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Reserve Step I Cards > Cardio > Flashcards

Cardio Flashcards

1
Q

What is moa of mineralocorticoid receptor antagonists? What diseases are they good for and who should they not be used for?

Give (2) examples

A

(Spironolactone and Eplerenone)

They prevent aldosterone from binding to its receptor in the distal renal tubules, leading to increased sodium excretion.

Indications: CHF and reduced left ventricular EF

Contraindications: Hyperkalemia and renal failure

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2
Q

What is NE extravasation and what is the treatment?

A

Blanching of vein into which NE is being infused due to NE leakage causing major a1 receptor activation and subsequent constriction.

Use phentolamine (alpha-receptor blocker)

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3
Q

Tetralogy of Fallot Pathophysiology and clinical presentation

A

VOIR:

  1. VSD
  2. Overiding aorta
  3. Infundibular pulmonary stenosis
  4. RVH

Presentation: Cyanosis; Improvement w/ squatting (increases SVR)

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4
Q

Define accuracy vs reliability

A

Accuracy: the degree to which the aerage measurment value matches that of the gold standard

Reliability: reproducibility of a result

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5
Q

What cranial nerves and what aortic arch derivatives are associated with each pharyngeal/aortic arch (1-6)

A
  1. CN V; Maxillary artery
  2. CN VII; Stapedial artery (regresses)
  3. CN IX; Common carotid and prox. internal carotid
  4. CN X (superior laryngeal); True aortic arch and Subcalvian arteries
  5. Obliterated
  6. CN X (recurrent branch); Pulmonary arteries and Ductus arteriosus
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6
Q

What are the normal adult pressures in the cardiac chambers, the pulmonary artery and the aorta (minimum and maximum)

A

RA: 0 and 8 mmHg

RV: 4 and 25 mmHg

PA: 9 and 25 mmHg

LA: 2 and 12 mmHg

LV: 9 and 130 mmHg

Aorta: systolic BP

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7
Q

How does A-fib look on an EKG? In this condition, what ultimately regulates the number of atrial pulses which reach the ventricle?

A
  • On EKG, it is characterized by: absent P waves, irregularly irregular R-R intervals, and narrow QRS
  • Ventricular response is based on transmission of the abnormal impulses through the AV node. The AV node refractory period regulates the number of impulses.
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8
Q

Dystrophic vs Metastatic calcification

What conditions do they each occur in?

A

Dystrophic: Occurs normally, w/ age, in damaged or necrotic tissues in the setting of normal calcium levels.

Metastatic: Occurs in normal tissue in the setting of hypercalcemia

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9
Q

Retinal Artery Occlusion

Presentation?

Pathogenesis?

What is the path most likely taken to occlude the artery?

A

Presentation: Acute, painless, monocular vision loss

Pathogenesis: Thromboembolic complications of athersclerosis in the internal carotid.

Path: Internal carotid –> Ophthalmic artery –> retinal artery

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10
Q

What is the MOA for ANP and BNP? How is this similar to sildenafil?

A

ANP and BNP are similar to NO. They activate guanyl cyclase which increases the levels of cGMP. cGMP leads to relaxation of vascular smooth muscle and vasodilation, via myosin light-chain dephosphorylation

Sildenafil is a phosphodiesterase inhibitor and therefore decreases degradation of cGMP, ultimately causing the same result.

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11
Q

Aortic Regurgitation

  1. Presentation
  2. Describe how the pulses may feel
  3. Describe the murmur and the best way to hear it
  4. What is the state of the pulse pressure?
A
  1. Presentation: progressive fatigue + dypsnea
  2. Pulses: “water-hammer” pulses (bounding femoral and carotids) and head-bobbing with each heartbeat (de Musset sign)
  3. Murmur:
  • Decrescendo murmur after A2
  • High-pitched, blowing quality
  • Best heard at left sternal border, at 3rd/4th intercostal space, with the patient sitting up and leaning forward
  1. The pulse pressure is widened
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12
Q

What are “Lichtenberg figures” and what are they associated with?

A

Erythematous cutaneous marks in a fern-leaf pattern.

They are pathognomonic of lightning strikes

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13
Q

MOA of Sotalol

A

It has both beta-adrenergic blocking properties and class 3 antiarrhtmic (K+ channel blocking) properties. It prolongs the PR interval and the QT interval.

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14
Q

What is the indication for an ace-inhibitor? For a thiazide?

