CV and Psych Flashcards

1
Q

_____% of adult population has a mental disorder
_____% of people with mental disorders have medical conditions
____% of people with medical conditions
______% of adults with medical ocnditions have mental disorders

A

25%
68%
58%
29%

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2
Q

What happens to Cardiac risk factors in pts with depression. What about post-MI mortatlity?

A

doubles.. much higher CV risk

associated with increased mortality post-MI

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3
Q

Depression has etiologies of increased morbidity and mortality.
Behavioral risk include:
Physiologic risk factors include:

A
• Behavioral risk factors
– Treatment non-adherence
– Lifestyle factors
– Personality types (A and D)
• Physiologic risk factors
– Autonomic nervous system dysfunction
– Inflammation/Platelet reactivity
– Hypothalamic pituitary adrenal (HPA) axis dysregulation
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4
Q
The link between beta-blockers and 
depression started with numerous case 
reports 
– There was a specific concern for the more \_\_\_\_\_\_\_ ones that more readily cross the blood-brain barrier
Should people stop taking B Blockers?
A

lipophilic
No, styematic studies failed to find increased rates of depression:
W/ beta-blockers we do see:
– Drowsiness, fatigue, lethargy, and sleep disorders

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5
Q

What drugs will increase lithium concentrations (lithium is classic med for bipolar)

A

anti HTNs like
Thiazide diuretics
Loop diuretics and ACEi have varied risk of lithuim toxicity

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6
Q

How does thiazide cause lithium toxicity?

A

Thiazide diuretics increase lithium levels
– Due to their site of action on the distal tubal which causes a compensatory proximal tubular reabsorption of sodium and lithium
– Lithium levels are often increased by 20% to 40%

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7
Q

What things are we more concerned with then ACEi and loop diuretics causing lithium toxicity?

A

– Patient factors such as volume status, renal
function, polypharmacy, and other medical
comorbidities are often more important
predisposing factors of lithium toxicity than these medications

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8
Q

A young patient you are seeing been on an Paroxetine, an SSRI, for some time to regulate her depression. She is 30 years old and has hypertension. A classmate recommends because she is you, a selective Bblocker like Metoprolol would be excellent. Do you agree?

A

– Metoprolol is extensively metabolized via 2D6 and Paroxetine, an inhibitor of 2D6, has been shown to effect metoprolol metabolism
• 2x increase in both maximum plasma
concentration and terminal elimination half-life
• Decrease in exercise heart rate and SBP

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9
Q

You are seeing a pt for hypertension that is on Mirtazapine to help with anxiety and depression. What type of drugs to tx his hypertension would be a bad mix with Mirtazapine as it is an alpha-2 antagonist?

A

Clonidine is antiHTN by acting on central alpha-2 receptors; at high doses, mirtazapine competes and may displace clonidine thus lose the antiHTN effect

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10
Q

Woman at funeral.. horrible substernal chest pain and SOB
• Vitals– T 99.0, BP 106/50 mmHg, HR 112 bpm, RR 32/min, POx 89% on room air.
Physical Examinations
– Diaphoretic
– Jugular venous distension
– Crackles in the bilateral basilar lung fields
Physical Examinations
– Diaphoretic
– Jugular venous distension
– Crackles in the bilateral basilar lung fields
NEXT STEP?

A

– Administered O2, ASA, NTG, beta-blocker and diuretic

Take urgently to cardiac catheterization

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11
Q

Funeral woman before was taken to cath lab and we get results:
– All coronary arteries were patent with no marked obstruction
– The LV had a large, severely hypokinetic
to akinetic segment
– All other myocardial segments contracted normally
– The estimated ejection fraction was 25%
Dx?

