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First aid Chs Part 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What anomaly has tricuspid leaflets that are displaced inferiorly in to the RV, a hypoplastic RV and tricuspid regurgitation or stenosis?

A

Ebstein Anomaly

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2
Q

What embryological anomaly is associated with maternal lithium use?

A

Ebstein anomaly

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3
Q

With what anomaly can you see a dilated RA leading to increased risk of Supraventricular tachycardia and WPW?

A

Ebstein anomaly

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4
Q

what’s the mnemonic for fetal erythropoiesis and what are the locations and times?

A 
Young Liver Synthesizes Blood
Yolk sac - 3-10 wks
Liver - 6 wk to birth
Spleen - 15 to 30 weeks
Bone marrow - 22 wks to adult
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5
Q

What’s the importance of the fact that fetal hemoglobin is a2g2 and adult hemoglobin is a2b2?

A

Gamma hemoglobin has decreased affinity for 2,3 DPG so fetal Hb has higher affinity for O2

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6
Q

Name places where bone marrow hematopoiesis occurs in infancy and childhood?

A
  • flat bones

- sternum, pelvis, ribs, cranial bones, vertebrae, long bones of the legs (tibia and femur)

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7
Q

Name places where bone marrow hematopoiesis occurs in adulthood?

A

Axial skeleton

- vertebrae, sternum, ribs and pelvis

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8
Q

In fetal circulation, what’s the force that directs blood through the ductus arteriosus and into the descending aorta?

A

Increased resistance in the pulmonary circulation

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9
Q

Name the 3 shunts used in fetal circulation

A
  1. Foramen Ovale (bypasses lungs)
  2. Ductus arteriosus (bypasses lungs)
  3. ductus venosus (bypasses hepatic circulation)
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10
Q

When a baby is born and takes first breath what causes the closure of the ductus arteriosus?

A

With the first breath, you get decreased resistance in the pulmonary vasculature leading to increased left atrial pressure vs right atrium. The increase in oxygen leads to a decreased in prostaglandins causing closure of ductus arteriosus

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11
Q

What will keep a PDA open?

A

PGE1 or PGE2

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12
Q

What will close a PDA?

A

NSAIDS like indomethacin

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13
Q

what vessel in a fetus has the highest O2 content?

A

Umbilical vein

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14
Q

How many umbilical arteries and veins are there?

A

2 umbilical arteries and one umbilical vein

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15
Q

What does the umbilical vein become and where is it contained?

A

Becomes the ligamentum teres hepatis - contained in falciform ligament

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16
Q

What does the umbilical arteries become?

A

Medial umbilical ligaments

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17
Q

What does the allantois become?

A

Urachus - median umbilical ligament

The urachus is the part of the allantoic duct between the bladder and the umbilicus

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18
Q

What does the notochord become?

A

nucleus pulposus of the intervertebral disc

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19
Q

What is the mnemonic for the 8 branches of the external carotid artery?

A

Some Attendings Like Freaking Out Potential Medical Students

Superior thyroid 
Ascending pharyngeal
Lingual
Facial
Occipital
Posterior auricular
Maxillary
Superficial temporal
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20
Q

What artery supplies the right ventricle?

A

Acute marginal artery

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21
Q

What artery supplies the posterior 1/3 of the interventricular septum and posterior walls of the ventricles?

A

Posterior descending/interventricular artery

This can branch off the RCA or Left circumflex artery

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22
Q

What artery supplies the anterior 2/3 of the interventricular septum, anterior papillary muscle and anterior surface of the LV?

A

LAD

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23
Q

What artery supplies the lateral and posterior walls of the LV?

A

Left circumflex artery

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24
Q

What artery usually supplies the SA and AV nodes?

A

RCA

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25
Q

What is the number 1 most likely area of coronary artery occlusion?

A

LAD

Widow maker

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26
Q

During what phase of the cardiac cycle do coronary arteries fill?

A

During diastole

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27
Q

What is the most posterior portion of the heart and what is a complication you can get from its enlargement?

A

Left atrium, enlargement can lead to dysphagia or hoarseness

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28
Q

What is the easy equation for cardiac output?

A

CO = SV x HR

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29
Q

What is the fick principle equation for cardiac output?

A

CO = (rate of O2 consumed)/ (arterial O2 content - venous O2 content)

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30
Q

What is the equation for mean arterial pressure?

A 
MAP = CO x TPR = QxR
MAP = 2/3 diastolic pressure + 1/3 systolic pressure
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31
Q

What is the equation for stroke volume?

A

SV = CO/HR = end diastolic volume - end systolic volume

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32
Q

What is the equation for pulse pressure?

A

pulse pressure = systolic pressure - diastolic pressure

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33
Q

what is the problem that occurs if the HR is too high?

