UWorld Step 1 - Deck 1 Exam
What is the first line treatment for panic disorder? SSRIs and/or CBT
Acute distress: benzodiazepines (except if history of EtOH/BZD abuse)
What warfarin reversal agents are available? In what Vitamin K: longer time - requires factor synthesis.
time frame? PCC (prothrombin complex concentrate) FFP: instantly gives back factors.
What is heparin's reversal agent? Protamine
What is psoas sign? passive extension of the hip leading to RLQ/R flank pain
What is the pathogenesis of praoxysmal nocturnal Lack of complement inactivating proteins (CD55, CD59) -> complement against
hemoglobinuria? RBCs -> hemolysis.
What is the treatment? Tx: monoclonal antibody against C5 - eculizumab
How do the following hormones act in hypoglycemia? Glucagon: stimulates hepatic glycogenolysis and gluconeogenesis
Glucagon Epinephrine: further stimulates G&G
Epinephrine Cortisol: binds to intracellular receptors - transported to nucleus - increases
Cortisol transcription of enzymes for gluconeogenesis, lipolysis, proteolysis
What are the functions of Type II pneumocytes? Surfactant production and regeneration. Can make Type I pneumocytes.
What is prerenal azotemia? a condition caused by decreased perfusion to the kidneys.
Azotemia: retention of nitrogenous waste products.
BUN/Cr ratio >20
What nerves travel through the temporal bone? CNVIII, CNVII (facial nerve).
When are these structures in danger? Facial trauma
What is cystinuria? Defective transporter for cola AAs - impaired renal and intestinal absorption
What amino acids are affected? COLA: cysteine, ornithine, lysine, arginine
What are the features? Features: cystine kidney stones (flat, yellow, hexagonal)
Hardy-Weinberg equilibrium: No mutation at the locus
What assumptions are being made? No natural selection occurring
No net migration
Randome mating
Large population
Hardy-Weinberg equilibrium: p^2 + 2pq + q^2 = 1
Equation? p= frequency of allele A
q = frequency of allele a
p+q = 1
Hardy-Weinberg equilibrium: males = q
X-linked disease frequency in males vs. females? females = q^2
What are factors that favor development of Elevated capillary hydrostatic pressure (arterial dilation, impaired venous return).
edema/impact interstitial fluid volume?
Name 4 Decreased plasma oncotic pressure (nephrotic syndrome, cirrhosis, malnutrition)
Sodium and water retention.
Lymphatic obstruction (impairs removal of excess interstitial fluid)
, UWorld Step 1 - Deck 1 Exam
What are factors that favor development of pleural Increased hydrostatic pressure gradient (heart failure)
effusions? x4
Decreased oncotic pressure gradient (nephrotic syndrome)
Which cause transudative formation vs. exudative?
Increased inflow vs. decreased outflow? Increased vascular permeability (infection)
Lymphatic obstruction.
What is the pathogenesis of peripheral edema in COPD? Chronic hypoxia -> pulmonary vasoconstriction -> increased pulmonary artery
pressure 0> cor pulmonale (R HF), increased CVP -> increased capillary
What is the initial compensatory mechanism? hydrostatic pressure -> peripheral edema.
Increased lymphatic drainage.
What are the four features of tetralogy of Fallot? Pulmonary infundibular stenosis.
R ventricular hypertrophy (boot shaped heart on CXR)
Hint: PROVe Overriding aorta
VSD
How do tet spells occur? Increased activity (O2 demand) - pulmonary stenosis increases RV pressure - R
What motion can improve a tet spell and how does it to L flow through VSD (deoxygenated blood into circulation) - desaturation,
work? cyanosis, crying.
Improve with squatting - increases SVR (kinks femoral arteries, increases LV
pressure), reduces R to L shunt, improves oxygenation
Why do we avoid around the clock administration of Want to avoid developing tolerance. Mechanism of tolerance is not understood.
nitrates for patients with exertional angina?
Free period at night - least cardiac work.
When would papillary muscle rupture occur post MI? 3-5 days
What is the blood supply for the anterolateral papillary AL: left anterior descending, left circumflex artery.
muscle?
PM: posterior descending.
Posteromedial papillary muscle?
Diastolic blood pressure is the (a) and is directly related a: baseline hydrostatic pressure in the arterial system
to (b). b: SVR and arterial blood volume
Pulse pressure is (a) SBP (left ventricular contraction) - DBP.
