6/18 UWorld Flashcards
Intoxication of what drug causes:
Violent behavior, dissociation, hallucinations, amnesia, nystagmus, ataxia
PCP = Hallucinogen
Intoxication of what drug causes:
Visual hallucinations, euphoria, dysphoria/panic, tachycardia/HTN
LSD - Hallucinogen
Intoxication of what drug causes:
Euphoria, agitation/psychosis, chest pain, seizures, tachycardia/HTN, mydriasis
Cocaine - stimulant
Intoxication of what drug causes:
Increased appetite, euphoria, dysphoria/panic, slow reflexes, impaired time perception, dry mouth, conjunctival injection
Marijuana = psychoactive
Intoxication of what drug causes:
Violent behavior, psychosis, diaphoresis, tachycardia/HTN, choreiform movements, tooth decay
Methamphetamine = stimulant
Intoxication of what drug causes:
Euphoria, depressed mental status, miosis, respiratory depression, constipation
Heroin = opioid
Withdrawal of what drug causes:
· Tremors, agitation, anxiety, delirium, psychosis
· Seizures, tachycardia, palpitations
Alcohol
Withdrawal of what drug causes:
Increased appetite, hypersomnia, intense psychomotor retardation, severe depression (“crash”)
Stimulants (cocaine / methamphetamine)
Withdrawal of what drug causes:
· Nausea, vomiting, abdominal cramping, muscle aches
· Dilated pupils, yawing, piloerection, lacrimation, hyperactive bowel sounds
Heroin = opioid
Why is there only minimal/rare risk of pulmonary infarction following a PE
Collateral circulation
Clot occludes the pulmonary artery, but the bronchial artery can continue to supply nutrients
Describe the effect of Class I anti-arrhythmics on EKG
- Class I antiarrhythmics widen the QRS complex on EKG (due to decreased AP conduction velocity)
- Because drug effect is stronger on channels with more depolarization (rapid heart rate), QRS will be even WIDER in patients with tachycardia
D
From what embryological derivative does the pituitary form? (endo, meso, or ectoderm)
- Ectoderm
- Anterior pituitary = surface ectoderm
- Posterior = neural tube
What is Rathke’s pough
Surface ectoderm where anterior pituitary sprouted from mouth
What are the differences in Troponin I and CK-MB seen after an MI
- Troponin I
- Rises after 4 hours
- Peaks at 24 hours
- Is elevated for 7-10 days
- Most specific to cardiac myocytes
- CK-MB
- Rises after 6-12 hours
- Peaks at 16-24 hours
- Return to normal after 48 hours
- Useful in diagnosing reinfarction following acute MI
What will you see < 4 hours after MI:
- Gross
- Microscopically
- Complications
- Gross changes:
- None
- Microscopic changes:
- None
- Complications:
- Cardiogenic shock (cannot provide blood to organs)
- Congestive heart failure (decreased ejection fraction)
- Arrhythmias
What will you see 4-24 hours after an MI:
- Gross
- Microscopically
- Complications
- Gross changes
- Dark discoloration
- Microscopic changes:
- Coagulative necrosis (nucleus removed from dead cells)
- Contraction bands (due to reperfusion injury from hypercontraction)
- Wavy fibers with narrow, elongated myocytes
- Complications:
- Arrhythmia
What will you see 1-3 days after an MI:
- Gross
- Microscopically
- Complications
- Gross changes:
- Yellow pallor (due to WBC)
- Microscopic changes
- Macrophages
- Complications
- Rupture of ventricular free wall can lead to cardiac tamponade
- Rupture of interventricular septum
- Rupture of papillary muscle (fed by R coronary artery) leading to mitral insufficiency
What will you see 4-7 days after an MI:
- Gross
- Microscopically
- Complications
- Gross changes:
- Yellow pallor (due to WBC)
- Microscopic changes
- Macrophages
- Complications
- Rupture of ventricular free wall can lead to cardiac tamponade
- Rupture of interventricular septum
- Rupture of papillary muscle (fed by R coronary artery) leading to mitral insufficiency
What will you see 1-3 weeks after an MI:
- Gross
- Microscopically
- Complications
- Gross changes:
- Red border emerges as blood vessel from normal tissue grow into necrotic tissue to form granulation tissue
- Microscopic changes:
- Granulation tissue with fibroblasts, collage, and blood vessels
- Complications:
- Arrhythmias
What will you see months after an MI:
- Gross
- Microscopically
- Complication
- Gross changes
- White scar
- Microscopic changes:
- Fibrosis
- Complications
- Aneurysm (scar is not as strong as myocardium)
- Mural thrombus and embolism (secondary to aneurysm)
- Dressler syndrome (antibodies against pericardium) occurring 6-8 weeks after infarction
- Chest pain, pericardial friction, and persistent fever
Treatment of MI before you know if it is an NSTEMI or STEMI
- ABCs (airway, breathing, circulation)
- MONA:
- Morphine (IV) – to relieve chest pain
- O2 supplemental (only if hypoxia present)
- Nitroglycerin (venodilator decreases preload)
- Aspirin – to decrease clotting
- Beta-blockers (Metoprolol)
- If no signs of heart failure or severe asthma
- Statins (Atorvastastin)
- Preferably before cath lab
- Antiplatelet therapy (Clopidogrel or Ticagrelor)
- To all patients
- Anticoagulant therapy to all patients
- Unfractionated heparin to patients undergoing catheterization
- Enoxaparin for patients not managed with catheterization
- Potassium and magnesium to decrease risk of arrhythmia
- Only if there are abnormalities
Treatment of STEMI vs. NSTEMI
- If STEMI:
- Percutaneous coronary intervention (PCI) = catheter
- If significant CAD on the catheter, then the patient may receive stenting or coronary artery bypass graft
- If PCI unavailable, treat with fibrinolysis within 90-120 minutes
- Avoid fibrinolysis with a NSTEMI
- Percutaneous coronary intervention (PCI) = catheter
- If NSTEMI:
- PCI only (no fibrinolytics)
Describe eccentric vs. concentric cardiac hypertrophy
Eccentric = sarcomeres added in series = dilated cardiomyopathy
Concentric = sarcomeres added in parallel = hypertrophic cardiomyopathy
