Cardiovascular Flashcards
Describe Paradoxical Splitting
“PAradoxical Splitting”
[Pulmonic Valve closes BEFORE Aortic Valve] which is abnormal
“Taking AP Classes were normal for me”
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Which conditions causes a [FIXED Widened S2 Splitting]?
Atrial Septic Defect
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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?
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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What makes up the Femoral Triangle (3)
- [Inguinal Ligament Superiorly]
- Sartorius M. Laterally
- [ADDuctor Longus M. Medially]
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What happens to [Cardiac-Vascular Function Curve] Intersection when there’s a:
A: [Change in Cardiac Output]
B: Give 2 examples
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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What do these Embryonic Structures form into:
[R Common Cardinal Vein] + [R Anterior Cardinal Vein]
SVC - Superior Vena Cava
“I need a SVC Card”
What does this Embryonic Structure form into:
Truncus Arteriosus (2)
[Trunk of Pulm (Pulmonary Trunk)]
&
[Ascending Aorta]
What does this Embryonic Structure form into:
Bulbus Cordis
[Smooth OUTFLOW TRACT] of BOTH Ventricles
“Bulbs are smooth”
What does this Embryonic Structure form into:
Primitive Atrium
”Trabaca is Primitive in his chamber”
Trabeculated L and R Atria
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What does this Embryonic Structure form into:
Primitive Ventricle
”Trabeca is Primitive in his chamber”
Trabeculated L and R Ventricles
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What does this Embryonic Structure form into:
Primitive Pulmonary Vein
[Smooth L Atrium]
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What does this Embryonic Structure form into:
Sinus Venosus - Left Horn
Coronary Sinus
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(found in the AV groove of the Posterior Heart)
What does this Embryonic Structure form into:
Sinus Venosus - Right Horn (2)
[Smooth R Atrium]
AKA [Sinus Venarum]
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Pathophysiology for [Tetralogy of Fallot]
[Anterior and Cephalad Deviation] of (Infundibular septum) during embryo —-> VOIR
“VOIR is to have See + Sight + Cry”
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Define Permissiveness
[1 Drug with no direct capabilities] Permits and enables a [capable drug] to reach a greater potential :-)
Describe [SHAC Syndrome - Supine hypOtensive Aortocaval Compression]
Pregnant Women > 20 weeks gestation can experience hypOtension when [gravid uterus] (while supine) compresses IVC –> [DEC Venous Return] –> DEC CO
What are the outcomes of Blunt Aortic Injury (2)
Tethered by [Ligamentum Arteriosum] and is fixed and immobile compared to adjacent [Descending Aorta]
A:
- Death
- [Chest or Back Pain] w/SOB and [Widened Mediastinum]
What embryonic Structure does the [Ductus Arteriosus] develop from?
6th Embryonic Aortic Arch
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There are 6 Structures that derive from the Aortic Arch.
Name them
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SacubiTrill MOA (2)
[Neprilysin Inhibitor] –> Prevents ANP degradation —>
*DEC TPR
*INC GFR –> INC Urinary Output
Name 3 EKG Signs of [Atrial Fibrillation]
- [irregularly irregular R-R intervals] (the already irregular R-R interval will occur at an irregular pace since atrial electrictivity is chaotic)
- Absent or [low-amp fibrillatory] P-waves
- Narrow QRS Complexes
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[Atrial Fibrillation] is the most common tachyarrhythmia. It is often precipitated by what 4 things?
“Smh, SAME Afib as before!”
- Acute Systemic Illness (Hyperthyroid / HF / HTN)
- Sympathetic Tone INC
- EtOH - excess
- Mitral Stenosis
Most common [Congenital Heart Defect]
Describe the Mumur.
A: VSD (Ventricular Septal Defect)
B: (when small) = [Holosystolic Harsh Blowing Murmur] auscultated @ [tricuspid area]
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Aortic Stenosis
Mumur
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[Crescendo-Descrescendo Systolic Ejection Murmur] auscultated @ [Heart Base w/radiation to carotids]
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What does [Hemosiderin-laden alveolar macrophages] likely indicate? Why is this?
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
Describe S3 gallop. What is it associated with? (3)
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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A: What do you use to treat Beta Blocker Overdose?
B: Why?
A: Glucagon
B: Activates [Cardiac GPCR] –> Activation of [Adenylate cyclase] —> INC [cAMP in cardiomyocytes]–> INC contractility and HR from Ca+ INC
How long does it take for cardiomyocytes to stop contracting after onset of a [COMPLETE ISCHEMIC EPISODE]?
60 Seconds
(After 30 min. the ischemic injury will become irreversible)
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Dysfunction of Platelets would manifest how? (2) How is Platelet Function measured?
Mucocuntaneous Bleeding (Epistaxis or Petechiae) ; Measured by Bleeding Time
Mitral / Tricuspid Regurgitation
Mumur
[Holosystolic High-Pitched Blowing Murmur]
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Causes of Mitral Regurgitation (3)
- [Ischemic Heart Dz (post MI)]
- MVP
- [LV Dilatation]
Familial Chylomicronemia Syndrome
Sx (5)
HHALX
- Acute Pancreatitis - recurrent
- HyperTriGlyceridemia (especially Chylomicrons)–>creamy supernatant
- [Lipdemia Retinalis]= milky retinal vasculature
- [SKIN Xanthomas- eruptive= yellow erythematous papules on extensor surfaces]
- HepatoSplenomegaly
Cardiac Tamponade MOD
Compression of Heart by Fluid in pericardial Space –> DEC CO and equilibration of diastolic pressures in all 4 chambers
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Describe Pulsus Paradoxus
DEC [Systolic BP] more than 10 mmHg during inspiration
“Pulsus for CAPOT”
What is Lipofuscin, and what is it a sign of
A: [lipid PerOxidation PRODUCT] commonly found in [AGING CELLS’ macrophages]
B: sign of “wear and tear” aging
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S4 Heart Sound is AKA an _____. What is the Etiology
Atrial Kick
A: [STIFF Hypertrophic Ventricle]
L atrium has to “KICK” hard against a STIFF Vt
A: Myocardial Hibernation
B: Describe the pathogenesis
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]
Mitral Stenosis
Mumur
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[Delayed Rumbling Diastolic murmur that follows an Opening Snap] - @ [Apex + LLDP (L Lateral Decubitus Position)]
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(Opening Snap comes from abrupt halt of leaflet motion in diastole after its rapid opening from the leaflet tips being fused together)
MAIN etiology for Claudication? Name 2 other less common etiologies
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]
Hypertrophic Obstructive CardioMyopathy (HOCM)
Mumur
[Holosystolic Harsh Murmur] auscultated @ [L Sternal 2nd/3rd ICS]
When does [Prinzmetal Variant Angina] typically present? (2)
A: At rest and [during midnight - early morning]
3 Common signs of CONSTRICTIVE Pericarditis
- Pericardial Knock= Sharp sound heard in early diastole
- Kussmaul Sign= Paradoxic [INC JVP during inspiration] since constricted R Vt can accomdate the INC blood
- Pulsus Paradoxus
MOD for [Carcinoid Syndrome Heart Disease]
[R sided endocardial fibrosis] —> [Pulmonic and Tricuspid Valve Stenosis] or [Restrictive Cardiomyopathy]
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CarcinoiD Syndrome: (Cutaneous Flushing)/Diarrhea/(SOB wheezing)
Pts with [Coarctation of Aorta] are INC risk of dying from what 3 things?