A

ACE-inhibitors: inhibit chronic angiotensin II-mediated remodeling that occurs in association w/ MI and CHF

Thiazides: useful as an initial treatment for essential HTN w/o CHF or diabetes

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15
Q
  1. Name the non-selective beta-blockers
  2. Name the selective beta-blockers
  3. Why would you choose selective over non-selective?
A
  1. Non-Selective- Propanolol, timolol, and nadolol
  2. Selective- metoprolol, atenolol, acebutolol and esmolol
  3. Selective only target B1, so if you have patients w/ COPD/asthma, you want to only use these.
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16
Q
  1. Name the anthracycline chemotherapeutic agents.
  2. What is their most severe side effect
  3. How does it present?
  4. How is this SE prevented?
A
  1. Doxorubicin, daunorubicin, epirubicin and idarubicin
  2. Their most severe side effect is a cumalitive dose-related dilated cardiomyopathy due to free-radical formation
  3. Presents w/ right and left ventricular CHF
  4. Prevented via dexrazoxane- iron-chelating drug which reduces free radical formation
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17
Q

Digoxin MOA

A

Digoxin directly blocks the Na/K+ pump in myocardial cells, leading to increased intracellular Na. This slows functioning of Na+/Ca+ exchanger, thereby keeping Ca+ trapped in the the myocardial cell as well, increasing contractility.

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18
Q

What is Trousseau sign? What does it indicate?

A

It is when superficial venous thromboses may appear in one site, resolve, and occur in another site. This often indicates visceral cancer.

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19
Q

Piercing of femoral artery above the inguinal ligament can signficantly increase the risk of what hemorrhage in what location?

A

Retroperitoneal

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20
Q

Buerger’s disease (thromboangiitis oblierans)

  1. Main population demographics
  2. Pathophysiology
  3. Presentation
  4. Tx
A
  1. Heavy smokers, males
  2. Path- Segmental thromboding vasculitis
  3. Presentation- Intermittent claudication which can lead to gangrene, autoamputation, and superficial nodular phlebitis. Also associated w/ Raynauds
  4. Tx: smoking cessation
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21
Q

Tricuspid Valve Endocarditis

  1. Most common bug associated?
  2. Usual patient population?
  3. Potential complications?
A
  1. Staph aureus is #1. Pseudomonas is #2
  2. IV drug users
  3. These patients can develop multiple septic emboli in lungs. Resulting pulmonary infarcts will be hemorrhagic due to dual blood supply.
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22
Q

Varicocele

  1. Pathophysiology?
  2. Presentation?
A
  1. Increased pressure in the left gonadal vein resulting in valve leaflet failure and varices of the testicular pampiniform plexus
  2. Presents with flank/abdominal pain and gross or microscopic hematuria
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23
Q

Niacin (nicotinic acid)

  1. Indication
  2. Adverse Effects
  3. What is the mechanism for the adverse effects and how can they be prevented?
A
  1. Used in the tx of hyperlipidemia. Effective in raising HDL cholesterol levels, and lowering LDLs and TGs
  2. SEs include cutaneous flushing, warmth and itching
  3. SEs are mediated by release of prostaglandins and can therefore be prevented by aspirin.
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24
Q

Blockage of what vein causes symptoms similar to those in SVC syndrome, except only on one side of the body? What are those symptoms?

A

Blocking of the Brachiocephalic vein

Shows one sided face-swelling, arm swelling and engorgement of subcutaneous veins .

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25
Q

In the pathogenesis of atherotic plaques, What is responsible for promoting migration of smooth muscle cells from the media into the intima, and subsequent proliferation?

A

The release of Platelet-derived growth factor (PDGF) by locally adherrent platelets, endothelial cells, and macrophages.

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26
Q

What is the most common condition predisposing a patient to infective endocarditis in…

  1. Adults in wealthier nations?
  2. Poorer nations/ children?
A
  1. Mitral valve prolapse/ mechanical valves
  2. Rheumatic fever
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27
Q

What is the “Number Needed to Treat”, and how is it calculated?

A

It’s the number of patients that need to be treated with a medicatin to avoid a negative outcome. It is 1 divided by the percent difference in outcome between the control and the experiment

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28
Q

What are the effects of nitrate? (3 general categories of effects)

Side Effects?

A
  • Primarily venodilators (but also vaso) that increase peripheralvenous capacitance
  • Reduce cardiac preload and afterload and LVEDP and volume, reducing work of heart
  • Modest effect on arteriolar dilation

Side Effects: HA, cutaneous flushing, hypotension

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29
Q

Thiazide diuretics

  1. MOA
  2. Effects
  3. AEs
A
  1. Inhibit Na+/Cl- co-transporter in the DCT, thereby decreasing reabsorption of NaCl
  2. Lower BP by decreasing intravascular volume, reduce CO, and lower systemic vascular resistance
  3. Dec. insulin secretion and glucose uptake, and increase LDL cholesterol and TG levels
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30
Q

Patent Ductus Arteriosus (PDA)

