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
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)
3
Q
Tetralogy of Fallot Pathophysiology and clinical presentation
A
VOIR:
- VSD
- Overiding aorta
- Infundibular pulmonary stenosis
- RVH
Presentation: Cyanosis; Improvement w/ squatting (increases SVR)
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
5
Q
What cranial nerves and what aortic arch derivatives are associated with each pharyngeal/aortic arch (1-6)
A
- CN V; Maxillary artery
- CN VII; Stapedial artery (regresses)
- CN IX; Common carotid and prox. internal carotid
- CN X (superior laryngeal); True aortic arch and Subcalvian arteries
- Obliterated
- CN X (recurrent branch); Pulmonary arteries and Ductus arteriosus
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
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.
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
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
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.
11
Q
Aortic Regurgitation
- Presentation
- Describe how the pulses may feel
- Describe the murmur and the best way to hear it
- What is the state of the pulse pressure?
A
- Presentation: progressive fatigue + dypsnea
- Pulses: “water-hammer” pulses (bounding femoral and carotids) and head-bobbing with each heartbeat (de Musset sign)
- 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
- The pulse pressure is widened
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
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.
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
15
Q
- Name the non-selective beta-blockers
- Name the selective beta-blockers
- Why would you choose selective over non-selective?
A
- Non-Selective- Propanolol, timolol, and nadolol
- Selective- metoprolol, atenolol, acebutolol and esmolol
- Selective only target B1, so if you have patients w/ COPD/asthma, you want to only use these.
16
Q
- Name the anthracycline chemotherapeutic agents.
- What is their most severe side effect
- How does it present?
- How is this SE prevented?
A
- Doxorubicin, daunorubicin, epirubicin and idarubicin
- Their most severe side effect is a cumalitive dose-related dilated cardiomyopathy due to free-radical formation
- Presents w/ right and left ventricular CHF
- Prevented via dexrazoxane- iron-chelating drug which reduces free radical formation
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.
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.
19
Q
Piercing of femoral artery above the inguinal ligament can signficantly increase the risk of what hemorrhage in what location?
A
Retroperitoneal
20
Q
Buerger’s disease (thromboangiitis oblierans)
- Main population demographics
- Pathophysiology
- Presentation
- Tx
A
- Heavy smokers, males
- Path- Segmental thromboding vasculitis
- Presentation- Intermittent claudication which can lead to gangrene, autoamputation, and superficial nodular phlebitis. Also associated w/ Raynauds
- Tx: smoking cessation
21
Q
Tricuspid Valve Endocarditis
- Most common bug associated?
- Usual patient population?
- Potential complications?
A
- Staph aureus is #1. Pseudomonas is #2
- IV drug users
- These patients can develop multiple septic emboli in lungs. Resulting pulmonary infarcts will be hemorrhagic due to dual blood supply.
22
Q
Varicocele
- Pathophysiology?
- Presentation?
A
- Increased pressure in the left gonadal vein resulting in valve leaflet failure and varices of the testicular pampiniform plexus
- Presents with flank/abdominal pain and gross or microscopic hematuria
23
Q
Niacin (nicotinic acid)
- Indication
- Adverse Effects
- What is the mechanism for the adverse effects and how can they be prevented?
A
- Used in the tx of hyperlipidemia. Effective in raising HDL cholesterol levels, and lowering LDLs and TGs
- SEs include cutaneous flushing, warmth and itching
- SEs are mediated by release of prostaglandins and can therefore be prevented by aspirin.
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 .
25
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?
The release of _Platelet-derived growth factor (PDGF)_ by locally adherrent platelets, endothelial cells, and macrophages.
26
What is the most common condition predisposing a patient to infective endocarditis in...
1. Adults in wealthier nations?
2. Poorer nations/ children?
1. Mitral valve prolapse/ mechanical valves
2. Rheumatic fever
27
What is the "Number Needed to Treat", and how is it calculated?
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
28
What are the effects of nitrate? (3 general categories of effects)
Side Effects?
* 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
29
Thiazide diuretics
1. MOA
2. Effects
3. AEs
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
30
**Patent Ductus Arteriosus (PDA)**
1. Pathology
2. Why is it patent
3. Clinical manifestations
4. Typical age at presentation
5. Tx.
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)
31
_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?
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
5. * 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
32
_Aortic Dissection_
1. Most important risk factor
2. What specific layer tears?
3. What genetic issue predisposes for aortic dissection?
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_
33
_Liver Angiosarcoma_
1. Pathology?
2. Describe the cellular change
3. Main carcinogens associated?
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)
34
MOA of B-Blockers
B-Blockers decrease AV nodal conduction, leading to an increased AV nodal refractory period
35
_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)
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
36
_Aspirin_
MOA
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.
37
_Clopidogrel_
1. MOA
2. Indication
_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.