HTN associated dz such as:
1) [L Vt Failure]
2) [Ruptured Aortic Aneurysm]
3) [Intracranial Hemorrhage] 2º to [Berry Saccular Aneurysm rupture]
Describe the Jugular Venous Pressure Points:
a
c
x
v
y
B: When is [x] absent?
*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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A: Dystrophic calcifcation is the Hallmark of _____ (3)
B: What is Plasma Ca+ in this DO?
A: [Dystrophic calcification] is the HALLMARK OF
- CELL INJURY
- CELL DEATH and
- Necrosis
B: Plasma Ca+ will be normal
This occurs naturally from aging
A: Which cells in an atherosclerotic plaque produce collagen and [ExtraCellular Matrix]?
B: What happens when these cells become ischemic and necrosed?
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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Describe [Strawberry Hemangioma]
[BENIGN CCM-Capillary Congenital Malformation] made of [unencapsulated capillaries]
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Which organs have [single end arterial] blood supply? (3) What does this make them susceptible to?
[Heart / Spleen / Kidneys]= makes them susceptible to [White infarcts]
[Jervell and Lange-Nielsen Syndrome]
[Jervell and Lange Nielsen]
auto recessive
[Sensorineural deafness]
+
[Long QT Syndrome]
7 common causes of Dilated Cardiomyopathy
“the PIG PAID for Dilated Cardiomyopathy”
- Post Myocarditis from [Coxsackie B Enterovirus]
- Alcoholic Cardiomyopathy from long term EtOH usage (direct toxicity vs. nutritional deficiency)
- [Doxorubicin and Daunarubicin Chemotherapy]= dose-dependent
- Peripartum - (late in pregnancy vs. 5 mo. post partum)
- Genetic= affects cytoskeleton
- Iron Overload: [Hereditary Hemochromatosis] or [Multiple Blood Transfusion Hemosiderosis] = Iron accumulates and interferes with metal-dependent enzyme system in myocytes
-
Idiopathic
* MOST COMMON CARDIOMYOPATHY*
A: Trousseau’s Syndrome
B: What other Dz is it similar to?
A: [Pancreatic or Lung ADC] –> releases products–> Hypercoagulability –> [NonBacterial Thrombotic Endocarditis] and [migratory thrombophlebitis]
B: Similar to MNTe (Marantics NonBacterial Thrombotic Endocarditis]
Post MI evolution
< 4 hours
A: Gross Changes
B: Microscopic Changes
C: Complications (3)
< 4 hours
C: [Cardiogenic Shock] / [Acute CHF] / Arrhthymia
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Post MI evolution
4-12 hours
A: Gross Changes
B: Microscopic Changes (2)
C: Complications
4-12 hours
B: [Beg. of CIN] / [Wavy Fibers]
C: Arrhythmia
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Post MI evolution
1-3 DAYS
A: Gross Changes
B: Microscopic Changes (2)
C: Complications
1-3 DAYS
A: No Gross
B:
- Neutrophil Infiltration
- [Loss of myocyte Nuclei]
C: [Fibrinous Pericarditis–> [sharp & pleuritic Chest Pain] + friction rub] (only with transmural infarcts)
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Post MI evolution
3-7 DAYS
A: Gross Changes
B: Microscopic Changes
C: Complications (3)
D: Lab
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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Post MI evolution
7-10 Days
A: Gross Changes
B: Microscopic Changes (2)
C: Complications
D: Lab
7-10 Days
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A:No Gross
B:
- [Early Granulation tissue w/collagen / fibroblast /MyeloFibroblast]
- Well developed Phagocytosis
C: No Complications
D: [Trop I] returns to baseline
Post MI evolution
2 - 8 WEEKS
A: Gross Changes
B: Microscopic Changes
C: Complications (3)
2 - 8 WEEKS
A: White Scar w/[Type 1 Dense Collagen]
B: Fibrosis
C: Aneurysm / [Mural Thrombus] / Dressler’s
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Valvular Vegetations of the AV valves
Aortic Regurgitation
Mumur
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[Early Diastolic Descrescendo Murmur-High Pitched Blowing noise] auscultated @ [L Sternal 2nd/3rd ICS]
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Name the proteins most likely responsible for these Localized Amyloidosis
- Cardiac Atria
- Thyroid
- Pancreatic Islets
- [Cerebrum and blood vessels]
- Pituitary gland
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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Identify
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Non-Caseating Granulomas
What cellular ultrastructural change indicates [irreversible myocardial cell injury]
Mitochondrial Vacuolization
Vacuoles and [Amorphous densities containing phospholipids] within the Mitochondria
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: Myeloperoxidase
B: Neutrophil Azurophilic Granules
C: Respiratory Burst for Bacterial Infections
Describe the process of how Endothelial Cell injury leads to Formation of an Atheroma
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Name the 7 most common manifestations of Marfan Syndrome
“Marfan BAATHES a lot! “
- Ectopia Lentis
- Arm-to-Height Ratio that’s INC
- Heart issues (MVP vs. [idiopathic Aortic cystic medial degeneration]–> Aortic Dissection and Aneurysm)
- Scoliosis vs. Kyphosis
- Breastbone w/structural abnormalities
- Arachnodactyly (Steinberg thumb & wrist)
- Tall / slender / flat feet
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Describe the circled below
______ are _______ that contain ________ - which are ________
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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What 3 maneuvers INCREASE intensity of Aortic Regurgitation
“AR your Hands & Breath [Leaning Forward] ?