It is directly related to (b)
b: stroke volume
What changes in blood pressure occur when you Reduced SVR: skeletal muscle arteriole vasodilation.
exercise?
SVR? Preload? SBP/DBP/PP? Increased preload: increased venous return, increased myocardial contractility.
DBP: largely unchanged.
Increased SBP and PP (from increased SV)
What is the timeframe for acute heart transplant 1-4 weeks
rejection?
host T-lymphocytes: dense interstitial lymphocytic infiltrate
What cells mediate this response/what would you see on
pathology?
Why does distributive shock result in increased cardiac Increased CO due to compensatory increase in sympathetic drive.
output? What happens to mixed venous oxygen
saturation as a result? SvO2 high because blood flow is too fast for complete O2 extraction by tissues.
What is the most common cause of familial dilated TTN - titin; autosomal dominant.
cardiomyopathy?
, UWorld Step 1 - Deck 1 Exam
What are the physical exam findings of a PDA? What is Continuous murmur at left sternal border. L->R shunt (pressure on L always
the pathophysiology behind the findings? greater than R).
How does the heart compensate? Bounding peripheral pulses. L-R shunt lowers SVR -> decreased DBP. Greater
difference between DBP and SBP
Increases LV output
Collagen Types: Be So Totally Cool, Read Books Type 1: 90% of all collagen; BONE, SKIN, TENDONS. Dentin, fascia, cornea.
Late wound repair. Decreased in osteogenesis imperfect
Type 2: CARTILAGE, vitreous body, nucleus pulosus.
Type 3: RETICULIN: skin blood vessels, uterus, fetal tissue, early wound repair -
Ehler's Danlos (vascular)
Type 4: BASEMENT membrane, lens. Defective in Alport syndrome, attacked by
autoantibodies in Goodpasture syndrome
What is the most common cause of acute pericarditis? Most common cause: Viral infection. Causative organism: coxsackievirus and
What are the features of acute pericarditis? echovirus.
Features: CP - intermittent, positional, pleuritic
What are symptoms of a pericardial effusion? SOB, DOE, pleuritic chest pain/tightness, Ewart's sign (bronchial breathing at left
base
What are the clinical signs of a pericardial effusion?
Tachycardia
Low voltage QRS/diminished heart sounds.
Electrical altercans: swinging motion of the heart. Beat to beat variation of QRS
complex.
What is the MOA of anthracyclines? Binds topoisomerase II to cleave DNA. Binds iron to generate free radicals.
How does doxorubicin cause cardiactoxicity? Dilated cardiomyopathy.
What classes of drugs have been shown to improve BBs, ACEi, angiotensin II receptor blocker, aldosterone antagonists.
long-term survival in heart failure?
What are the laboratory differences between drug- DIL: ANA and anti-histone antibodfies. NO anti-dsDNA antibodies.
induced lupus and SLE?
What drugs can cause drug-induced lupus? Hydralazine, procainamide, isoniazid, minocycline, quinidine.
Cardiovascular Equations: Series: Rtotal = R1 + R2 + ... Rx
Total resistance of vessels in series = Parallel: 1/Rtotal = 1/R1 + 1/R2 +...1/Rx
Total resistance of vessels in parallel =
What is the mechanism behind ACEi cough? ACE breaks down bradykinin and substance P. ACEi inhibits breakdown. Build up
of bradykinin and substance P causes lung irritation.
How does implantable pacemaker or cardioverter- The right ventricular lead passes through the tricuspid valve. The lead can
defibrillator lead to right heart failure? damage the leaflets or prevent them from fulling closing.
Signs of right heart failure: elevated JVP, jugular vein distention, lower extremity
edema, ascites.
How would beta blockers affect an ECG? Prolongs the PR interval by slowing AV node conduction.
It will not impact the QRS complex.
, UWorld Step 1 - Deck 1 Exam
Describe the effects of alpha-1 agonists on blood Alpha 1 -> vascular smooth muscle contraction -> increase SBP and DBP ->
pressure, heart rate, and conduction. baroreceptors in carotid sinus and aortic arch -> reflex vagal influence ->
inhibition of pacemaker activity in SA node -> slowed AV conduction ->
decreased cardiac contractility.
Where does traumatic aortic rupture most often occur? Aortic isthmus. Tethered by the ligamentum arteriosum - immobile
Where do changes in partial pressure of oxygen and Venous blood - muscle tissue extracts more O2 and produces more carbon
carbon dioxide occur in exercise? dioxide.
What are the echocardiographic findings of HCM? Overall increase in LV size.