  1. Pathology
  2. Why is it patent
  3. Clinical manifestations
  4. Typical age at presentation
  5. Tx.
A
  1. Vascular connection between the main pulmonary artery and the aorta still remains after birth
  2. Patent due to prostaglandin E2 production by the placenta
  3. Clinical features vary by size: Small: continuous machine-like murmur w/ no other symptoms. Large: progressive pulmonary HTN, reversal of shunt (now right-to-left), ultimately leading to HF and cyanosis (Eisenmenger syndrome), particularly in lower extemities.
  4. Childhood
  5. Tx: Indomethacin (prostaglandin E@ inhibitors)
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31
Q

Hypertrophic Cardiomyopathy

  1. Key potential clinical consequences (2)?
  2. Histo
  3. Pathology
  4. Dx of this consequence?
  5. What actions make those sx better or worse?
A
  1. Left ventricular outflow obstruction; sudden death in stressful situation
  2. Extreme myofiber disarray w/ interstitial fibrosis
  3. Mutations in genes encoding cardiac sarcomere proteins
  4. Harsh crescendo-decrescendo systolic ejection-type murmur best heard along left sternal border and apex
    • Mechanisms dec. preload or afterload increase obstruction – such as sudden standing or nitro.
    • Mechanisms inc. preload or afterload decrease obstruction – such as squatting, sustained hand grip, or passive leg raise
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32
Q

Aortic Dissection

  1. Most important risk factor
  2. What specific layer tears?
  3. What genetic issue predisposes for aortic dissection?
A
  1. HTN is most important risk factor
  2. Tunica intima is the layer which tears away
  3. Marfan’s which leads to cystic medial degeneration
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33
Q

Liver Angiosarcoma

  1. Pathology?
  2. Describe the cellular change
  3. Main carcinogens associated?
A
  1. Rare malignant vascular endothelial cell neoplasm associated w/ carcinogen exposure
  2. Neoplasm composed of CD-31 PECAM1 (platelet endothelial cell adhesion molecule). Indicates that a tumor has risen from vascular endothelial cells.
  3. Implicated chemicals include arsenic (pesticides), thorotrast (contrast), and polyvinyl chloirde (industry plastic)
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34
Q

MOA of B-Blockers

A

B-Blockers decrease AV nodal conduction, leading to an increased AV nodal refractory period

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35
Q

Pulsus Paradoxus

  1. What is it?
  2. How is it detected?
  3. Why does it happen?
  4. What disease processes is it associated with? (4)
A
  1. An exaggerated drop (>10mmHg) in systolic BP during inspiration
  2. Detected when taking the BP, by listening to the difference between when korotkoff sounds are first heard during expiration and the pressure at which they are heard throughout all phases of respiration
  3. Inspiration inc. venous return and normally this expands RV into pericardium but if this expansion can’t happen, the interventricular septum pushes into the LV, dropping LV EDV and subsquently the stroke volume
  4. Pericardial disease, acute cardiac tamponade, asthma, COPD
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36
Q

Aspirin

MOA

A

Aspirin impairs prostaglandin synthesis by irreversibly inhibiting COX. Inhibition of COX-1 in platelets prevents synthesis of thromboxane A2, a potent stimulator of platelet aggregation and vasoconstriction.

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37
Q

Clopidogrel

  1. MOA
  2. Indication
A

MOA: Irreversibly blocks the P2Y component of ADP receptors on the platelet surface and prevents platelet aggregation

Indication: Just as effective as aspirin for prevention of CV events and should be used if patient has aspirin allergy.

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38
Q

What is the most common location on the aorta for a traumatic aortic rupture (blunt aortic injury)?

A

The aortic isthmus (located just past the aortic arch)

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39
Q

Statins

  1. Indication
  2. MOA
  3. Side effects
  4. What sort of things can help lead to adverse effects from Statins
A
  1. Indications: Tx of hypercholesterolemia
  2. Inhibit HMG-CoA reductase, thus blocking hepatic cholesterol synthesis. This forces the liver to increase surface expression of LDL receptors, thus pulling LDL from circulation
  3. SE: Myopathy, rhabdomyolysis, and hepatoxicity
  4. Drugs that interfere w/ statin metabolization, particuarly via cytochrome p450 enzymes (ex. fibrates)
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40
Q

Streptococcus gallolyticus (formely S. Bovis) can cause endocarditis and bactermia. When this bug is cultured in the blood, workup for what, is absolutely essential?

A

Colonic malignancy with colonoscopy

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41
Q

Describe the Sx of Digoxin Toxicity

(what ion is often elevated?)

A
  • Typically presents w/ cardiac arrhythmias and nonspecific GI, neuro and visual (color change) sx
  • Elevated K+ is another sign of digoxin toxicity (due to inhibition of Na-K-ATPase)
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42
Q

AV Shunts

  1. What affect do they have on preload/afterload?
  2. What might the physical exam reveal?
A
  1. AV shunt increases the preload and decreases the afterload by routing blood directly from the arterial system to the venous system
  2. Physical exam may reveal pulsatile mass w/ thrill on palpation. Ausculation reveals a constant bruit over the site.
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43
Q

What is the most common congenital heart lesion?

