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[3] Step 1 USMLE > Cardiovascular > Flashcards

Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

Describe Paradoxical Splitting

A

“PAradoxical Splitting”

[Pulmonic Valve closes BEFORE Aortic Valve] which is abnormal

“Taking AP Classes were normal for me”

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2
Q

Which conditions causes a [FIXED Widened S2 Splitting]?

A

Atrial Septic Defect

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3
Q

A: 1st Choice Replacement Vessel for [L Anterior Descending Coronary Artery] occlusion

B1: Which Vessel is used for MULTIPLE coronary arteries/vessels occlusions

B2: Where is the vessel in B1 located and what are 2 ways it’s accessed?

A

1st Choice: [Left ITM (Internal Thoracic Mammary) Artery]

B1: MULTIPLE OCCLUSIONS = [Great Saphenous Vein]

B2: Inferolateral to [pubic tubercle] and

accessed in the [medial leg] or [femoral triangle of upper thigh]

[Great Saphenous Vein] empties into the Femoral Vein

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4
Q

What makes up the Femoral Triangle (3)

A
  1. [Inguinal Ligament Superiorly]
  2. Sartorius M. Laterally
  3. [ADDuctor Longus M. Medially]
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5
Q

What happens to [Cardiac-Vascular Function Curve] Intersection when there’s a:

A: [Change in Cardiac Output]

B: Give 2 examples

A

A: If there’s a [Change in Cardiac Output] —> Intersection slides along [VVV Curve -**Venous/Volume/Vascular]

Ex: Catecholamines / (HF - MI)

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6
Q

What do these Embryonic Structures form into:

[R Common Cardinal Vein] + [R Anterior Cardinal Vein]

A

SVC - Superior Vena Cava

“I need a SVC Card”

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7
Q

What does this Embryonic Structure form into:

Truncus Arteriosus (2)

A

[Trunk of Pulm (Pulmonary Trunk)]

&

[Ascending Aorta]

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8
Q

What does this Embryonic Structure form into:

Bulbus Cordis

A

[Smooth OUTFLOW TRACT] of BOTH Ventricles

“Bulbs are smooth”

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9
Q

What does this Embryonic Structure form into:

Primitive Atrium

A

​”Trabaca is Primitive in his chamber”

Trabeculated L and R Atria

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10
Q

What does this Embryonic Structure form into:

Primitive Ventricle

A

​”Trabeca is Primitive in his chamber”

Trabeculated L and R Ventricles

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11
Q

What does this Embryonic Structure form into:

Primitive Pulmonary Vein

A

[Smooth L Atrium]

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12
Q

What does this Embryonic Structure form into:

Sinus Venosus - Left Horn

A

Coronary Sinus

(found in the AV groove of the Posterior Heart)

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13
Q

What does this Embryonic Structure form into:

Sinus Venosus - Right Horn (2)

A

[Smooth R Atrium]

AKA [Sinus Venarum]

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14
Q

Pathophysiology for [Tetralogy of Fallot]

A

[Anterior and Cephalad Deviation] of (Infundibular septum) during embryo —-> VOIR

“VOIR is to have See + Sight + Cry”

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15
Q

Define Permissiveness

A

[1 Drug with no direct capabilities] Permits and enables a [capable drug] to reach a greater potential :-)

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16
Q

Describe [SHAC Syndrome - Supine hypOtensive Aortocaval Compression]

A

Pregnant Women > 20 weeks gestation can experience hypOtension when [gravid uterus] (while supine) compresses IVC –> [DEC Venous Return] –> DEC CO

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17
Q

What are the outcomes of Blunt Aortic Injury (2)

A

Tethered by [Ligamentum Arteriosum] and is fixed and immobile compared to adjacent [Descending Aorta]

A:

  1. Death
  2. [Chest or Back Pain] w/SOB and [Widened Mediastinum]
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18
Q

What embryonic Structure does the [Ductus Arteriosus] develop from?

A

6th Embryonic Aortic Arch

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19
Q

There are 6 Structures that derive from the Aortic Arch.

Name them

A
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20
Q

SacubiTrill MOA (2)

A

[Neprilysin Inhibitor] –> Prevents ANP degradation —>

*DEC TPR

*INC GFR –> INC Urinary Output

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21
Q

Name 3 EKG Signs of [Atrial Fibrillation]

A
  1. [irregularly irregular R-R intervals] (the already irregular R-R interval will occur at an irregular pace since atrial electrictivity is chaotic)
  2. Absent or [low-amp fibrillatory] P-waves
  3. Narrow QRS Complexes
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22
Q

[Atrial Fibrillation] is the most common tachyarrhythmia. It is often precipitated by what 4 things?

A

“Smh, SAME Afib as before!”

  1. Acute Systemic Illness (Hyperthyroid / HF / HTN)
  2. Sympathetic Tone INC
  3. EtOH - excess
  4. Mitral Stenosis
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23
Q

Most common [Congenital Heart Defect]

Describe the Mumur.

A

A: VSD (Ventricular Septal Defect)

B: (when small) = [Holosystolic Harsh Blowing Murmur] auscultated @ [tricuspid area]

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24
Q

Aortic Stenosis

Mumur

A

[Crescendo-Descrescendo Systolic Ejection Murmur] auscultated @ [Heart Base w/radiation to carotids]

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25
Q

What does [Hemosiderin-laden alveolar macrophages] likely indicate? Why is this?

A

L Vt Dysfunction

L HF –> Pulmonary Edema and RBC extravasation from INC permeability of [capillary wall]. Macrophages phagocytose RBC and the iron is converted —> Hemosiderin

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26
Q

Describe S3 gallop. What is it associated with? (3)

A

A: [low-frequency sound JUST after S2]

B: Associated with:

1) [Pts > 40]:
* -(*[L Vt Systolic HF—> [Dilated Vt]]

vs.

  • [mitral regurgitation—>[INC Vt filling Rate] –> [Dilated Vt]]):
    2) Athletes/ [Pts younger than 40] / Preggos = Normal
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27
Q

A: What do you use to treat Beta Blocker Overdose?

B: Why?

A

A: Glucagon

B: Activates [Cardiac GPCR] –> Activation of [Adenylate cyclase] —> INC [cAMP in cardiomyocytes]–> INC contractility and HR from Ca+ INC

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28
Q

How long does it take for cardiomyocytes to stop contracting after onset of a [COMPLETE ISCHEMIC EPISODE]?

A

60 Seconds

(After 30 min. the ischemic injury will become irreversible)

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29
Q

Dysfunction of Platelets would manifest how? (2) How is Platelet Function measured?

A

Mucocuntaneous Bleeding (Epistaxis or Petechiae) ; Measured by Bleeding Time

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30
Q

Mitral / Tricuspid Regurgitation

Mumur

A

[Holosystolic High-Pitched Blowing Murmur]

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31
Q

Causes of Mitral Regurgitation (3)

A
  1. [Ischemic Heart Dz (post MI)]
  2. MVP
  3. [LV Dilatation]
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32
Q

Familial Chylomicronemia Syndrome

Sx (5)

A

HHALX

  1. Acute Pancreatitis - recurrent
  2. HyperTriGlyceridemia (especially Chylomicrons)–>creamy supernatant
  3. [Lipdemia Retinalis]= milky retinal vasculature
  4. [SKIN Xanthomas- eruptive= yellow erythematous papules on extensor surfaces]
  5. HepatoSplenomegaly
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33
Q

Cardiac Tamponade MOD

A

Compression of Heart by Fluid in pericardial Space –> DEC CO and equilibration of diastolic pressures in all 4 chambers

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34
Q

Describe Pulsus Paradoxus

A

DEC [Systolic BP] more than 10 mmHg during inspiration

“Pulsus for CAPOT”

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35
Q

What is Lipofuscin, and what is it a sign of

A

A: [lipid PerOxidation PRODUCT] commonly found in [AGING CELLS’ macrophages]

B: sign of “wear and tear” aging

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36
Q

S4 Heart Sound is AKA an _____. What is the Etiology

A

Atrial Kick

A: [STIFF Hypertrophic Ventricle]

L atrium has to “KICK” hard against a STIFF Vt

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37
Q

A: Myocardial Hibernation

B: Describe the pathogenesis

A

A: Myocardium that Hibernates (DEC its activity) due to coronary ischemia but is invigorated and improved after [Coronary ReVascularization]

B: Coronary Ischemia –> [Myocardial Ischemia] –> [Myocardial Hibernation] —> [L Vt Systolic HF]

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38
Q

Mitral Stenosis

Mumur

A

[Delayed Rumbling Diastolic murmur that follows an Opening Snap] - @ [Apex + LLDP (L Lateral Decubitus Position)]