38
What is the most common location on the aorta for a traumatic aortic rupture (blunt aortic injury)?
The **aortic _isthmus_** (located just past the aortic arch)
39
_Statins_
1. Indication
2. MOA
3. Side effects
4. What sort of things can help lead to adverse effects from Statins
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)
40
*Streptococcus gallolyticus* (formely S. Bovis) can cause **endocarditis** and **bactermia**. When this bug is cultured in the blood, workup for _what_, is absolutely essential?
**_Colonic malignancy_** with colonoscopy
41
Describe the Sx of Digoxin Toxicity
| (what ion is often elevated?)
* 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)
42
_AV Shunts_
1. What affect do they have on preload/afterload?
2. What might the physical exam reveal?
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.
43
What is the **most common** _congenital heart lesion_?
1. Dx/ Presentation?
2. Effect on blood oxygenation
3. Prognosis?
_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
44
_Prinzmetal's (variant) Angina_
1. Pathology?
2. When does it occur?
3. Dx?
4. Tx?
5. What drug can make it worse?
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*
45
How is tolerance to nitrates avoided?
You must provide a nitrate-free interval every day in patients w/ long acting nitrates.
46
How is nitric oxide synthesized?
It is synthesized from arginine by NO synthase
47
What are the _only_ cells within atherosclerotic plaque which are capable of synthesizing collagen isoforms and ECM?
Vascular Smooth Muscle Cells (VSMCs)
48
When given with a Statin, what drug is most likely to lead to myopathy or even rhabdomyolosis? Why?
Fibrates (like Gemfibrozil). They impair the hepatic clearance of Statins leading to excessive blood levels.
49
_Aortic stenosis_
1. Common murmur
2. Sx
3. Main causes
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
50
_Carcinoid Syndrome_
1. What is it?
2. What can it progress to?
3. How does a blood/urine test tell us about severity?
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**
51
Main Side Effect difference between ACE-I's and ARBs
ACE-I's raise the level of Bradykinin causing non-productive cough.
ARBs do not.
The two drugs are very similar otherwise
52
How does the effect of Rheumatic Heart Disease on the mitral valve vary as the patient's age changes?
_First few decades of life_: MR
_Middle-aged_: MS (most common cause of MS)
_Elders_: Mixed mitral disease (S and R)
53
MOA of class 3 antiarrhytmic agents
They block K+ efflux from cardiac myocytes and prolong phase 3 of the myocyte AP
54
SE profile for _ACE-Inhibitors_ (2)
1. Bradykinin induced cough and angioedema if there is accumulation
2. First dose hypotension due to volume depletion
55
_Phenoxybenzamine_
1. MOA
2. Indication
3. Effect
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
_Isoproterenol_
1. MOA
2. Effect
1. Non-selective Beta-_agonist_
2. Increases myocardial contractility and decreases systemic vascular resistance
57
_Dopamine:_ What is the effect of...
1. Low doses?
2. Medium doses?
3. Very high doses?
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
_Antiarrhythmic drugs_
Drugs + Predominant actions
**Class IA, IB, IC**
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
What are the type II Anti-arrhythmics?
Beta-blockers
60
_Antiarrhythmic drugs_
Drugs + Predominant actions
**Class III**
**Amiodarone, Dronedarone, Dofetilide, Sotalol** (also class II)
*Prolongs APD by blocking K+ channels* (no effect on AP conduction velocity)
61
_Antiarrhythmic drugs_
1. Drugs + Predominant actions
2. Potential SEs
**Class IV**
**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
Relationship between blood flow and radius
Blood flow is directly proportional to vessel radius raised to the fourth power.
63
_Jervell and Lange-Nielsen Syndrome_
1. Pathology
2. Clinical presentation
3. Mode of inheritance
4. What other disease is this similar to?
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
What sometimes occurs between days 2-4 following a transmural MI? Why?
**Early-onset pericarditis** develops in 10-20% of patients. It represents an inflammatory reaction to adjacent cardiac muscle necrosis.
65
_Cystic Medial Degeneration_
1. Characteristics
2. What does it predispose you for?
3. Who is it common in?
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
_Adult type Aortic Coarctation_
1. Key triad
2. View on imaging
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
Permissiveness
**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
_Cutaneous, strawberry-type capillary hemangiomas_
1. Pathology
2. Prognosis
1. Benign congenital tumor of unencapsulated aggregates of closely packed, thin-walled capillaries
2. Initial growth followed by regression (excellent prognosis)
69
Why does listening to heart sounds at end expiration make them more audible?
Decreased lung volume, bringing the heart closer to the chest wall.
70
What are the (2) mechanisms by which beta-blockers lower blood pressure?
1. Reducing myocardial contractility and HR
2. Decreasing renin release by the kidney
71
What phase of the AP corresponds with the QRS of the EKG?