- with Hand Grip
- when Breath is held after exhalation
- with Patient leaning forward
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List the common causes of Restrictive Cardiomyopathy (8)
RAMILIES
- Radiation Fibrosis
- Amyloidosis (heterogenous misfolded proteins)
- Sarcoidosis= [Noncaseating granuloma formation] in multiple organs 2º to [CD4 Helper T] attack on unidentified antigen
- Metastatic Tumor
- Inborn metabolism errors
- Endomyocardial fibrosis= Common in [African/Tropic children]
- [Loeffler Endomyocardial fibrosis] = (Has [Peripheral blood eosinophilia and infiltrate])
- Idiopathic
Describe [Libman Sacks Endocarditis]
[Non-bacterial wart-like vegations] accumulate on either side of a heart valve –> Fibrotic Valve Thickening–> MI
Associated with SLE Lupus
[BUerger Thromboangiitis Obliterans] Tx
Smoking Cessation
Lichtenberg Figure
Erythematous Cutaneous [fern-leaf pattern] from Lightning Strike
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Identify the manifestation and name what dz it’s associated with
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[Nailbed Subungal Splinter Hemorrhage] - Bacterial Endocarditis
“Bacteria FROM JANE”
3 Major signs of Coarctation of Aorta
- Upper body HTN–> HA & Epistaxis
- Diminished LE pulses (from inadequate LE perfusion)
- [Enlarged Intercostal Artery Collaterals]
Occlusion of the [R Coronary Artery] would cause:
Transmural ischemia in what part of the heart?
[R Vt inferior wall] —> [R Vt MI and HF]
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Occlusion of the [Proximal LAD Artery] would cause:
Transmural ischemia in what part of the heart?
Anteroseptal
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Occlusion of the [L Circumflex Artery] would cause:
Transmural ischemia in what part of the heart?
[L Vt Lateral Wall]
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Chest CT Scan + IV contrast
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A: 3 Heart Structural Effects of Aging
B: At what age do these changes onset?
- Sigmoid shaped septum
- Hypertrophied Myocyte
- DEC LV Chamber Size
B: AFTER 65
Which Murmur?
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(Auscultation Site is attached)
B: Maneuvers that INC (2)
Mitral Regurgitation
[Holosystolic High-Pitched Blowing Murmur]
“MR. Hand me a Squat”
B: INC with…
1) Hand Grip
2) Squatting
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Which Murmur? (Is Not VSD)
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(Auscultation Site is attached)
B: Maneuvers that INC
Tricuspid Regurgitation
[Holosystolic High-Pitched Blowing Murmur]
B: INC with… Inspiration
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Which Murmur?
(Auscultation Site is attached)
B: Maneuvers that INC (2)
C: Maneuvers that DEC
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Aortic Stenosis
[Crescendo-Descrescendo Systolic Ejection Murmur]
“Lean forward…& then Squat with that Ass, that’ll turn it up!”
B: INC with…
- Leaning Forward
2) Squatting
C: DEC with…handgrip (INC afterload)
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Mitral Valve Prolapse
Murmur
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“He was MVP…OF COURSE he had a Mid Clique to hang with”
[Late Systolic Crescendo Murmur + MidSystolic Click] @ Apex
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Which Murmur?
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(Auscultation Site is attached)
Mitral Valve Prolapse
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[Late Systolic Crescendo Murmur + MidSystolic Click]
Which Murmur?
B: Name the Auscultation Site
C: Maneuvers that INC sound
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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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Which Murmur?
(Auscultation Site is attached)
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Hypertrophic Cardiomyopathy
[Holosystolic Harsh Murmur] auscultated @ [L Sternal 2nd/3rd ICS]
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Which Murmur?
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(Auscultation Site is attached)
Ventricular Septal Defect
[Holosystolic Harsh Blowing Murmur]
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Which Murmur?
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(Auscultation site is attached)
Patent Ductus Arteriosus
[Machinery Continuous Murmur] ausculated over [L infraclavicular region]
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Which murmurs are heard at the Apex? (3)
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ALL THINGS Mitral!
- Mitral Regurgitation
- Mitral Stenosis (Apex + LLDP)
- Mitral Valve Prolapse
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Which murmurs are heard at the Tricuspid Area? (4)
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- Tricuspid Regurgitation
- Tricuspid Stenosis
- VSD
- ASD (from flow across Tricuspid valve initially—>progresses to Pulmonic regurgitation from pulmonic valve damage)
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Which murmurs are heard at the Pulmonic Area? (2)
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- Pulmonic Stenosis
- [Physiologic Flow Murmur]
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Which murmurs are heard at the [L Sternal 2nd/3rd ICS] ? (3)
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- Aortic Regurgitation
- Pulmonic Regurgitation
- (HOCM) Hypertrophic Cardiomyopathy
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Which murmurs are heard at the Aortic Area? (2)
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- Aortic Stenosis
- Aortic Valve Sclerosis
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[Aortic Cystic Medial Degeneration] is often seen in ____ pts with ____ syndrome.
B: Describe [Cystic Medial Degeneration] (2)
[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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When do Ventricles release BNP? (2)
(BNP) AND (ANP) are both released during [Heart Failure -Vt Hypertrophy and/or Vt Dilitation
What microscopic changes occur during [REVERSIBLE (sublethal) Ischemic injury] to cardiac myocytes (4)
“It’s not lethal yet (sublethal/Reversible) So Relax And Layback”
- Swelling of Mitochondria
- Relaxation of Myofibrils
- [ATP & Glycogen DEC]
- Lactate Accumulation
Paradoxical Embolism occurs when _____
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)
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: “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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Describe Angiosarcoma
[Rare Blood Vessel Malignancy] usually in [Head/Neck/Breast] but can originate from Liver as well
Clinical Presentation for LARGE PDA (2)
- 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
- HF (SOB + Fatigue)
Note: LARGE PDA can progress from small PDA if untreated
Which Drugs cause [Coronary Artery CORONARY STEAL] (2). Why is this?