  1. Dx/ Presentation?
  2. Effect on blood oxygenation
  3. Prognosis?
A

Ventricular Septal Defects

  1. Small VSDs have a loud, “blowing”, holosystolic murmur at the mid/lower left sternal border (louder with handgrip). Murmur is usually inaudible until 4-10 days when pulmonary vascular resistance declines enabling left-to-right shunt.
  2. Right ventriclular blood has increased O2 content
  3. Most are clinically insignficant and close spontaneously
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44
Q

Prinzmetal’s (variant) Angina

  1. Pathology?
  2. When does it occur?
  3. Dx?
  4. Tx?
  5. What drug can make it worse?
A
  1. Episodic, transient attacks of coronary vasospasm
  2. Usually occurs at rest and during late night/early morning
  3. Temporary transumral MI w/ ST elevation on EKG
  4. Tx with vasodilators and CCBs
  5. Ergonovine can provoke vasospasm and can aid in diagnosis
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45
Q

How is tolerance to nitrates avoided?

A

You must provide a nitrate-free interval every day in patients w/ long acting nitrates.

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46
Q

How is nitric oxide synthesized?

A

It is synthesized from arginine by NO synthase

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47
Q

What are the only cells within atherosclerotic plaque which are capable of synthesizing collagen isoforms and ECM?

A

Vascular Smooth Muscle Cells (VSMCs)

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48
Q

When given with a Statin, what drug is most likely to lead to myopathy or even rhabdomyolosis? Why?

A

Fibrates (like Gemfibrozil). They impair the hepatic clearance of Statins leading to excessive blood levels.

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49
Q

Aortic stenosis

  1. Common murmur
  2. Sx
  3. Main causes
A
  1. Crescendo-decrescendo murmur right sternal border
  2. Typically asymptomatic. If advanced can present w/ exertion and inlcude syncope, dizzyness, angina or even HF
  3. Main causes: abnormal valve w/ calcification (e.g. bicuspid aortic); calcified normal valve; or rhemuatic heart disease
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50
Q

Carcinoid Syndrome

  1. What is it?
  2. What can it progress to?
  3. How does a blood/urine test tell us about severity?
A
  1. Fibrous thickening with endocardial plaques limited to the right heart
  2. May progress to pulmonic stenosis and/or restrictive cardiomyopathy
  3. Severity correlates with plasma levels of serotonin and urinary excretion of the serotonin metabolite, 5-hydroxyindoleacetic acid
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51
Q

Main Side Effect difference between ACE-I’s and ARBs

A

ACE-I’s raise the level of Bradykinin causing non-productive cough.

ARBs do not.

The two drugs are very similar otherwise

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52
Q

How does the effect of Rheumatic Heart Disease on the mitral valve vary as the patient’s age changes?

A

First few decades of life: MR

Middle-aged: MS (most common cause of MS)

Elders: Mixed mitral disease (S and R)

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53
Q

MOA of class 3 antiarrhytmic agents

A

They block K+ efflux from cardiac myocytes and prolong phase 3 of the myocyte AP

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54
Q

SE profile for ACE-Inhibitors (2)

A
  1. Bradykinin induced cough and angioedema if there is accumulation
  2. First dose hypotension due to volume depletion
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55
Q

Phenoxybenzamine

  1. MOA
  2. Indication
  3. Effect
A
  1. Irreversible a1 and a2 antagonist that effectively reduces the arterial vasoconstriction induced by NE.
  2. Pheochromocytoma
  3. Because it is irreversible, even very high concentrations of NE (like those seen in pheochromocytoma) cannot overcome its effects
56
Q

Isoproterenol

  1. MOA
  2. Effect
A
  1. Non-selective Beta-_agonist_
  2. Increases myocardial contractility and decreases systemic vascular resistance
57
Q

Dopamine: What is the effect of…

  1. Low doses?
  2. Medium doses?
  3. Very high doses?
A
  1. Low dose: stimulate D1 receptors in the renal and mesenteric vasculature
  2. Medium dose: stimulate B-1 receptors, increasing cardiac contractility
  3. High dose: stimulate a-1 receptors, producing generalized vasoconstriction
58
Q

Antiarrhythmic drugs

Drugs + Predominant actions

Class IA, IB, IC

A
  1. IA: Dispyramide, Procainamide, Quinidine- slows AP conduction velocity; prolongs APD
  2. 1B: Lidocaine, Mexiletine, Phenytoin- Shortens APD (no effect on AP conduction velocity)
  3. 1C: Flecainide, Propafenone- Slows AP conduction velocity; minimal effect on APD

“Double Quarter Pounder; Light Mayo and Pickles; Fries Please”

59
Q

What are the type II Anti-arrhythmics?