QT?
QRS = Phase 0
QT = Phase 3
72
What receptors is epinephrine capable of affecting?
a1, B1, and B2
73
Following focal ischemia in an MI, how long until there is a **loss of cardiomyocyte contractility?**
Loss of focal contractility occurs within _60secs_!
74
_Fenoldopam_
1. MOA
2. Indication
3. Effects (3)
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
_Fibrates_
1. MOA
2. Effect
3. Compare this to fish oil
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
_Dihydropyridine CCBs (Anti-hypertensives)_
1. Main examples
2. Indications
3. SEs
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
What sort of procedure is associated with _enterococcal endocarditis_
Genitourinary instrumentation or catherization (enterococcus is a component of normal colonic and GU flora)
78
Main phase "0" difference between regular cardiac cell and a pacemaker cell
Regular cardiac cell: 0 = Na+ rush
Pacemaker: 0 = Ca2+ rush
79
_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?
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
In patients with mitral regurg, what is the most reliable ausculatory finding to assess severity
The presence of a left-sided **_S3 gallop_**. This indicates high regurgitant volume and left ventricular volume overload
81
Why is it that calcium channel blockers affect smooth and cardiac muscle, but not skeletal?
**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
Ortner syndrome
When mitral stenosis causes left atrial dilatation sufficient to impinge on the left laryngeal nerve
83
Myocardial hibernation
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
_Drug-induced Lupus Erythematosus_
1. Presentation
2. Dx
3. What is almost never seen?
4. Drugs normally implicated
1. New onset of lupus symptoms
2. Anti-nuclear antibodies (ANA) and anti-histone antibodies
3. Anti-dsDNA **_ALMOST NEVER SEEN_**
4. _HIP_: **_H_**ydralazine, **_I_**soniazid, **_P_**rocainamide
85
What is usually the most key component of the pathogenesis of AAAs?
Transmural aortic wall inflammation
86
Lipofuscin
Yellow-brown, granular product of lipid peroxidation and considered to be a sign of "wear and tear"/aging.
87
_Prostacyclin vs Thromboxane A2_
Compare their effects
**_Prostacyclin_**: vasodilates, *inhibiting platelet aggregation* and increasing vascular permeability
**_Thromboxane A2_**: prostaglandin which enhances platelet aggregation and causes vasoconstriction
88
_Kawasaki Disease_
1. What type of disease is this?
2. Presentation
3. Potential consequence
4. Tx
1. Medium-vessel vasculitis
2. **CRASH** and **burn**
* **_C_**onjuctival injection, **_R_**ash, **_A_**denopathy, **_S_**trawberry tongue, **_H_**and/foot changes (edema and erythema) and _fever_
3. Risk of **coronary artery aneurysm**
4. Tx w/ *IV and aspirin*
89
_Diphteria_
1. Epidemiology
2. Micro/pathology
3. Clinical Sx (4)
4. Complications (3)
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
_Vascular and Immunologic Manifestations of Infective Endocarditis_
(3) Vascular
(2) Immunological
_Vascular_:
1. Systemic emboli
2. Mycotic aneurysm
3. Janewy lesions (**nontender**- palms/soles)
_Immunologic_:
1. Osler nodes (**Painful**- toes/fingertips)
2. Roth spots
91
_Coronary Sinus_
1. What does it serve as?
2. Under what condition might it be dilated?
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
_Paroxysmal Supraventricular Tachycardia_
1. Presentation
2. Tx
3. Potential SEs of tx (4)
1. Sudden onset palpitations
2. Tx w/ adenosine
3. _SE_: (1) Flushing, (2) chest burning (from bronchospasm), (3) hypotension, (4) AV block
93
_Giant Cell Arteritis_
1. Also known as?
2. Main Sxs (4)
3. What does the artery look like on biopsy?
1. aka _Temporal_ arteritis
2. **Jaw Claudication**, HA, facial pain, and vision loss
3. Temporal artery biopsy demonstrates granulomatous inflammation of the media
94
_Torsades de Pointes_
1. Pathology
2. What are the most common precipitants? (3 categories + examples)
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
_Paradoxical Embolism_
1. Pathology
2. Dx
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
Of all major vascular beds, which (2) are most susceptible to athersclerosis?
1. Lower abdominal aorta
2. Coronary arteries
97
_Mitral Stenosis_
1. What is the best/most reliable asuculatory indicator of the severity?
1. The interval between A2 and the opening snap (OS). **Shorter interval = more severe stenosis**
98
_Right Ventricular MI_
1. Presentation
2. Pathology
3. What does the hemodynamic assessment reveal? (CVP? Wedge pressure? CO?)
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
How is carotid sinus massage useful for termination of paroxysmal SVT?
