Dislipidemia

Family Hx

Smoking

Obesity

HTN

DM

Men >45, Women >55

1)  There is none between the extent of CAD and severity of anginal symptoms.

2) There is none between severity and duration of anginal sx to prognosis.

1)  Coronary blood flow

2) Oxygen carrying capacity in blood (do CBC --> anemic?)

1)  Cocaine

2) Ergot alkaloids

1) Anginal hx with no changes in the last 2 months in...

Frequency

Duration

Time of Day

Severity

Episodic pain <5-15 min

Provoked by exertion

Relieved by rest or NTG

-->Is predictable and has limitations

1) What is Chronic Stable angina's classic presentation?

2) What classic descriptor do women usually have?

1) Pain that is substernal, retrosternal with radiation to neck or left arm.

2) A feeling of anxiety.

Physical exertion

emotions

cold

heat

humidity

high fatty/chol meals

sexual intercourse (more in men)

1) What do women usually present with for chronic stable angina?

2) What is the usual cause for Prinzmetal's angina and who shows this type?

1)Exertional dyspnea

Fatigue

Exhaustion

2)Coronary artery spasm, women

A = Aspirin and Antianginal therapy (Nitrates)

B= Beta-blocker and blood pressure

C = Cigarette smoking and Cholesterol

D = Diet and Diabetes

E = Education and Exercise

1) What are the symptomatic relief therapies for chronic stable angina?

2) And for antiplatelet therapy?

1) Nitrates, B-blockers, Ca Channel blockers

2) Aspirin

1) What drugs should you think of giving with chronic stable angina?

2) What is an alternative med?

1) Beta-blockers

Aspirin

ACE-I

NTG - PRN

2) Ca channel blockers

1) What is the triple combination therapy for chronic stable angina?

2) And when is it used?

1) B-blocker, calcium channel blocker, long-acting nitrates with aspirin

2) With persistent angina on dual therapy

Both (is both preload/venous and afterload/arterial)

 - They also can reverse coronary vasospasm for Prinzmetal's angina

1) What is the problem of nitrates with extended use?

2) What are some adverse effects of nitrates?

3) How are nitrates stored?  Why?

1) Tolerance

2) HA (most common), Light-headedness, dizziness, tachy

3) In a brown bottle in cool and dry place.  Very labile compound.  Must refill frequently.

1) What is a short acting nitrate?

2) Long acting?

1) NTG - SL .4-.6 mg (tablet)

NTG - Spray .4-.8 mg (exp. but not affected by environment)

2) ISDN, ISMN

1) What is the MofA of Beta-blockers?

2) What are the beneficial effects of BBs?

1) Inhibits binding of catecholamines

2) Lower heart rate

Increase diastolic filling time (increase heart rest which lowers Oxygen demand)

1) Beta-1 receptors are found where and what do they do?

2) Beta-2 receptors are found where and what do they do?

1) Heart:  increase HR, increase contractility, increase AVN conduction

2) Lungs and Vascular:  Bronchodilation, vasodilation

Selective:  Atenolol, Metoprolol

Non-selective:  Propranolol

All are effective in preventing angina.

1) What is an adverse effect (there are many) with BBs?

2) what is a major precaution with Beta-blockers?

1) Sinus bradycardia, intensification of insulin-induced hypoglycemia

2) BB withdrawl syndrome (usage increases # of Beta receptors)

2nd degree Mobits

Allergy to the BBs

Hypotensive

Prinzmetal's angina

Bradycardia

1) What is the MofA for the Ca Channel blockers?

2) What is a physiologic effect?

1) Blocks influx of Ca into cardiac/smooth muscle which results in decreased excitation-contraction mechanism.

2) Slows AV nodal conduction

1) What are some adverse effects of Ca Channel blockers?

How can you stop Ca channel blockers?

1) Ankle edema

HF

Proarrhythmia

2) Abruptly (unlike the BBs --> slowly)

The Dihydropyridines

Nefedipine (short acting)

Nicardipine (medium acting)

Amlodipine (long acting)

Felodipine

The Non-diydropyridine

Verapamil

Diltiazem

1) What is significantly increased when used in conjunction with calcium channel blockers?

2) What should you do?

1) HMG-CoA reductase inhibitors (=Statins)

2) May need to lower statin dose and watch for liver failure or signs of rhabdomyolysis

Dihydropyridine

Hypotension

HA

Ankle edema

Short acting (Nifedipine; Nicardipine

Tachycardia

Flushing

Dizziness

1) What med should you use for chronic stable angina experienced <1/week?

2) Experienced >2-3/week?

1) NTG

2) NTG (not sub-lingual), BB, CCB

For variant angina:

1) What can you use for acute episodes?

2) What can you use for chronic episodes?

3) What do you not want to use because it could exacerbate coronary artery spasm?

1) Nitrates

2) CCB

3)  BB

1) How are most of the Acute coronary syndromes caused?

2) What is the spectrum?

1) From a disrupted atherosclerotic plaque.

2) Unstable Angina

Non-Q wave MI

Q-wave MI

Angina at rest (>20 min)

New-onset (<2 months) exertional

Recent (<2 months) acceleration of angina -- (increase in severity of at least one ACC class to at least class III)

Plaque disruption

Acute thrombosis

Vasoconstriction

Acute:  Oxygen,NTG, BB, ACE-I, Antiplatelet therapy, Anticoag therapy

Maintenance:  Antiplatelet therapy, BB, CCB, Lipid-lowering agents, ACE-I

ST segment elevation during chest pain

Intermittent chest pain at rest and in early morning hours

Rapidly relieved by NTG

Syncope (rare)

Raynaud's

Migraines

1) What does an ST elevation MI imply?