Reduced LV cavity size.
Asymmetric LV wall thickness - greatest in septum
Normal/increased LVEF
LA enlargement
Poorly developed coronary capillary network in hypertrophied areas (chronic
ischemia)`
What structures cause the left ventricular outflow Interventricular septum and mitral valve leaflet.
obstruction observed in HCM?
Renal Artery Stenosis: Etiology: atherosclerotic narrowing of renal artery -> less oxygenation and
Etiology? nutrients; fibromuscular dysplasia (women)
Risk Factors?
Presentation (x4) RF: atherosclerotic disease (CAD, carotid stenosis), smoking, DM, HTN
Pathology: gross and microscopic
Presentation: refractory HTN, recurrent flash pulmonary edema, abdominal bruit,
AKI with starting ACEi
Pathology:
Gross: atrophied kidney
Microscopic: crowded glomeruli, tubular atrophy, interstitial fibrosis, focal
inflammatory infiltrate.
What is the definition of refractory hypertension? Persistent HTN after initiation of multiple antihypertensive medications.
What are the three main anti-inflammatory cytokines? IL4, IL10, TGFB
What ligand and receptor are involved in the extrinsic Fas-ligand and Fas receptor - apoptosis in cell with Fas receptor.
pathway of apoptosis?
1) Binding -> trimerization -> Fas-associated death domain.
Describe the steps after activation. 2) Activation of caspases 8 and 10
3) Executioner caspase -> initiates apoptosis
Leukocyte adhesion deficiency: Autosomal recessive. Absence of CD18 antigents - no integrin formation.
Pathogenesis and inheritance
Features Features: recurrent skin/mucosal infections WITHOUT PUS, poor wound healing,
delayed umbilical cord separation, marked peripheral leukocytosis with
neutrophilia.
What type of antibody is rheumatoid factor? What does it IgM
bind to? How does it and anti-CCP cause rheumatoid Fc component of IgG
arthritis? Immune complex formation on synovium and cartilage cause complement
activation - chronic inflammation and joint destruction.
What is the main difference between selective IgA Main difference: SIgA forms IgE antibodies against IgA -> anaphylaxis with
deficiency and C1 inhibitor deficiency? transfusions!
What are the similarities? Similarities: angioedema
C1 is hereditary angioedema
What is the first line treatment for panic disorder? SSRIs and/or CBT
Acute distress: benzodiazepines (except if history of EtOH/BZD abuse)
What warfarin reversal agents are available? In what Vitamin K: longer time - requires factor synthesis.
time frame? PCC (prothrombin complex concentrate) FFP: instantly gives back factors.
What is heparin's reversal agent? Protamine
What is psoas sign? passive extension of the hip leading to RLQ/R flank pain
What is the pathogenesis of praoxysmal nocturnal Lack of complement inactivating proteins (CD55, CD59) -> complement against
hemoglobinuria? RBCs -> hemolysis.
What is the treatment? Tx: monoclonal antibody against C5 - eculizumab
How do the following hormones act in hypoglycemia? Glucagon: stimulates hepatic glycogenolysis and gluconeogenesis
Glucagon Epinephrine: further stimulates G&G
Epinephrine Cortisol: binds to intracellular receptors - transported to nucleus - increases
Cortisol transcription of enzymes for gluconeogenesis, lipolysis, proteolysis
What are the functions of Type II pneumocytes? Surfactant production and regeneration. Can make Type I pneumocytes.
What is prerenal azotemia? a condition caused by decreased perfusion to the kidneys.
Azotemia: retention of nitrogenous waste products.
BUN/Cr ratio >20
What nerves travel through the temporal bone? CNVIII, CNVII (facial nerve).
When are these structures in danger? Facial trauma
What is cystinuria? Defective transporter for cola AAs - impaired renal and intestinal absorption
What amino acids are affected? COLA: cysteine, ornithine, lysine, arginine
What are the features? Features: cystine kidney stones (flat, yellow, hexagonal)
Hardy-Weinberg equilibrium: No mutation at the locus
What assumptions are being made? No natural selection occurring
No net migration
Randome mating
Large population
Hardy-Weinberg equilibrium: p^2 + 2pq + q^2 = 1
Equation? p= frequency of allele A
q = frequency of allele a
p+q = 1
Hardy-Weinberg equilibrium: males = q
X-linked disease frequency in males vs. females? females = q^2
What are factors that favor development of Elevated capillary hydrostatic pressure (arterial dilation, impaired venous return).
edema/impact interstitial fluid volume?