A

Beta-blockers

60
Q

Antiarrhythmic drugs

Drugs + Predominant actions

Class III

A

Amiodarone, Dronedarone, Dofetilide, Sotalol (also class II)

Prolongs APD by blocking K+ channels (no effect on AP conduction velocity)

61
Q

Antiarrhythmic drugs

  1. Drugs + Predominant actions
  2. Potential SEs

Class IV

A

Verapamil; Dilitiazem

  1. Slows sinus node discharge rate; slows AV nodal conduction and prolongs refractoriness
  2. Can lead to severe bradycardia and hypotension (especially in combo with a beta-blocker)
62
Q

Relationship between blood flow and radius

A

Blood flow is directly proportional to vessel radius raised to the fourth power.

63
Q

Jervell and Lange-Nielsen Syndrome

  1. Pathology
  2. Clinical presentation
  3. Mode of inheritance
  4. What other disease is this similar to?
A
  1. Congenital long-QT syndrome; thought to result from mutations in a K+ channel protein
  2. Syncopal episodes; sudden cardiac death (torsades de pointes);
  3. Autosomal recessive condition
  4. Similar to Romano-Ward syndrome
64
Q

What sometimes occurs between days 2-4 following a transmural MI? Why?

A

Early-onset pericarditis develops in 10-20% of patients. It represents an inflammatory reaction to adjacent cardiac muscle necrosis.

65
Q

Cystic Medial Degeneration

  1. Characteristics
  2. What does it predispose you for?
  3. Who is it common in?
A
  1. Myxomatous (weakening of connective tissue) changes with pooling of proteoglycans in the media layer of large arteries
  2. Aortic dissections/ Aneurysms
  3. Younger patients with Marfan Syndrome
66
Q

Adult type Aortic Coarctation

  1. Key triad
  2. View on imaging
A
  1. (1) upper body hypertension; (2) diminished lower extremity pulses; (3) enlarged intercostal artery collaterals
  2. Notching of ribs as a result of the enlarged, tortuous intercostal arteries
67
Q

Permissiveness

A

When one hormone allows another to exert its maximal effect (ex. cortisol allows NE to work even better although cortisol has no direct vascular effect itself)

68
Q

Cutaneous, strawberry-type capillary hemangiomas

  1. Pathology
  2. Prognosis
A
  1. Benign congenital tumor of unencapsulated aggregates of closely packed, thin-walled capillaries
  2. Initial growth followed by regression (excellent prognosis)
69
Q

Why does listening to heart sounds at end expiration make them more audible?

A

Decreased lung volume, bringing the heart closer to the chest wall.

70
Q

What are the (2) mechanisms by which beta-blockers lower blood pressure?

A
  1. Reducing myocardial contractility and HR
  2. Decreasing renin release by the kidney
71
Q

What phase of the AP corresponds with the QRS of the EKG?

QT?

A

QRS = Phase 0

QT = Phase 3

72
Q

What receptors is epinephrine capable of affecting?

A

a1, B1, and B2

73
Q

Following focal ischemia in an MI, how long until there is a loss of cardiomyocyte contractility?

A

Loss of focal contractility occurs within 60secs!

74
Q

Fenoldopam

  1. MOA
  2. Indication
  3. Effects (3)
A
  1. MOA: selective peripheral D1 receptor agonist
  2. Indication: given IV ti lower BP in HTN crisis, especially in patients with renal insufficiency
  3. Effects: (1)Arteriolar dilation, (2) increased renal perfusion, and (3) promotion of diuresis/ natriuresis
75
Q

Fibrates

  1. MOA
  2. Effect
  3. Compare this to fish oil
A
  1. Activates peroxisome proliferator-activated receptor alpha (PPAR-a).
  2. This leads to decreased hepatic VLDL production and increased Lipoprotein lipase activity, thus lowering triglyceride levels
  3. Fish oil supplements w/ O3FA dec. VLDL and ApoB production
76
Q

Dihydropyridine CCBs (Anti-hypertensives)

  1. Main examples
  2. Indications
  3. SEs
A
  1. Amlodipine and Nifedipine
  2. Effective for monotherapy or in combination with other agents for Tx of HTN
  3. Peripheral Edema and Dizziness/ Lightheadedness
77
Q

What sort of procedure is associated with enterococcal endocarditis

A

Genitourinary instrumentation or catherization (enterococcus is a component of normal colonic and GU flora)

78
Q

Main phase “0” difference between regular cardiac cell and a pacemaker cell

A

Regular cardiac cell: 0 = Na+ rush

Pacemaker: 0 = Ca2+ rush

79
Q

ASD

  1. What is the usual pathology?
  2. What other cardiac condition is often also present?
  3. Dx
  4. Potential consequence
  5. What genetic disease is also associated?
A
  1. Failure of the endocardial cushions of the atrioventricular canal to fuse completely during embryonic development can lead to a lower interatrial septum defect
  2. Malformation of mitral valve leading to mitral regurg is often present
  3. Wide, fixed splitting of the second heart sound (S2)
  4. Pulmonary HTN
  5. Down syndrome
80
Q

In patients with mitral regurg, what is the most reliable ausculatory finding to assess severity

A

The presence of a left-sided S3 gallop. This indicates high regurgitant volume and left ventricular volume overload

81
Q

Why is it that calcium channel blockers affect smooth and cardiac muscle, but not skeletal?

