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IP-9 Final exam > ED/CAD > Flashcards

ED/CAD Flashcards

1
Q

What is ED

A

Inability to attain or maintain an erection sufficient for vaginal intercourse.

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2
Q

Explain the epidemiology associated with ED

A

Affects men over 40. Prevalence increases with advancing age.

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3
Q

Development of ED has been linked to which other comorbidities

A

Diabetes, hypertension, hyperlipidemia, metabolic syndrome, depression and lower UT symptoms

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4
Q

ED is associated with an increased risk of…

A

CVD, CAD, stroke and all cause mortality.

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5
Q

What 3 things might be a predictor of ED?

A

Smoking, obesity, and limited/absence of physical exercise.

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6
Q

Explain the physiology of an erection

A

NO, released from the endothelium and parasympathetic nerve terminals is the primary NT involved in penile erection. NO-dependent relaxation of cavernosal smooth muscle compresses veins in the penis, occluding venous return and results in erection.

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7
Q

Explain why ED is a mixed psychogenic and organic nature

A

Performance anxiety relates to fear of failure during intercourse and organic causes includes neurogenic, endocrinological, vasculogenic, drug induced depression and local penile factors.

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8
Q

Explain the functions of androgens in ED

A

Androgens enhance sexual desire. Testosterone is important in the regulation of NO synthase and PDE5 inside the penis.

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9
Q

Drugs associated with ED. Which 2 classes are most common?

A

Antiandrogens: GnRH agonists
Antihypertensives (most common): Thiazide diuretics, B-blockers, CCB
Antiarrhythmics: Digoxin, amiodarone, disopyramide
Statins: Although controversial
Psychotropic drugs (most common): TCA, SSRI, phenothiazines, butyrophenones
Recreational drugs: MJ, opiates, cocaine, nicotine, alcohol.

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10
Q

What are the first and second most common risk factors of AD?

A

1st: Age
2nd: Type II diabetes

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11
Q

Main goals of assessment of ED?

A

Establish whether the disorder truly is ED, identify the cause of the disorder, and ascertain risk factors and potentially life-threatening comorbid disorders associated with ED.

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12
Q

Explain low risk and provide recommended treatment

A

Low risk is less than 3 major risk factors-controlled hypertension, mild valvular disease, LVD (NHYA I and II)
Sexual activity can be continued and oral PDE-5 inhibitor can be given.

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13
Q

Explain intermediate risk and provide recommended treatment

A 
At least 3 CAD risk factors: Mild stable angina, asymptomatic (>6-8 weeks) after MI, moderate stable angina, MI for over 2 weeks, but less than 6 weeks, NHYA class III, history of stroke, history of TIA.
Treatment: In depth CV assessment to re-categorize the patient before providing treatment
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14
Q

Explain high risk and provide recommended treatment

A 
High risk: Unstable or refractory angina, uncontrolled HTN, CHF class IV, MI < 2 weeks ago, high-risk arrhythmias, obstructive hypertrophic cardiomyopathies, or moderate-severe valve disease. 
Treatment: Stop sexual activity and stabilize cardiovascular condition first the proceed to ED treatment (REFER to cardiologist)
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15
Q

What are the 2 basic lab tests that should be performed when ED is suspected?

A

Fasting blood sugar and testosterone. Because ED is s strong predictor of vascular disease, clinicians should order lipids also.

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16
Q

Indications for referral to a specialist in ED

A

Psychiatric problems, CNS disorders, complex endocrine disorders, severe CVD, lifelong EF, penile fibrosis, congenital penile anomalies, PDE-5 inhibitor failure

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17
Q

What lifestyle modifications can help improve ED?

A

Smoking and alcohol cessation, work out to prevent obesity.

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18
Q

What is the mechanism of action of the PDE-5 inhibitors?

A

By inhibiting the enzyme PDE-5 we get increased levels of cGMP which decreased intracellular calcium, maintains smooth muscle relaxation and results in rigid erection.

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19
Q

PDE4 inhibitors are contraindicated in whom?

A

Those taking nitrates because of the severe risk of hypotension.
Also, caution should be taken when using these medications in patients with CVD (uncontrolled HTN and unstable angina) and in patients taking a-blockers.

20
Q

Most common adverse effects with the PDE5 inhibitors?

A

Headache and flushing, dyspepsia, nasal congestion and dizziness. Tadalafil can cause myalgia and pain at different body sites.

21
Q

How does the Lancet article define PDE5 failure?

A

Inability to attain or maintain erection during sex on at least 4 consecutive occasions, in spite of optimum drug dosing.

22
Q

What are first, second and third line treatments for ED?

A

1st line: PDE-5 inhibitors
2nd line: Intracavernosal injection or vacuum constrictive devices
3rd line: Penile prosthesis

23
Q

Who is most likely a candidate for intracavernosal injections?

A

Those who failed or disliked PDE-5 inhibitors, and those with spinal cord injuries or post-radical prostatectomy.

24
Q

List the intracavernosal injections and their most common adverse effects

A

Alprostadil, papaverine, phentolamine and vasoactive intestinal polypeptide. Side effects include priapism and penile fibrosis.

25
Q

How do vacuum constrictive devices work and what are the side effects associated with it?

A

By applying continuous negative pressure to the shaft, it helps draw blood into the corpora cavernosa. Side effects include petechiae, penile numbness and delayed ejaculation.