It leads to increased parasympathetic tone causing temporary inhibition of the SA node and the prolongation of AV node refractory period
100
_Osler-Weber-Rendu Syndrome_
1. What is the other name?
2. Genetics
3. Clinical Presentation
4. Possible consequences
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
_Lidocaine_
1. What class drug?
2. MOA?
3. Effect?
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
Fick Principle
An alternative means for calculating cardiac output.
CO = O2 consumption/ AV O2 difference
103
Which cell types have B1 receptors?
Cardiac tissue and renal juxtaglomerular cells
104
a-1 blockers are useful for the treatment of ... (2 conditions)
What natural secretion has these same effects?
HTN and benign prostatic hyperplasia (relaxes the bladder)
**ANP/BNP** has the same effects
105
Which blood vessel carries blood with the _lowest content of oxygen_ in the body
Coronary sinus
106
Describe the process of _Infective Endocarditis_ (4)
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
_Polyarteritis nodosa_
1. Pathology
2. What organ is normally spared?
3. Presentation
4. Potential consequences
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
Coordinate each artery with the leads associated with them
1. LAD
2. LCX
3. RCA
1. Anterior and Septal
2. Left lateral
3. Inferior and Right
109
What are the afferent and efferent limbs leading to/away the carotid bodies?
_Afferent_: **G****lossopharyngeal nerve**
_Efferent_: **Vagus nerve**
110
What is the main side effect which limits the long-term efficacy of arteriolar vasodilators. Give (2) main examples of these drugs
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
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?
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
What bones meet at the pterion? What vessel lies underneath it?
Frontal, parietal, temporal, and sphenoid bones
**Middle meningeal artery** (branch of the maxillary artery)
113
Which bug is associated with right-sided endocarditis in IV drug users?
Staph aureus
114
What (2) drugs are selective vasodilators of coronary vessels? How can they affect the heart _negatively_ during ischemic events?
**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
Compare cardiac tissue conduction velocity between the:
AV node, purkinje system, ventricular muscle, and atrial system
**_P**_ark _**At**_ _**Vent**_ure _**Av_**enue
*Fastest*- Purkinje system, Atrial system, Ventricular system, AV node- *slowest*
116
_Nitroprusside_
1. MOA
2. Effect
3. Indication
1. Short-acting balanced venous and arterial vasodilator
2. Decreases both preload and afterload, thus maintaining stroke volume
3. Indicated for hypertensive HF
117
_Dobutamine_
1. MOA
2. Indication
3. Effect (3)
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
What percentage of vessel must be blocked to qualify as stable angina?
\> or equal to 75%
119
Formula for half life
Vd x .7/CL
120
Formula for Maintenance dose
Cpss (steady-state plasma concentration) x CL/[bioavailability fraction]
121
Formula for Loading dose
Vd x Cpss (steady state plasma concentration)/ [bioavailability fraction]
122
**Kussmaul sign**
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
Order the class one subcategories based on sodium-channel-binding strength (as measured by use dependence)
1C \> 1A \> 1B (least use dependent)
124
Structural cardiac changes due to aging are generally not prominent before the age of...
65y/o
125
_Familial chylomicronemia syndrome_
1. Which protein is defected? (2)
2. Which lipoprotein is elevated?
3. Major manifestations?
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
_Verrucous endocarditis_
1. Who does it occur in?
2. What is it?
3. Potential consequence?
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
What is an appendage, in the context of the heart?
It is a small saclike structure that is particularly susceptible to thrombus formation
128
What is the most common genetic cause for:
Hypertrophic cardiomyopathy?
Dilated cardiomyopathy?
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
How is the pathogenesis of Non-bacterial thrombotic endocarditis (_NBTE_) related to that of _Trousseau's_?
They can both be induced by disseminated cancers, usually due to some hypercoagulable state.
130
What does _Prussian blue stain_ detect?
Intracellular iron
131
What is responsible for swelling in myocardial cells during ischemia?
Ion pump failure due to ATP loss, leading to increased intracellular Na+ and Ca2+
132
Describe the hemodynamic profile of aortic regurg (3 key differences from normal)
1. Higher pressure peaks (more blood in LV)
2. Loss of dichrotic notch
3. Steeper fall in aortic pressure
133
Path and Presentation of patients with 21-hydroxylase deficiency
Deficient cortisol and aldosterone synthesis + adrenal androgen overproduction
_Males_: normal genitalia + vomiting, hypoTN, hyponatremia, hyperkalemia
_Females_: ambiguous genitalia (+ sx above)
134
_Antiphospholipid Antibody Syndrome_
1. Type/ cause of antibodies
2. Sx (2)
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
Why do patients with _Antiphospholipid antibody syndrome_ often get false positive syphillus exams?
Presence of anticardiolipin antibody (which is tested for in Treponema pallidum, but is also present in this dz)
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Decks in class (10)
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