2) What does a non-ST elevation MI imply?

3) Unstable angina implies?

1) Transmural infarction (not definitive)

2) Non-transmural

3) No cardiac enzymes were released

AMI Definition = Death of myocardial tissue.

Criteria?  1) Chest discomfort suggest of AMI

2) EKG findings consistent with AMI

3) Characteristic elevation of cardiac enzymes

1) In an AMI, what area has the highest mortality?

2) What is the most common cause of AMI?

1) Anterior wall infarction

2) Atherosclerosis

1) Prior MI

2) History CAD (family hx)

3) Malignant arrythmias

Chest pain that lasts >30 minutes

Not relieved with NTG

New EKG changes:  ST elevation in two contiguous leads

Presence of an increase in cardiac enzymes

What are the level elevations, peaks, return to baseline time for the following cardiac enzymes:

Myoglobin?

Troponin I (CTnI)?

CKMB?

Myoglobin:  initial elevation (1-4 hr)

Peak (4-12 hr)

Return to baseline (10-24 hr)

CTnI:  2-6 hr

10-24 hr

7-10 days

CKMB:  4-6 hr

18-24 hrs

36-48 hrs

1) When is the highest risk for sudden death to occur with AMI?

2) What is the AMI therapeutic plan?

1) Within the first 24 hours

2) ASA, NTG, Morphine, Heparin, BB (Lopressor or Brevibloc (short)

1) What is a complication of NTG tx for AMI?

2) In what situation is NTG contraindicated?

1) Hypoxia (causing a V/Q mismatch)

2) RV infarct

Dry hacking cough (S3 present ---> cough from HF)

Angioedema

1) For AMI, what is the most common of death in the first 4-12 hours?

2) What is the treatment for this?

1) Ventricular fibrillation

2) Lidocaine or amiodarone

1) What type of murmurs may begin after an AMI?

2) What is the tx for them?

1) Mitral and aortic regurgitation

2) Surgery NOW!!

1) What is a AMI supportive anti-anxiety med you can use?

2) What are not effective?

1) Benzodiazepines (lower oxygen demand)

2) Anti-depressants

Sudden onset, severe intensity within seconds to minutes.  New HA in elderly or HIV+.

Wonder about Berry aneurysms, cerebral bleeds or sub-arachnoid hemorrhage.

1) What should you assess in a TTH?

2) When should you consider imaging?

1) Full eye exam

Neurological screen

2) Neuro findings + or atypical presentation

(Bleeds = non-contrast CT)

(Masses = MRI)

1) With TTH, what are some initial medications for tx?

2) How long do they take to work?

1) ASA, Acetaminophen, NSAIDs

2) 30 minutes for ASA, 60 min. for acetominophen and NSAIDs

1) What are some longer acting NSAIDs?

2) What are some common NSAID SE?

1) Orudis, Toradol

2) Nausea, dyspepsia, inhibits platelet aggregation (bleeding)

Tylenol III (acetominophen and Codeine)

Darvocette

1) What are some opioid SE?

2) What is butalbital good for?  Caffeine?

1) Sedation, nausea, psych effects (hallucinations)

2) Lowers anxiety; Caffeine enhances drug absorption

TCAs (amitriptyline/nortriptyline) are better than SSRIs.

TCA SE:  Drymouth, drousiness

1) Who are migraines more common in?  Who should you seed a secondary cause in?

2) Who is it more common in?

1) Peek 25-50.  Seek sec. cause in pts >50.

2) Women except prior to puberty then it is boys.

1) The brainstem reflex provides what symptoms in a migraine?

2) The Autonomic reflex provides what symptoms in a migraine?

1) Nausea/vomiting/photo,phonophobia

2) Nasal congestion, rhinorrhea, lacrimation

NSAIDs

Demerol (with vistaril for nausea)

Stadol (NS)

Nubain

Severe unilateral with orbital, supraorbital or temporal pain.

Lasts < 2 hours

ASA d/t Reye's syndrome

Triptans not approved.

1. visceral - dull ache poorly localized

2. parietal - sharp intense localized

3. referred pain

1. inflammation - infection

2. ischemia - torsion

3. tension - peritoneum

IV fluids

Antispasmodics

Antibiotics (surgical prophylaxis)

severe incr. pain

bile stained vomitus

involuntary guarding

distention with tympany

acute fluid or blood loss

-single dose parenterally

-2 hours prior to incision

-discontinue within 48 hrs.

-E. coli

-B. fragilis

-S. pneumo.

-H. influenzae

-oropharyngeal organisms

-bacterial

-mycoplasma, viral or legionella

-Macrolides

-doxycycline (mycoplasma)

quinolones #1

or (3rd gen. cephalosporin or B-L inhibitors) plus add a macrolide

-Start within 4 hours of admission

-3rd gen. cephalosporin or B-L inhibitor

and quinalone

-by day 3 with good response

-during first 72 hrs

-After 48 hrs in institutionalized setting

-post-surgical or ventilator pts.

-Gram-neg. bacilli

-S. pneumo

-SA

-anaerobes

-Broad spectrum

aspiration pneumonia

foul smelling, purulent sputum

-over 65

-under 65 if smoker or asthma