A

Takotsubo cardiomyopathy

–> pt can have full recover

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12
Q
Mortality Rates and Schizophrenia
• Standardized mortality ratio
– All cause mortality rate: 
• Natural cause: 
• Unnatural cause: 
Main trend in mortality rates of schizophrenics
A

2.58 (so 2.5xs higher mortality then normal)
2.41
7.50
Mortality rates are INCREASING

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13
Q

What trend do we see with modifiable CVD risk factors in patients with Schizophrenia and Bipolar?

A

very much elevated, especially schizophrenics:

much higher for smoking in both, as well as obesity and metabolic syndrome

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14
Q

The diagnosis of schizophrenia associated with 34% increase risk of mortality following MI… why is this?

A

Suboptimal medical care; many pts with schizophrenia aren’t getting treated for the diesases they have such as: dyslipidemia, HTN and DM

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15
Q

describes a group of cardiometabolic risk factors associated with insulin resistance

A

Metabolic Syndrome

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16
Q

Metabolic syndrome is much higher in which populations of people according to the CATIE study

A

mental illness we see a double in metabolic sydrome, even more so in women with mental illness

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17
Q

What are some general etiologic concerns in pts with schizophrenia

A
General etiology concerns
– Schizophrenia
• Suspicion
• Stigma
• Negative symptoms
• Executive dysfunction
• Medications
– Lifestyle
• Sedentary lifestyle
• Lack of regular physical activity
• Poor food intake
• Substance use
• High rates of smoking
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18
Q

Olanzipine is used to tx bipolar and schizophrenia and has what concerning side effect?

A

weight gain; increased metabolic syndrome

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19
Q

What is the correlation between obesity, mental illness and medication

A

obesity is 2x more common in mental ill…
Clinical course of weight gain
– Weight gain tends to slow after the first year of treatment
– Longer-term progressive increases have been reported

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20
Q

• Risk factors for antipsychotic-induced
weight gain
– Demographic risk factors

A
  • Younger age
  • Lower initial BMI
  • Personal or family history of obesity
  • Non-white ethnic background
  • Cannabis use
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21
Q

• Risk factors for antipsychotic-induced
weight gain
– Clinical risk factors:

A
  • Choice of antipsychotic

* First episode psychosis/Previous antipsychotic exposure

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22
Q

What antipsychotic shows most weight gain after 10 weeks? the least?

A

Olanzapine worst followed by Clozapine

Ziprasidone was least wt gain and Risperidone wasn’t bad either

23
Q

What CVD risk factors did the CATIE group of individuals have that was much higher then normal?

A

increase HDL, smoking, DM and HTN

*overall have higher CVD risk!

24
Q

What modifiable CV risk factors need to be assessed in pts to eval for metabolic disease?

A
– Weight
– BMI
– Waist circumference
– Fasting lipids
– Fasting glucose
– Blood pressure
25
Q

Why are modifiable risk factors such an important intervention in as far as CV disease?

A
• Reduction of modifiable risk factors has 
long-term benefits
• Strategies
– Antipsychotic choice/change
– Lifestyle modifications
– Medication augmentation
• Even modest reductions in any one of 
the modifiable risk factors for 
cardiometabolic diseases can lead to 
substantial benefits
26
Q

A patient on Hyokalemia can end up with

A

prolongation of QT; anything above 500 msec is concerning

27
Q

What are symptoms of lithuim toxicity

A

– Coarse upper-extremity tremor, impaired attention, and confusion/ delerium
high normal levels is 1.2 mmol/L
–can cause sever renal damage so you’ll see elevated

28
Q

What would you do for a pt with severe lithium toxicity?

A

hemodialysis

29
Q

asymptomatic non-sustained polymorphic ventricular tachycardia (toursades) are often preceded by:

A

preceded by a prolonged QT

30
Q

What is most important in repolarization of myocardium?