A

Diastolic filling will be incomplete so your cardiac output will decrease

Ex: ventricular tachycardia

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34
Q

what’s the difference between how cardiac output is maintained early in exercise vs later in exercise?

A

Early in exercise: CO is maintained by increased HR and increased SV

Late in exercise: CO is maintained by increased HR only because the SV plateaus

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35
Q

What is the term used for the harder the heart pumps, the more that is pushed out?

A

Contractility

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36
Q

Name the 3 cardiac output variables?

A

SV CAP

Stroke Volume is affected by: Contractility, Afterload, Preload

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37
Q

Name 4 things that INCREASE contractility and therefore stroke volume

A
  1. increased intracellular calcium
  2. decreased extracellular sodium
  3. catecholamines (increase the activity of the calcium pump in the sarcoplasmic reticulum)
  4. Digitalis (leads to both 1. and 2.)
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38
Q

Name 5 things that DECREASE contractility and therefore stroke volume

A
  1. beta-1 blockers - result in decreased cAMP
  2. heart failure
  3. acidosis
  4. hypoxia or hypercapnea
  5. non-dihydropyridine CCB like verapamil
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39
Q

What is seen with stroke volume in an anxious exercising pregnant patient?

A

you see INCREASED stroke volume in anxiety, exercise, and pregnancy

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40
Q

What is another name for ventricular end diastolic volume?

A

Preload

When the ventricles are their fullest right before they contract then the atrial P is = to the central venous pressure

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41
Q

What is another name for the mean arterial pressure/TPR?

A

Afterload

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42
Q

name a vasodilator?

A

Hydralazine - decreases afterload

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43
Q

Name 3 things that increase preload

A
  1. exercise slightly due to muscles contracting and pushing more blood up to the heart
  2. increased blood volume
  3. excitement - increased Sympathetics
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44
Q

What is the percent of ejection fraction normally?

A

greater than or equal to 55%

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45
Q

What is the equation of Ejection fraction?

A

EF = SV/EDV = (EDV - ESV) / EDV

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46
Q

What is ejection fraction an index for?

A

ventricular contractility

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47
Q

what is the equation for a change in pressure?

A

Change in pressure = flow x resistance = QxR

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48
Q

What vessels account for most of TPR?

A

arterioles

This regulates capillary flow

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49
Q

What is resistance directly and indirectly proportionate to?

A

Directly proportionate to viscosity and vessel length and inversely proportional to the radius to the 4th power

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50
Q

Name 3 things that cause increased viscosity and therefore increased resistance?

A
  1. Polycythemia
  2. hyperproeinemic states (like multiple myeloma)
  3. hereditary spherocytosis

note that viscosity is decreased in anemia

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51
Q

What is the S1 sound?

A

Mitral and tricuspid valve closing - this is loudest at the mitral area

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52
Q

What is the S2 sound?

A

Aortic and pulmonary valve closing. Loudest at the left sternal border

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53
Q

WHat is the S3 sound? What is it associated with?

A

Heard early in diastole during rapid ventricular filling phase.
Associated with increased filling pressure like in mitral regurg or CHF and it’s more common in dilated ventricles - but more normal in children and pregnant women

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54
Q

What is the S4 heart sound? What is it associated with?

A

Atrial kick - occurs in late diastole. High atrial pressure

Associated with ventricular hypertrophy - the LA must push against a stiff LV wall

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55
Q

What does the a wave in jugular venous pulse (right heart) stand for?

A

Atrial contraction

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56
Q

What does the c wave in jugular venous pulse (right heart) stand for?

A

RV contraction - the closed tricuspid valve bulging into the atrium

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57
Q

What does the x descent in jugular venous pulse (right heart) stand for?

A

atrial relaxation and downward displacement of the closed tricuspid valve during ventricular contraction

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58
Q

What does the v wave in jugular venous pulse (right heart) stand for?

A

Increased right atrial pressure due to filling against a closed tricuspid valve

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59
Q

What does the y descent in jugular venous pulse (right heart) stand for?

A

blood flow from the RA to RV

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60
Q

What does the brief increased in pressure or dichrotic notch mean?

A

it’s a brief reversal of flow from the aorta back into the LV which actually helps the aortic valve to close - it’s due tot he elastic revoic of the semilunar valve and aorta

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61
Q

What are some diseases that may give you a jacked up dichrotic notch on a diagram?

A

Diseases that effect the elasticity of the aorta - Marfan syndrome or syphilis

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62
Q

What is seen in normal splitting?

A

In normal splitting, you have delayed closure of the pulmonic valve during inspiration so inspiration has a wider split between A2 and P2

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63
Q

What type of splitting is seen in delayed RV emptying (pulmonic stenosis, RBBB)?