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
How does Reperfusion Injury cause its damage (5), and what is the ultimate result?
“MICCO injured himself from Reperfusing”
- [Oxygen Free Radical Generation] by endothelial cells
- [Mitochondrial damage(not vacuolization) - Severe & Irreversible]
- [Inflammation - which attracts neutrophils–>more injury]
- [Complement & Cell membrane damage]
Ultimate Result = Cell Membrane Damage —> Elevated [Creatine Kinase] if brain/heart/muscle are affected
What should you suspect if [Right Vt] is Hypertrophied ( >3-4 mm) and Dilated?
[Cor Pulmonale 2° to Pulm HTN]
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Post MI evolution
12-24 hours
A: Gross Changes
B: Microscopic Changes (3)
C: Complications
D: Lab
12-24 hours
MCN CAT: M/CNC/A/T
A: Myocardial Mottling
B:
- [CIN Continues]
- Nuclei Pyknosis
- [Contraction Band Necrosis]
C: Arrhythmia
D: [Trop I] and [CkMB] peaks at 24 hours
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Post MI evolution
10 - 14 Days
A: Gross Changes
B: Microscopic Changes (2)
C: Complications
10 - 14 Days
{Use TriChrome Stain}
A: No Gross
B:
- [Granulation tissue with neovascularization and Fibroblast]
- Red Border from Granulation tissue entering from edge of infarct
C: No Complications
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In which Arteries do Atherosclerotic Plaques develop? (7)
[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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What is the single most important risk factor for developing Aortic DISSECTION
HTN
(causes intimal tears)
scan shows intimal flap torn away from Aortic wall
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Pathogensis of Aortic Aneurysm
[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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What does a [FIXED and Widened S2 Spliting] likely indicate?
[ASD] murmur
= [FIXED and widened S2 Spliting (since pulmonic will always take longer to close if there’s extra fluid in R vt)
A: Describe the Heart changes in JONES syndrome from Rheumatic Fever (2)
B: What are the 2 dangerous developments of this?
Mitral Stenosis from
- Mitral Valve Leaflet Distortion 2° to fusion of leaflet edges
- L Atria with [diffuse fibrous thickening]
B: Afib –> [Embolic Stroke]
Describe the [OWR - Osler Weber Rendu syndrome]
[Hereditary Hemorrhagic Telangiectasia] described as pink and spider-like lesions
A: Explain the physiology for [Carotid Sinus] massage
B: Where, in the CNS, does the nerve responsible for this physiology terminate?
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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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: [Shorter Duration of Diastole 2° to Tachycardia] -Max blood flow to coronary arteries occurs during Diastole
B:
- Flow-mediated Dilation
- VasoDilators (Adenosine / NO)
What is the Coronary Sinus, and what’s unique about it’s O2 content
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
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How does [AV Shunts] affect Preload and Afterload
* INC Preload–> [High Output Cardiac Failure]
*DEC afterload (since they’ll be less blood in Arterial system once it travels to the venous system)
A: Which Collagen type do you find in Mature Scars?
B: Is this type of Collagen Abundant?
A: Type 1 Collagen
B: Most prevalent Collagen in Body
Describe Collagen Type 1
A: Location (3)
B: Associated DO
[be so totally] Cool, Read Books
Type 1 = MOST PREVALENT (especially in mature scars)
A: bone / skin / tendon
B: [Osteogensis Imperfecta type 1]
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: [Total Flow] = [Flow Velocity] x [Cross Sectional Area]
B: [(Area 1) x (Velocity 1)] = [(Area 2) x (Velocity 2)]
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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: 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]
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List the 2 Formulas for Cardiac Output
- [CO = HR x SV]
- [CO = (O2 consumption) ÷ (AV O2 Difference)] = Fick Principle
List, from FASTEST to slowest, [Conduction Speed] between:
- Atria
- AV node
- Purkinje Fibers
- Ventricles
Park At Venture Avenue
PURKINJE > Atrial > Ventricle > [AV node]
[Aortic / pharyngeal Arch 1]
A: Key Derivative from this Arch
B: Associated Cranial Nerve with this Arch
“1st arch is Maximal “
A: Maxillary artery (portion of it)
B: [Trigeminal CN5]
[Aortic / pharyngeal Arch 2]
A: Key Derivative from this Arch
B: Associated Cranial Nerve with this Arch
“Second = Stapedial”
A: Stapedial artery (WHICH COMPLETELY REGRESSES EVENTUALLY)
B: [Facial CN7] “Don’t be 2 faced”
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[Aortic / pharyngeal Arch 3]
A: Key Derivatives from this Arch (2)
B: Associated Cranial Nerve with this Arch
“C = 3rd letter in Alphabet & 3x3 = 9”
A: [Common Carotid] / [Internal Carotid - proximal part]
B: [Glossopharyngeal CN9]
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[Aortic / pharyngeal Arch 4]
A: Key Derivatives from this Arch (2)
B: Associated Cranial Nerve with this Arch
A: [True Aortic Arch] / [R Subclavian Artery]
B: [Vagus CN10 - Superior Laryngeal branch]
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[Aortic / pharyngeal Arch 5]
A: Key Derivatives from this Arch
B: Associated Cranial Nerve with this Arch
EVERYTHING FROM THIS ARCH OBLITERATES!
[Aortic / pharyngeal Arch 6]
Key Derivatives from this Arch (2)
[Ductus Arteriosus] & [Pulmonary Arteries]
” 666 is Recurrent”
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What 2 Heart Defects are associated with Cryptogenic Stroke
A:
- ASD
- Patent Foramen Ovale (occurs in 25% of normal adults)
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Clinical Presentation for [TGA - Transposition of Great Arteries] (3)
Neonate with…
- [Aorta lies ANTERIOR and to the RIGHT of Pulm Artery]
- Cyanosis
- Tachypnea
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Which Artery is injured from a fracture to the Pterion? Name the Parent Artery of this vessel
A: [Middle meningeal a. - frontal branch] (courses thru Foramen Spinosum deep to the Pterion)
B: MAXILLARY ARTERY (Derivative of 1st Aortic/pharyngeal arch)
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Identify
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Identify
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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]
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Where is the SA node located?
