USMLE STEP 1 – CARDIO UPDATED STUDY GUIDE
QUESTIONS AND CORRECT ANSWERS
C
α1 Agonist Effects
-Vascular SM contraction
-Myadrisis
-↑↑ Urethral sphincter
-↑↑ BP
-Inhibition of Pacemaker activity leading to slowed conduction through the
AV Node (After stimulation of Carotid baroreceptors)
Right Dominant Circulation PDA arises from RCA
Left Dominant Circulation PDA arises from LCX
Standing from Supine Position Physiological Changes
-↓↓ Venous Return
-↓↓ Baroreceptor activity
-↓↓ Cerebral Bloow Flow
**The body responds to these changes by ↑↑ BP + ↑↑ Pulse + ↑↑ Cardiac
Output**
Na+/Ca2+ Exchanger Antiporter which helps to re-establish the baseline Resting Potential which is
a key step during Phase 4 of the AP
Nesiritide MOA
-BNP Analogue
Effects
-Vasodilation
-↑↑ Urinary flow
Congenital Bicuspid Valve Early-onset Aortic Stenosis
ASD ECG
-Right Axis deviation
-Right Ventricular Hypertrophy
Cardiac Valves Cardiac Valves
A - Aortic Valve A-
B - Pulmonary Valve B-
C - Tricuspid Valve C-
D - Mitral Valve D-
, Granulomatosis w/ Polyangitis C-Anca "+"
Dx
-Lungs affected
-Kidneys affected
-Nose affected
Histo
-Necrotizing Arteritis w/ Epithelioid Histiocytes
Polyarteritis Nodosa Hep B-associated
Dx
-Kidneys affected
-Spares the Lungs
Histo
-Fibrinoid necrosis w/ Luminal narrowing
Transposition of the Great Vessels CXR
-Narrow Mediastinal shadow
Widely-split S2 ASD or Pulmonic Stenosis auscultation
Baroreceptor Firing Produces an increase in Parasympathetic impulses to the SA + AV Nodes
Effects
-Temporary inhibition of SA Node activity
-Slowed conduction through AV Node
-Prolonged AV Node Refractory Period
Mitral Regurgitation Etiology
-Rupture of the Papillary muscles
QUESTIONS AND CORRECT ANSWERS
C
α1 Agonist Effects
-Vascular SM contraction
-Myadrisis
-↑↑ Urethral sphincter
-↑↑ BP
-Inhibition of Pacemaker activity leading to slowed conduction through the
AV Node (After stimulation of Carotid baroreceptors)
Right Dominant Circulation PDA arises from RCA
Left Dominant Circulation PDA arises from LCX
Standing from Supine Position Physiological Changes
-↓↓ Venous Return
-↓↓ Baroreceptor activity
-↓↓ Cerebral Bloow Flow
**The body responds to these changes by ↑↑ BP + ↑↑ Pulse + ↑↑ Cardiac
Output**
Na+/Ca2+ Exchanger Antiporter which helps to re-establish the baseline Resting Potential which is
a key step during Phase 4 of the AP
Nesiritide MOA
-BNP Analogue
Effects
-Vasodilation
-↑↑ Urinary flow
Congenital Bicuspid Valve Early-onset Aortic Stenosis
ASD ECG
-Right Axis deviation
-Right Ventricular Hypertrophy
Cardiac Valves Cardiac Valves
A - Aortic Valve A-
B - Pulmonary Valve B-
C - Tricuspid Valve C-
D - Mitral Valve D-
, Granulomatosis w/ Polyangitis C-Anca "+"
Dx
-Lungs affected
-Kidneys affected
-Nose affected
Histo
-Necrotizing Arteritis w/ Epithelioid Histiocytes
Polyarteritis Nodosa Hep B-associated
Dx
-Kidneys affected
-Spares the Lungs
Histo
-Fibrinoid necrosis w/ Luminal narrowing
Transposition of the Great Vessels CXR
-Narrow Mediastinal shadow
Widely-split S2 ASD or Pulmonic Stenosis auscultation
Baroreceptor Firing Produces an increase in Parasympathetic impulses to the SA + AV Nodes
Effects
-Temporary inhibition of SA Node activity
-Slowed conduction through AV Node
-Prolonged AV Node Refractory Period
Mitral Regurgitation Etiology
-Rupture of the Papillary muscles