A

Cardiac and smooth muscle cells depend on extracellular calcium influx into cells via L-type calcium channels. Skeletal muscle cells do not, because they have a direct mechanical coupling of the L-type channel and the RyR.

82
Q

Ortner syndrome

A

When mitral stenosis causes left atrial dilatation sufficient to impinge on the left laryngeal nerve

83
Q

Myocardial hibernation

A

A state of chronic myocardial ischemia in which myocardial metabolism and function is reversibly reduced in order to match a reduction in coronary blood flow, thus preventing myocardial necrosis

84
Q

Drug-induced Lupus Erythematosus

  1. Presentation
  2. Dx
  3. What is almost never seen?
  4. Drugs normally implicated
A
  1. New onset of lupus symptoms
  2. Anti-nuclear antibodies (ANA) and anti-histone antibodies
  3. Anti-dsDNA ALMOST NEVER SEEN
  4. HIP: Hydralazine, Isoniazid, Procainamide
85
Q

What is usually the most key component of the pathogenesis of AAAs?

A

Transmural aortic wall inflammation

86
Q

Lipofuscin

A

Yellow-brown, granular product of lipid peroxidation and considered to be a sign of “wear and tear”/aging.

87
Q

Prostacyclin vs Thromboxane A2

Compare their effects

A

Prostacyclin: vasodilates, inhibiting platelet aggregation and increasing vascular permeability

Thromboxane A2: prostaglandin which enhances platelet aggregation and causes vasoconstriction

88
Q

Kawasaki Disease

  1. What type of disease is this?
  2. Presentation
  3. Potential consequence
  4. Tx
A
  1. Medium-vessel vasculitis
  2. CRASH and burn
    • Conjuctival injection, Rash, Adenopathy, Strawberry tongue, Hand/foot changes (edema and erythema) and fever
  3. Risk of coronary artery aneurysm
  4. Tx w/ IV and aspirin
89
Q

Diphteria

  1. Epidemiology
  2. Micro/pathology
  3. Clinical Sx (4)
  4. Complications (3)
A
  1. Endemic in developing countries
  2. Corynebacterium diphtheriae colonize repiratory tract and secrete diphtheria toxin (inhibits protein synthesis via ribosylation of EF-2)
  3. (1) Pseudomembrane; (2) cervical adenopathy (3)sore throat (4) fever
  4. (1) Suffocation due to edema/pseudomembrane aspiration; (2) Heart failure/ (3) neuro toxicity from the toxin
90
Q

Vascular and Immunologic Manifestations of Infective Endocarditis

(3) Vascular
(2) Immunological

A

Vascular:

  1. Systemic emboli
  2. Mycotic aneurysm
  3. Janewy lesions (nontender- palms/soles)

Immunologic:

  1. Osler nodes (Painful- toes/fingertips)
  2. Roth spots
91
Q

Coronary Sinus

  1. What does it serve as?
  2. Under what condition might it be dilated?
A
  1. Serves as the endpoint of venous drainage from the coronary blood supply, draining directly into the right atrium
  2. Will be dilated by any factor that dilates the right atrium (most commonly pulmonary HTN)
92
Q

Paroxysmal Supraventricular Tachycardia

  1. Presentation
  2. Tx
  3. Potential SEs of tx (4)
A
  1. Sudden onset palpitations
  2. Tx w/ adenosine
  3. SE: (1) Flushing, (2) chest burning (from bronchospasm), (3) hypotension, (4) AV block
93
Q

Giant Cell Arteritis

  1. Also known as?
  2. Main Sxs (4)
  3. What does the artery look like on biopsy?
A
  1. aka Temporal arteritis
  2. Jaw Claudication, HA, facial pain, and vision loss
  3. Temporal artery biopsy demonstrates granulomatous inflammation of the media
94
Q

Torsades de Pointes

  1. Pathology
  2. What are the most common precipitants? (3 categories + examples)
A
  1. Polymorphic v.tach that occurs in the setting of a congenital or acquired prolonged QT interval
  2. Medications such as certain (1) antiarrhythmics (sotalol, quinidine); (2) antipsychotics (haloperidol); (3) antibiotics (macrolides, fluoroquinolones)
95
Q

Paradoxical Embolism

  1. Pathology
  2. Dx
A
  1. When a thrombus from the venous system crosses into arterial circulation (as oppose to the pulmonary) via an abnormal connection between the right and left cardiac chambers
  2. May see fixed splitting of S2 if a shunt is present
96
Q

Of all major vascular beds, which (2) are most susceptible to athersclerosis?

