  • LDL
  • Total Cholesterol
  • Smoker
  • DM (equivalent vs. RF)
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3
Q

Framingham Risk Score

A
  • Age
  • Gender
  • Smoker
  • SBP
  • HDL
  • Total Cholesterol

Total number points = percentage risk

> 15% high risk
10-15% moderate risk
< 10% low risk

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4
Q

Treatment
ASCVD

A

First line: Diet, exercise, weight loss, smoking cessation

Second line: Pharmacological

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5
Q

Statins
are also known as

A

HMG CoA reductase inhibitors

3-hydroxy 3-methyl glutaryl co enzyme A reductase

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6
Q

Statins
MOA

A
  1. Inhibit HMGCoA Reductase
    -rate limiting step in cholesterol synthesis
    - lower LDL and lower TC
    - ALSO: lower TG, increase HDL
  2. Stabilization Plaque
    - Decrease cholesterol deposit
    - decrease calcification
    - Decrease inflammation
  3. Increase endothelial function
    - Vasodilation
    - Anti-platelet (prevent platelet activation)
    - Anti-coagulation (prevent thrombin formation)
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7
Q

Statin Benefits

A

Reduce HF, MI, CVE, and sudden cardiac death

  • Lower LDL, Total C
  • increase HDL
  • lower TG
  • stabilize plaque
  • decrease inflammation
  • decrease calcification
  • decrease cholesterol deposition
  • increase endothelial function
  • increase vasodilation
  • decrease platelet aggregation
  • decrease coagulation
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8
Q

How does inhibiting HMG CoA reductase decrease LDL in the bloodstream?

A

Inhibition HMG CoA reductase

  • liver cannot synthesize cholesterol
  • decrease endogenous LDL synthesis
  • liver expresses more LDL receptors
  • uptake of LDL increased
  • unable to synthesize apolipoprotein B
  • this decreases VLDL and TG synthesis
  • HDL increases to get cholesterol from the non-hepatic tissues and bring it back to the liver
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9
Q

Statin
Indication

A
  • Diabetes Mellitus
  • Hypercholesterolemia / dyslipidemia
  • post-MI
  • primary and secondary prevention ASCVD and CAD
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10
Q

Statin
Pharmacokinetics

A

Metabolized by CYP3A4
- CYP3A4 inhibitors increase to toxic level
- Ex. Macrolide Abx., Azoles., CCB

Asians 2x level at same dosage
- reduced dosage needed

Give at night
- liver synthesizes cholesterol at night

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11
Q

Statin SE/AE

A

GI: Nausea, vomiting, flatulence, cramps, constipation

MSK: myopathy, myosititis 10%, rhabdomyolysis

Liver: hepatitis and liver failure

Teratogenic

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12
Q

What increases the risk of rhabdomyolysis
Statin therapy

A
  • age
  • frail
  • malnourished
  • alcohol
  • CYP3A4 inhibitors
  • Asian
  • hypothyroidism
  • Low Vitamin D
  • Low Coenzyme Q
  • High statin dosage
  • Rovustatin (highest risk rhabdomyolysis)
  • Fibrates, niacin, exetimibe
  • CKD, DM, Thyroid disease
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13
Q

Strategy for myopathy
Statins

A
  • 10% patients will get myopathy (muscle aches, weakness)

Strategy
1. lower dose
2. switch statin

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14
Q

When to D/C Statin

A

S&S hepatitis or liver failure
- LFT > 3x normal
- anorexia, nausea, vomiting, dark urine
- D/C statin

S&S Rhabdomyolysis
- CK elevated
- K+ elevated > 3x normal
- BUN:Cr elevated
- D/C statin
- Tea coloured urine = myoglobin in urine

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15
Q

Statin
Therapeutic Monitoring

A

Baseline:
- Lipid pannel (LDL, TG, TC, HDL)
- LFT (> 3x normal, reduce dose, repeat)
- CK (> 3 x normal, reduce dose, repeat)
- Cr (reduce dose)
- TSH

Monitoring:
- LFT 4-6 weeks after starting
- repeat every 6 to 12 months

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16
Q

High Intensity statin therapy
Examples

A

Lower cholesterol > 50%

Atorvastatin40-80mg

Rosuvastatin 20mg

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17
Q

Moderate intensity statin therapy
Examples

A

lower cholesterol 30-50%

  • atorvastatin 10mg
  • rosuvastatin 10mg
  • simvastatin 20-40mg
  • pravastatin 40mg
  • lovastatin 40mg
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18
Q

low intensity statin therapy
Examples

A

lower cholesterol < 30%

  • simvastatin 10mg
  • pravastatin 10mg
  • lovastatin 20mg
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19
Q

Statin
Contraindications/precautions

A

Contraindication:
- viral or alcoholic hepatitis
- pregnancy
- hx. rhabdomyolysis
- niacin (vitamin B3)