(Opening Snap comes from abrupt halt of leaflet motion in diastole after its rapid opening from the leaflet tips being fused together)

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39
Q

MAIN etiology for Claudication? Name 2 other less common etiologies

A

Atherosclerosis of Larger Arteries —>[Fixed Stenotic Intimal Atheroma (lipid filled)] —> Blood Flow Obstruction (especially during exercise)

Less common:

  • [Giant Cell Temporal Arteritis]
  • [BUerger Thromboangiitis Obliterans]
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40
Q

Hypertrophic Obstructive CardioMyopathy (HOCM)

Mumur

A

[Holosystolic Harsh Murmur] auscultated @ [L Sternal 2nd/3rd ICS]

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41
Q

When does [Prinzmetal Variant Angina] typically present? (2)

A

A: At rest and [during midnight - early morning]

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42
Q

3 Common signs of CONSTRICTIVE Pericarditis

A
  1. Pericardial Knock= Sharp sound heard in early diastole
  2. Kussmaul Sign= Paradoxic [INC JVP during inspiration] since constricted R Vt can accomdate the INC blood
  3. Pulsus Paradoxus
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43
Q

MOD for [Carcinoid Syndrome Heart Disease]

A

[R sided endocardial fibrosis] —> [Pulmonic and Tricuspid Valve Stenosis] or [Restrictive Cardiomyopathy]

CarcinoiD Syndrome: (Cutaneous Flushing)/Diarrhea/(SOB wheezing)

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44
Q

Pts with [Coarctation of Aorta] are INC risk of dying from what 3 things?

A

HTN associated dz such as:

1) [L Vt Failure]
2) [Ruptured Aortic Aneurysm]
3) [Intracranial Hemorrhage] 2º to [Berry Saccular Aneurysm rupture]

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45
Q

Describe the Jugular Venous Pressure Points:

a

c

x

v

y

B: When is [x] absent?

A

*Jugular Venous Pressure:

a: atrial contraction

c: [closure of tricuspid valve] from [RV contraction]

x: atrial RelaXation – absent during [tricuspid regurgitation]

v: villing of atrial w/venous blood

y: emptYing of atria into Vt

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46
Q

A: Dystrophic calcifcation is the Hallmark of _____ (3)

B: What is Plasma Ca+ in this DO?

A

A: [Dystrophic calcification] is the HALLMARK OF

  • CELL INJURY
  • CELL DEATH and
  • Necrosis

B: Plasma Ca+ will be normal

This occurs naturally from aging

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47
Q

A: Which cells in an atherosclerotic plaque produce collagen and [ExtraCellular Matrix]?

B: What happens when these cells become ischemic and necrosed?

A

A: [Vascular Smooth Muscle Cells] produce collagen and [ExtraCell Matrix] when stimulated by cytokines from infiltrated macrophages

B: When VSMC die, fibromuscular cap becomes weak –> rupture –> Thrombosis

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48
Q

Describe [Strawberry Hemangioma]

A

[BENIGN CCM-Capillary Congenital Malformation] made of [unencapsulated capillaries]

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49
Q

Which organs have [single end arterial] blood supply? (3) What does this make them susceptible to?

A

[Heart / Spleen / Kidneys]= makes them susceptible to [White infarcts]

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50
Q

[Jervell and Lange-Nielsen Syndrome]

A

[Jervell and Lange Nielsen]

auto recessive

[Sensorineural deafness]

+

[Long QT Syndrome]

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51
Q

7 common causes of Dilated Cardiomyopathy

A

“the PIG PAID for Dilated Cardiomyopathy”

  1. Post Myocarditis from [Coxsackie B Enterovirus]
  2. Alcoholic Cardiomyopathy from long term EtOH usage (direct toxicity vs. nutritional deficiency)
  3. [Doxorubicin and Daunarubicin Chemotherapy]= dose-dependent
  4. Peripartum - (late in pregnancy vs. 5 mo. post partum)
  5. Genetic= affects cytoskeleton
  6. Iron Overload: [Hereditary Hemochromatosis] or [Multiple Blood Transfusion Hemosiderosis] = Iron accumulates and interferes with metal-dependent enzyme system in myocytes
  7. Idiopathic
    * MOST COMMON CARDIOMYOPATHY*
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52
Q

A: Trousseau’s Syndrome

B: What other Dz is it similar to?

A

A: [Pancreatic or Lung ADC] –> releases products–> Hypercoagulability –> [NonBacterial Thrombotic Endocarditis] and [migratory thrombophlebitis]

B: Similar to MNTe (Marantics NonBacterial Thrombotic Endocarditis]

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53
Q

Post MI evolution

< 4 hours

A: Gross Changes

B: Microscopic Changes

C: Complications (3)

A

< 4 hours

C: [Cardiogenic Shock] / [Acute CHF] / Arrhthymia

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54
Q

Post MI evolution

4-12 hours

A: Gross Changes

B: Microscopic Changes (2)

C: Complications

A

4-12 hours

B: [Beg. of CIN] / [Wavy Fibers]

C: Arrhythmia

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55
Q

Post MI evolution

1-3 DAYS

A: Gross Changes

B: Microscopic Changes (2)

C: Complications

A

1-3 DAYS

A: No Gross

B:

  1. Neutrophil Infiltration
  2. [Loss of myocyte Nuclei]

C: [Fibrinous Pericarditis–> [sharp & pleuritic Chest Pain] + friction rub] (only with transmural infarcts)

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56
Q

Post MI evolution

3-7 DAYS

A: Gross Changes

B: Microscopic Changes

C: Complications (3)

D: Lab

A

3-7 DAYS

A: Yellow Pallor

B: Macrophage phagocytosis of dead debris –> weakens cardiac tissue

C: Cardiac Tissue Weakning (Vt Free Wall Rupture) / (papillary m. rupture) / (interventricular septal rupture)

D: [CkMB] returns to Baseline at Day 3

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57
Q

Post MI evolution

7-10 Days

A: Gross Changes

B: Microscopic Changes (2)

C: Complications

D: Lab

A

7-10 Days

A:No Gross

B:

  • [Early Granulation tissue w/collagen / fibroblast /MyeloFibroblast]
  • Well developed Phagocytosis

C: No Complications

D: [Trop I] returns to baseline

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58
Q

Post MI evolution

2 - 8 WEEKS

A: Gross Changes

B: Microscopic Changes

C: Complications (3)

A

2 - 8 WEEKS

A: White Scar w/[Type 1 Dense Collagen]

B: Fibrosis

C: Aneurysm / [Mural Thrombus] / Dressler’s

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59
Q
A

Valvular Vegetations of the AV valves

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60
Q

Aortic Regurgitation

Mumur

A

[Early Diastolic Descrescendo Murmur-High Pitched Blowing noise] auscultated @ [L Sternal 2nd/3rd ICS]

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61
Q

Name the proteins most likely responsible for these Localized Amyloidosis

  • Cardiac Atria
  • Thyroid
  • Pancreatic Islets
  • [Cerebrum and blood vessels]
  • Pituitary gland
A

If a protein is misfolding and forming [Beta-pleated sheets] in the …

  • Cardiac Atria= [ANP]
  • Thyroid= Calcitonin
  • Pancreatic Islets= [Amylin Islet protein]
  • [Cerebrum and blood vessels]= [Beta-amyloid protein]
  • Pituitary gland= Prolactin
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62
Q

Identify

A

Non-Caseating Granulomas

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63
Q

What cellular ultrastructural change indicates [irreversible myocardial cell injury]

A

Mitochondrial Vacuolization

Vacuoles and [Amorphous densities containing phospholipids] within the Mitochondria

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64
Q

A: Which compound is responsible for the Green color of sputum associated w/ [productive cough]?

B: Where is it found?

C: What is this compound use for?

A

A: Myeloperoxidase

B: Neutrophil Azurophilic Granules

C: Respiratory Burst for Bacterial Infections

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65
Q

Describe the process of how Endothelial Cell injury leads to Formation of an Atheroma

A
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66
Q

Name the 7 most common manifestations of Marfan Syndrome

A

“Marfan BAATHES a lot! “

  1. Ectopia Lentis
  2. Arm-to-Height Ratio that’s INC
  3. Heart issues (MVP vs. [idiopathic Aortic cystic medial degeneration]–> Aortic Dissection and Aneurysm)
  4. Scoliosis vs. Kyphosis
  5. Breastbone w/structural abnormalities
  6. Arachnodactyly (Steinberg thumb & wrist)
  7. Tall / slender / flat feet
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67
Q

Describe the circled below

______ are _______ that contain ________ - which are ________

A

Aschoff Bodies are [Interstitial Myocardial Granulomas] tht contain [ACM-Anitschkow Caterpillar Macrophages] - which are full of cytoplasm and [ribbon-like chromatin]

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68
Q

What 3 maneuvers INCREASE intensity of Aortic Regurgitation

A

“AR your Hands & Breath [Leaning Forward] ?