A

outward flow of K+

31
Q

Describe what happens in these phases of repolarization
Phase 1
Phase 2
Phase 3

A

Phase 1 Repolarization begins; Opening of K channels (outward K flow)
Phase 2: Plateau phase/Repolarization continuesOpening of Ca channels (inward Ca flow)
Phase 3: Repolarization; Opening of fast K rectifier channels (outward K flow)

32
Q

Includes the ventricluar depolarization and repolarization; (more repolarization then depolarization)

A

QT interval

33
Q

Rule of thumb for length of QT interval

A

should be less then half of the preceding RR interval

34
Q

Whats the simple two step approach to measure QT interval with lead II or V5

A

A simple two step approach (lead II or V5)

  1. The end of the T wave was defined as the intersection of a tangent to the steepest slope the T wave and the baseline
  2. QTc was defined as QT/√RR from the RR interval between the measured and the preceding complex
35
Q

QTc prolongation increases risk of:

A

TdP

36
Q

has become a surrogate marker to predict drug-related cardiac morbidity and mortality

A

• QTc prolongation

37
Q

Normal QT for women

for men

A

women: 500msed

38
Q

Non modifiable risk factors for QT prolongation

A

Genetic LQTS, Age >65, Female, Circadian rhythm, CV disease

39
Q

Modifiable risk factors for QT prolongation

A

Bradycardia, Electrolyte abnormalities (HypoMagnesium and HypoKalemia)
Pharmacokinetic and phamacogenetic

40
Q

Characteristics of torsades de pointes

A
  • Polymorphic ventricular tachycardia
  • Change in amplitude and morphology (i.e., twisting) of the QRS
  • Ventricular rate: 160-240bpm
41
Q

Pt with this can present as asymptomatic, self-limiting dizziness, palpitations or syncope or even sudden cardiac death
*usually short lived and terminates spontaneously

A

Toursades de Pointes

42
Q

Citalopram over 40 mg/day increases risk for

A

QT prolongation withough metabolic inhibition

43
Q

the greatest risk for the development of TdP

occur when

A

multiple recognizable risk factors cluster in

a single patient

44
Q

Prompt action is required, if after administration of an at-risk drug, the QTc becomes prolonged to..

A

– Greater 500 msec or

– An increase of at least 60 msec compared with the predrug baseline value

45
Q

Appropriate actions include to a pt that has a prolongued QT dt meds is:

A

– Alternative pharmacotherapy
– Assessment of potentially aggravating drug-drug interactions
– Correction of electrolyte abnormalities

46
Q
– Amitriptyline
– Nortriptyline
– Chlorpromazine
– Imipramine
– Desipramine
– Doxepin 
are all
A

TCAs

47
Q

When do we prescribe TCAs?

A
– Chronic pain
– Peripheral neuropathy
– Depression
– Anxiety disorders
– Migraine prophylaxis
– Cyclic vomiting syndrome
48
Q

Pt comes in with suspected OD of unknown substatnce… what do you do?

A
The “ABCs”
“DON’T”
Decontamination
Focused Therapy
Obtain 
Consultation
49
Q

What do we see on an ECG dt a TCA overdose?

A

prolongued QRS

50
Q

TCA makes up only 12% of toxic exposures to drugs… and yet;

A

makes up over 50% of deaths from toxicity

51
Q

You suspect TCA overdose but it’s hard to measure TCA levels acutely so you order an ECG (need to do this if you suspect TCA OD!)
Electrocardiogram (ECG)
What signs on the ECG suggest TCA poisoning?

A

– QRS prolongation (>100msec)
– Abnormal morphology of QRS (slurred S wave in leads I and AVL)
– QT and PR prolongation
– Right axis deviation
– AV or bundle branch blocks
– Abnormal size and ration of R and S waves in lead AVR

52
Q

How do we tx someone with TCA poisoning?

A

• Airway/Breathing/Circulation
to tx Hypotension use an IVF bolus and Vasopressor support (-adrenergic agonist) if
refractory to sodium bicarbonate

53
Q

What does sodium bicarbonate do for someone with TCA poisoning?

A

– Resolution of QRS prolongation
– Recovery from hypotension
– Treatment of existing arrhythmias