[Junction of (R Atrium) and (SVC)]
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Identify
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Remember:
- [R middle Lung lobe] is adjacent to [R Atrium]
- R side of Heart of CXR is [R Atrium]
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A: Cannulation above the inguinal ligament INC risk of developing what condition?
B: What is this condition the most common cause of?
RETROPERITONEAL HEMORRHAGE—> Unexpected Mortality post cardiac-cathertization
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Name the Autoregulator Factors for the Heart (4)
- NO (MOST IMPORTANT AND AUTOREGULATES HEART’S LARGE/MEDIUM VESSELS)
- -Adenosine (small coronary arterioles*)
- DEC O2
- CO2
Which Heart Chamber does a [TEE - TransEsophageal Echocardiography] face when placed?
L Atrium!
Probe is placed in mid-esophagus facing anteriorly, which faces L Atrium
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[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: [(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
Identify
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Where are the 3 leads of a Biventricular PACEMAKER placed?
- R Atrium (via L subclavian vein –> SUP Vena Cava–> R Atrium)
- R Ventricle (via L subclavian vein–> SUP Vena Cava–> R Atrium –> R Vt)
- L Ventricle (via R atrium —> [Coronary Sinus within the AV groove] of Post Heart –> L Vt)
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What part of the heart forms the [diaphragmatic surface]?
[L Vt - INFERIOR WALL]
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What areas of the heart do these Coronary Arteries perfuse?
[LCX - Left CircumfleX] (2)
[LCX] - from [L Main Coronary Artery]
- [L Vt - Lateral AND Posterior Surface]
- [Anterolateral Papillary muscle]
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What areas of the heart does this Coronary Artery perfuse?
[R Coronary A.] (3)
[R Coronary A.]
- SA Node
- PDA -[Posterior Descending Interventricular Artery] (70% population) —> PERFUSES AV NODE
- [R Marginal Acute A.]
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What areas of the heart do these Coronary Arteries perfuse?
[PDA - Posterior Descending Artery] (3)
[PDA]
- [Post 1/3 of Interventricular septum]
- [Post Vt Walls (including Diaphragmatic surface of heart)]
- [Posteromedial Papillary muscle]
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What areas of the heart do these Coronary Arteries perfuse?
[LAD - Left Anterior Descending] (3)
[LAD] - from [L Main Coronary Artery]
- [ANT 2/3 of Interventricular septum]
- [Anterolateral Papillary muscle]
- [L Vt - Anterior Surface]
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What areas of the heart do these Coronary Arteries perfuse?
[R Marginal Acute A.]
Right Ventricle
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A: What does the Red arrow indicate?
B: What does the White arrow indicate?
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A: [L Main Coronary Artery] originating from [L coronary cusp] from Aortic Root and continuous anteriorly as …
B: [LAD]
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What 2 diseases is Streptococcus Gallolyticus Bovis associated with?
- [SBE-SubAcute Bacterial Endocarditis] (Aortic Regurgitation) (SBE also caused by Strep Viridans)
- [GI Lesions –> Colon CA]
AKA S. Bovis
A: Clinical Manifestations of DiGeorge Syndrome (5)
B: Genetic Cause
C: Embryologic cause
“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
List the most important steps for preventing [CVC-Central Venous Catheter] Infections (5)
‘CVC’s need a good BRACH b4 being inserted!”
- Hand Washing prior to insertion
- Barrier precautions during Central line insertion
- Chlorhexidine for skin disinfection
- Avoid [Femoral catheter insertions] (instead use SubClavian or Internal Jugular Vein)
- Remove Catheter when no longer needed for good
In terms of Accuracy and Precision, what is another term for Precision?
RELIABILITY
- R is just a P with a kickstand!*
- Precision = Reliability*
Bicuspid Aortic Valve
Mumur
[Early Systolic High-frequency click] @ [R Border 2nd ICS]
Monoamine Oxidase is a ___ enzyme that degrades excess ______ and detoxifies _______
Monoamine Oxidase is a Mitochondrial enzyme that degrades excess [monoamine NTS in presynpatic n. temrinals] and detoxifies [Dietary Tyramine in the GI tract]
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Explain Coronary Dominance
The Dominating coronary a. tht perfuses the [PDA-PosteriorDescending interventricularArtery]
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Describe the path a thrombus would take in order to cause [RAO-Retinal Artery Occlusion] (3)
[Internal Carotid Artery] –> [Opthalmic Artery] –> [Retinal Artery]
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Atrial Fibrillation INC risk of ______ Thromboembolism
B: What location is the source of [Afib thrombus formation]?
Atrial Fibrillation INC risk of Systemic Thromboemoblism
B: L Atrial Appendage
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What is a good parameter for certain BP medication non-compliance? Describe it.
A: PRA - Plasma Renin Activity
B: PRA measures the amount of [Angiotensin 1] made in a certain time = assess [Renin-Angiotensin-Aldosterone Axis].
A: Describe Fetal Circulation starting with Placenta
B: Which Structure has the MOST OXYGENATED BLOOD?
B: Umbilical VEIN
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Remember: Single Umbilical A. = Chromosomal & Congenital anomalies
What happens to [Cardiac-Vascular Function Curve] Intersection when there’s a:
A: [Change in Venous Return]
B: Give 2 examples of each
A: If there’s [Change in Venous Return (venous/volume/vascular)] —> Intersection slides along [Cardiac Output Curve]
Ex: [Acute Hemorrhage] / Sympathetics / [Fluid Infusion]
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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: 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 ⬆︎]
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3 classic Clinical Manifestations of [Tetralogy of Fallot]
A:
- [Systolic Ejection Murmur] from [RVOT -R Vt Outflow Obstruction]
- Squatting relieves sx (INC afterload–> [DEC amount of R to L shunt]
- [Cyanotic Tet Spells]
“VOIR is to have See + Sight & Cry”
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Describe the 3 Clinical Manifestations of [PDA- Patent Ductus Arteriosus]
[R–> Left Shunting] causes….
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- [Machinery Continuous Murmur] over [L infraclavicular region]
- Palpable Thrill over [L infraclavicular region]
- HF sx (Failure To Thrive and Respiratory Distress)
What protein is Defective (2) in [Familial Chylomicronemia Syndrome] and why does Heparin exacerbate this?
