Difficult Exam Flashcards

1
Q

What is histopathology of Aortic Aneurysm?

A

-Cystic Medial Degeneration
-Loss of Elastin
-Loss of smooth muscle cells
-Increased Collagen in the adventitia layer

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2
Q

3 Pathologic/Histologic abnormalities in MVP?

A

-Myxomatous proliferation of the mitral valve (Increased Spongiosum layer)
-Increased production of Mucopolysaccharide
-Fibrosis on the surface of the mitral leaflet
-Thinning and elongation of the chordae

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3
Q

Describe the histopathologic findings of IMH?

A

-Tear in the medial layer which leads to hemorrhage. No false lumen is created. Can be traumatic or atraumatic.

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4
Q

Histopathology of HoCM?

A

-Septal hypertrophy with sarcomere disarray and surrounding interstitial fibrosis.
-Additional findings: Large and bizarre nuclei, thrombosis and obliteration of the small vessels

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5
Q

What seen on Myocarditis biopsy?

A

-Inflammatory cell infiltrate or positive viral genome on EMB

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6
Q

What is seen on biopsy of Rheumatic Carditis?

A

-Aschoff bodies (Hallmark granulomatous lesions) in the Proliferative phase (1 to 6 months post illness)

-Inflammation of endocardium with macrophage and lymphocytic infiltration and fibroid degeneration of collagen and veruccous vegetations (Small uniformly sized thrombotic vegetations that don’t produce valve destruction) Exudative Phase (First few weeks)

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7
Q

What are the three characteristics disrupted in the failing myocyte?

A

Cellular membrane

Sarcoplasmic Reticulum

Contractile proteins

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8
Q

What are 3 anatomic hallmarks of LV remodeling?

A

-Alterations in cellular biology

-Myocardial changes: Necrosis, Apoptosis,

-Alterations in LV geometry: Dilation, wall thinning

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9
Q

What are two acute mechanisms by which smoking acutely increases risk of MI?

A

-Increases BP and sympathetic tone

-Reduction in myocardial oxygen supply

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10
Q

5 ways that smoking chronically results in more MI?

A

-Inflammatory effects (Increases levels of CRP, fibrinogen and homocysteine)

-Accelerates atherothrombosis and atherosclerotic progression

-Enhances oxidation of LDL cholesterol

-Impairs endothelium-dependent coronary artery vasodilation / Vasospasm

-Provokes spontaneous platelet activation

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11
Q

How to diagnose Takotsubo? By Mayo, ESC 2016 and INTERTak

A

Mayo Criteria
1) Transient LV dysfunction with RWMAs
2) No obstructive CAD
3) New ECG abnormalities or elevation in cardiac troponin
4) Absence of pheo/myocarditis

ESC 2016 Criteria
1) Transient RWMA/LV dysfunction usually but not always preceded by a stressful trigger.
2) RWMAs extend beyond single epicardial territory
3) Absence of culprit ASCVD
4) New and reversible ECG abnormalities
5) Elevated BNP
6) Positive troponin but small elevation
7) Recovery in 3-6 months

InterTAK (Preferred, will go with this on Exam)
1) Transient LV dysfunction beyond a single epicardial vascular distribution
2) An emotional/physical trigger is usual but no obligatory
3) Neurologic or Pheochromocytoma may serve as a trigger
4) New ECG abnormalities
5) Elevated biomarkers
6) Significant CAD can be present
7) No myocarditis
8) Post menopausal women are usually effected

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12
Q

3 Pathophysiologic features of microvascular angina?

A

Abnormal Vasodilation: Endothelial dysfunction is primarily due to imbalance in NO production and consumption

Pro thrombotic state: Increase platelet and leukocyte activation

Arterial remodelling: Endothelial dysfunction also increase activation of cytokines that increase the permeability of the vessel wall to oxidized lipoproteins and inflammatory mediators

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13
Q

What are the two mechanisms of SCAD?

A

-Intimal tear or bleeding into the Vasa vasorum with intramedial hemorrhage. This creates a false lumen by an enlarging hematoma

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14
Q

What are 3 histologic features of radiation induced coronary disease

A

-Diffuse interstitial fibrosis and collagen deposition

-Luminal narrowing of both arteries and arterioles due to accumulation of myofibroblasts and resultant intimal proliferation

-Intimal proliferation with aggregation of lipid-rich macrophages.