Caution:
- NAFLD
- Fibrates
- Ezetimibe
- frail, elderly, hypothyroidism, vitamin D deficiency, Coenzyme Q deficiency

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20
Q

Ezetimibe
Indication

A

Second line add on therapy if statin is not working

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21
Q

Bile Acid Sequestrants
Examples

A
  1. Colesevelam
  2. Cholestyramine
  3. Colstipol
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22
Q

Indication
Bile Acid Sequestrants

A

Moderate-Intermediate Risk
- Statin + ezetimibe
- Bile acid sequestrant if do not tolerate ezetimibe

3rd line adjunct

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23
Q

Therapeutic Effect
Bile Acid Sequestrant

A

Reduce cholesterol 50% when combined with statin

  1. Decrease LDL
24
Q

MOA
Bile Acid Sequestrants

A

Bile acid sequestrants are resins

  • Bind and prevent absorption bile
  • Liver produces more LDL receptors (to increase endogenous synthesis)
  • Increase uptake LDL
25
Q

SE/AE
Bile Acid Sequestrants

A
  1. GI upset: bloating, nausea, constipation

*Not absorbed systemically
*safe in all populations

26
Q

Patient Monitoring & Education
Bile Acid Sequestrants

A

Baseline
- LDL, HDL, TC, TG

Monitoring
- 1 month follow up
- Lipid levels

Patient education
- Take drugs 1 hour before, 4 hours afterwards
- decrease absorption fat soluble vitamins and drugs
- drink lots of water
- increase fibre intake

27
Q

Ezetimibe
Therapeutic Indication

A

Intermediate/High Risk
- Statin + Ezetimibe (second line added on)

High Risk
- Statin + Ezetimibe (second line add on)

*bile acid sequestrant is an alternative therapy
*Add on PCSK9 if still not controlled

28
Q

Ezetimibe
MOA

A

Prevents dietary cholesterol absorption by brush boarder cells of the SI

Liver increase synthesis of LDL receptors, increased uptake LDL from circulation

  • Reduced LDL, TG, apolipoprotein B
  • Reduction > 20% when combined with statin

*No evidence reduces ASCVD

29
Q

Pharmacokinetics
Ezetimibe

A

Prodrug converted by SI and liver
- not CYP450

Active drug: Ezetimibe glucuronide

Eliminated in Bile

*no dose adjustment needed for renal impairment / elderly

30
Q

SE/AE
Ezetimibe

A
  1. Hepatitis
  2. Pancreatitis (when combined with fibrates, increase gallstones)
  3. Myopathy
  4. Rhabdomyolysis
  5. Thrombocytopenia

*risk increases when combined with statins or fibrates

31
Q

Monitoring
Ezetimibe

A

Baseline
- LDL, HDL, TC, TG
- LFTs
- CBC and diff

Monitor
- 1 month follow up

32
Q

Physiological Function
PCSK9

A

Normally

PCSK9 binds to LDL receptors and blocks the uptake of cholesterol from the bloodstream

33
Q

PCSK9 Inhibitors
MOA

A

Monoclonal antibodies that bind to PCSK9
Blocks interaction between PCSK9 and LDL receptors
LDL receptors are free to take up cholesterol

34
Q

PCSK9 Examples

A
  1. Evolocumab
  2. Alirocumab

Proprotein convertase subtilisin/kexin type 9 inhibitors

35
Q

PCSK9
Indications

A

Intermediate-moderate risk
- Statin therapy + ezetimibe (second adjunct) / bile acide sequestrant
- Does not work to lower
- addition PCSK9 inhibitor

High Risk
- Statin therapy + ezetimibe (second adjunct) / bile acid sequestrant
- does not work to lower
- Addition PCSK9

*Third line adjunct

36
Q

PCSK9 inhibitors
Pharmacokinetics

A

Subcutaneous injection
10-20 day half life

37
Q

PCSK9 inhibitors
SE/AE

A
  1. Hypersensitivity (rash, urticaria, vasculitis, angioedema)
  • requires hospitalization
  1. Immunogenicity to monoclonal antibody
  • antibodies against the drug
  • inactivate drug
  1. Injection site reaction

*no drug interactions
*costly

38
Q

Fibric acid Derivative
Examples

A
  1. Gemfibrozil
  2. Fenofibrate
  3. Fenofibric acid
  4. Benzafibrate
39
Q

Fibrates
MOA

A

Activates peroxisome proliferator activated receptor alpha (PPAR alpha)

Increases lipolysis
Increase chylomicrons in the blood
Increase cholesterol in the bile for excretion

  • Lowers TG 20-90%
  • minimal effect LDL (lower), HDL (increase)
40
Q

Fibrate
Indication

A

Hypertriglyceridemia
- Lowers TG by up to 90%

(Normal TG < 1.7mmol/L)