Name 4 Decreased plasma oncotic pressure (nephrotic syndrome, cirrhosis, malnutrition)
Sodium and water retention.
Lymphatic obstruction (impairs removal of excess interstitial fluid)
, UWorld Step 1 - Deck 1 Exam
What are factors that favor development of pleural Increased hydrostatic pressure gradient (heart failure)
effusions? x4
Decreased oncotic pressure gradient (nephrotic syndrome)
Which cause transudative formation vs. exudative?
Increased inflow vs. decreased outflow? Increased vascular permeability (infection)
Lymphatic obstruction.
What is the pathogenesis of peripheral edema in COPD? Chronic hypoxia -> pulmonary vasoconstriction -> increased pulmonary artery
pressure 0> cor pulmonale (R HF), increased CVP -> increased capillary
What is the initial compensatory mechanism? hydrostatic pressure -> peripheral edema.
Increased lymphatic drainage.
What are the four features of tetralogy of Fallot? Pulmonary infundibular stenosis.
R ventricular hypertrophy (boot shaped heart on CXR)
Hint: PROVe Overriding aorta
VSD
How do tet spells occur? Increased activity (O2 demand) - pulmonary stenosis increases RV pressure - R
What motion can improve a tet spell and how does it to L flow through VSD (deoxygenated blood into circulation) - desaturation,
work? cyanosis, crying.
Improve with squatting - increases SVR (kinks femoral arteries, increases LV
pressure), reduces R to L shunt, improves oxygenation
Why do we avoid around the clock administration of Want to avoid developing tolerance. Mechanism of tolerance is not understood.
nitrates for patients with exertional angina?
Free period at night - least cardiac work.
When would papillary muscle rupture occur post MI? 3-5 days
What is the blood supply for the anterolateral papillary AL: left anterior descending, left circumflex artery.
muscle?
PM: posterior descending.
Posteromedial papillary muscle?
Diastolic blood pressure is the (a) and is directly related a: baseline hydrostatic pressure in the arterial system
to (b). b: SVR and arterial blood volume
Pulse pressure is (a) SBP (left ventricular contraction) - DBP.
It is directly related to (b)
b: stroke volume
What changes in blood pressure occur when you Reduced SVR: skeletal muscle arteriole vasodilation.
exercise?
SVR? Preload? SBP/DBP/PP? Increased preload: increased venous return, increased myocardial contractility.
DBP: largely unchanged.
Increased SBP and PP (from increased SV)
What is the timeframe for acute heart transplant 1-4 weeks
rejection?
host T-lymphocytes: dense interstitial lymphocytic infiltrate
What cells mediate this response/what would you see on
pathology?
Why does distributive shock result in increased cardiac Increased CO due to compensatory increase in sympathetic drive.
output? What happens to mixed venous oxygen
saturation as a result? SvO2 high because blood flow is too fast for complete O2 extraction by tissues.
What is the most common cause of familial dilated TTN - titin; autosomal dominant.
cardiomyopathy?
, UWorld Step 1 - Deck 1 Exam
What are the physical exam findings of a PDA? What is Continuous murmur at left sternal border. L->R shunt (pressure on L always
the pathophysiology behind the findings? greater than R).
How does the heart compensate? Bounding peripheral pulses. L-R shunt lowers SVR -> decreased DBP. Greater
difference between DBP and SBP
Increases LV output
Collagen Types: Be So Totally Cool, Read Books Type 1: 90% of all collagen; BONE, SKIN, TENDONS. Dentin, fascia, cornea.
Late wound repair. Decreased in osteogenesis imperfect
Type 2: CARTILAGE, vitreous body, nucleus pulosus.
Type 3: RETICULIN: skin blood vessels, uterus, fetal tissue, early wound repair -
Ehler's Danlos (vascular)
Type 4: BASEMENT membrane, lens. Defective in Alport syndrome, attacked by
autoantibodies in Goodpasture syndrome
What is the most common cause of acute pericarditis? Most common cause: Viral infection. Causative organism: coxsackievirus and
What are the features of acute pericarditis? echovirus.
Features: CP - intermittent, positional, pleuritic
What are symptoms of a pericardial effusion? SOB, DOE, pleuritic chest pain/tightness, Ewart's sign (bronchial breathing at left
base
What are the clinical signs of a pericardial effusion?
Tachycardia
Low voltage QRS/diminished heart sounds.
Electrical altercans: swinging motion of the heart. Beat to beat variation of QRS
complex.