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15
Q

**Give 3 pathologic/Histopathologic findings in progressive calcified aortic valve stenosis

A

-Fibrous damage resulting in thickening

-Calcium deposition leading to thickening

-Atherosclerosis in valve tissue of patients resulting in cellular proliferation, inflammation, lipid accumulation and increased margination of macrophages and T lymphocytes

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16
Q

Histopathology of Giant Cell Myocarditis?

A

-Lymphocyte infiltration (predominantly CD4 T cells), myocyte necrosis/loss and viral inclusions on EMB, and large multinucleated cells. The cytoplasm of these cells can contain star shaped asteroid bodies.

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17
Q

What is histopathology of Sarcoidosis?

A

Noncaseating granulomas without myocyte necrosis

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18
Q

Review Coronary Artery Layers

A
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19
Q

What are histopathologic features of radiation induced coronary disease?

A

-Diffuse interstitial fibrosis and collagen deposition along with luminal narrowing of both arteries and arterioles due to accumulation of myofibroblasts and resultant intimal proliferation

You need 30 gray of radiation exposure and athero starts to develop 10-20 years post exposure

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20
Q

Review effects of Vaping on the Heart (AHA 2022) (7)

A

-Accelerated CAD
-Myocardial Fibrosis
-Decreased Myocardial blood flow
-Decreased Endothelial flow
-Decreaed NO production
-Increased Blood pressure and Arterial Tone
-Increased Oxidative Stress

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21
Q

What is Jones criteria for Rheumatic fever? What is treatment?

A

Major:
-Sydenham’s chorea
-Carditis
-Migratory arthralgias
-Subcutaneous nodules
-Erythema Migrans

Minor:
-Fever
-Polyarthralgias
-ESR > 30
-Prolonged PR interval

Pen V 200 mg BID (As per AHA)
Sulfadiezine 1000 mg daily (As per AHA)

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22
Q

What is pathophysiology/criteria for Type 1 MI ? (4)

A

-Related to atherosclerotic plaque rupture
-Resulting intraluminal thrombus in 1 or more coronary arteries
-Leading to decreased flow or distal platelet emboli
-Ensuing myocyte necrosis

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23
Q

What is criteria for Type 1 MI?

A

-Rise and fall of troponin with at least one value above the 99th percentile URL with one of the following:

-Symptoms of ischemia
-New ST-T changes, LBBB, pathologic Q waves
-Loss of viable myocardium or RWMAs
-Angiography or autopsy showing intracoronary thrombus

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24
Q

What is the Dallas Criteria?

A

For diagnosing Myocarditis definitively:

-Inflammatory infiltrates of the myocardium with necrosis of adjacent myocytes not typical of the ischemic damage of coronary disease

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25
Q

What are 4 mechanisms for LV dysfunction in TCMO?

A

Depletion of myocardial energy stores

Abnormal Calcium handling

Oxidative stress in atrial and ventricular myocardium

downregulation and decreased responsiveness of beta adrenergic receptors

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26
Q

What are four pathogenic processes of NSTEACS?

A

-Rupture of unstable atheromatous plaque

-Coronary arterial vasoconstriction

-Imbalance between supply and demand of myocardium for oxygen

-Gradual intraluminal narrowing of an epicardial coronary artery because of progressive atherosclerosis or post stent restenosis

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27
Q

**What are three mechanisms for thrombus formation in setting of coronary plaque?

A

Rupture of Coronary Plaque fibrous plaque ->

Exposes thrombogenic material in the lipid rich core to blood and triggers platelet activation through exposure of subendothelial collagen and vWF -> thrombin generation ->

Tissue factor exposed at site of injury results in thrombin generation -> Thrombin converts fibrinogen to fibrin and potentiates platelet aggregation

Summary:
1) Platelet activation and aggregration
2) Thrombin activation
3) Coagulation cascade

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28
Q

What are 4 types of Takotsubo (Variants) ?

A

Apical

Midventricular

Basal

Focal Type

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29
Q

What are two mechanisms of SCAD?

A

-Spontaneous Hemorrhage

-Tear (No Hemorrhage)

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30
Q

What are 5 risk factors for pace maker post TAVR?

A

-Male

-RBBB

-LAFB

-First degree AV block

-Self expanding valve

-Depth of Implantation

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31
Q

3 things that can provoke Vasospasm?

A

-Hyperventilation

-Early morning (Higher Vagal Tone)

-Precipitated with Cocaine/Smoking

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32
Q

Name 5 changes on Echo in Pregnancy? (5)

A

-Increased LV mass

-LV dilation

-Increased stroke volume

-Increased Valvular gradients

-Increased regurgitation

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33
Q

What are risk factors for ICH with Lytic ?

A

Age
Female
Hypertension (SBP > 160mmhg)
Black
Prior Stroke
Use of Alteplase

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34
Q

What are 4 non pharm things in long term management of SCAD?

A

-CR Program with 50-70% HRR

-Weight lifting < 20 lbs women and < 50 lbs men

-BP control < 130/80mmhg

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35
Q

What are the high risk Aortopathy criteria in Pregnancy?

A

-BAV > 5

-MFS > 4.5

  • Turners > 25mm/m2
  • Vascular EDS

-LD with any Aortic dilation

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36
Q

What are three primary pericardial tumors? three most common mets?

A

-Mesotheliomas, Teratoma, Paraganglionomas

-Mets: Lung, Breast, Esophageal, Lymphoma

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37
Q

What are cardiac abnormalities associated with Freidrich’s Ataxia?

A

HCM, Conduction system disease

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38
Q

What is the cardiac abnormality associated with Tuberous Sclerosis?

A

Cardiac Rhabdomyoma

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39
Q

What is the cardiac abnormalities associated with HHT?

A

AV malformations resulting in high output HF

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40
Q

How many Korotkoff sounds are there? Describe them:

A

5 sounds

  1. Clear tapping sounds heard for at least 2 straight beats (this is SBP)
  2. Softening of the tapping sounds with the addition of a swishing sound
  3. Return of tapping sounds as heard with a phase 1 but with an increase in sharpness and intensity
  4. Abrupt muffling of sounds
  5. Disappearance of sounds (this is DBP)
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41
Q

Which populations is the 5 Korotkoff sound not interpretable? (So you have to use the 4th as a measure of DBP) (2)

A

-Pregnancy
-Severe AI

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42
Q

Label the following in descending O2 content
-Pulmonary vein, SVC, IVC, Coronary Sinus

A

-Pulmonary Vein (most oxygenated vessel in body)

-IVC (Renal shunting)

-SVC

-Coronary sinus (Heart extracts maximally at rest)

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43
Q

What are the 4 possibilities you can get from ABI?

A

> 1.4 : Non compressible (age, DM, CKD)

1-1.4 : Normal

0.9 - 0.99: Borderline

< 0.9: Abnormal

44
Q

What is the NASPE code?

A

Note- 4th position is rate responsiveness

45
Q

What are three mechanisms of how ACE inhibitors decrease cardiovascular disease?

A
  1. Improves LV remodeling through inhibition of RASS/Angiotensin
  2. Decreased Afterload
  3. Increased Bradykinin release which results in improved NO, fibrinolysis, decreased thrombocyte activity
46
Q

What is pathology of Coronary Vasospasm?

A

-Focal or diffuse spasm of the smooth muscle layer of the arterial wall

-Caused by vascular smooth muscle hyper-reactivity

-Caused by imbalance in vagal and sympathetic tone

Tends to occur in younger women with lack of traditional RFs except for smoking. Associated with Raynauds and cocaine use.

47
Q

Name 5 echocardiographic changes in pregnancy? (5)

A

-Increased LV size (LVEDD)

-Increased SV/Gradients

-Increased Atria size

-Increased RV size

-Increased valvular regurgitation

48
Q

**What is sarcomere comprised of?

A

Thick and Thin filaments

-Myosin is the main component of the thick filament (2 heavy and 4 light chains)

-Actin is the main component of the thin filament (Troponins are found on in the thin filament to facilitate Actin and Myosin interaction)

49
Q

What does ischemia do to myosin/actin on the molecular level?

A

Results in depletion in ATP which leads to failure of detachment from Actin and Myosin (manifests as diastolic dysfunction)

50
Q

**5 indications for ICD in Sarcoidosis?

A

LVEF < 35% (1)

VT/Arrest (1)

Indication for PPM (2a)

History of syncope (2a)

Inducible sustainable VT (2a)

51
Q

What are three mechanisms that NSAIDS result in HF?

A

-Increased sodium retention

-Increased afterload/vasoconstriction

-Worsening renal function

52
Q

5 beneficial effects of BNP?

A

-Diuresis

-Natriuresis

-Vasodilation

-Endothelin antagonism

-Aldosterone antagonism

53
Q

4 harmful effects of supplemental oxygen?

A

-Depress CO

-Increased PCWP

-Increased Afterload/vasocontriction

-Oxidized free radicals

54
Q

Who to screen for Diabetes? Three ways to make diagnosis?

A

-Age > 40 no RF’s -> screen every 3 years

-Risk factors present (Family history, GDM/Prediabetes, CV RF’s , end organ damage) -> annually screen

-FPG > 7, Hba1c > 6.5%, 2h OGTT > 11.1

55
Q

When to start diabetes meds based on Hba1c?

A

-A1c > 1.5% target

-If less than that, try three months of lifestyle management

56
Q

What are 8 biological mechanisms that reduced CAD?

A

-Antiatherogenic effects (decreasing other CV RFs)

-Anti inflammation

-Effects on vascular endothelial function

-Effects on blood clotting

-Autonomic functional changes

-Anti ischemic effects (HR and SBP fixed submaximal work rates, increases myocardial perfusion and decreased in ischemia post MI)

-Antiarrhythmic effects

-Reduction in age-related disability

57
Q

Driving restriction for Ascending and Descending aneursym?

A

Private: Ascending > 6cm, Descending >6.5cm

Commercial: Ascending > 5.5cm, Descending > 6cm

58
Q

What are 3 biological mechanisms for in stent restenosis?

A

-Lumen re-narrowing due to negative remodeling

-Intimal restenosis

-Focal tissue growth within stent or at margins

59
Q

What are 3 cardiac contraindications to alcohol septal ablation?

A

-LBBB (risk of PPM)

-LV thickness > 30mm (likely not effective) or < 15mm (increase risk of rupture/VSR)

-Contrast extends beyond target myocardium (presence of collaterals, this will lead to larger myocardial injury))

-Tend to not prefer in Patients younger than 21 years old

60
Q

Name 6 absolute contraindications to transplant?

A

-Fixed pulmonary hypertension > 3 WU, irreversible does not decrease < 2.5 WU with vasodilation

-LE < 2y despite transplant

-Clinically significant symptomatic severe CVD

-Active substance use

-Multiple demonstrations of inability to comply with drug therapy

-Multisystem disease with severe extracardiac organ dysfunction

61
Q

What are 7 contraindications to PMBC?

A

> Moderate MR

LA Thrombus

Anatomy unfavourable

Previous failed PMBC

Indication for OHS

Mild MS

Contraindication for transseptal puncture

62
Q

What are 3 etiologies of LFLG AS?

A

-Low EF: Any CMO

-Paradoxical: Amyloidosis, Sigmoid septum, Small chamber size/HTN

-Concomitant Mitral Regurgitation

63
Q

What are 2 reasons to revascularize in SCAD?

A

-High risk anatomy (LMCA or proximal 2 vessel disease)

-Ongoing ischemia or instability

64
Q

Name 12 contraindications to transplant

A

a. Systemic illness with life expectancy < 2 years
b. Irreversible PH with PVR > 3 WU
c. Clinically severe symptomatic cerebrovascular disease
d. Multiple demonstration with inability to comply with drug therapy
e. Multisystem disease with severe extracardiac organ dysfunction
f. BMI > 35
g. Age > 70
h. Diabetes with poor control
i. Active infection
j. Active neoplasm
k. Tobacco use within 6 months
l. Substance abuse within 6 months

65
Q

What are three major biochemical pathways that produce vasonconstriction?

A

-Endothelin

-SNS: NE/Angiotensin/Thromboxane/Angiotensin

-Acetylcholine

66
Q

**Name 3 biochemical pathways that produce vasodilation in normal arteries?

A

-Nitric Oxide

-Prostacyclin pathway

-Bradykinin/Adenosine

67
Q

What are 4 findings of mitral stenosis on CXR

A

LA enlargement: Left heart border becomes straightened

Elevated bronchus and splaying of the carina

Calcification of the MV annulus

Enlargement of the main PA due to pulmonary hypertension

68
Q

What are the two most common causes of death in pregnant women with coarctation?

A

-Aortic rupture or Dissection

-Rupture of cerebral aneurysm with ICH

69
Q

What are 2 class 1 indications for Tricuspid Stenosis?

A

-Severe TS at time of operation for left sided valve disease

-Isolated symptomatic severe TR

70
Q

3 reasons that surgical closure of an ASD is recommended as opposed to percutaneous?

A

-AVSD repair

-Unroofed coronary sinus

-Sinus venosus defect

-Also if >38mm in size and <5mm from AV valves

71
Q

What are three criteria for prior MI

A

Any of the following:

-Pathologic Q waves
-Imaging evidence of a region of loss of viable myocardium that is thin and fails to contract in the absence of a non ischemic cause
-Pathologic findings of a prior MI

72
Q

WHO classes for pregnancy correlate to what risk?

A

1: 5%

2: 10%

3: 20%

4: 40-100%

73
Q

What are the 4 features of SCAD on cath?

A

-No CAD

-Radiolucent flap

-Contrast staining

-presence of a non iatrogenic dissection plane

74
Q

When can patients have sex post MI?

A

when patients can exercise 3-5 METS without angina, arrhythmia or ischemia

75
Q

What are 7 absolute contraindications to Persantine?

A

-Bronchospastic lung disease with active wheezing

-Sinus node disease or 2nd/3rd degree heart block without a functioning pacemaker

-SBP < 90mmhg

-Uncontrolled HTN > 200/110

-Recent use of dipyramidole

-Hypersensitivty to adenosine

-ACS within 48 hours

76
Q

What are 4 contraindications to LVADs

A

-RV failure
-Active bleeding or bleeding diathesis
-Limiting Life expectancy
-Large VSD
-Active substance/drug use
-Inabilite to comply

77
Q

5 findings that portend a good prognosis in PPCM?

A

-Non black

-LVEF > 30%

-LVEDD < 60mm

-Post partum diagnosis

-Low BNP/Troponin

78
Q

5 alterations in biology for the failing Myocyte ?

A

-Cardiac Myocyte Hypertrophy

-Alterations in Excitation-Contraction coupling

-Beta-adrenergic desensitization

-Reduced SR calcium release

-Abnormalities in contractile and regulatory proteins

79
Q

What is definition of reinfarction vs. recurremt MI

A

Within 28 days or after

80
Q

What is the mechanism of RVOT VT? Fascicular?

A

-Myocyte Calcium overload triggering delayed after depolarizations

-Fascicular: Reentry in the Purkinje fibers

81
Q

What are 5 cardiac effects of SGLT2 inhibitors?

A

-Decrease myocardial hypertrophy and fibrosis
-Reverse cardiac remodeling
-Decrease Myocardial oxidative stress
-Improved energetics
-Improved endothelial function

82
Q

What are 5 beneficial effects of Icosapent Ethyl

A

-Triglyceride reduction
-Cell membrane stabilization
-Improved Lipid oxidation
-Anti-inflamatory
-Improved endothelial function

83
Q

What are three classifications of Anthracycline toxicity?

A

-Acute: Myocarditis, QTc prolongation -> Reversible

-Early-Onset Chronic Progressive: irreversible CMO within 1 year

-Late-Onset Chronic Progressive: irreversible CMO onset after 1 year

84
Q

Name 4 pathophysiologic mechanisms of PPCM?

A

-Increased Prolactin
-Oxidative stress
-Immune mechanisms
-Viral infections

85
Q

What 3 populations with ATTR CA should not be prescribed Tafamadis?

A

-NYHA IV, 6MWT < 100m, severe functional disability

These were excluded in ATTRACT trial

86
Q

5 reasons to admit for HF?

A

-NYHA III/IV
-SPO2 < 91%
-SBP < 90mmhg
-HR > 90 bpm
-RR > 20

87
Q

What are 3 accepted regimens for Afib and PCI post ACS? Elective?

A

-ACS: Apixaban 5mg BID, Rivaroxaban 2.5mg BID, Warfarin + ASA/Plavix (1day - 6 month) -> Dual Pathway

-Elective: Apixaban 5mg BID, Rivaroxaban 15mg daily, Edoxaban 60mg, Dabigatran 110 or 150 bid, Warfarin (Dual pathway)

88
Q

Review the Class 1 indications for LYTIC in STEMI

A
89
Q

How to diagnose CPVT?