A
  1. Lower abdominal aorta
  2. Coronary arteries
97
Q

Mitral Stenosis

  1. What is the best/most reliable asuculatory indicator of the severity?
A
  1. The interval between A2 and the opening snap (OS). Shorter interval = more severe stenosis
98
Q

Right Ventricular MI

  1. Presentation
  2. Pathology
  3. What does the hemodynamic assessment reveal? (CVP? Wedge pressure? CO?)
A
  1. Presents with hypotension, elevated JV pressure, clear lungs
  2. Most often occurs in the setting of acute inferior wall MI
  3. CVP= inc.; Wedge pressure = dec.; CO = dec.
99
Q

How is carotid sinus massage useful for termination of paroxysmal SVT?

A

It leads to increased parasympathetic tone causing temporary inhibition of the SA node and the prolongation of AV node refractory period

100
Q

Osler-Weber-Rendu Syndrome

  1. What is the other name?
  2. Genetics
  3. Clinical Presentation
  4. Possible consequences
A
  1. Hereditary hemorrhagic telangiectasia
  2. Autosomal dominat
  3. Presence of telangiectasias in the skin and mucous membraes of the lips, oropharynx, respiratory tract, GI tract and urinary tract
  4. Rupture of these vessels may cause epistaxis (nosebleeds), GI bleed, or hematuria
101
Q

Lidocaine

  1. What class drug?
  2. MOA?
  3. Effect?
A
  1. IB antiarrhythmic
  2. Binds (mostly) to inactivated sodium channels and rapidly dissociates
  3. Effective in suppressing v.tach induced by rapidly depolarizing and ischemic myocardium.
102
Q

Fick Principle

A

An alternative means for calculating cardiac output.

CO = O2 consumption/ AV O2 difference

103
Q

Which cell types have B1 receptors?

A

Cardiac tissue and renal juxtaglomerular cells

104
Q

a-1 blockers are useful for the treatment of … (2 conditions)

What natural secretion has these same effects?

A

HTN and benign prostatic hyperplasia (relaxes the bladder)

ANP/BNP has the same effects

105
Q

Which blood vessel carries blood with the lowest content of oxygen in the body

A

Coronary sinus

106
Q

Describe the process of Infective Endocarditis (4)

A
  1. Disruption of normal endocardial surface (usually in areas of maximum turbulence)
  2. Focal adherence of fibrin and platelets, forming sterile fibrin-platelet nidus
  3. Colonization by microorganisms (strep to damaged areas; staph to damaged or normal areas)
  4. Formation of macroscopic vegetations made of debris
107
Q

Polyarteritis nodosa

  1. Pathology
  2. What organ is normally spared?
  3. Presentation
  4. Potential consequences
A
  1. Segmental, transmural, necrotizing nflammation of medium to small sized arteries in any organ
  2. Lungs are spared
  3. Can be cutaneous manifestations, including livedo reticularis and palpable purpura
  4. Inflammation can result in ischemia, infarcation, or hemorrhage and bead-like aneurysm formation
108
Q

Coordinate each artery with the leads associated with them

  1. LAD
  2. LCX
  3. RCA
A
  1. Anterior and Septal
  2. Left lateral
  3. Inferior and Right
109
Q

What are the afferent and efferent limbs leading to/away the carotid bodies?

A

Afferent: Glossopharyngeal nerve

Efferent: Vagus nerve

110
Q

What is the main side effect which limits the long-term efficacy of arteriolar vasodilators. Give (2) main examples of these drugs

A

Ex: Hydralazine and minoxidil

There can be reflex sympathetic stimulation (leading to inc. HR, contractility, and CO) and also stimulation of the RAA system leading to sodium and fluid retention/edema

111
Q

Name the precursor protein/peptide responsible for localized amyloidosis for each of the following organs:

  1. Cardiac atria
  2. Thyroid gland
  3. Pancreatic islets
  4. Cerebrum/cerebral blood vessels
  5. Pituitary gland
  6. Multi-organ amyloid deposition?
A
  1. Cardiac atria: atrial natriuretic peptide
  2. Thyroid gland: calcitonin
  3. Pancreatic islets: islet amyloid protein
  4. Cerebrum/cerebral blood vessels: B-amyloid protein
  5. Pituitary gland: prolactin
  6. Multi-organ amyloid deposition? Immune globulin light chains
112
Q

What bones meet at the pterion? What vessel lies underneath it?

A

Frontal, parietal, temporal, and sphenoid bones

Middle meningeal artery (branch of the maxillary artery)

113
Q

Which bug is associated with right-sided endocarditis in IV drug users?

A

Staph aureus

114
Q

What (2) drugs are selective vasodilators of coronary vessels? How can they affect the heart negatively during ischemic events?