A: [Lipoprotein Lipase (LPL) Deficiency] or [ApoC2]
B: exacerbated by [Exogenous Heparin] since LPL is naturally bound to Heparin
Sx = HHALX
Which demographics are likely to develop Lipofuscin? (3)
Aging / Cachectic / Malnurished pts
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[HOCM - HyperObstructive CardioMyopathy] MOD
[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]
Upregulators of Cytochrome P450 Enzymes (8)
Chronic alcoholics Steal Phen-Phen & Never Refuse Greasy Carbs
- Chronic alcohol use
- St.John’s wort
- Phenytoin
- Phenobarbital
- Nevirapine
- Rifampin
- Griseofulvin
- Carbamazepine
Inhibitors of Cytochrome P450 Enzymes (11)
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)
What Substrates does the Cytochrome P450 enzymes work on? (6)
Can Always Think When Outdoors, Son….i need it!
Cyclosporine (Liver AND small intestine)
AntiEpileptics
Theophylline
Warfarin
OCP
Statins (NOT PRAVASTATIN)
What type of Cardiovascular predispositions do Down Syndrome pts have? (2)
- Atrial Septal defect
- Vt Septal Defect
2 Conditions that cause Paradoxical Splitting
“PAradoxical Splitting”
- LBBB
- Aortic Stenosis
“Taking AP Classes were normal for me”
4 anatomic abnormalities associated with [Tetralogy of Fallot]
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”
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How does Cortisol utilize Permissiveness?
Cortisol upregulates [alpha-1 adrenergic receptors] on vascular and bronchial smooth m. –> better response to Catecholamines(such as NorEpi)–> MORE Vasoconstriction
What are the Sx of [SHAC Syndrome] (4)
Syncope / Nausea / Dizziness / Fetal Demise (when severe)
Blunt Aortic Injury
Rapid Deceleration while restrained/seatbelted (occurs in MVC) causes Aortic Isthmus to tear —> Aortic Rupture
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Which pts benefit from SacubiTrill
Heart Failure Pts
A: What is the Typical Heart Rate for [aFib with RVR]
B: What does the Ventricular Rate depend on in [Atrial Fibrillation]
A: 90-170 bpm
B: AV Node Refractory Period
A: What is Lymphangiosarcoma
B: What predisposes a pt to Lymphangiosarcoma
A: MALIGNANT neoplasm of the [endothelial lining of lymphatic channels]
B: Persistent Lymphedema w/chronic Dilation of lymphatic channels
Heart Manifestations of VSD (2)
- [INC R Vt O2 Sat] with [NORMAL L Vt O2 Sat]
- LARGE VSD –> Heart Failure
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Aortic Stenosis
Manifestations (5)
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*) [Pulsus parvus et tardus]= weak pulses with delayed peak
*) SAD: [Syncope / Angina / (Dyspnea on exertion)]
*) [S4 Atrial Kick]
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Causes of Aortic Stenosis (3)
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[Age-Related calcification ( >65 y/o)]
vs.
[Bicuspid Aortic Valve] calcification ( >50 y/o)]
vs.
[Rheumatic Fever Endocarditis (Fish Mouth)]
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Describe the histology for [Hemosiderin-laden alveolar macrophages]
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
Auscultation Site for S3 gallop (3)
[Apex + (LLDP) + (End Exhalation)]
End Exhalation brings heart closer to chest wall
Best indicator for severity of valve Regurgitation?
Presence of an additional S3 (indicates Vt Dilitation in addition to regurgitaiton)
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Auscultation site for Mitral vs. Tricuspid Regurgitation each
- Mitral Regurgitation:* [Apex w/radiation to axilla]
- Tricuspid Regurgitation:* [Tricuspid Area w/radiation to R Sternal border]
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Causes of Tricuspid Regurgitation
[RV Dilatation]
Which Dz’s cause EITHER OR Mitral vs. Tricuspid Regurgitation (2)
Rheumatic Fever and [Infective Endocarditis]
Clinical Manifestation of Cardiac Tamponade (3)
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“Heavy Bleeding in PericardialSpace
- [Beck Triad: hypOtension / JVD / Distant Heart Sounds]
- [HR INC but CO DEC]
- Pulsus Paradoxus (Pulsus for CAPOT)
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EKG Manifestation of Cardiac Tamponade (2)
[low-voltage QRS] + [Electrical Alternans from Heart swinging in fluid]
Describe Lipofuscin (3)
Yellow-brown / fine granular / perinuclear pigment
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What conditions cause Pulsus Paradoxus (5)
“Pulsus for CAPOT”
- Croup
- Asthma
- Pericarditis
- Obstructive sleep apnea
- Tamponade
What Conditions are associated with S4 Atrial Kick (2)
- Aortic Stenosis
- Restrictive Cardiomyopathy (includes HOCM)
A: Explain the opening snap for Mitral Stenosis
B: Best Tool for assessing Degree of Mitral Stenosis
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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]
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Mitral Stenosis is associated with which condtion
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Rheumatic Fever
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Which 2 bedside maneuvers ⬆︎ Intensity of the HOCM mumur?
“Val [Stood Up] to Hulk HOCM, the MVP, which ⬆︎ his anxiety”
Valsalva
[Standing Up]
(both ⬇︎ Preload AND ⬇︎ Afterload)
Hypertrophic Obstructive CardioMyopathy (HOCM)
Mode of Inheritance
AUTO DOM
How does [Prinzmetal Variant Angina] manifest on EKG. Why is this?
[Temporary transmural myocardial ischemia (typically near atherosclerosis)] –> manifest as transient ST-elevations
A: What drug provokes [Prinzmetal Variant Angina] episodes and possibly aids in diagnosis?
B: How do you treat [Prinzmetal Variant Angina]
A: ErGonovine (stimulates [alpha adrenergic] and serotonergic receptors–>coronary spasm induction)
B: Nitrates and CCB
Clinical Presentation of [Carcinoid Heart Disease] (3)
[Cutaneous Flushing] / Diarrhea / Bronchospasms
What 3 Congenital defects are also associated with [Coarctation of Aorta]?
[Turner Syndrome] (pre-PDA)
[Berry Saccular Aneurysm]
[Bicuspid Aortic Valve]
Histology for [Dystrophic Calcification]
Dark-purple aggregates that may develop outer layers known as psammoma bodies
A: [Strawberry Hemangioma] Demographic
B: Prognosis
A: Infants
B: Grows proportionally with child and regresses by age 5-8
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Which 2 organs have DUAL blood supply?