A

-Age < 40, no other reason for VT and bidirectional VT

-Pathogenic mutation

-If Bidirectional VT and FDR with CPVT

90
Q

5 Echo features for Tamponade?

A

-60 / 30% inflow variation across AV valves

-RV end diastolic collapse

-RA collapse 1/3 of Cardiac cycle

-Plethoric IVC that does not collapse significantly

-Systolic flow dominant for Hepatic vein and reversal of diastolic flow in expiration

91
Q

Name 3 differences between BNP and NT Pro BNP? Review metabolic pathway

A

-BNP is biologically active, NT-proBNP is inert.

-BNP has a shorter half life, NT-proBNP is more sensitive (circulates longer in the bloodstream).

-BNP levels may increase in patients taking neprilysin (neprilysin can break down BNP, but if inhibited, levels may increase). It has no effect on NT-proBNP

92
Q

What is confirmed stent thrombosis?

A

Thrombosis confirmed within the stent of 5mm before or after the stent

93
Q

What is the ICD recommendation for CPVT?

A

-ICD is recommended in patients with Arrest, Recurrent Syncope or VT despite Beta Blocker (Class 1)

94
Q

What are two things that can be done in CPVT when they have symptoms despite maximum beta blocker? (Other than ICD)

A

-Flecainide (2a)

-Left Cardiac Sympthathetic Denervation (2a)

95
Q

Name 2 class 1 indications for pacemaker implantation in PCCD?

A

-Intermittent or permanent third degree or high grade AV block

-Symptomatic Mobitz I or II AV block

96
Q

Define facilitated PCI and a Pharmaco-invasive strategy

A

-Facilitated: Adjuvant therapies such as fibrinolytic or GIIbIIIa inhibitors given while in transit for primary PCI

-Pharmacoinvasive: Strategy where patients with STEMI are lysed with immediate transfer for shock or failed lysis, and routine transfer post successful lysis

97
Q

3 mechanisms of thrombus formation in coronary plaque

A
  1. Plaque rupture with exposure of thrombogenic necrotic core material -> Platelet, Fibrin and coagulation cascade activation.
  2. Thrombi forming on lesions without rupture (Plaque erosions), most often on pathological intimal thickening of fibroaatheromas.
  3. Protruding Nodular calcifications serving as a site for thrombus.
98
Q

Where in the fibrous cap does plaque rupture tend to occur? (2)

A

-Where it is thinnest

-Where it is most infiltrated by foam cells

99
Q

What is a foam cell?

A

Macrophage in the vessel wall that’s consumed Lipoproteins, giving it a foamy appearance

100
Q

3 features of unstable plaque?

A

Thin fibrous cap

Large necrotic core

Inflammation within the necrotic core

101
Q

What are 5 stages of plaque progression?

A

Fatty streak -> Foam cell invasion -> Lipid pools -> Development of fibrous cap -> Increased calcification of fibrous cap

102
Q

How to adjust colchicine based on following renal function:
< 10:
10-35:
35-50:

A

< 10: Dont use

10-35: 0.5mg q2-3 days

35-50: 0.5mg daily

> 50: 0.5 BID

103
Q

Name 7 CI for PMBC

A

-MVA > 1.5
-LA thrombus
-More than mild MR
-Severe or bicommissural calcification
-Absence of commissual fusion
-Severe concomitant valvular disease requiring surgery
-Concomitant CAD or CABG

104
Q

Name 4 benign cardiac tumors, and 4 malignant

A

-Benign: Myxoma > Lipoma > Papillary Fibroelastoma > Hemangioma

-Malignant: Angiosarcoma > Rhabdomyosarcoma > Mesothelioma > Fibrosarcoma

105
Q

What is most common primary malignant pericardial tumor?

A

Mesothelioma > Teratoma > Paraganglioma

106
Q

Review how TNK is mixed and given

A

https://www.tnkase.com/dosing-and-administration/dosing-administration-and-reconstitution.html#:~:text=INJECT%20entire%20contents%20(10%20mL,stand%20undisturbed%20for%20several%20minutes.&text=GENTLY%20SWIRL%20until%20contents%20are,DO%20NOT%20SHAKE.