  • with Hand Grip
  • when Breath is held after exhalation
  • with Patient leaning forward
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69
Q

List the common causes of Restrictive Cardiomyopathy (8)

A

RAMILIES

  1. Radiation Fibrosis
  2. Amyloidosis (heterogenous misfolded proteins)
  3. Sarcoidosis= [Noncaseating granuloma formation] in multiple organs 2º to [CD4 Helper T] attack on unidentified antigen
  4. Metastatic Tumor
  5. Inborn metabolism errors
  6. Endomyocardial fibrosis= Common in [African/Tropic children]
  7. [Loeffler Endomyocardial fibrosis] = (Has [Peripheral blood eosinophilia and infiltrate])
  8. Idiopathic
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70
Q

Describe [Libman Sacks Endocarditis]

A

[Non-bacterial wart-like vegations] accumulate on either side of a heart valve –> Fibrotic Valve Thickening–> MI

Associated with SLE Lupus

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71
Q

[BUerger Thromboangiitis Obliterans] Tx

A

Smoking Cessation

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72
Q

Lichtenberg Figure

A

Erythematous Cutaneous [fern-leaf pattern] from Lightning Strike

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73
Q

Identify the manifestation and name what dz it’s associated with

A

​[Nailbed Subungal Splinter Hemorrhage] - Bacterial Endocarditis

“Bacteria FROM JANE”

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74
Q

3 Major signs of Coarctation of Aorta

A
  1. Upper body HTN–> HA & Epistaxis
  2. Diminished LE pulses (from inadequate LE perfusion)
  3. [Enlarged Intercostal Artery Collaterals]
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75
Q

Occlusion of the [R Coronary Artery] would cause:

Transmural ischemia in what part of the heart?

A

[R Vt inferior wall] —> [R Vt MI and HF]

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76
Q

Occlusion of the [Proximal LAD Artery] would cause:

Transmural ischemia in what part of the heart?

A

Anteroseptal

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77
Q

Occlusion of the [L Circumflex Artery] would cause:

Transmural ischemia in what part of the heart?

A

[L Vt Lateral Wall]

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78
Q

Chest CT Scan + IV contrast

A
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79
Q

A: 3 Heart Structural Effects of Aging

B: At what age do these changes onset?

A
  • Sigmoid shaped septum
  • Hypertrophied Myocyte
  • DEC LV Chamber Size

B: AFTER 65

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80
Q

Which Murmur?

(Auscultation Site is attached)

B: Maneuvers that INC (2)

A

Mitral Regurgitation

[Holosystolic High-Pitched Blowing Murmur]

“MR. Hand me a Squat”

B: INC with…

1) Hand Grip
2) Squatting

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81
Q

Which Murmur? (Is Not VSD)

(Auscultation Site is attached)

B: Maneuvers that INC

A

Tricuspid Regurgitation

[Holosystolic High-Pitched Blowing Murmur]

B: INC with… Inspiration

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82
Q

Which Murmur?

(Auscultation Site is attached)

B: Maneuvers that INC (2)

C: Maneuvers that DEC

A

Aortic Stenosis

[Crescendo-Descrescendo Systolic Ejection Murmur]

“Lean forward…& then Squat with that Ass, that’ll turn it up!”

B: INC with…

  1. Leaning Forward
    2) Squatting

C: DEC with…handgrip (INC afterload)

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83
Q

Mitral Valve Prolapse

Murmur

A

“He was MVP…OF COURSE he had a Mid Clique to hang with”

[Late Systolic Crescendo Murmur + MidSystolic Click] @ Apex

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84
Q

Which Murmur?

(Auscultation Site is attached)

A

Mitral Valve Prolapse

[Late Systolic Crescendo Murmur + MidSystolic Click]

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85
Q

Which Murmur?

B: Name the Auscultation Site

C: Maneuvers that INC sound

A

Mitral Stenosis

[Delayed Rumbling Diastolic murmur that follows an Opening Snap]

B: [Apex + LLDP (L Lateral Decubitus Position)]

C: Maneuvers that [INC Afterload]

-handgrip

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86
Q

Which Murmur?

(Auscultation Site is attached)

A

Hypertrophic Cardiomyopathy

[Holosystolic Harsh Murmur] auscultated @ [L Sternal 2nd/3rd ICS]

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87
Q

Which Murmur?

(Auscultation Site is attached)

A

Ventricular Septal Defect

[Holosystolic Harsh Blowing Murmur]

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88
Q

Which Murmur?

(Auscultation site is attached)

A

Patent Ductus Arteriosus

[Machinery Continuous Murmur] ausculated over [L infraclavicular region]

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89
Q

Which murmurs are heard at the Apex? (3)

A

ALL THINGS Mitral!

  1. Mitral Regurgitation
  2. Mitral Stenosis (Apex + LLDP)
  3. Mitral Valve Prolapse
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90
Q

Which murmurs are heard at the Tricuspid Area? (4)

A
  1. Tricuspid Regurgitation
  2. Tricuspid Stenosis
  3. VSD
  4. ASD (from flow across Tricuspid valve initially—>progresses to Pulmonic regurgitation from pulmonic valve damage)
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91
Q

Which murmurs are heard at the Pulmonic Area? (2)

A
  1. Pulmonic Stenosis
  2. [Physiologic Flow Murmur]
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92
Q

Which murmurs are heard at the [L Sternal 2nd/3rd ICS] ? (3)

A
  1. Aortic Regurgitation
  2. Pulmonic Regurgitation
  3. (HOCM) Hypertrophic Cardiomyopathy
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93
Q

Which murmurs are heard at the Aortic Area? (2)

A
  1. Aortic Stenosis
  2. Aortic Valve Sclerosis
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94
Q

[Aortic Cystic Medial Degeneration] is often seen in ____ pts with ____ syndrome.

B: Describe [Cystic Medial Degeneration] (2)

A

[Aortic Cystic Medial Degeneration] is often seen in YOUNGER pts with Marfan Syndrome

B: Myxomatous changes (connective tissue weakening) + [pooling of proteoglycans] in the [Tunica Media of Large Arteries]

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95
Q

When do Ventricles release BNP? (2)

A

(BNP) AND (ANP) are both released during [Heart Failure -Vt Hypertrophy and/or Vt Dilitation

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96
Q

What microscopic changes occur during [REVERSIBLE (sublethal) Ischemic injury] to cardiac myocytes (4)

A

“It’s not lethal yet (sublethal/Reversible) So Relax And Layback”

  • Swelling of Mitochondria
  • Relaxation of Myofibrils
  • [ATP & Glycogen DEC]
  • Lactate Accumulation
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97
Q

Paradoxical Embolism occurs when _____

A

Occurs when thrombus from venous system (DVT) crosses into arterial system via [ASD / VSD / PDA] in lieu of going to lungs.

[ASD] murmur = [Wide and FIXED S2 Spliting (since pulmonic will always take longer to close if there’s extra fluid in R vt)

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98
Q

List the associated cardiac pathology which each inherited disorder

A: Down Syndrome

B: DiGeorge Syndrome (2)

C: Friedreich’s Ataxia

D: Marfan Syndrome

E: Tuberous Sclerosis

F: Turner’s Syndrome (2)

A

A: “Put the cusions Down” = [Endocardial Cusion Defects: (Ostium Primum ASD) + (Regurgitant AV valves)]

B: [Tetralogy of Fallot] + [Aortic Arch abnormalities]

C: Hypertrophic Cardiomyopathy (“sweet, big heart”)

D: [Aortic Cystic Medial Dengeration]

E: [Cardiac Rhabdomyomas —> Valvular Obstruction]

F: [Aortic CoArctation] vs. [Biscuspid Aortic Valve]

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99
Q

Describe Angiosarcoma

A

[Rare Blood Vessel Malignancy] usually in [Head/Neck/Breast] but can originate from Liver as well

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100
Q

Clinical Presentation for LARGE PDA (2)

A
  1. Large PDA Shunt will eventually –> (Eisenmenger R to L shunt) –> PDA delivers DeOxygenated blood distal to [L subclavian a.]–> LE cyanosis & clubbing with NO BP/pulse discrepancies
  2. HF (SOB + Fatigue)

Note: LARGE PDA can progress from small PDA if untreated

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101
Q

Which Drugs cause [Coronary Artery CORONARY STEAL] (2). Why is this?

A

A: [Adenosine vs. Dipyridamole] = VasoDilators

B: These 2 drugs selectively vasodilate coronary arteries in non-ischemic myocardium –> steals blood flow from [occluded coronary arteries] which perfuse ischemic areas –> EXACERBATES ISCHEMIA

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102
Q

How does Reperfusion Injury cause its damage (5), and what is the ultimate result?

A

“MICCO injured himself from Reperfusing”

  1. [Oxygen Free Radical Generation] by endothelial cells
  2. [Mitochondrial damage(not vacuolization) - Severe & Irreversible]
  3. [Inflammation - which attracts neutrophils–>more injury]
  4. [Complement & Cell membrane damage]

Ultimate Result = Cell Membrane Damage —> Elevated [Creatine Kinase] if brain/heart/muscle​ are affected

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103
Q

What should you suspect if [Right Vt] is Hypertrophied ( >3-4 mm) and Dilated?

A

[Cor Pulmonale 2° to Pulm HTN]

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104
Q

Post MI evolution

12-24 hours

A: Gross Changes

B: Microscopic Changes (3)

C: Complications

D: Lab

A

12-24 hours

MCN CAT: M/CNC/A/T

A: Myocardial Mottling

B:

  1. [CIN Continues]
  2. Nuclei Pyknosis
  3. [Contraction Band Necrosis]

C: Arrhythmia

D: [Trop I] and [CkMB] peaks at 24 hours

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105
Q

Post MI evolution

10 - 14 Days

A: Gross Changes

B: Microscopic Changes (2)

C: Complications

A

10 - 14 Days

{Use TriChrome Stain}

A: No Gross

B:

  1. [Granulation tissue with neovascularization and Fibroblast]
  2. Red Border from Granulation tissue entering from edge of infarct

C: No Complications

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106
Q

In which Arteries do Atherosclerotic Plaques develop? (7)

A

[Large Elastic Arteries (-CIA: Carotid, iLiac, Aorta)]

&

[Medium Muscular Arteries (Coronary & Popliteal)]

&

[Circle of Willis]

[Abd Aorta] > Coronary > Popliteal > [Internal Carotid] > [COW]

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107
Q

What is the single most important risk factor for developing Aortic DISSECTION

A

HTN

(causes intimal tears)

scan shows intimal flap torn away from Aortic wall

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108
Q

Pathogensis of Aortic Aneurysm

A

[Chronic Transmural Inflammation] of Aortic wall —> [Loss of Elastin and Smooth Muscle] –> [Abnormal Collagen remodeling] –> [progressive Weakening of Aorta] –> Wall Expansion

[Chronic Transmural Inflammation] can come from Atherosclerosis but ⬆︎ risk of rupture comes from smoking!

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109
Q

What does a [FIXED and Widened S2 Spliting​] likely indicate?

A

[ASD] murmur

= [FIXED and widened S2 Spliting (since pulmonic will always take longer to close if there’s extra fluid in R vt)

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110
Q

A: Describe the Heart changes in JONES syndrome from Rheumatic Fever (2)

B: What are the 2 dangerous developments of this?

A

Mitral Stenosis from

  1. Mitral Valve Leaflet Distortion 2° to fusion of leaflet edges
  2. L Atria with [diffuse fibrous thickening]

B: Afib –> [Embolic Stroke]

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111
Q

Describe the [OWR - Osler Weber Rendu syndrome]

A

[Hereditary Hemorrhagic Telangiectasia] described as pink and spider-like lesions

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112
Q

A: Explain the physiology for [Carotid Sinus] massage

B: Where, in the CNS, does the nerve responsible for this physiology terminate?

A

A: [Hering nerve] of [Carotid Sinus] starts to fire when BP in [Carotid Sinus] INC –> [Glossopharyngeal CN9] to [DEC BP / HR / [induce syncope] ]

B: [Solitary nucleus of medulla]

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113
Q

A: What is the major limiting factor to Coronary blood flow during Exercise?

B: How does the Body compensate for this during Exercise? (2)

A

A: [Shorter Duration of Diastole 2° to Tachycardia] -Max blood flow to coronary arteries occurs during Diastole

B:

  1. Flow-mediated Dilation
  2. VasoDilators (Adenosine / NO)
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114
Q

What is the Coronary Sinus, and what’s unique about it’s O2 content

A

A: Vein that collects [DeOxygenated Blood FROM HEART MUSCLE] –> [Dumbs into IVC]–> [R Atrium]

B: Has the [LOWEST O2 Content in Body] since Myocardial O2 extraction is VERY high

Remember: Heart muscle is perfused during Diastole

115
Q

How does [AV Shunts] affect Preload and Afterload

A

* INC Preload–> [High Output Cardiac Failure]

*DEC afterload (since they’ll be less blood in Arterial system once it travels to the venous system)

116
Q

A: Which Collagen type do you find in Mature Scars?

B: Is this type of Collagen Abundant?

A

A: Type 1 Collagen

B: Most prevalent Collagen in Body

117
Q

Describe Collagen Type 1

A: Location (3)

B: Associated DO

A

[be so totally] Cool, Read Books

Type 1 = MOST PREVALENT (especially in mature scars)

A: bone / skin / tendon

B: [Osteogensis Imperfecta type 1]

118
Q

Blood is in incompressible fluid

A: State the [Law of Conservation of Mass] formula

B: Which formula is used for constant flow through a tube

A

A: [Total Flow] = [Flow Velocity] x [Cross Sectional Area]

B: [(Area 1) x (Velocity 1)] = [(Area 2) x (Velocity 2)]

119
Q

List the Pressures for the following Heart chambers:

A: Central Venous Pressure

B: [R Atrium] (2)

C: [R Ventricle]

D: Pulmonary Artery (2)

E: [Pulm Wedge / L Atrium] (2)

F: [L Ventricle]

G: Aorta

H: Brachial Artery

A

A: CVP = 2

B: [R Atrium] = 2 (8 / 0 range)

C: [R Ventricle] = 25 / 2

D: Pulmonary Artery = 25 / 10 (15 Mean)

E: [Pulm Wedge / L Atrium] = 6 (12 / 2 range)

F: [L Ventricle] = 120 / 6

G: Aorta = 120 / 70

H: Brachial Artery = [95 Mean]

120
Q

List the 2 Formulas for Cardiac Output

A
  1. [CO = HR x SV]
  2. [CO = (O2 consumption) ÷ (AV O2 Difference)] = Fick Principle
121
Q

List, from FASTEST to slowest, [Conduction Speed] between:

  • Atria
  • AV node
  • Purkinje Fibers
  • Ventricles
A

Park At Venture Avenue

PURKINJE > Atrial > Ventricle > [AV node]

122
Q

[Aortic / pharyngeal Arch 1]

A: Key Derivative from this Arch

B: Associated Cranial Nerve with this Arch

A

“1st arch is Maximal “

A: Maxillary artery (portion of it)

B: [Trigeminal CN5]

123
Q

[Aortic / pharyngeal Arch 2]

A: Key Derivative from this Arch

B: Associated Cranial Nerve with this Arch

A

“Second = Stapedial”

A: Stapedial artery (WHICH COMPLETELY REGRESSES EVENTUALLY)

B: [Facial CN7] “Don’t be 2 faced”

124
Q

[Aortic / pharyngeal Arch 3]

A: Key Derivatives from this Arch (2)

B: Associated Cranial Nerve with this Arch

A

“C = 3rd letter in Alphabet & 3x3 = 9”

A: [Common Carotid] / [Internal Carotid - proximal part]

B: [Glossopharyngeal CN9]

125
Q

[Aortic / pharyngeal Arch 4]

A: Key Derivatives from this Arch (2)

B: Associated Cranial Nerve with this Arch

A

A: [True Aortic Arch] / [R Subclavian Artery]

B: [Vagus CN10 - Superior Laryngeal branch]

126
Q

[Aortic / pharyngeal Arch 5]

A: Key Derivatives from this Arch

B: Associated Cranial Nerve with this Arch

A

EVERYTHING FROM THIS ARCH OBLITERATES!

127
Q

[Aortic / pharyngeal Arch 6]

Key Derivatives from this Arch (2)

A

[Ductus Arteriosus] & [Pulmonary Arteries]

” 666 is Recurrent”

128
Q

What 2 Heart Defects are associated with Cryptogenic Stroke

A

A:

  1. ASD
  2. Patent Foramen Ovale (occurs in 25% of normal adults)
129
Q

Clinical Presentation for [TGA - Transposition of Great Arteries] (3)

A

Neonate with…

  1. [Aorta lies ANTERIOR and to the RIGHT of Pulm Artery]
  2. Cyanosis
  3. Tachypnea
130
Q

Which Artery is injured from a fracture to the Pterion? Name the Parent Artery of this vessel

A

A: [Middle meningeal a. - frontal branch] (courses thru Foramen Spinosum deep to the Pterion)

B: MAXILLARY ARTERY (Derivative of 1st Aortic/pharyngeal arch)

131
Q

Identify

A
132
Q

Identify

A

A: Duodenum (lies at level L2)

B: IVC (Remember that R renal vein drains into IVC)

C: [Abd Aorta] (Bifurcation of Abd Aorta occurs at level L4)

D: iLeum (LOOKS LIKE FIGURE 8 SOMETIMES)

E: [L Renal Vein]

133
Q

Where is the SA node located?

A

[Junction of (R Atrium) and (SVC)]

134
Q

Identify

A

Remember:

  • [R middle Lung lobe] is adjacent to [R Atrium]
  • R side of Heart of CXR is [R Atrium]
135
Q

A: Cannulation above the inguinal ligament INC risk of developing what condition?

B: What is this condition the most common cause of?

A

RETROPERITONEAL HEMORRHAGE—> Unexpected Mortality post cardiac-cathertization

136
Q

Name the Autoregulator Factors for the Heart (4)

A
  • NO (MOST IMPORTANT AND AUTOREGULATES HEART’S LARGE/MEDIUM VESSELS)
  • -Adenosine (small coronary arterioles*)
  • DEC O2
  • CO2
137
Q

Which Heart Chamber does a [TEE - TransEsophageal Echocardiography] face when placed?

A

L Atrium!

Probe is placed in mid-esophagus facing anteriorly, which faces L Atrium

138
Q

[ST Elevations] or [Q waves] in these leads indicate INFARCT in which areas?

A: [V1 - V2]

B: [V3 - V4]

C: [V5 - V6]

D: [Lead 1 / aVL]

E: [Lead 2 / 3 / avF]

A

A: [(V1 - V2) = Anteroseptal - LAD]

B: [(V3 - V4) = Anteroapical - distal LAD]

C: [(V5 - V6) = AnteroLateral - LAD vs. LCX]

D: [Lead 1 / aVL] = [Lateral - LCX]

E: [Lead 2 / 3 / avF] = [InFerior - RCA] - DONT GIVE BETA BLOCKERS

139
Q

Identify

A
140
Q

Where are the 3 leads of a Biventricular PACEMAKER placed?

A
  1. R Atrium (via L subclavian vein –> SUP Vena Cava–> R Atrium)
  2. R Ventricle (via L subclavian vein–> SUP Vena Cava–> R Atrium –> R Vt)
  3. L Ventricle (via R atrium —> [Coronary Sinus within the AV groove] of Post Heart –> L Vt)
141
Q

What part of the heart forms the [diaphragmatic surface]?

A

[L Vt - INFERIOR WALL]

142
Q

What areas of the heart do these Coronary Arteries perfuse?

[LCX - Left CircumfleX] (2)

A

[LCX] - from [L Main Coronary Artery]

  1. [L Vt - Lateral AND Posterior Surface]
  2. [Anterolateral Papillary muscle]
143
Q

What areas of the heart does this Coronary Artery perfuse?

[R Coronary A.] (3)

A

[R Coronary A.]

  1. SA Node
  2. PDA -[Posterior Descending Interventricular Artery] (70% population) —> PERFUSES AV NODE
  3. [R Marginal Acute A.]
144
Q

What areas of the heart do these Coronary Arteries perfuse?

[PDA - Posterior Descending Artery] (3)

A

[PDA]

  1. [Post 1/3 of Interventricular septum]
  2. [Post Vt Walls (including Diaphragmatic surface of heart)]
  3. [Posteromedial Papillary muscle]
145
Q

What areas of the heart do these Coronary Arteries perfuse?

[LAD - Left Anterior Descending] (3)

A

[LAD] - from [L Main Coronary Artery]

  1. [ANT 2/3 of Interventricular septum]
  2. [Anterolateral Papillary muscle]
  3. [L Vt - Anterior Surface]
146
Q

What areas of the heart do these Coronary Arteries perfuse?

[R Marginal Acute A.]

A

Right Ventricle

147
Q

A: What does the Red arrow indicate?

B: What does the White arrow indicate?

A

A: [L Main Coronary Artery] originating from [L coronary cusp] from Aortic Root and continuous anteriorly as …

B: [LAD]

148
Q

What 2 diseases is Streptococcus Gallolyticus Bovis associated with?

A
  1. [SBE-SubAcute Bacterial Endocarditis] (Aortic Regurgitation) (SBE also caused by Strep Viridans)​
  2. [GI Lesions –> Colon CA]

AKA S. Bovis

149
Q

A: Clinical Manifestations of DiGeorge Syndrome (5)

B: Genetic Cause

C: Embryologic cause

A

“CATCH 22 & Pa3”

Cardiac (Aortic Arch abnormalitites)

Abnormal face (Bifid Uvula/low set ears)

Thymus Aplasia

Cleft Palate

[HypOcalcemia from PTH deficiency] may–> Carpopedal Spasms

22q.11.2 deletion

Pharyngeal arch - 3rd/4th both fail to develop

150
Q

List the most important steps for preventing [CVC-Central Venous Catheter] Infections (5)

A

‘CVC’s need a good BRACH b4 being inserted!”

  1. Hand Washing prior to insertion
  2. Barrier precautions during Central line insertion
  3. Chlorhexidine for skin disinfection
  4. Avoid [Femoral catheter insertions] (instead use SubClavian or Internal Jugular Vein)
  5. Remove Catheter when no longer needed for good
151
Q

In terms of Accuracy and Precision, what is another term for Precision?

A

RELIABILITY

  • R is just a P with a kickstand!*
  • Precision = Reliability*
152
Q

Bicuspid Aortic Valve

Mumur

A

[Early Systolic High-frequency click] @ [R Border 2nd ICS]

153
Q

Monoamine Oxidase is a ___ enzyme that degrades excess ______ and detoxifies _______

A

Monoamine Oxidase is a Mitochondrial enzyme that degrades excess [monoamine NTS in presynpatic n. temrinals] and detoxifies [Dietary Tyramine in the GI tract]

154
Q

Explain Coronary Dominance

A

The Dominating coronary a. tht perfuses the [PDA-PosteriorDescending interventricularArtery]

155
Q

Describe the path a thrombus would take in order to cause [RAO-Retinal Artery Occlusion] (3)

A

[Internal Carotid Artery] –> [Opthalmic Artery] –> [Retinal Artery]

156
Q

Atrial Fibrillation INC risk of ______ Thromboembolism

B: What location is the source of [Afib thrombus formation]?

A

Atrial Fibrillation INC risk of Systemic Thromboemoblism

B: L Atrial Appendage

157
Q

What is a good parameter for certain BP medication non-compliance? Describe it.

A

A: PRA - Plasma Renin Activity

B: PRA measures the amount of [Angiotensin 1] made in a certain time = assess [Renin-Angiotensin-Aldosterone Axis].

158
Q

A: Describe Fetal Circulation starting with Placenta

B: Which Structure has the MOST OXYGENATED BLOOD?

A

B: Umbilical VEIN

Remember: Single Umbilical A. = Chromosomal & Congenital anomalies

159
Q

What happens to [Cardiac-Vascular Function Curve] Intersection when there’s a:

A: [Change in Venous Return]

B: Give 2 examples of each

A

A: If there’s [Change in Venous Return (venous/volume/vascular)] —> Intersection slides along [Cardiac Output Curve]

Ex: [Acute Hemorrhage] / Sympathetics / [Fluid Infusion]

160
Q

What happens to [Cardiac-Vascular Function Curve] Intersection when there’s a:

A: [Change in Total Peripheral Resistance]

B: Give 2 examples of each

A

A: If there’s a change in [Total Peripheral Resistance] —> Intersection FLEXES Up or Down

Ex: Vasopressors / Exercise(DEC TPR to get blood to musculature) /

[Exercise and AV Shunt DEC TPR ⬇︎–> Intersection FLEXES UP ⬆︎]

161
Q

3 classic Clinical Manifestations of [Tetralogy of Fallot]

A

A:

  1. [Systolic Ejection Murmur] from [RVOT -R Vt Outflow Obstruction]
  2. Squatting relieves sx (INC afterload–> [DEC amount of R to L shunt]
  3. [Cyanotic Tet Spells]

“VOIR is to have See + Sight & Cry”

162
Q

Describe the 3 Clinical Manifestations of [PDA- Patent Ductus Arteriosus]

A

[R–> Left Shunting] causes….

  • [Machinery Continuous Murmur] over [L infraclavicular region]
  • Palpable Thrill over [L infraclavicular region]
  • HF sx (Failure To Thrive and Respiratory Distress)
163
Q

What protein is Defective (2) in [Familial Chylomicronemia Syndrome] and why does Heparin exacerbate this?

A

A: [Lipoprotein Lipase (LPL) Deficiency] or [ApoC2]

B: exacerbated by [Exogenous Heparin] since LPL is naturally bound to Heparin

Sx = HHALX

164
Q

Which demographics are likely to develop Lipofuscin? (3)

A

Aging / Cachectic / Malnurished pts

165
Q

[HOCM - HyperObstructive CardioMyopathy] MOD

A

[Beta myosin heavy-chain mutation] –> Defective cardiosarcomeres–> [Hypertrophied myocytes that are haphazardly arranged]

+

Abnormal [ANT motion of (ANT leaflet mitral valve) toward [Hypertrophied interventricular septum]

166
Q

Upregulators of Cytochrome P450 Enzymes (8)

A

Chronic alcoholics Steal Phen-Phen & Never Refuse Greasy Carbs

  • Chronic alcohol use
  • St.John’s wort
  • Phenytoin
  • Phenobarbital
  • Nevirapine
  • Rifampin
  • Griseofulvin
  • Carbamazepine
167
Q

Inhibitors of Cytochrome P450 Enzymes (11)

A

AAA RACKS IN GQ Magazine

INHIBIT me from doing my job!

Acute Alcohol Abuse

Ritonavir (HIV Protease inhibitor)

Amiodarone

[Cimetidine & Ciprofloxacin]

Ketoconazole

Sulfonamides

INH (Isoniazid)

Grapefruit Juice

Quinidine

Macrolides (except Azithro)

168
Q

What Substrates does the Cytochrome P450 enzymes work on? (6)

A

Can Always Think When Outdoors, Son….i need it!

Cyclosporine (Liver AND small intestine)

AntiEpileptics

Theophylline

Warfarin

OCP

Statins (NOT PRAVASTATIN)

169
Q

What type of Cardiovascular predispositions do Down Syndrome pts have? (2)

A
  1. Atrial Septal defect
  2. Vt Septal Defect
170
Q

2 Conditions that cause Paradoxical Splitting

A

“PAradoxical Splitting”

  1. LBBB
  2. Aortic Stenosis

“Taking AP Classes were normal for me”

171
Q

4 anatomic abnormalities associated with [Tetralogy of Fallot]

A

VOIR

(Vt Septal Defect / Overriding Aorta / [Infundibular Pulmonary Stenosis] / [R Vt Hypertrophy with [R –> L shunt] = Boot shaped on CXR ]

“VOIR is to have See + Sight & Cry”

172
Q

How does Cortisol utilize Permissiveness?

A

Cortisol upregulates [alpha-1 adrenergic receptors] on vascular and bronchial smooth m. –> better response to Catecholamines(such as NorEpi)–> MORE Vasoconstriction

173
Q

What are the Sx of [SHAC Syndrome] (4)

A

Syncope / Nausea / Dizziness / Fetal Demise (when severe)

174
Q

Blunt Aortic Injury

A

Rapid Deceleration while restrained/seatbelted (occurs in MVC) causes Aortic Isthmus to tear —> Aortic Rupture

175
Q

Which pts benefit from SacubiTrill

A

Heart Failure Pts

176
Q

A: What is the Typical Heart Rate for [aFib with RVR]

B: What does the Ventricular Rate depend on in [Atrial Fibrillation]

A

A: 90-170 bpm

B: AV Node Refractory Period

177
Q

A: What is Lymphangiosarcoma

B: What predisposes a pt to Lymphangiosarcoma

A

A: MALIGNANT neoplasm of the [endothelial lining of lymphatic channels]

B: Persistent Lymphedema w/chronic Dilation of lymphatic channels

178
Q

Heart Manifestations of VSD (2)

A
  • [INC R Vt O2 Sat] with [NORMAL L Vt O2 Sat]
  • LARGE VSD –> Heart Failure
179
Q

Aortic Stenosis

Manifestations (5)

A

*) [Pulsus parvus et tardus]= weak pulses with delayed peak

*) SAD: [Syncope / Angina / (Dyspnea on exertion)]

*) [S4 Atrial Kick]

180
Q

Causes of Aortic Stenosis (3)

A

[Age-Related calcification ( >65 y/o)]

vs.

[Bicuspid Aortic Valve] calcification ( >50 y/o)]

vs.

[Rheumatic Fever Endocarditis (Fish Mouth)]

181
Q

Describe the histology for [Hemosiderin-laden alveolar macrophages]

A

Golden cytoplasmic granules that turn blue with [Prussian blue stain]

L HF –> Pulmonary Edema and RBC extravasation from INC permeability of [capillary wall]. Macrophages phagocytose RBC and the iron is converted —> Hemosiderin

182
Q

Auscultation Site for S3 gallop (3)

A

[Apex + (LLDP) + (End Exhalation)]

End Exhalation brings heart closer to chest wall

183
Q

Best indicator for severity of valve Regurgitation?

A

Presence of an additional S3 (indicates Vt Dilitation in addition to regurgitaiton)

184
Q

Auscultation site for Mitral vs. Tricuspid Regurgitation each

A
  • Mitral Regurgitation:* [Apex w/radiation to axilla]
  • Tricuspid Regurgitation:* [Tricuspid Area w/radiation to R Sternal border]
185
Q

Causes of Tricuspid Regurgitation

A

[RV Dilatation]

186
Q

Which Dz’s cause EITHER OR Mitral vs. Tricuspid Regurgitation (2)

A

Rheumatic Fever and [Infective Endocarditis]

187
Q

Clinical Manifestation of Cardiac Tamponade (3)

A

“Heavy Bleeding in PericardialSpace

  • [Beck Triad: hypOtension / JVD / Distant Heart Sounds]
  • [HR INC but CO DEC]
  • Pulsus Paradoxus (Pulsus for CAPOT)
188
Q

EKG Manifestation of Cardiac Tamponade (2)

A

[low-voltage QRS] + [Electrical Alternans from Heart swinging in fluid]

189
Q

Describe Lipofuscin (3)

A

Yellow-brown / fine granular / perinuclear pigment

190
Q

What conditions cause Pulsus Paradoxus (5)

A

“Pulsus for CAPOT”

  1. Croup
  2. Asthma
  3. Pericarditis
  4. Obstructive sleep apnea
  5. Tamponade
191
Q

What Conditions are associated with S4 Atrial Kick (2)

A
  1. Aortic Stenosis
  2. Restrictive Cardiomyopathy (includes HOCM)
192
Q

A: Explain the opening snap for Mitral Stenosis

B: Best Tool for assessing Degree of Mitral Stenosis

A

A: Opening Snap comes from abrupt halt of leaflet motion in diastole after its rapid opening from the leaflet tips being fused together)

B: DEC interval between S2 and Opening Snap = INC severity of [Mitral Stenosis]

193
Q

Mitral Stenosis is associated with which condtion

A

Rheumatic Fever

194
Q

Which 2 bedside maneuvers ⬆︎ Intensity of the HOCM mumur?

A

“Val [Stood Up] to Hulk HOCM, the MVP, which ⬆︎ his anxiety”

Valsalva

[Standing Up]

(both ⬇︎ Preload AND ⬇︎ Afterload)

195
Q

Hypertrophic Obstructive CardioMyopathy (HOCM)

Mode of Inheritance

A

AUTO DOM

196
Q

How does [Prinzmetal Variant Angina] manifest on EKG. Why is this?

A

[Temporary transmural myocardial ischemia (typically near atherosclerosis)] –> manifest as transient ST-elevations

197
Q

A: What drug provokes [Prinzmetal Variant Angina] episodes and possibly aids in diagnosis?

B: How do you treat [Prinzmetal Variant Angina]

A

A: ErGonovine (stimulates [alpha adrenergic] and serotonergic receptors–>coronary spasm induction)

B: Nitrates and CCB

198
Q

Clinical Presentation of [Carcinoid Heart Disease] (3)

A

[Cutaneous Flushing] / Diarrhea / Bronchospasms

199
Q

What 3 Congenital defects are also associated with [Coarctation of Aorta]?

A

[Turner Syndrome] (pre-PDA)

[Berry Saccular Aneurysm]

[Bicuspid Aortic Valve]

200
Q

Histology for [Dystrophic Calcification]

A

Dark-purple aggregates that may develop outer layers known as psammoma bodies

201
Q

A: [Strawberry Hemangioma] Demographic

B: Prognosis

A

A: Infants

B: Grows proportionally with child and regresses by age 5-8

202
Q

Which 2 organs have DUAL blood supply?

A

Lungs and Liver = NOT SUSCEPTIBLE TO INFARCTS

203
Q

[Jervell and Lange-Nielseon Syndrome]

Mode of inheritance

A

auto recessive

204
Q

PGN of [Jervell and Lange-Nielseon Syndrome] (3)

A

[Prolonged QT] –> Torsades De Pointes –> [Syncope and Sudden Cardiac Death]

205
Q

Dilated Cardiomyopathy Clinical Findings (3)

A

“the PIG PAID for Dilated Cardiomyopathy”

HF / S3 / [Systolic Regurgitant Murmur]

MOST COMMON CARDIOMYOPATHY

206
Q

3 Main Causes of Aortic Regurgitation

A
  • [Aortic Root Dilitation]
  • [Bicuspid Aortic Valve]
  • Endocarditis (i.e. Rheumatic Fever)
207
Q

Aortic Regurgitation Clinical Presentation (2)

A
  1. [Widened Pulse Pressure (may manifest as head bobbing with each heart beat = [de Musset sign])]

+

  1. [Large Stroke Volumes (may manifest as head / heart pounding )]
208
Q

A: What dz are these formations associated with?

B: What is the Cardiac Dz Progression?

A

Aschoff Bodies

A: Acute Rheumatic Fever - 2º to Strep A

B: Mitral Regurgitation —> Mitral Stenosis

209
Q

What Dz is associated with [Libman Sacks Endocarditis]

A

Systemic Lupus Erythematosus

210
Q

A: 2 Demographics at risk for [BUerger Thromboangiitis Obliterans]

B: These pts show a hypersensitivity to what?

A

A: [Heavy Smokers] / [Males

B: [Intradermal injection of Tobacco Extract]

211
Q

Describe [BUerger Thromboangiitis Obliterans] and what 3 things it leads to

A

[STMV- Segmental Thrombosing (Medium vessel) Vasculitis] that leads to:

  • Intermittent claudication –> Extremity Gangrene
  • Corkscrew Collaterals on imaging
  • -*Raynaud Phenomenon
212
Q

Name the manifestations of Bacterial Endocarditis (7)

A

“Bacteria FROM JANE”

Fever

[Retinal Roth Spots - Immunologic phenomena]

[Osler “Ouch” Nodes- Immunologic phenomena]

[Mumur that’s new]

[Janeway lesions on palms/sole]

Anemia

[Nailbed Subungal Splinter Hemorrhages] - shown in image

[Emboli from valvular vegetations]

213
Q

Occlusion of the [R Coronary Artery] would cause:

A: ST elevation in which leads? (3)

B: Any other associations?

A

A: Leads 2 / 3 / avF

B: Sinus Node Dysfunction (also supplied by RCA)

214
Q

Occlusion of the [Proximal LAD Artery] would cause:

ST elevation in which leads? (4)

A

V1 - 4

215
Q

Occlusion of the [L Circumflex Artery] would cause:

ST elevation in which leads? (4)

A

V5 / V6 / Lead 1 / aVL

216
Q

Causes of MVP (3). MVP can predispose to what condition?

A

“He was MVP…OF COURSE he had a Mid Clique to hang with”

  1. Myxomatous Degeneration (Marfan vs. [Ehlers Danlos])
  2. Rheumatic Fever
  3. Chordae Rupture

Usually benign but can predispose to infective endocarditis

217
Q

Which Maneuvers make MVP murmur delayed

A

Squatting

218
Q

Which Maneuvers make MVP murmur occur earlier (2)

A

“They were all Standing and Bearing Down before the MVP got there”

Occurs earlier with…

1) Standing
2) Valsalva

219
Q

Maneuvers that INC HOCM murmur (2)

A

Hypertrophic Cardiomyopathy

[Harsh Holosystolic Murmur] auscultated @ [L Sternal 2nd/3rd ICS]

INC with… [Manuevers that DEC PA-Preload ANDAfterload]

  • Valsalva
  • Standing
220
Q

Maneuvers that DEC HOCM murmur (2)

A

Hypertrophic Cardiomyopathy

[Harsh Holosystolic Murmur] auscultated @ [L Sternal 2nd/3rd ICS]

:DEC with..

  • No Valsalva
  • sitting
221
Q

What 2 conditions does [Aortic Cystic Medial Degeneration] potentially lead to?

A

[Aortic Dissection] and [Aortic Aneurysm]

[Basket Weave Pattern**] on Histo

222
Q

Describe the Histology for [Aortic Cystic Medial Degeneration]

A

[Elastic Tissue Fragmentation (from Myxomatous changes)]

–> [Basket Weave Pattern]

223
Q

Angiosarcoma Risk Factors (6)

A

“Angie was only attracted to SLAVER’s”

  1. [Elderly on sun exposed areas]
  2. Sun Exposure
  3. Radiation therapy
  4. Lymphedema PostMastectomy (LymphAngiosarcoma)
  5. Vinyl Chloride (HEPATIC Angiosarcoma)
  6. Arsenic (HEPATIC Angiosarcoma)
224
Q

A: Prognosis for Angiosarcoma

B: Which markers do these tumors express (2)

A

“Angie was only attracted to SLAVER’s”

A: VERY AGRESSIVE TUMOR and difficult to resect due to delay in dx

B: [CD31 and endothelial cell markers]

225
Q

Which demographic is most at risk for developing Cor Pulmonale idiopathically?

A

[Females ages 20-40]

226
Q

Which demographics develops Cor Pulmonale secondarily? (2)

A

COPD pts / smokers –> [Obliteration of pulmonary vasculature] –> Cor Pulmonale

227
Q

List the 5 vessels from MOST to least susceptible to Atherosclerotic Plaques

A

[Abd Aorta] > Coronary > Popliteal > [Internal Carotid] > [Circle Of Willis]

228
Q

Which mucous membranes are affected by OWR - Osler Weber Rendu syndrome.

What’s the worst complication?

A

Telangiectasias on…

  1. [Skin/Lips/Oronasopharygeal]
  2. GI
  3. Respiratory
  4. Urinary

May rupture –> Bleeds

229
Q

[OWR - Osler Weber Rendu syndrome] Mode of Inheritance

A

AUTO DOM

230
Q

Complications of [OWR - Osler Weber Rendu syndrome] (3)

A

Rupturing of Telangiectasia –>

Epistaxis

GI bleeding

Hematuria

DO of blood vessels –> AV malformations –> Telangiectasia

231
Q

What therapeutic tool is associated with the Coronary Sinus

A

[L Vt Pacemaker Lead] traverses thru [Coronary Sinus that lies within the AV Groove] to reach L Vt

Remember: Heart muscle is perfused during Diastole

232
Q

When can the Coronary Sinus become Dilated?

A

[Pulmonary HTN] –> [R Vt AND R Atrial Pressure INC] —> [Coronary Sinus Dilatation]

Remember: Heart muscle is perfused during Diastole

233
Q

Describe AV Shunt. Name 2 ways they’re formed

A

A: Abnormal communication from [Artery –> vein] that bypasses arterioles

B:

  • Iatrogenic (AV Fistula for Hemodialysis)
  • Penetrating injuries
234
Q

Describe Collagen Type 2

A: Location

B: Associated DO

A

[be so totally] Cool, Read Books

Type 2 “Cartwolage”

A: Cartilage (including hyaline and vitreous body)

B: none

235
Q

Describe Collagen Type 3

A: Location (3)

B: Associated DO

A

[be so totally] Cool, Read Books

Type 3 “Read ThreE D”

A: Reticulin (blood vessels / granulation tissue / fetal tissue)

B: [Ehlers Danlos]

236
Q

Describe Collagen Type 4

A: Location (2)

B: Associated DO (2)

A

[be so totally] Cool, Read Books

Type 4 “Type 4 is under the floor”

A: [Basement Membrane and lens]

B: [Alport Syndrome] & Goodpasture

237
Q

[Aortic / pharyngeal Arch 6]

Associated Cranial Nerve with this Arch

A

[CN10 Vagus - Recurrent Laryngeal branch]

” 666 is Recurrent”

238
Q

How are Cryptogenic Stroke lesions typically closed?

A
  1. ASD
  2. Patent Foramen Ovale (occurs in 25% of normal adults)

[Umbilical cord clamping and DEC Pulm vascular resistance] –> [DEC R Atrial pressure] and [INC L Atrial pressure] –> closes [Septum Primum] flap against [Septum Secundum] –> Closes [Formaen Ovale]

239
Q

What causes [TGA - Transposition of Great Arteries] embryogenically?