Lungs and Liver = NOT SUSCEPTIBLE TO INFARCTS
[Jervell and Lange-Nielseon Syndrome]
Mode of inheritance
auto recessive
PGN of [Jervell and Lange-Nielseon Syndrome] (3)
[Prolonged QT] –> Torsades De Pointes –> [Syncope and Sudden Cardiac Death]
Dilated Cardiomyopathy Clinical Findings (3)
“the PIG PAID for Dilated Cardiomyopathy”
HF / S3 / [Systolic Regurgitant Murmur]
MOST COMMON CARDIOMYOPATHY
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3 Main Causes of Aortic Regurgitation
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- [Aortic Root Dilitation]
- [Bicuspid Aortic Valve]
- Endocarditis (i.e. Rheumatic Fever)
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Aortic Regurgitation Clinical Presentation (2)
- [Widened Pulse Pressure (may manifest as head bobbing with each heart beat = [de Musset sign])]
+
- [Large Stroke Volumes (may manifest as head / heart pounding )]
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A: What dz are these formations associated with?
B: What is the Cardiac Dz Progression?
Aschoff Bodies
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A: Acute Rheumatic Fever - 2º to Strep A
B: Mitral Regurgitation —> Mitral Stenosis
What Dz is associated with [Libman Sacks Endocarditis]
Systemic Lupus Erythematosus
A: 2 Demographics at risk for [BUerger Thromboangiitis Obliterans]
B: These pts show a hypersensitivity to what?
A: [Heavy Smokers] / [Males
B: [Intradermal injection of Tobacco Extract]
Describe [BUerger Thromboangiitis Obliterans] and what 3 things it leads to
[STMV- Segmental Thrombosing (Medium vessel) Vasculitis] that leads to:
- Intermittent claudication –> Extremity Gangrene
- Corkscrew Collaterals on imaging
- -*Raynaud Phenomenon
Name the manifestations of Bacterial Endocarditis (7)
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“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]
Occlusion of the [R Coronary Artery] would cause:
A: ST elevation in which leads? (3)
B: Any other associations?
A: Leads 2 / 3 / avF
B: Sinus Node Dysfunction (also supplied by RCA)
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Occlusion of the [Proximal LAD Artery] would cause:
ST elevation in which leads? (4)
V1 - 4
Occlusion of the [L Circumflex Artery] would cause:
ST elevation in which leads? (4)
V5 / V6 / Lead 1 / aVL
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Causes of MVP (3). MVP can predispose to what condition?
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“He was MVP…OF COURSE he had a Mid Clique to hang with”
- Myxomatous Degeneration (Marfan vs. [Ehlers Danlos])
- Rheumatic Fever
- Chordae Rupture
Usually benign but can predispose to infective endocarditis
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Which Maneuvers make MVP murmur delayed
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Squatting
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Which Maneuvers make MVP murmur occur earlier (2)
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“They were all Standing and Bearing Down before the MVP got there”
Occurs earlier with…
1) Standing
2) Valsalva
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Maneuvers that INC HOCM murmur (2)
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Hypertrophic Cardiomyopathy
[Harsh Holosystolic Murmur] auscultated @ [L Sternal 2nd/3rd ICS]
INC with… [Manuevers that DEC PA-Preload ANDAfterload]
- Valsalva
- Standing
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Maneuvers that DEC HOCM murmur (2)
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Hypertrophic Cardiomyopathy
[Harsh Holosystolic Murmur] auscultated @ [L Sternal 2nd/3rd ICS]
:DEC with..
- No Valsalva
- sitting
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What 2 conditions does [Aortic Cystic Medial Degeneration] potentially lead to?
[Aortic Dissection] and [Aortic Aneurysm]
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[Basket Weave Pattern**] on Histo
Describe the Histology for [Aortic Cystic Medial Degeneration]
[Elastic Tissue Fragmentation (from Myxomatous changes)]
–> [Basket Weave Pattern]
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Angiosarcoma Risk Factors (6)
“Angie was only attracted to SLAVER’s”
- [Elderly on sun exposed areas]
- Sun Exposure
- Radiation therapy
- Lymphedema PostMastectomy (LymphAngiosarcoma)
- Vinyl Chloride (HEPATIC Angiosarcoma)
- Arsenic (HEPATIC Angiosarcoma)
A: Prognosis for Angiosarcoma
B: Which markers do these tumors express (2)
“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]
Which demographic is most at risk for developing Cor Pulmonale idiopathically?
[Females ages 20-40]
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Which demographics develops Cor Pulmonale secondarily? (2)
COPD pts / smokers –> [Obliteration of pulmonary vasculature] –> Cor Pulmonale
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List the 5 vessels from MOST to least susceptible to Atherosclerotic Plaques
[Abd Aorta] > Coronary > Popliteal > [Internal Carotid] > [Circle Of Willis]
Which mucous membranes are affected by OWR - Osler Weber Rendu syndrome.
What’s the worst complication?
Telangiectasias on…
- [Skin/Lips/Oronasopharygeal]
- GI
- Respiratory
- Urinary
May rupture –> Bleeds
[OWR - Osler Weber Rendu syndrome] Mode of Inheritance
AUTO DOM
Complications of [OWR - Osler Weber Rendu syndrome] (3)
Rupturing of Telangiectasia –>
Epistaxis
GI bleeding
Hematuria
DO of blood vessels –> AV malformations –> Telangiectasia
What therapeutic tool is associated with the Coronary Sinus
[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
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When can the Coronary Sinus become Dilated?
