Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ASCVD Risk Factors

A
  • Age
  • Black
  • HTN
  • HDL
  • LDL
  • Total Cholesterol
  • Smoker
  • DM (equivalent vs. RF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatment
ASCVD

A

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

Second line: Pharmacological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Statins
are also known as

A

HMG CoA reductase inhibitors

3-hydroxy 3-methyl glutaryl co enzyme A reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Statin
Indication

A
  • Diabetes Mellitus
  • Hypercholesterolemia / dyslipidemia
  • post-MI
  • primary and secondary prevention ASCVD and CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Statin SE/AE

A

GI: Nausea, vomiting, flatulence, cramps, constipation

MSK: myopathy, myosititis 10%, rhabdomyolysis

Liver: hepatitis and liver failure

Teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Strategy for myopathy
Statins

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

Strategy
1. lower dose
2. switch statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

High Intensity statin therapy
Examples

A

Lower cholesterol > 50%

Atorvastatin40-80mg

Rosuvastatin 20mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Moderate intensity statin therapy
Examples

A

lower cholesterol 30-50%

  • atorvastatin 10mg
  • rosuvastatin 10mg
  • simvastatin 20-40mg
  • pravastatin 40mg
  • lovastatin 40mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

low intensity statin therapy
Examples

A

lower cholesterol < 30%

  • simvastatin 10mg
  • pravastatin 10mg
  • lovastatin 20mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ezetimibe
Indication

A

Second line add on therapy if statin is not working

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bile Acid Sequestrants
Examples

A
  1. Colesevelam
  2. Cholestyramine
  3. Colstipol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Indication
Bile Acid Sequestrants

A

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

3rd line adjunct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
SE/AE Bile Acid Sequestrants
1. GI upset: bloating, nausea, constipation *Not absorbed systemically *safe in all populations
26
Patient Monitoring & Education Bile Acid Sequestrants
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
Ezetimibe Therapeutic Indication
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
Ezetimibe MOA
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
Pharmacokinetics Ezetimibe
Prodrug converted by SI and liver - not CYP450 Active drug: Ezetimibe glucuronide Eliminated in Bile *no dose adjustment needed for renal impairment / elderly
30
SE/AE Ezetimibe
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
Monitoring Ezetimibe
Baseline - LDL, HDL, TC, TG - LFTs - CBC and diff Monitor - 1 month follow up
32
Physiological Function PCSK9
Normally PCSK9 binds to LDL receptors and blocks the uptake of cholesterol from the bloodstream
33
PCSK9 Inhibitors MOA
Monoclonal antibodies that bind to PCSK9 Blocks interaction between PCSK9 and LDL receptors LDL receptors are free to take up cholesterol
34
PCSK9 Examples
1. Evolocumab 2. Alirocumab Proprotein convertase subtilisin/kexin type 9 inhibitors
35
PCSK9 Indications
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
PCSK9 inhibitors Pharmacokinetics
Subcutaneous injection 10-20 day half life
37
PCSK9 inhibitors SE/AE
1. Hypersensitivity (rash, urticaria, vasculitis, angioedema) - requires hospitalization 2. Immunogenicity to monoclonal antibody - antibodies against the drug - inactivate drug 3. Injection site reaction *no drug interactions *costly
38
Fibric acid Derivative Examples
1. Gemfibrozil 2. Fenofibrate 3. Fenofibric acid 4. Benzafibrate
39
Fibrates MOA
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
Fibrate Indication
Hypertriglyceridemia - Lowers TG by up to 90% (Normal TG < 1.7mmol/L) *No effect on death from ASCVD and CVE
41
Fibrates SE/AE
1. GI: Nausea, abdominal pain, diarrhea 2. Hepatitis 3. myopathy, rhabdomyolysis 4. pancreatitis, gallstones 5. Severe skin reactions
42
Fibrates Contraindications
Liver disease Gallbladder disease Pancreatic disease Kidney disease (increase Cr, eliminated by kidney) Rhabdomyolysis
43
Fibrates Patient monitoring
Baseline TG, LDL, HDL, TC Monitor SE: gallbladder disease, liver disease, myopathy
44
Who do you screen for dyslipidemia?
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
How often do you screen for dyslipidemia
Annually low-high risk Every 5 years individuals without risk factors
46
What test are involved in screening
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
What is preferred to LDL for predicting risk of ASCVD?
Non-HDL-C - TG, Chylomycrons, VLDL, IDL, LDL, lipoproteins ApolipoproteinB - attachment and deposition into tissue
48
When do you fast for lipids?
TG > 4.5mmol/L fasting is required food influences TG level
49
Primary Prevention Treatment Pathways
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
Statin Indications
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
Primary Prevention Treatment pathways
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
Secondary prevention Treatment pathways
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
Primary prevention
1. lifestyle 2. statin 3. statin + ezetimibe / bile acid sequestrant
54
Secondary prevention
1. lifestyle 2. statin 3. statin + ezetimibe 4. Statin + ezetimibe + PCSK9 inhibitor
55
Niacin MOA
Decrease HDL catabolism results in increased HDL level 15-20% *low HDL assocaited with increased mortality from CAD
56
Niacin SE
GI: ulceration Skin: flushing, dry Liver: hepatitis Hyperglycemia Hyperuricemia
57
Niacin Contraindications
Diabetes Gout Liver disease GI ulcers

Year 1: Patho/Pharm (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions