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315 Cards in this Set
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Lecture 118: CV 4
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Heart failure
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What is the most common type of TE fistula?
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• Type C
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What are the major regulatory enzymes of citric acid cycle?
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• Citrate synthase
• Isocitrate dehydrogenase (rate limiting) • a-Ketoglutarate dehydrogenase: co- factors: tender love and tender for no one |
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What infections are caused by Chlamydia and Chlamydophila species? What is the treatment for most of these infections?
• Chlamydophila psittaci |
o Pneumonia with exposure to birds
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• Chlamydophila pneumoniae
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o Interstitial (walking, atypical) pneumonia
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• Chlamydia trachomatis Types A, B, C
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o Trachoma eye infection (Africa)
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• Chlamydia trachomatis Types D-K
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o STDs, PID, urethritis
o Neonatal conjunctivitis |
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• Chlamydia trachomatis Types L1, L2, L3
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o Lymphogranuloma venereum
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• Treatment
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o Macrolides
o Tetracycline |
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• Left-sided Heart Failure
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o Dyspnea on exertion (DOE)
o Cardiac dilation o Pulmonary edema: Paroxysmal nocturnal dyspnea, Orthopnea |
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• Right-sided Heart Failure
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o Peripheral edema (sacral edema)
o Jugular venous distension (JVD) o Hepatic congestion :Nutmeg liver on biopsy *Remember—nutmeg liver also seen in Budd Chiari syndrome |
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BNP (Brain/B type Natrieutic peptide)
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BNP >100 = CHF (may show up on test)
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Treatment for Acute CHF
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“LMNOP”
o Loops oMorphine o Nitrates o Oxygen o Positioning and Pressors: Have patient sit on edge of bed so blood pools in legs rather than lungs |
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Digoxin toxicity
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oCholinergic effects
- Vomiting - Diarrhea - Blurry yellow vision (CLASSIC SE) o Abdnormal EKG - Bradycardia - Antidote of these is Atropine |
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Digoxin toxicity treatment
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o Correct hypokalemia
o Correct magnesium o Atropine, temporary pacemaker (tx. bradycardia) o Lidocaine (tx. tachycardia) o Anti-digoxin antibody fragments |
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What are the signs of right-sided-heart failure?
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• Peripheral signs and symptoms
o Lower extremity edema o Jugular venous distension o Hepatosplenomegaly |
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What are the signs of left-sided-heart failure?
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• Dyspnea on exertion
• Orthopnea • Paroxysmal nocturnal dyspnea • Pulmonary congestion symptoms |
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How does poor cardiac output result in an increase in aldosterone?
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• Decreased CO → low BP
• Juxtaglomerular cells secrete renin • Activates the RAS → aldosterone levels |
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What medications are used to treat chronic heart failure?
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•Improve Survival
o ACE inhibitors and ARBs o Aldosterone antagonists o B-blockers •Symptomatic relief o Diuretics o Digoxin o Nitrates and other vasodilators |
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What medications are used to treat acute heart failure?
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“LMNOP”
o Loops o Morphine o Nitrates o Oxygen o Positioning and Pressors |
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What is the mechanism of action of the cardiac glycosides (e.g., digoxin)?
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• Inhibits the Na+/K+ ATPase, which increases intracellular Ca+2
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Cor pulmonale
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Right heart failure due to pulmonary disease
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Nutmeg liver
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Right heart failure
Budd-Chiari syndrome |
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Which two beta blockers are indicated for the treatment of chronic heart failure?
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• Carvedilol
• Metoprolol: Long-acting metoprolol |
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Which beta blocker is indicated for acute decompensated CHF?
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• NONE – they are contraindicated
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Lecture 119: CV 5
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Edema & Shock
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Which Rickettsial species has properties unique from the other Rickettsial organisms? What are those unique properties?
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Coxiella burnetii
o Negative Weil-Felix o No vector o Aerosol transmission o Endospore o No rash o Interstitial pneumonia |
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What is the classic presentation of congenital pyloric stenosis?
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• Palpable epigastric olive mass
• Poor feeding • Projectile vomiting • Hypochloremic metabolic alkalosis • Hypokalemia • 2 weeks of age |
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Explain why a deficiency of the enzyme that is the rate-limiter for the HMP shunt can result in hemolytic anemia.
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• Rate-limiting enzyme is G6PD which generate NADPH.
• Without NADPH, RBCs are more susceptible to oxidative damage which leads to hemolysis |
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Capillary Fluid Exchange: Mechanisms of edema
HIGH YIELD – 5 star topic • Increased capillary pressure |
o CHF
o Venous thrombosis o Anything that obstructs venous out flow (tight clothes, cast, etc) |
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• Decreased plasma colloid osmotic pressure
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o Nephrotic syndrome
o Liver disease o Protein malnutrion o Protein losing enteropathy |
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• Increased capillary permeability: Increased filtration constant Kf
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o Sepsis & infection: Release of histamine and bradykinin causes vessels to become more leaky and fluids leave the vessles causing edema
o Toxins o Burns |
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• Increased interstitial colloid pressure
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o Caused by increased protein in the interstitium
o Lymphatic blockage: - Cancer - Surgery - Radiation |
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• Pitting edema vs. non-pitting edema
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o Pitting edema due to increased fluid or decreased colloid
- Gravity dependent, often seen lower extremities - Water balloon - Edema caused by increased capillary pressure or decreased plasma proteins cause transduative fluid (basically water, low protein content) o Non-pitting -A lot of colloid in interstitial fluid - Edema caused by increased capillary permeability protein rich fluid (exudate) |
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• Edema from Na & H20 retention
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o Renal failure
o RAAS |
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How do SVR and CO change in the following types of shocks?
Hypovolemia |
SVR: Increased
CO: Decreased Rx: IV fluids, blood |
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Heart failure
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SVR: Increased (compensatory)
CO: Decreased Rx:“LMNOP” |
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Sepsis/anaphylaxis
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SVR: Decreased (vasodilation)
CO: Increased (compensatory) Rx: Antibiotics, IV fluids, Norepinephrine |
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Neurogenic
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SVR: Decreased
CO: Decreased Rx: IV fluids, steroids |
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How do the following circumstances impact the Starling forces of fluid movement through capillaries?
• Heart failure |
o Increased capillary pressure
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• Liver failure
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o Decreased oncotic pressure
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• Renal failure
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o Decrease plasma protein
o Decrease plasma colloid osmotic pressure |
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• Infections and toxins
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o Increase capillary permeability
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• Nephritic syndrome
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o Decrease plasma protein
o Decrease plasma colloid osmotic pressure |
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• Lymphatic blockage
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o Increased osmotic pressure
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• Burns
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o Increased capillary permeability
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• Diuretic administration
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o Osmotic agent to prevent water reabsorption
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• IV infusion of albumin or clotting factors
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o Increased plasma proteins
o Increased plasma colloid osmotic pressure |
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• Venous insufficiency
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o Increased capillary pressure
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How does the vascular resistance and stroke volume differ in hypovolemic shock compared to septic shock?
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Hypovolemic shock: Increased vascular resistance, Decreased SV
Septic shock: Decreased vascular resistance, Increased SV |
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What are some of the causes of cardiogenic shock?
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• MI
• PE • Arrhythmia (V tach, V fib) • Cardiac tamponade |
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How is the skin of a patient different in cardiogenic shock compared to septic shock?
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• Cardiogenic shock
o Cold o Clammy o Cyanotic • Septic shock o Initially warm and flushed |
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What other severe problems often coexist with septic shock in ICU patients?
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• DIC
• Acute pancreatitis • Acute renal failure • Liver failure • ARDS • Intestinal ileus • Adrenal insufficiency |
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What serum lab marker is helpful in assessing the appropriate oxygenation of tissues?
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• Lactic acid
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Lecture 120: CV 6
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Cardiac Cycle
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What is the primary energy source in a patient that has not eaten in two days?
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• Fatty acids
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When placing a femoral venous catheter, while palpating the pulsatile femoral artery, where is the femoral catheter placed in relation to the artery?
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• Medial to the artery
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Where in the cell would you find each of the following enzymatic processes taking place?
• Fatty acid degradation |
o Mitochondria
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• Fatty acid synthesis
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o Cytoplasm
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• Glycolysis
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o Cytoplasm
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• TCA cycle
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o Mitochondria
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• Electron transport chain (oxidative phosphorylation)
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o Mitochondria
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• Gluconeogenesis
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o Mitochondria
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• Protein synthesis (RER)
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o Cytoplasm
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• Urea cycle
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o Mitochondria and cytoplasm
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• Steroid synthesis (SER)
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o Cytoplasm
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• Heme synthesis
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o Mitochondria and cytoplasm
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Pressure volume loop (very high yield)
o Increase afterload (hypertension) o Increase contractility o Increased preload |
o Increase afterload (hypertension)
- Increased in aortic pressure - Decreased SV - Increased ESV o Increase contractility - Increased SV - Increased EF - Decreased ESV o Increased preload - Increased SV |
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When does isovolumetric contraction take place?
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• During the QRS
• After AV valve closes • Before the Aortic valve opens |
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How does an increase in afterload affect the stroke volume of the heart assuming contractility remains the same?
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• Decreases the SV
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What impact does an increase in contractility have on stroke volume assuming preload and after load remain constant?
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• Increase the SV
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What heart sound is associated with dilated congestive heart failure? What heart sound is associated with chronic hypertension?
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• Dilated CHF: S3
• Chronic hypertension: S4 |
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What gives rise to the jugular venous a, c, and v waves?
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• a wave: Atrial contraction
• c wave: ventricular contraction • v wave: atria filling against closed tricuspid valve |
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Where does the QRS complex fall in relation to valvular dynamics?
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• Mitral valve closure
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Lecture 121: CV 7
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Heart Murmur
5 Stars ***** |
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What protozoa/helminthes match each of the following statements?
• Contracted by eating undercooked fish and causes an inflammation of the biliary tract |
o Clonorchis sinensis
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• Most common protozoal infection in US
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o Toxoplasma gondii
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• Cause of Chagas disease
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o Trypanosome cruzi
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• Most common helminthic infection in the US
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o Enterobius vermicularis
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• Snail host, “swimmers itch”
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o Schistosoma mansoni
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• Diarrhea in campers and hikers
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o Giardia lamblia
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• Transmitted in raw meat or infected cat feces
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o Toxoplasma
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What effect does stress have on adipocytes?
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o Sympathetic stimulation
- Epi and NE released from adrenal medulla o Activates hormone-sensitive TG lipase in fat cells - Rapid breakdown of TGs - Mobilization of fatty acids used to muscles are energy o Release of ACTH from anterior pituitary |
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What are the 4 obligate aerobic bacteria?
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“Nagging Pests Must Breath”
• Nocardia • Pseudomonas aeruginosa • Mycobacterium tuberculosis • Bacillus species |
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Blood flow across the valves
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Diastole—filling of ventricles
Open valves—mitral valve & tricuspid Closed—aortic & pulmonic valve Systole—ventricles contracting Open valves—pulmonic & aortic Closed—mitral & tricuspid |
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Diastolic murmurs
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Mitral/Tricuspid stenosis
Aortic/Pulmonic regurgitation |
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Systolic murmurs
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Aortic/pulmonic stenosis
Mitral/Tricuspid regurgitation |
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Bedside Maneuvers: Breathing
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o Inspiration
- Causes negative intrathoracic pressure - Pulls the blood from the vena cava into the right atrium - Therefore during inspiration there will be a lot of right atrial filling - Triscupid mumurs will be loudest at this time o Expiration - Mitral mumurs will be loudest because more blood going to left atrium |
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Bedside Maneuvers: Hand grip
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o Tell pt to hold this for 60 secs causes increased afterload and systemic vascular resistance
o Mitral regurg will get louder |
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Bedside Maneuvers: Louder with Valsalva
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o Increases thoracic pressurereduces venous return to right heart and systemic BP (if done long enough)
o Reduces preload and afterload o Most mumurs are reduced o 2 murmurs get louder: Mitral prolapse o Murmur of hypertrophic cardiomyopathy |
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Bedside Maneuvers: Softer with standing → squatting
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o Compression of veins: venous return increases
o Compression of arteries: increases peripheral vascular resistance & afterload o 2 murmurs get softer: Mitral prolapse o Murmur of hypertrophic cardiomyopathy |
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Aortic Stenosis
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• Ejection click
o Due to calcified leaflets coming to an abrupt halt • Murmur during systole between S1 & S2 • No murmur at the beginning of systole! o No blood flowing through the aortic valve yet o Pressure must get great enough to force AV open • Crescendo- Descrescendo • Radiates into carotids • Weak delayed pulses |
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Aortic Stenosis Associated S/S
KNOW!!! |
o Syncope
o Angina o Dyspnea |
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What are the most common causes of aortic valvular stenosis?
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• Congenital bicuspid aortic valve
• Senile (degenerative) calcification • Chronic rheumatic valvular disease • Unicuspid aortic valve • Syphilis |
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Mitral regurgitation
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• Immediately following S1 (closure of mitral & tricuspid valves)
• During systole the mitral valve should be closed and there shouldn’t be any blood flow across it • Holosystolic o Occurs through systole o S1--> S2 (aortic and pulmonary valve closure) •High pitched • Heard best at apex • Can radiate to left axial • Heart best in left later decubitus position • Enhanced by increased PVR & afterload o Hand gripping o Squatting |
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Causes of mitral regurgitation
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o Rheumatic heart dz most common cause (mitral valve must common to be damaged by rheumatic fever)
o Endocarditis o Ischemic heart dz o Left ventricle dilatation o Mitral valve prolapse |
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Mitral Valve prolapse
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• Floppy valve leaflets
• Midsystolic click with crescendo towards S2 • Enhanced by valsalva and quieter by squatting |
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Tricsupid regurgitation
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• Similar to MV
• Holosystolic • Louder with inspiration • Causes: Rheumatic, Endocarditis, IV drug users** |
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Ventricular Septal Defect
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• Holosystolic
• Heard best in tricuspid area • Gets louder with respiration • Seen in newborns |
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Murmurs heard best in the Left Lateral Decubitus position
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• Mitral regurgitation
• Mitral stenosis • Left-sided S3 • Left-sided S4 |
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Aortic Regurgitation
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•Occurs during S2
•Wide pulse pressure o Example 120/40 o Systolic pressure (normal) o Diastolic pressure (low): Because blood is flowing backing Exam findings: - Strong and bounding pulse - Water-hammer pulse - Head bobbing o Causes (dilatation of aortic root) -Syphilis - Marfans - Bicuspid aortic valve - Rheumatic fever |
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Mitral stenosis
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• Opening snap
• Does not occur immediately following S2 • Enhanced by maneuvers that increase blood return to left atrium o Expiration • Similar to S2 split, but S2 split is enhanced in expiration • Chronic mitral stenosis ---> left aortic dilatation |
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Patent Ductus Arteriosus
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• Continuous machine- like murmur
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Which heart murmur is associated with weak pulses (pulus parvus atardus)?
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• Aortic stenosis
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What defect is associated with the following type of murmur?
Crescendo-decrescendo systolic murmur best heard in the 2nd-3rd right interspace close to the sternum |
Aortic stenosis
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Early diastolic decrescendo murmur heard best along the left side of the sternum
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Pulmonic regurgitation
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Late diastolic decrescendo murmur heard along the left side of the sternum
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Tricuspid stenosis
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Pansystolic (aka holosystolic or uniform) murmur best heard at the apex and often radiates to the left axilla
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Mitral regurgitation
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Late systolic murmur usually preceded by a mid-systolic click
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Mitral prolapse
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Crescendo-decrescendo systolic murmur est heard in the 2nd and 3rd left interspaces close to the sternum
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Pulmonic stenosis
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Pansystolic (aka holosystolic or uniform) murmur best heard along the left lower sterna border and generally radiates to the right lower sterna border
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Tricuspid regurgitation
VSD |
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Rumbling late diastolic murmur with an opening snap
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Mitral stenosis
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Continuous machine-like murmur (in systole and diastole)
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Patent ductus arteriosus (PDA)
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High-pitched diastolic murmur associated with a widened pulse pressure
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Aortic regurgitation
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What murmurs are heard best in the left lateral decubitus position?
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• Mitral regurgitation and mitral stenosis
• Left-sided S3 and S4 heart sounds |
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Bounding pulses, head bobbing, diastolic murmur
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Aortic regurgitation
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Most common congenital heart murmur
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Mitral valve prolapse
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Lecture 122: CV 8
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Electrophysiology
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Why do the kidneys retain fluid in heart failure patients?
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• Renal hypoperfusion → RAS
• Under perfusion is recognized by JG apparatus • Renin is secreted • Renin converts AT → AT-1 • ACE converts AT-1 → AT-2 • AT-2 signals the adrenals to secrete aldosterone • Aldosterone causes sodium and water reabsorption |
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Which hereditary hyperbilirubinemia matches each of the following statements?
• Mildly decreased UDPGT |
o Gilbert syndrome
o Crigler-Najjar, type II |
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• Completely absent UDPGT
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o Crigler-Najjar, type I
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• Grossly black liver
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o Dubin-Johnson syndrome
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• Responds to Phenobarbital
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o Crigler-Najjar, type II
o Gilbert syndrome |
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• Treatment includes plasmpheresis and phototherapy
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o Crigler-Najjar, type I
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• Asymptomatic unless under physical stress (alcohol, infection)
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o Gilbert syndrome
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What is a disulfiram-like reaction? What drugs cause a disulfiram-like reaction?
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o Inhibition of acetaldehyde dehydrogenase:
Flushing Sweating Nausea Headache Hypotension Drugs causing a Disulfiram-like reaction o Metronidazole o Cephalosporins: Cefotetan, Cefamandole, Cefoperazone o 1st generation sulfonylureas: Tolbutamide |
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Phases of a myocardial action potential and describe which ion channels are responsible for each phase.
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• Phase 0= rapid upstroke—voltage- gated Na+ channels open
• Phase 1= initial repolarization—inactivation of voltage-gate Na+ channel; VG K+ channels begin to open • Phase 2= plateau—Ca2+ influx through VG Ca2+ channels balances K+ efflux; Ca2+ influx triggers Ca2+ release from SR and myocyte contraction • Phase 3=rapid repolarization—massive K+ efflux due to opening of VG slow K+ channels and closure of VG Ca2+ • Phase 4= resting potential—high K+ permeability |
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Flow of ions during a pacemaker AP
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•Phase 0= upstroke—opening of Ca2+ channels; fast Na+ channels are permanently inactivated because of the less negative resting voltage of these cells; results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles
• Phase 2= plateau is absent • Phase 3= inactivation of Ca2+ channels and increased activation of K+ channels increased K+ efflux • Phase 4= slow diastolic depolarization—membrane potential spontaneously depolarizes as Na+ conductance increases (If different from INa in phase 0 of ventricular action potential) o Accounts for automaticity of SA & AV node; o The slope of phase 4 in the SA node determines heart rate o Ach/ adenosine decrease the rate of diastolic depolarization and decreases HR, while catecholamines increases depolarization and increases HR o Sympathetic stimulation increases the chance that If channels are open and this increases HR |
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What physiology accounts for the automaticity of the AV and SA nodes?
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• Phase 4 gradual sodium conductance
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Lecture 123: CV 9
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Antiarrhythmics
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At what age should patients begin receiving screening colonoscopies?
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• 50 year of age for most patients
• Family history of colon cancer o 40 years of age o 10 years before youngest 1st degree relative was diagnosed • Familial adenomatous polyposis (FAP) o Every 12 months beginning at age 10-12 •Lynch syndrome o 20-25 years of age o 10 years before youngest 1st degree relative was diagnosed •Inflammatory bowel disease (IBD) o 8-10 years after the initial diagnosis |
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A patient develops ARDS from an occupational inhalation of nitrogen dioxide. What histologic change is seen in a patient recovering from ARDS?
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• Proliferation of type II pneumocytes
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What lab value is used to monitor the following medications: heparin, warfarin, enoxaparin?
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• Heparin – PTT
• Warfarin – PT/INR • Enoxaparin – factor Xa activity |
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Antiarrhythmic Classes
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“No Bad Boy Keeps Clean”
o Class I: Na+ channel blockers o Class II: B-blockers o Class III: K+ channel blockers o Class IV: Ca+2 channel blockers |
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Class I Antiarrhythmics (Na+ channel blockers)
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• Decrease length of phase 0—elongates refractory period
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Class IA
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“Double Quarter-Pounder”
Disopyramide Quinidine Procainamide |
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Class IB
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“Lettuce, Tomato, Mayo, Pickles”
Lidocaine Tocainide Mexiletine Phenytoin |
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Class 1C
|
“Fries Please”
Flecainide Propafenone |
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B-Blockers (Class II)
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• Propranolol
• Esmolol • Metoprolol • Atenolol • Timolol • Clinical use o V-tach o SVT o Atrial fibrillation o Atrial flutter |
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B- Blockers Side Effects:
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o Impotence
o Exacerbation of asthma o Bradycardia o AV block o CHF exacerbation o CNS effects o Mask effects of hypoglycemia |
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Treatment for overdose of B- Blockers
*High Yield* |
Glucagon
|
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K+ Channel Blockers (Class III)
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o Amiodarone
o Sotalol o Ibutilide o Bretylium o Dofetilide |
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Side effects of Amiodarone
|
• Pulmonary fibrosis (check PFTs)
• Hepatotoxicity (check LFTs) • Hypo- or hyperthyroidism (check TFTs) • Corneal deposits • Skin deposits:Photodermatitis • Neurologic effects • Constipation • CV effects: Bradycardia, Heart block, Heart failure |
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Ca+2 Channel Blockers (Class IV)
|
• Non-dihydropyridine (heart)
o Verapamil o Diltiazem • Dihydropyridine o Nifedipine |
|
Ca2+ channel blockers SE
|
o Constipation
o Flushing o Edema o CV - Heart failure - AV block - Sinus node depression - Torsades |
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Drugs that cause photosensitivity
|
“SAT”
Sulfonamides Amiodarone Tetracycline |
|
Drug-induced lupus
|
• Sulfonamides
• Hyrdralazine • Isoniazid • Procainamide • Phenytoin |
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What is the mechanism of action of each class of antiarrhythmic?
|
“No Bad Boy Keeps Clean”
o Class I: Na+ channel blockers o Class II: B-blockers o Class III: K+ channel blockers o Class IV: Ca+2 channel blockers |
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Which antiarrhythmic has the side effect of cinchonism?
|
Quinidine
Side effects: Cinchonism (Headache, Tinnitus), Thrombocytopenia, Torsades de Points |
|
What are the potential side effects of amiodarone use?
|
Amiodarone
Side effects: Pulmonary fibrosis, Hyper/hypothyroidism, Hepatotoxicity, Blue-grey skin discoloration, Photodermatitis, Bradycardia, Heart block, Corneal deposits, Neurologic, Constipation |
|
What is the mechanism of action of adenosine as an antiarrhythmic?
|
Adenosine
MOA: Increases the outward K+ current, Hyperpolarization of cells, Decreasing intracellular calcium |
|
To which class of antiarrhythmics does each of the following agents belong?
• Sotalol |
o Class III
|
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• Propranolol
|
o Class II
|
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• Bretylium
|
o Class III
|
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• Quinidine
|
o Class I
|
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• Verapamil
|
o Class IV
|
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• Procainamide
|
o Class I
|
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• Lidocaine
|
o Class I
|
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• Diltiazem
|
o Class IV
|
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Lecture 124: CV 10
|
Electrocardiography
|
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Identify the hepatitis B status of the following patients based on their hepatitis B serologic markers.
HepBsAg: Negative HepBsAb: Positive HepBcAB: Positive |
Recovery
|
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HepBsAg: Negative
HepBsAb: Negative HepBcAB: Positive |
Window phase
|
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HepBsAg: Positive
HepBsAb: Negative HepBcAB: Positive IgM |
Acute disease
|
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HepBsAg: Positive
HepBsAb: Negative HepBcAB: Positive IgG |
Chronic disease
|
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HepBsAg: Negative
HepBsAb: Positive HepBcAB: Negative |
Immunized
|
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With what type of congenital heart defect would increasing afterload be beneficial?
|
•Any congenital heart defect that has a Right-to-Left shunt
o Tetralogy of Fallot o Transposition of the great vessels o Truncus arteriosus o Eisenmenger syndrome (VSD, ASD, PDA) |
|
What drugs are known for inhibiting cytochrome P450?
|
“CRACK AMIGOS”
o Cimetidine o Ritonavir (protease inhibitors) o Amiodarone o Ciprofloxacin o Ketoconazole o Acute alcohol use o Macrolides o Isoniazid o Grapefruit juice Omeprazole o Sulfonamides |
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How does the cause of a narrow QRS complex differ from the cause of a wide QRS complex?
|
• Wide QRS complex could cause
o Premature ventricular contraction (PVC) o Ventricular tachycardia o Bundle branch block |
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What is the ECG axis given the QRS deflections in each of the following scenarios?
• Positive in lead I, positive in lead II |
o Normal axis
|
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• Positive in lead I, negative in lead III
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o Left axis deviation, or normal axis
|
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• Negative in lead I, positive in lead III
|
o Right axis deviation
|
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• Positive in lead I, negative in aVR
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o Normal axis
|
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How does hyperkalemia affect the shape of T waves?
|
• Hyperkalemia: Tall peaked T-waves
|
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Lecture 125: CV 11
|
Arrhythmias
|
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What is the target HgbA1C for every diabetic patient?
|
< 7.0
|
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What are the five hereditary thrombosis syndromes?
|
• Factor V Leiden
• Prothrombin 20210 mutation • Protein C deficiency • Protein S deficiency • Antithrombin deficiency |
|
Which Mycobacterium spp fits each of the following descriptions?
• Causes leprosy |
o Mycobacterium leprae
|
|
• Causes pulmonary TB-like symptoms in COPD patients
|
o Mycobacterium kansasii
|
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• Causes cervical lymphadenitis in children
|
o Mycobacterium scrofulaceum
|
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• Causes a disseminated disease in AIDS patients
|
o MAI or MAC
|
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• Hand infection in aquarium
|
o Mycobacterium marinum
|
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Lewis Notes (HIGHEST YIELD for standalone questions )
• A-fib |
o Irregularly irregular
|
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• A-flutter
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o Sawtooth pattern
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• 1st degree block
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o PT > 200ms
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• Mobitz type I
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o Increased PR until dropped beat
|
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• Mobitz type II
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o No warning dropped beat
|
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• 3rd degree
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o Atria and ventricle beat independently
|
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• WPW
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o Delta waves
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• Ventricular escape
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o Wide QRS after long pause
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• V-tach
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o Wide QRS and tachycardia
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• Torsades
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o Undulating amplitude of QRS
|
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• V-fib
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o Erratic rhythm
|
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What is the initial treatment for ventricular fibrillation?
|
• CPR and Defibrillation
|
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What is the initial treatment for ventricular tachycardia when there is no pulse?
|
• CPR and Defibrillation
|
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What is the hallmark of a third degree heart block?
|
• No coordination between P-waves and QRS segments
|
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What drugs are known to prolong the QT interval, increasing the likelihood of torsades in those at risk?
|
• Drugs that prolong the QT interval
o Anti-infectives: Macrolides, Chloroquine o Anti-psychotics: Haloperidol, Risperidone o Anti-HIV: Protease inhibitors (-navirs) o Anti-arrhythmics: Class IA, Class III |
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What are the two different types of second degree AV block? How do they differ?
|
• Second Degree (Mobitz I) heart block: Progressive lengthening of the PR interval then dropped beat
• Second Degree (Mobitz II) heart block: Dropped beat without lengthening of PR interval |
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Why is warfarin anticoagulation important in patients with chronic atrial fibrillation?
|
• Reduce the risk of thrombotic stroke or PE
|
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Lecture 126: CV12
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Regulation of BP
|
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What is the difference between primary biliary cirrhosis and primary sclerosing cholangitis?
|
• Primary Biliary Cirrhosis
o Autoimmune disease o Associated with CREST scleroderma o Positive AMA o Middle-aged females • Primary Sclerosing Cholangitis o Unknown etiology o Positive pANCA (60%) o Males over 40 o Associated with ulcerative colitis and cholangiocarcinoma o ERCP – alternating beading & stricturing |
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How does increasing the diameter of a vessel by two times affect the resistance of that vessel?
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• Decrease resistance by a power of 16
|
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What substances are known teratogens? List as many as you can recall.
|
• ACE inhibitors
• Valproate, Phenytoin • Lithium • Tetracycline, aminoglycosides • Warfarin • Excessive vitamin A • Smoking, alcohol, cocaine • Diethylstilbestrol (DES) |
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What substances act on smooth muscle myosin light-chain kinase? How does this effect blood pressure?
|
• Dihydropyridine CCBs
• Epinephrine B2 receptors • Prostaglandin E2 • These substances effect blood pressure by o Relax vascular smooth muscle o Decrease blood pressure |
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Describe the chain of events in which hypotension causes a reflex tachycardia.
|
• Baroreceptors in the carotid sinus sense low BP
• Low BP results in less stretch of the carotid sinus • Increased sympathetic output • Decreased parasympathetic output • Reflex tachycardia |
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Lecture 126: CV 12
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Regulation of BP
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Lecture 127: CV 13
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Hypertension
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A tall, thin male teenager has abrupt onset dyspnea and left-sided chest pain. Percussion on the affected side reveals hyperresonance, and breath sounds are diminished. What is the diagnosis?
|
• Spontaneous pneumothorax
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An 80-year-old man presents with a systolic crescendo-decrescendo murmur. What is the most likely cause?
|
• Aortic stenosis
|
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What are the differences between hexokinase and glucokinase?
|
•Hexokinase
o Everywhere o Insulin: doesn’t induce o Low Km o Low Vmax •Glucokinase o Liver, pancreas (B cells) o Insulin: induces o High Km o High Vmax |
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Causes of aortic dissection
|
o HTN
o Disease of the aorta: Cystic medial necrosis (Marfan syndrome) |
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What BP values mark the diagnosis of hypertension? What values mark prehypertension?
|
• Hypertension – BP ≥ 140/90
• Prehypertension – BP ≥ 120/80 |
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What would you most suspect the cause of hypertension to be in a patient with each of the following clinical clues?
• Paroxysms of increased sympathetic tone: anxiety, palpitations, diaphoresis |
o Pheochromocytoma
|
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• Age of onset between 20 and 50
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o Primary HTN
|
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• Elevated serum creatinine and abnormal urinalysis
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o Renal disease
|
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• Abdominal bruits
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o Renal artery stenosis
|
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• BP in arms > legs
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o Coarctation of the aorta
|
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• Family history of HTN
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o Primary HTN
|
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• Tachycardia, heat intolerance, diarrhea
|
o Hyperthyroidism
|
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• Hyperkalemia
|
o Renal failure
|
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o Renal failure
|
o Pheochromocytoma
|
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• Abrupt onset in a patient younger than 20 or older than 50, and depressed serum K+ levels
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o Hyperaldosteronemia
|
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• Central obesity, moon-shaped face, hirsutism
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o Cushing syndrome
|
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• Normal urinalysis and normal serum K+ levels
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o Primary HTN
|
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• Young individual with acute onset tachycardia
|
o Cocaine or amphetamines
|
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• Hypokalemia
|
o Renal artery stenosis
|
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• Proteinuria
|
o Renal disease
|
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What chest x-ray finding is a possible sign for aortic dissection?
|
• Widened mediastinum
|
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What category of BP medications is preferred in the treatment of aortic dissection?
|
• B-Blocker
|
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Lecture 128: CV 14
|
Antihypertensives
|
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Which group of medications inhibits the rate limiting enzyme of cholesterol synthesis?
|
• HMG-CoA reductase inhibitors
|
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What are the primary mechanisms of action of the different classes of antiarrhythmics?
|
• Class I: Na+ channel blockers
• Class II: B-Blockers • Class III: K+ channel blockers • Class IV: Ca+2 channel blockers |
|
Name 8 different indirect cholinergic agonists and state the use for each.
• Neostigmine |
o Neurogenic ileus
o Neuromuscular junction blockade reversal agent o Myasthenia gravis |
|
• Pyridostigmine
|
o Myasthenia gravis
|
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• Edrophonium
|
o Diagnose myasthenia gravis
|
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• Physostigmine
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o Atropine overdose
|
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• Echothiophate
|
o Glaucoma
|
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• Donepezil
|
o Alzheimer disease
|
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• Galantamine
|
o Alzheimer disease
|
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• Rivastigmine
|
o Alzheimer disease
|
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Treatment of HTN
*******HIGGGGGGGH YIELD TOPIC******** |
• ACE inhibitors
• Vasodilator: Hydralazine, Minoxidil • Calcium channel blockers |
|
• Clinical uses of ACE Inhibitors
|
o HTN
o CHF o Post MI o Diabetic renal disease |
|
• Side Effects of ACE Inhibitors
|
o Cough: Possibly due to elevated levels of bradykinin (KNOW)
o Angioedema o Raise serum K+ o Decrease GFR o Teratogenic |
|
Angiotensin Receptor Blockers (ARBs)
• -sartan |
• Clinical uses of ARBs
o HTN o CHF o Post MI o Diabetic renal disease • Side Effects of ARBs o Teratogenic o Raise serum K+ o DON’T CAUSE A COUGH o Angioedema |
|
Aliskiren
|
• Inhibits renin
• ONLY indicated for HTN (not CHF or MI) |
|
Hydralazine
|
• Arteriole vasodilator
• Mainly used by severe HTN or HTN urgency/emergency • Side effects of Hydralazine o Reflex tachycardia o Fluid retention o Nausea o Headache o Drug-induced lupus |
|
Drug-induced Lupus
|
“SHIPP”
o Sulfasalazine o Hydralazine o Isoniazid o Procainamide o Phenytoin |
|
Drugs to use during Pregnancy
|
“Hypertensive Moms Love Nifedipine”
o Hydralazine o Methyldopa o Labetalol o Nifedipine |
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Which antihypertensive class or drug fits each of the following side effects?
First dose orthostatic hypotension |
a1-blockers
|
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Ototoxic (especially with aminoglycosides)
|
Loop diuretics
|
|
Hypertrichosis
|
Minoxidil
|
|
Cyanide toxicity
|
Nitroprusside
Sodium nitroprusside |
|
Dry mouth, sedation, severe rebound HTN
|
Clonidine
|
|
Bradycardia, impotence, asthma exacerbation
|
B- Blocker
|
|
Reflex tachycardia
|
Nitrates
Hydralazine Dihydropyridines |
|
Cough
|
ACE inhibitors
|
|
Avoid in patients with sulfa allergy
|
Loop diuretics
Thiazide diuretics |
|
Possible angioedema
|
ACE inhibitors
|
|
Possible development of drug-induced lupus
|
Hydralazine
|
|
Hypercalcemia, hypokalemia
|
Thiazides
|
|
Which antihypertensives are particularly beneficial to heart failure patients?
|
• ACE inhibitors
• ARBs • Aldosterone antagonists • B-Blockers o Carvedilol o Metoprolol o Bisoprolol |
|
Which antihypertensives are safe to use in pregnancy?
|
“Hypertensive Moms Love Nifedipine”
o Hydralazine o Methyldopa o Labetalol o Nifedipine |
|
Lecture 129: CV 15
|
Atherosclerosis
|
|
Describe how the murmur of mitral regurgitation is different from the murmur of aortic regurgitation.
|
•Mitral regurgitation (MR): Holosystolic
• Aortic regurgitation: Diastolic |
|
Which 2 bacteria are well known for being obligate intracellular bacteria? Why can’t these bacteria replicate extracellularly?
|
•Rickettsia: Cant make its own ATP
• Chlamydia: Can’t make its own ATP • Intracellular because it’s Really Cold •Legionella •Rickettsia and Chlamydia can’t replicate extracellularly b/c they can’t make ATP |
|
What marker of inflammation produced by the liver and within atherosclerotic plaques is a strong predictor of MI risk?
|
• C-reactive protein (CRP)
|
|
Arteriosclerosis
|
Arteriosclerosis – hardening of arteries
o Medial calcific sclerosis: Media of arteries o Arteriolosclerosis: Hyaline thickening of small arteries o Atherosclerosis: Intima of arteries, Large & medium vessels |
|
Pathogenesis of atherosclerosis
|
• Endothelial injury
• Accumulation of lipoprotein • Monocyte adhesion to the endothelium • Platelet adhesion • Factor release • Smooth muscle cell proliferation and ECM production • Lipid accumulation |
|
Coronary Arteries
HIGH YIELD TOPIC – 3 star*** |
Right coronary artery
Posterior descending artery Right marginal artery Left coronary artery Left circumflex artery Left marginal artery Left anterior descending (or interventricular) artery Diagonal branch |
|
What is the most likely cause of chest pain in each of the following scenarios?
• ST segment elevation only during brief episodes of chest pain |
o Prinzmetal’s angina
|
|
• Patient is able to point to localize the chest pain using one finger
|
o Musculoskeletal chest pain
|
|
• Chest wall tenderness on palpation
|
o Musculoskeletal chest pain
|
|
• Rapid onset sharp chest pain that radiates to the scapula
|
o Aortic dissection
|
|
• Rapid onset sharp pain in a 20-year-old and associated with dyspnea
|
o Spontaneous pneumothorax
|
|
• Occurs after heavy meals and improved by antacids
|
o GERD
o Esophageal spasm |
|
• Sharp pain lasting hours-days and is somewhat relieved by sitting forward
|
o Pericarditis
|
|
• Pain made worse by deep breathing and/or motion
|
o Musculoskeletal chest pain
|
|
• Chest pain in a dermatomal distribution
|
o Herpes zoster (rash follows pain)
|
|
• Most common cause of non-cardiac chest pain
|
o Musculoskeletal chest pain or GERD
|
|
What are the most common locations for atherosclerosis, and what disorders result from plaques in these locations?
|
• Abdominal aorta: AAA
• Coronary arteries: angina, MI • Popliteal arteries: claudication/PVD • Carotid arteries: TIA, strokes, dementia |
|
A patient with poorly-managed HTN has acute, sharp substernal pain that radiates to the back and progresses over a few hours. Death occurs in a few hours. Diagnosis?
|
• Aortic dissection
|
|
What is the most likely cause of chest pain in each of the following scenarios?
• Acute onset dyspnea, tachycardia, and confusion in the hospitalized patient |
o PE
|
|
• Rapid onset of sharp pain in the 20-year-old and associated with dyspnea
|
o Spontaneous pneumothorax
|
|
• Pain began the day following an intensive new exercise program
|
o Musculoskeletal chest pain
|
|
• ST segment elevation only during brief episodes of chest pain
|
o Prinzmetal’s angina
|
|
• Sharp pain lasting for hours to days and is somewhat relieved by sitting forward
|
o Pericarditis
|
|
• Chest wall tenderness on palpation
|
o Musculoskeletal chest pain
|
|
Lecture 130: CV 16
|
Antifungal Therapy and Lipid- Lowering Agents
|
|
Which calcium channel blockers can be used to treat both hypertension and tachyarrhythmia?
|
• Diltiazem
• Verapamil |
|
What are the systolic heart murmurs?
|
• Mitral and tricuspid regurgitation
• Aortic stenosis • VSD • Mitral prolapsed • PDA |
|
What problem is most closely associated with the following statements?
50-year-old female presents with pruritius without jaundice, lab reveals (+) AMA |
Primary biliary cirrhosis
|
|
A patient with GI bleeding has buccal pigmentation
|
Peutz-Jeghers syndrome
|
|
60-year-old woman with rheumatoid arthritis and no alcohol history presents with fatigue and right abdominal pain, lab studies reveal high levels of ANA and no ASMA, elevated serum IgG levels, and no viral serologic markers
|
Autoimmune hepatitis
|
|
Liver biopsy on a 23-year-old female with elevated levels of LKM-1 antibodies, no alcohol history, and no viral serologic markers reveals infiltration of the portal and periportal area with lymphocytes
|
Autoimmune hepatitis
|
|
Fatal disease of unconjugated bilirubin resulting from a complete lack of UDPGT activity
|
Crigler-Najjar, Type I
|
|
Nonfatal disease of unconjugated bilirubin resulting from low levels of UDPGT active
|
Gilbert disease
Crigler-Najjar, type II |
|
Elevated levels of serum ferritin and increased transferrin saturation
|
Hemochromatosis
|
|
Alpha-fetoprotein levels > 1000 pg/mL
|
Hepatocellular carcinoma
|
|
Elevated serum copper, decreased serum ceruloplasmin, and elevated 24-hr urinary copper
|
Wilson disease
|
|
Liver disease + lung emphysema
|
a- Antitrypsin deficiency
|
|
ERCP reveals alternating strictures and dilation
|
Primary sclerosing cholangitis
|
|
Statins
KNOW SE |
o HMG CoA reductase inhibitor
o Agents Lovastatin Pravastatin Simvastatin Atorvastatin Rosuvastatin o Side Effects Hepatotoxicity Myalgias Myositis Rhabdomyolysis can lead Renal failure |
|
Niacin
KNOW SE |
o Clinical use: Raises HDL
o Side Effects: Flushing |
|
Bile Acid Binding Resins
|
Cholestyramine: Binds C. diff toxin
Colestipol Colesevelam |
|
Cholesterol Absorption Blocker (Ezethimibe)
KNOW SE |
o MOA: Prevents cholesterol reabsorption at the small intestine brush border
o Side effects: Increase in LFTs |
|
Fibrates
KNOW SE |
o Agents: Gemfibrozil, Clofibrate, Fenofibrate, Bezafibrte
o MOA: Lowering TGs, More effective than statins o Side Effects: Myositis |
|
Omega-3 fatty acids
|
o Agents: Fish oil (Salmon, Halibut, Coldwater ocean), Flaxseed oil
o MOA: Lowering TGs |
|
Which lipid-lowering agent matches each of the following descriptions?
• SE: facial flushing |
o Niacin (counteracted with aspirin)
|
|
• SE: elevated LFTs, myositis
|
o Statins
o Fibrates |
|
• SE: GI discomfort, bad taste
|
o Bile acid binding resins
|
|
• Best effect on HDL
|
o Niacin
|
|
• Best effect on triglycerides/VLDL
|
o Fibrates
o Omega-3 fatty acids |
|
• Best effect on LDL/cholesterol
|
o Statins
|
|
• Binds C. diff toxin
|
o Cholestyramine
|
|
A 50-year-old man starts on lipid-lowering medication. Upon his first dose, he develops a rash, pruritus, and diarrhea. What drug is he taking?
|
• Niacin
|
|
How can the flushing reactions of niacin be prevented?
|
• Aspirin or NSAID 30 minutes before niacin
• Avoid alcohol/hot beverages • Take at bedtime • Be persistent: Flushing usually goes away after 1 week of using niacin |