What is the MOA of anthracyclines? Binds topoisomerase II to cleave DNA. Binds iron to generate free radicals.
How does doxorubicin cause cardiactoxicity? Dilated cardiomyopathy.
What classes of drugs have been shown to improve BBs, ACEi, angiotensin II receptor blocker, aldosterone antagonists.
long-term survival in heart failure?
What are the laboratory differences between drug- DIL: ANA and anti-histone antibodfies. NO anti-dsDNA antibodies.
induced lupus and SLE?
What drugs can cause drug-induced lupus? Hydralazine, procainamide, isoniazid, minocycline, quinidine.
Cardiovascular Equations: Series: Rtotal = R1 + R2 + ... Rx
Total resistance of vessels in series = Parallel: 1/Rtotal = 1/R1 + 1/R2 +...1/Rx
Total resistance of vessels in parallel =
What is the mechanism behind ACEi cough? ACE breaks down bradykinin and substance P. ACEi inhibits breakdown. Build up
of bradykinin and substance P causes lung irritation.
How does implantable pacemaker or cardioverter- The right ventricular lead passes through the tricuspid valve. The lead can
defibrillator lead to right heart failure? damage the leaflets or prevent them from fulling closing.
Signs of right heart failure: elevated JVP, jugular vein distention, lower extremity
edema, ascites.
How would beta blockers affect an ECG? Prolongs the PR interval by slowing AV node conduction.
It will not impact the QRS complex.
, UWorld Step 1 - Deck 1 Exam
Describe the effects of alpha-1 agonists on blood Alpha 1 -> vascular smooth muscle contraction -> increase SBP and DBP ->
pressure, heart rate, and conduction. baroreceptors in carotid sinus and aortic arch -> reflex vagal influence ->
inhibition of pacemaker activity in SA node -> slowed AV conduction ->
decreased cardiac contractility.
Where does traumatic aortic rupture most often occur? Aortic isthmus. Tethered by the ligamentum arteriosum - immobile
Where do changes in partial pressure of oxygen and Venous blood - muscle tissue extracts more O2 and produces more carbon
carbon dioxide occur in exercise? dioxide.
What are the echocardiographic findings of HCM? Overall increase in LV size.
Reduced LV cavity size.
Asymmetric LV wall thickness - greatest in septum
Normal/increased LVEF
LA enlargement
Poorly developed coronary capillary network in hypertrophied areas (chronic
ischemia)`
What structures cause the left ventricular outflow Interventricular septum and mitral valve leaflet.
obstruction observed in HCM?
Renal Artery Stenosis: Etiology: atherosclerotic narrowing of renal artery -> less oxygenation and
Etiology? nutrients; fibromuscular dysplasia (women)
Risk Factors?
Presentation (x4) RF: atherosclerotic disease (CAD, carotid stenosis), smoking, DM, HTN
Pathology: gross and microscopic
Presentation: refractory HTN, recurrent flash pulmonary edema, abdominal bruit,
AKI with starting ACEi
Pathology:
Gross: atrophied kidney
Microscopic: crowded glomeruli, tubular atrophy, interstitial fibrosis, focal
inflammatory infiltrate.
What is the definition of refractory hypertension? Persistent HTN after initiation of multiple antihypertensive medications.
What are the three main anti-inflammatory cytokines? IL4, IL10, TGFB
What ligand and receptor are involved in the extrinsic Fas-ligand and Fas receptor - apoptosis in cell with Fas receptor.
pathway of apoptosis?
1) Binding -> trimerization -> Fas-associated death domain.
Describe the steps after activation. 2) Activation of caspases 8 and 10
3) Executioner caspase -> initiates apoptosis
Leukocyte adhesion deficiency: Autosomal recessive. Absence of CD18 antigents - no integrin formation.
Pathogenesis and inheritance
Features Features: recurrent skin/mucosal infections WITHOUT PUS, poor wound healing,
delayed umbilical cord separation, marked peripheral leukocytosis with
neutrophilia.
What type of antibody is rheumatoid factor? What does it IgM
bind to? How does it and anti-CCP cause rheumatoid Fc component of IgG
arthritis? Immune complex formation on synovium and cartilage cause complement
activation - chronic inflammation and joint destruction.
What is the main difference between selective IgA Main difference: SIgA forms IgE antibodies against IgA -> anaphylaxis with
deficiency and C1 inhibitor deficiency? transfusions!
What are the similarities? Similarities: angioedema
C1 is hereditary angioedema