A

Failure of [Fetal Aorticopulmonary septum] to sprial normally during [Truncus Arteriosus Septation]

240
Q

What Mothers are at high risk of having Neonates with [TGA - Transposition of Great Arteries]?

A

Diabetic Mothers

241
Q

What Bone segments make up the Pterion? (4)

A

Frontal, Sphenoid, Temporal, Parietal

242
Q

What is the Ultimate result of a [fractured Pterion]?

A

[Epidural Hematoma]

243
Q

Where is the [R Vt] located

A

[L sternal 4th ICS - Anterior Heart]

244
Q

Where is the [Pulmonary Trunk] located?

A

[L sternal 2nd/3rd ICS]

245
Q

What structure makes up most of the heart’s posterior surface? How is this structure related to dysphagia?

A

[L Atrium] ([[Mitral Stenosis vs. aFib] –> [L atrial enlargement] –> can compress esophagus –> dysphagia)

246
Q

Name the Autoregulator Factors for the Brain

A

[CO2 (pH)]

247
Q

Name the Autoregulator Factors for the Kidneys (2)

A

[Myogenic & Tubuloglomerular feedback]

248
Q

Name the Autoregulator Factors for the Lungs

A

[DEC O2]

249
Q

Name the Autoregulator Factors for the Skeletal Muscle (6)

A

Sk. Muscle = [Lactate / Adenosine / K+ / H+ / CO2 / (Sympathetic tone when at rest)]

250
Q

What perfuses the [diaphragmatic heart surface]? What is its PARENT artery?

A

[PDA-PosteriorDescending interventricularArtery]

251
Q

What was the former name of Streptococcus Gallolyticus, and where does it “live”?

A

S Bovis; Lives in Colon Normal Flora

252
Q

Pts with Bicuspid Aortic Valve are at INC risk of what 3 things?

A

[Stenosis vs. Insufficiency vs. Infection]

253
Q

How is Monoamine Oxidase associated with Tyramine HTN Crisis

A

Pts who are taking MAOI-MonoAmine Oxidase Inhibitors for depression but eat:

1) Aged cheese
2) Cured meats (Sausage)
3) Draft Beer

will develop Tyramine HTN Crisis (Tyramine is an Indirect Sympathomimetic)

254
Q

List the Population breakdown for Coronary Dominance (3)

A
  • 70% population use [R Coronary Artery] to perfuse PDA = RIGHT DOMINANT CIRCULATION
  • 20% population use BOTH [R Coronary Artery] AND [L Circumflex Artery] to perfuse PDA = CoDominant Circulation
  • 10% population use [L Circumflex Artery] to perfuse PDA= Left Dominant Circulation
255
Q

If a pt with Left Dominant Circulation has [AV node ischemia], which artery is responsible?

A

[AV node] is perfused by PDA and in Left Dominant Ciruclation populations (10%), PDA is perfused by [L Circumflex Artery]

256
Q

Clinical Presentation of a [RAO-Retinal Artery Occlusion] (2)

A

[Acute, painless, (monocular vision loss)]

+

[Macula cherry red spot with a surrounding white retina]

257
Q

What factors INC [PRA - Plasma Renin Activity] (2). How is it used to assess BP med non-compliance?

A

1) low Na+ intake
2) certain BP meds - HCTZ vs. Angiotensin blockers

PRA should INC when pt is started on BP medications (HCTZ vs. Angiotensin blockers) and if it doesn’t = med non-compliance

258
Q

How does [____Stenosis] determine the degree of severity in [Tetrology of Fallot]

A

Degree of [Infundibular Pulmonary Stenosis] determines degree of symptoms since [INC stenosis] –> [INC R–>L Vt Shunt] –> INC [Cyanotic Tet Spells]

“VOIR is to have See + Sight + Cry”

259
Q

PDA Tx (2)

A

Indomethacin (PGE2 inhibitor)

vs.

[Surgical Ligation in older pts]

260
Q

2 Main Causes of [PDA]

A

Prematurity & [Congenital Rubella]

261
Q

Which organs is Lipofuscin normally found (4)

A

Heart

Liver

Kidney

Colon

262
Q

HOCM Sx (3)

A
  • [Syncope during exercise]
  • [Sudden Cardiac Death] 2º to Vt Arrhythmia
  • [S4 Atrial Kick]
263
Q

[Familial Chylomicronemia Syndrome] Mode of Inheritance

A

auto recessive

264
Q

[Familial Hypercholesterolemia (2A)] Mode of Inheritance

A

AUTO DOM

265
Q

Common Causes of [Constrictive Pericarditis] - 5

A

‘Ur an Idiot to constrict my Radio & T-V”

Uremia

Idiopathic

Radiation

TB

Viruses

266
Q

What’s the most frequent [1° Cardiac Peds Tumor]?

A

[Tuberous Sclerosis: Rhabdomyoma] –> Valvular Obstruction

267
Q

ALPHA 1 RECEPTOR

Tissues - Actions (3)

A

“Gimme an alpha 1 VID”

(1) Most Vascular smooth muscle- contracts (inc. vascular resistance)
(2) Dilator Pupillary muscle- contracts (myDriasis)
(3) Internal Urethral Sphincter- contracts

268
Q

ALPHA 2 RECEPTOR

Tissues- Actions (5)

A

“You’ll find alpha 2 receptors on a PPEAA”

(1) [Adrenergic and cholinergic nerve terminals]- inhibits NTS release–> [CNS-mediated BP DEC]
(2) Platelets- stimulates aggregation
(3) Pancreas- DECREASES Insulin Release
(3) Adipocytes - DEC Lipolysis
(4) Eye - DEC Intraocular pressure

269
Q

BETA 1 RECEPTOR

Actions (2)

A

(1) Heart- INC rate and force by [INC [Na+ I(f) channels] in phase 0 of AV node] –> shortens PR interval
(2) JGA cells- Stimulates renin release

270
Q

BETA 2 RECEPTOR

Tissues-Actions (4)

A

“B Team Team 2 Rarely Loves Play Time”

(1) Relaxes RUV - (Respiratory, Uterine and Vascular) smooth muscle
(2) Liver- stimulates glycoGenolysis
(3) Pancreatic B cells- stimulates insulin release
(4) Tremor activation by @ [voluntary m. somatic n. terminals]

271
Q

BETA 3 RECEPTOR Tissues-Actions

A

Fat cells- stimulates Lipolysis

(B1 and B2 may also contribute)

272
Q

DOPAMINE 1 RECEPTOR

Tissues-Actions

A

Renal and other splanchnic blood vessels- vasoDilates (reduces resistance)

D for Dopamine Receptor

273
Q

DOPAMINE 2 RECEPTOR

Tissues-Actions

A

Nerve terminals- inhibits adenylyl cyclase

274
Q

What target organ does the M1 Receptor work in

A

“[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges”

Brain

275
Q

What target organ does the M2 Receptor work in

A

“[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges”

Heart

276
Q

What target organ does the M3 Receptor work in (6)

A

“[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges”

“M3’s BEGS for Private Lounges”

Bladder(contraction) / Eyes / GI / Skin / [Peripheral Vasculature] / Lungs

277
Q

Name the 4 Medications that Prevent LV Remodeling in HF pts

A

“BANA helps HF pts live Loonger”

Beta Blockers (Metoprolol / Carvedilol)

[ACEk2 inhibitors AND ARBs]

[Nitrates + Hydralazine]

[Aldosterone Blockers (Spironolactone / Eplerenone)]

278
Q

When does Lymphangiosarcoma present

A

~10 years after [radical mastectomy w/axillary lymph node dissection]

279
Q

M INC Severity of [Carcinoid Heart Disease] correlates with what compound?

A

[INC Urinary/Plasma 5HiAA (5HydroxyindoleAcetic Acid)] = INC Severity

CarcinoiD Syndrome: (Cutaneous Flushing)/Diarrhea/(SOB wheezing)

280
Q

When do you hear a loud P2?

A

Pulmonary HTN

281
Q

[T or F] ASA, alone, is sufficient to treat DVT/PE in high risk pts

A

NO

282
Q

[Fetal Alcohol Syndrome] is asociated with which Congenital Heart Defect

A

VSD (the most common)

283
Q

Where is the AV node located?

A

near Interatrial septum around the coronary sinus opening

284
Q

Acute Coronary Syndrome consist of what 3 conditions

A

“We have ACS in the USA”

  1. [Unstable vulnerable Angina]
  2. Sudden Cardiac Death
  3. Acute MI

[3] Step 1 USMLE (8 decks)

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