[Pulmonary HTN] –> [R Vt AND R Atrial Pressure INC] —> [Coronary Sinus Dilatation]
Remember: Heart muscle is perfused during Diastole
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Describe AV Shunt. Name 2 ways they’re formed
A: Abnormal communication from [Artery –> vein] that bypasses arterioles
B:
- Iatrogenic (AV Fistula for Hemodialysis)
- Penetrating injuries
Describe Collagen Type 2
A: Location
B: Associated DO
[be so totally] Cool, Read Books
Type 2 “Cartwolage”
A: Cartilage (including hyaline and vitreous body)
B: none
Describe Collagen Type 3
A: Location (3)
B: Associated DO
[be so totally] Cool, Read Books
Type 3 “Read ThreE D”
A: Reticulin (blood vessels / granulation tissue / fetal tissue)
B: [Ehlers Danlos]
Describe Collagen Type 4
A: Location (2)
B: Associated DO (2)
[be so totally] Cool, Read Books
Type 4 “Type 4 is under the floor”
A: [Basement Membrane and lens]
B: [Alport Syndrome] & Goodpasture
[Aortic / pharyngeal Arch 6]
Associated Cranial Nerve with this Arch
[CN10 Vagus - Recurrent Laryngeal branch]
” 666 is Recurrent”
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How are Cryptogenic Stroke lesions typically closed?
- ASD
- 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]
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What causes [TGA - Transposition of Great Arteries] embryogenically?
Failure of [Fetal Aorticopulmonary septum] to sprial normally during [Truncus Arteriosus Septation]
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What Mothers are at high risk of having Neonates with [TGA - Transposition of Great Arteries]?
Diabetic Mothers
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What Bone segments make up the Pterion? (4)
Frontal, Sphenoid, Temporal, Parietal
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What is the Ultimate result of a [fractured Pterion]?
[Epidural Hematoma]
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Where is the [R Vt] located
[L sternal 4th ICS - Anterior Heart]
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Where is the [Pulmonary Trunk] located?
[L sternal 2nd/3rd ICS]
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What structure makes up most of the heart’s posterior surface? How is this structure related to dysphagia?
[L Atrium] ([[Mitral Stenosis vs. aFib] –> [L atrial enlargement] –> can compress esophagus –> dysphagia)
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Name the Autoregulator Factors for the Brain
[CO2 (pH)]
Name the Autoregulator Factors for the Kidneys (2)
[Myogenic & Tubuloglomerular feedback]
Name the Autoregulator Factors for the Lungs
[DEC O2]
Name the Autoregulator Factors for the Skeletal Muscle (6)
Sk. Muscle = [Lactate / Adenosine / K+ / H+ / CO2 / (Sympathetic tone when at rest)]
What perfuses the [diaphragmatic heart surface]? What is its PARENT artery?
[PDA-PosteriorDescending interventricularArtery]
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What was the former name of Streptococcus Gallolyticus, and where does it “live”?
S Bovis; Lives in Colon Normal Flora
Pts with Bicuspid Aortic Valve are at INC risk of what 3 things?
[Stenosis vs. Insufficiency vs. Infection]
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How is Monoamine Oxidase associated with Tyramine HTN Crisis
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)
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List the Population breakdown for Coronary Dominance (3)
- 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
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If a pt with Left Dominant Circulation has [AV node ischemia], which artery is responsible?
[AV node] is perfused by PDA and in Left Dominant Ciruclation populations (10%), PDA is perfused by [L Circumflex Artery]
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Clinical Presentation of a [RAO-Retinal Artery Occlusion] (2)
[Acute, painless, (monocular vision loss)]
+
[Macula cherry red spot with a surrounding white retina]
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What factors INC [PRA - Plasma Renin Activity] (2). How is it used to assess BP med non-compliance?
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
How does [____Stenosis] determine the degree of severity in [Tetrology of Fallot]
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”
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PDA Tx (2)
Indomethacin (PGE2 inhibitor)
vs.
[Surgical Ligation in older pts]
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2 Main Causes of [PDA]
Prematurity & [Congenital Rubella]
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Which organs is Lipofuscin normally found (4)
Heart
Liver
Kidney
Colon
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HOCM Sx (3)
- [Syncope during exercise]
- [Sudden Cardiac Death] 2º to Vt Arrhythmia
- [S4 Atrial Kick]
[Familial Chylomicronemia Syndrome] Mode of Inheritance
auto recessive
[Familial Hypercholesterolemia (2A)] Mode of Inheritance
AUTO DOM
Common Causes of [Constrictive Pericarditis] - 5
‘Ur an Idiot to constrict my Radio & T-V”
Uremia
Idiopathic
Radiation
TB
Viruses
What’s the most frequent [1° Cardiac Peds Tumor]?
[Tuberous Sclerosis: Rhabdomyoma] –> Valvular Obstruction
ALPHA 1 RECEPTOR
Tissues - Actions (3)
“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
ALPHA 2 RECEPTOR
Tissues- Actions (5)
“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
BETA 1 RECEPTOR
Actions (2)
(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
BETA 2 RECEPTOR
Tissues-Actions (4)
“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]
BETA 3 RECEPTOR Tissues-Actions
Fat cells- stimulates Lipolysis
(B1 and B2 may also contribute)
DOPAMINE 1 RECEPTOR
Tissues-Actions
Renal and other splanchnic blood vessels- vasoDilates (reduces resistance)
D for Dopamine Receptor
DOPAMINE 2 RECEPTOR
Tissues-Actions
Nerve terminals- inhibits adenylyl cyclase
What target organ does the M1 Receptor work in
“[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges”
Brain
What target organ does the M2 Receptor work in
“[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges”
Heart
What target organ does the M3 Receptor work in (6)
“[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
Name the 4 Medications that Prevent LV Remodeling in HF pts
“BANA helps HF pts live Loonger”
Beta Blockers (Metoprolol / Carvedilol)
[ACEk2 inhibitors AND ARBs]
[Nitrates + Hydralazine]
[Aldosterone Blockers (Spironolactone / Eplerenone)]
When does Lymphangiosarcoma present
~10 years after [radical mastectomy w/axillary lymph node dissection]
M INC Severity of [Carcinoid Heart Disease] correlates with what compound?
[INC Urinary/Plasma 5HiAA (5HydroxyindoleAcetic Acid)] = INC Severity
CarcinoiD Syndrome: (Cutaneous Flushing)/Diarrhea/(SOB wheezing)
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When do you hear a loud P2?
Pulmonary HTN
[T or F] ASA, alone, is sufficient to treat DVT/PE in high risk pts
NO
[Fetal Alcohol Syndrome] is asociated with which Congenital Heart Defect
VSD (the most common)
Where is the AV node located?
near Interatrial septum around the coronary sinus opening
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Acute Coronary Syndrome consist of what 3 conditions
“We have ACS in the USA”
- [Unstable vulnerable Angina]
- Sudden Cardiac Death
- Acute MI