Psychiatry of CV - Heinrich Flashcards

1
Q

Depression worsens CVD outcomes. Recall some etiologies explaining why this may be the case.

A

Behavioral risk factors such as treatment non-adherence, poor lifestyle, and (maybe) personality typing.

Physiologic risk factors such as ANS dysfunction, HPA dysfunction, and immune/platelet dysfunction.

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2
Q

What implications might beta-blockers have on depression?

Any other neuropsych implications?

A

No proven increase in rates of depression, even for the lipophilic beta-blockers.

Some neuropsych side effects do occur: Lethargy, fatigue, drowsiness, sleep disorders. Eh.

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3
Q

How is lithium affected by hypertensive medications?

A

Thiazide diuretics increase lithium levels (promote tubular reabsorption).

Loop diuretics and ACE-Is may increase lithium toxicity.

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4
Q

Describe a couple of common interactions between antihypertensive medications and antidepressants.

A

Beta blockers (eg metoprolol) are often metabolized by 2D6, which is downregulated by paroxetine (an SSRI). This can cause dangerous decreases in heart rate and BP…

Clonidine and Mirtazapine have opposing effect on the alpha-2 receptor. Mirtazapine may displace clonidine.

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5
Q

How can stress trigger acute cardiac episodes?

Name an example of this.

What drug is especially useful for this illness?

A

Catecholaminergic surge from extreme emotion or stress can cause episodes, perhaps through vasoconstriction or nodal influence.

Takotsubo cardiomyopathy.

Beta-blockers.

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6
Q

How does schizophrenia affect clinical outcomes?

What CV diseases is it a risk factor for?

A

Schizophrenia increases all-cause mortality by 2-3x. Unnatural causes by 7.5x!

Pretty much anything: Obesity, diabetes, hypertension, dyslipidemia…

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7
Q

Why is schizophrenia a major risk factor for metabolic syndrome?

A

Schizophrenics may have worse lifestyles, resulting from their social stigmas as well as depression.

Just as importantly, antipsychotic medications often cause weight gain.

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8
Q

Describe the trend of weight gain with antipsychotic use.

Which are the worst about this? The best?

A

Weight gain is most rapid during first year of treatment. Worse in hte young, initially thin, cannabis users, non-whites and those with a family history of obesity.

Clozapine & Olanzapine cause the most gain. Aripiprazole and Ziprasidone cause the least.

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9
Q

What are NHANES III and CATIE?

A

Both are public health studies–NHANES more general, CATIE specifically investigating antipsychotics.

CATIE found worse outcomes for schizophrenics in all factors.

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10
Q

In a discussed case, a psychiatric patient experienced prolonged Q-T syndome and TdP as the result of her medication. Which was responsible?

A

Ziprasidone caused her initial episode, but the second episode didn’t improve until fluconazole/trazodone were discontinued. Takeaway: Many drugs can affect the Q-T interval.

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11
Q

QT prolongation occurs as a result of alteration of phase ___ of the action potential, in which ___ channels are open.

A

3; K+

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12
Q

What is the “teach the tangent” method to calculating QT interval?

How can the QTc be found from this?

A

Determine the “end” of the T wave by drawing a tangent to its steepest slope and taking the intersection point of the baseline. Measure from there to the start of the Q wave.

QTc = QT / sqrt(RR)

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13
Q

What is the importance of the QT interval?

What QT intervals are considered normal?

A

QT interval determines risk of developing Torsades de Pointes, and is a “surrogate marker to predict (drug-related) cardiac morbidity and mortality”

<440ms in men, <450ms in women.

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14
Q

What are the modifiable risk factors that influence QT prolongation?

What are the non-modifiable risk factors that influence QT prolongation?

A

Modifiable: Bradycardia, Electrolyte abnormalities, drug regimen.

Non-modifiable: Age (worse >65), Gender (worse female), circadian rhythm (worse at night/morning), genetic LQTS and CVDs.

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15
Q

When does QT prolongation become alarming/need intervention?

How can it be treated?

A

When the QTc exceeds 500ms, or increases 60ms above the patient’s (pre-drug) baseline.

Modify the drug regimen and correct electrolyte abnormalities.

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16
Q

What are the appropriate diagnostic and treatment measure to take when a patient presents with acute poisoning?

A

Diagnosis: Besides Hx & PE, identify toxidrome and conduct toxin assays.

Treatment: ABCs, DONT (dextrose, oxygen, naloxone, thiamine), decontamination. (focused therapy?)

17
Q

What are the indications of TCAs?

How popular are they? Why?

A

For pain, depression, neuropathy, anxiety, migraine prophylaxis, and “cyclic vomiting syndrome”.

Not at all. They have many side effects, and high mortality associated with use.

18
Q

Why does TCA overdose affect heart function?

How does this present?

How is it treated?

A

Blocks the cardiac fast sodium channels (in addition to many, many other receptors)

Prolonged and abnormal QRS complex. QT/PR prolongations. Blocks. Right axis deviation?

Sodium bicarbonate.