26
Q

Rank the PDE5 inhibitors from shortest to longest duration… same for half-life

A

Sildenafil (4 hours), vardenafil (4-5 Levitra or 4-6 hours Staxyn), avanafil (4-5 hours), tadalafil (24-36 hours)

27
Q

Rank the PDE5 inhibitors from fastest to slowest onset

A

Avanalfil (0.5-0.8 hours), Sildenafil (0.5-1 hour), vardenafil (0.7-0.9 hours Levitra, 1..5 hours Staxyn), tadalafil (2 hours)

28
Q

Initial dose for each of the PDE5 inhibitors

A

Sildenafil 50mg 30-60 minutes before
Vardenafil: 10mg PO (levitra) 10mg SL for Staxyn
Tadalafil: 10mg PO at least 30 min before (2.5mg PO QD)
Stendra (avanafil): 100mg PO 15-30 minutes before

29
Q

Explain how inhibiting other PDE isoforms can cause other adverse effects. Which medications inhibit these other isoforms?

A

Tadalafil also inhibits PDE 11 which can cause lower back and limb muscle pain.
Sildenafil also inhibits PDE 6 in the photoreceptor cells in rods and cones leading to increased sensitivity to light, blurred vision or loss of blue-green color discrimination.

30
Q

How long should nitrates be withheld before administering a PDE5 inhibitor? Why is this a concern?

A

Nitrates are contraindicated in patients taking PDE5 inhibitors due to life threatening severe hypotension. Nitrates should be withheld for 24 hours after PDE5 inhibitor administration (48 hours for Cialis) and should not be taken for 1 week after administration of a nitrate.

31
Q

What recommendations should be given to men initiating a PDE5 inhibitor who have been stable on a-blockers?

A

Initiate PDE5 inhibitor at the lowest starting dose.

32
Q

When should testosterone levels be measured?

A

In all men with diagnosis of organic ED and especially in those who failed PDE5 inhibitor therapy. Total testosterone (TT) level before 11 am because testosterone levels wean over the day so even men with normal testosterone levels will look low if levels are taken in the afternoon. TT levels should be measured on 2 separate mornings.

33
Q

Recognize testosterone levels and when we treat

A

TT level > 350 ng/dL does not require substitution. TT < 230 ng/dL usually benefit from TRT. Any levels in-between may be considered for a 3-6 month trial

34
Q

FDA issued a warning regarding ______ with respect to men treated with TRT

A

Increased risks of MI and stroke

35
Q

Risk factors for ACS

A

Age (>45 men >55 women), hypertension, hyperlipidemia, smoking, physical inactivity, unhealthy diet, obesity, diabetes, family history of chest pain, heart disease or stroke,

36
Q

Differentiate UA, NSTEMI and STEMI based on symptoms, ECG and diagnostic test results

A

UA and NSTEMI are similar conditions but differ in severity. NSTEMI and UA may look similar on the ECG (ST depression, T-wave inversion or normal). NSTEMI and STEMI will have increased cardiac enzyme levels. UA will have no biomarkers. STEMI will have an elevated ST segment on the ECG.

37
Q

Identify signs and symptoms of ACS

A

Classic symptom is chest pain. N/V, sweating and SOB may also occur. Chest pain normally present at rest and the pain may radiate to shoulder, back, down the left arm or even to the jaw. Not all MI patients will present with chest pain.

38
Q

Treatment for a STEMI

A

Intranasal oxygen if O2 < 90%, SL NTG, aspirin, beta-blocker, anticoagulation and immediate reperfusion therapy.
Reperfusion therapy can include PCI, fibrinolytic (-plases; clot busters) if chest pain occurred less than 12 hours ago and they were unable to reach PCI within 2 hours after first medical contact.
Regardless of repercussion technique used everyone should receive anticoagulant (Heparin, LMWH or fondaparinux).
Anti-platelet therapy: On top of the ASA, one of the p2y12 inhibitors.

39
Q

What medication is approved for patients with unstable angina undergoing PCI? what is this drugs mechanism of action?

A

Bivalirudin- a direct thrombin inhibitor

40
Q

Treatment of UA and NSTEMI

A

Intranasal oxygen if < 90%, SL NTG, ASA, oral B-blocker, anticoagulant and possibly a GP IIb/IIIa inhibitor (eptifibitide).
Fibrinolytic therapy is never administered, GP IIb/IIIa for high risk patients only.
Early invasive strategy (medium to high risk patients) and ischemia guided therapy (low risk patients) based on their TIMI score.

41
Q

Every patient who experiences an MI should be discharged on what medications?

A

Aspirin, B-blocker, ACEi, high intensity statin, P2Y12 inhibitor (most patients).

42
Q

How can you tell if someone has stable ischemic heart disease (SIHD)?

A

When a patient has been free of recurrent ACS for >1 year beyond the most recent ACS episode.

43
Q

Dual antiplatelet therapy (DAPT) is not recommended for…

A

SIHD patients wihtout a history of ACS, stent implantation or CABG within the last 12 months.

44
Q

How long should DAPT be continued?

A

For at least 1 month if they have a bare metal stent and for at least 6 months if they receive a drug eluting stent.

45
Q

Explain what factors are considered when deciding whether or not the patient should be continued on DAPT

A

A P2Y12 inhibitor added to aspirin therapy will reduce the risk of ischemia but will increase the risk of bleeding. So, if the benefits of preventing another heart attack outweigh the increased bleeding risk then DAPT can be considered. If bleeding is the primary concern, only the aspirin should be continued.

46
Q

The DAPT score tool has been developed to help weight the risks vs. benefits associated with DAPT. Explain what scores we are looking for and what they mean

A

A score of 2 or more indicates it is reasonable to continue DAPT. A score < 2 demonstrates DAPT should be d/c and only ASA should be continued.

IP-9 Final exam (3 decks)

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