A

Adenosine and dipyridamole

They can lead to coronary steal because they vasodilate everything in the heart. The vessels going to ischemic areas are already maximumly dilated so they only lose out on blood.

115
Q

Compare cardiac tissue conduction velocity between the:

AV node, purkinje system, ventricular muscle, and atrial system

A

_P_ark _At_ _Vent_ure _Av_enue

Fastest- Purkinje system, Atrial system, Ventricular system, AV node- slowest

116
Q

Nitroprusside

  1. MOA
  2. Effect
  3. Indication
A
  1. Short-acting balanced venous and arterial vasodilator
  2. Decreases both preload and afterload, thus maintaining stroke volume
  3. Indicated for hypertensive HF
117
Q

Dobutamine

  1. MOA
  2. Indication
  3. Effect (3)
A
  1. B-agonist (predominant activity on B1 receptors)
  2. Management of refractory HF w/ severe LV systolic dysfunction/ cardiogenic shock
  3. (1) Positive inotropic effect (2) weakly positive chronotropic effect (3) mild vasodilation
  4. Some increased O2 consumption due to increased chronotropy
118
Q

What percentage of vessel must be blocked to qualify as stable angina?

A

> or equal to 75%

119
Q

Formula for half life

A

Vd x .7/CL

120
Q

Formula for Maintenance dose

A

Cpss (steady-state plasma concentration) x CL/[bioavailability fraction]

121
Q

Formula for Loading dose

A

Vd x Cpss (steady state plasma concentration)/ [bioavailability fraction]

122
Q

Kussmaul sign

A

Paradoxical rise in JVP during inspiration, because volume-restricted right ventricle is unable to accomadte the inspiratory increase in venous return.

Associated with constrictive pericarditis

123
Q

Order the class one subcategories based on sodium-channel-binding strength (as measured by use dependence)

A

1C > 1A > 1B (least use dependent)

124
Q

Structural cardiac changes due to aging are generally not prominent before the age of…

A

65y/o

125
Q

Familial chylomicronemia syndrome

  1. Which protein is defected? (2)
  2. Which lipoprotein is elevated?
  3. Major manifestations?
A
  1. Defected: Lipoprotein lipase; ApoC-II
  2. Elevated: Chylomicrons
  3. Manifestations: Acute pancreatitis; lipemia retinalis (milky lipids in retinal vasculature); eruptive skin xanthomas; hepatosplenomegaly
126
Q

Verrucous endocarditis

  1. Who does it occur in?
  2. What is it?
  3. Potential consequence?
A
  1. Occurs in up to 25% of patients with SLE
  2. Can cause small cardiac valvular vegetations on either side of a valve, resulting in fibrotic valve thickening and deformity
  3. May cause acute coronary syndrom in young patients with normal coronary arteries
127
Q

What is an appendage, in the context of the heart?

A

It is a small saclike structure that is particularly susceptible to thrombus formation

128
Q

What is the most common genetic cause for:

Hypertrophic cardiomyopathy?

Dilated cardiomyopathy?

A
  1. Hypertrophic: Autosomal dominant mutations in cardiac sarcomere proteins (usually beta-myosin heavy chain)
  2. Dilated: Autosomal dominant mutations of myocyte cytoskeleton (dystrophin) or mitochondrial enzymes
129
Q

How is the pathogenesis of Non-bacterial thrombotic endocarditis (NBTE) related to that of Trousseau’s?

A

They can both be induced by disseminated cancers, usually due to some hypercoagulable state.

130
Q

What does Prussian blue stain detect?

A

Intracellular iron

131
Q

What is responsible for swelling in myocardial cells during ischemia?

A

Ion pump failure due to ATP loss, leading to increased intracellular Na+ and Ca2+

132
Q

Describe the hemodynamic profile of aortic regurg (3 key differences from normal)

A
  1. Higher pressure peaks (more blood in LV)
  2. Loss of dichrotic notch
  3. Steeper fall in aortic pressure
133
Q

Path and Presentation of patients with 21-hydroxylase deficiency

A

Deficient cortisol and aldosterone synthesis + adrenal androgen overproduction

Males: normal genitalia + vomiting, hypoTN, hyponatremia, hyperkalemia

Females: ambiguous genitalia (+ sx above)

134
Q

Antiphospholipid Antibody Syndrome

  1. Type/ cause of antibodies
  2. Sx (2)
A
  1. Antiphospholipid antibodies (either primary or due to SLE)
  2. Venous or arterial thromboembolism (in the presence of paradoxical inc. PTT) + recurrent pregnancy loss
135
Q

Why do patients with Antiphospholipid antibody syndrome often get false positive syphillus exams?

A

Presence of anticardiolipin antibody (which is tested for in Treponema pallidum, but is also present in this dz)

Reserve Step I Cards (10 decks)

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