*No effect on death from ASCVD and CVE

41
Q

Fibrates
SE/AE

A
  1. GI: Nausea, abdominal pain, diarrhea
  2. Hepatitis
  3. myopathy, rhabdomyolysis
  4. pancreatitis, gallstones
  5. Severe skin reactions
42
Q

Fibrates
Contraindications

A

Liver disease
Gallbladder disease
Pancreatic disease
Kidney disease (increase Cr, eliminated by kidney)
Rhabdomyolysis

43
Q

Fibrates
Patient monitoring

A

Baseline
TG, LDL, HDL, TC

Monitor
SE: gallbladder disease, liver disease, myopathy

44
Q

Who do you screen for dyslipidemia?

A

Men/women >/= 40 years of age

Anyone with the following (at any age):
dyslipidemia (or FHx)
atheroscelerosis
AAA
MI
Stroke (FHx CVD)
smoking
HTN (or pregnancy HTN)
DM
erectile dysfunction
CKD
inflammatory diseases (RA, SLE, PsA, AS, IBD)
COPD

45
Q

How often do you screen for dyslipidemia

A

Annually low-high risk

Every 5 years individuals without risk factors

46
Q

What test are involved in screening

A
  1. history
  2. physical examination
  3. lipid pannel
    - TC
    - HDL
    - non HDL C = TC - HDL (atherogenic lipids, CVR*)
    - LDL
    - TG
  4. FBG and A1C
  5. Lipoprotein (*genetic risk CVD)
  6. Apolipoprotein B (*CVR)
47
Q

What is preferred to LDL for predicting risk of ASCVD?

A

Non-HDL-C
- TG, Chylomycrons, VLDL, IDL, LDL, lipoproteins

ApolipoproteinB
- attachment and deposition into tissue

48
Q

When do you fast for lipids?

A

TG > 4.5mmol/L
fasting is required
food influences TG level

49
Q

Primary Prevention
Treatment Pathways

A

Primary prevention
- prevent ASCVD development

Screen for dyslipidemia
1. FRS (age, gender, smoking, TC, HDL, SBP) / 10
2. lipid pannel (LDL, non-HDL-C)
3. lipoprotein levels (ApoB)

  1. High Risk > 20%
    - statin + Behaviour
  2. Moderate risk 10-20% + CVRF present / dyslipidemia
    - statin + behaviour
  3. Low risk < 10% and LDL < 5mmol/L
    - behaviour modification only

*If statin > 5mmol/L start statin + behaviour
*If DM start statin (equivalent to having ASCVD)

50
Q

Statin
Indications

A
  1. ASCVD or ASCVD risk factors
    - anything that causes atherogenesis
    - inflammatory diseases
    - CVD
    - HTN
    - DM
    - CKD
    - Stroke, TIA
    - AAA
    - PAD
  2. Dyslipidemia
    - LDL > 5mmol/L
    - apoB > 1.45mmol/L
    - nonHDLC > 5.8mmol/L
  3. FRS > 20% or FRS 10-20% with CVRF or FRS < 10% with dyslipidemia as defined above
51
Q

Primary Prevention
Treatment pathways

A
  1. Low risk
    LDL < 5mmol/L
    FRS < 10%
    - behavioural modification only
    LDL > 5mmol/L
    - Statin therapy
  2. Intermiediate or high risk
    - first line: statin therapy

LDL > 2, apoB > 0.8 non HDL > 2.6 (remains elevated)
- second line: ezetimibe
- alternative second line: bile acid sequestrant
*PCSK9 inhibitors are not used for primary prevention

52
Q

Secondary prevention
Treatment pathways

A
  1. Low risk
    - statin
    - second line ezetimibe or PCSK9 inhibitor
  2. intermediate
    - statin
    - second line ezetimibe/bile acid
    - third adjunct if remains elevated PCSK9
  3. high risk
    - statin
    - second line adjunct ezetimibe +- PCSK9
53
Q

Primary prevention

A
  1. lifestyle
  2. statin
  3. statin + ezetimibe / bile acid sequestrant
54
Q

Secondary prevention

A
  1. lifestyle
  2. statin
  3. statin + ezetimibe
  4. Statin + ezetimibe + PCSK9 inhibitor
55
Q

Niacin
MOA

A

Decrease HDL catabolism
results in increased HDL level 15-20%

*low HDL assocaited with increased mortality from CAD

56
Q

Niacin
SE

A

GI: ulceration
Skin: flushing, dry
Liver: hepatitis
Hyperglycemia
Hyperuricemia

57
Q

Niacin
Contraindications

A

Diabetes
Gout
Liver disease
GI ulcers

Year 1: Patho/Pharm (45 decks)

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