A

Wide splitting

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64
Q

What type of splitting is seen in an atrial septal defect?

A

Fixed splitting

This occurs because regardless of whether you’re breathing in or out the pulmonic closure is delayed because of the left to right shunt causing an increase in RA and RV volumes

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65
Q

What type of splitting is seen in conditions that delay LV emptying like in aortic stenosis or LBBB?

A

Paradoxical splitting

This occurs because the normal order of valve closures is reverse so P2 is heard before a delayed A2 sound. So on inspiration, P2 closes later and moves closer to A2 thereby “paradoxically” eliminating the split

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66
Q

A patient presents with a NSTEMI splitting of S2 that narrows with inspiration and audibly eliminates the split - what does the patient most likely have?

A

Paradoxical splitting - most likely due to a LBBB

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67
Q

Why can S3 be a normal sound heart in children and pregnancy?

A

Due to increased preload and blood flow and filling pressure

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68
Q

What heart sound can be heart in dilated cardiomyopathy, CHF, mitral regurgitation, or L to R shunting?

A

S3

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69
Q

What heart sound can be heard in hypertrophic cardiomyopathy? aortic stenosis? chronic HTN with LVH? Post MI?

A

S4

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70
Q

when a patient breathes in, does that decrease or increase the filling of the heart?

A

When a patient inspires, that drops the intrathoracic pressure and increases the venous return to the right side of the heart

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71
Q

what is the result of hand gripping?

A

increased afterload

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72
Q

What is the result of valsalva? and what causes a similar result?

A

Valsalva decreases venous return - so does standing

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73
Q

What is the result of rapid squatting?

A

Increased venous return, increased preload and you can get increased afterload with prolonged squatting

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74
Q

What maneuver will increase the intensity of hypertrophic cardiomyopathy murmurs?

A

Valsalva (decreased venous return)

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75
Q

An 18 yo man presents with a systolic murmur heart best at the apex which increases with standing and decreases with squatting - what is the murmur due to?

A

Hypertrophic cardiomyopathy

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76
Q

A patient presents with a systolic murmur that is loudest at the apex and radiates toward the axilla. what is it?

A

Mitral regurgitation

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77
Q

A patient presents with a systolic murmur that radiates tot he right sternal border what is it?

A

Tricuspid regurgitation

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78
Q

An infant presents with a holosystolic harsh-sounding murmur that’s loudest at the triscupid area and is accentuated with a hand grip maneuver due to increased afterload - what is it?

A

A VSD

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79
Q

A patient presents with a systolic murmur following an ejection click. It’s heart loudest at the heart base and it radiates to the carotids - what is it?

A

Aortic stenosis

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80
Q

A patient presents with pulsus parveus et tardus what is the systolic murmur?

A

Aortic stenosis

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81
Q

What can be a result of aortic stenosis?

A

SAD - syncope, angina, and dyspnea on exertion

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82
Q

A patient presents with a late systolic murmur with a mid systolic click - what is the murmur?

A

Mitral valve prolapse

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83
Q

What can myxomatous degeneration, rheumatic fever or chordae rupture all lead to?

A

Mitral valve prolapse

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84
Q

a patient presents with a high pitched blowing diastolic decrescendo murmur - what is the murmur?

A

Aortic regurgitation

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85
Q

A patient presents with a chronic aortic regurgitation murmur - what are some things you will see on PE?

A

you can see bounding pulses and heat bobbing. The murmur will worsen with hand grip and the intensity will decreased with vasodilators

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86
Q

Name 4 possible causes of aortic regurgitation?

A
  1. aortic root dilation
  2. bicuspid aortic valve
  3. endocarditix
  4. rheumatic fever
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87
Q

A patient presents with a diastolic murmur with an opening snap and low pitched rumbling - what is it?

A

Mitral stenosis

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88
Q

what is the most common cause of mitral stenosis?

A

rheumatic fever

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89
Q

what is a common cause of a PDA?

A

Congenital rubella

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90
Q

What causes the plateau during a cardiac muscle action potential?

A

The balance between calcium influx and potassium efflux

Myocyte contraction occurs here because you have the calcium coming in leading to calcium induced calcium release from the sarcoplasmic reticulum

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91
Q

What type of channels allow for spontaneous depolarization of the cardiac nodal cells?

A

If channels (funny current channels responsible for a slow mixed Na/K inward current)

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92
Q

what determines the heart rate in the SA node?

A

The slope of phase 4

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93
Q

what effect do acetylcholine and adenosine have on heart rate and the rate of diastolic depolarization?

A

Decreases both

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94
Q

What two things can cause a U wave to appear of EEG?

A

Hypokalemia or bradycardia

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95
Q

Name the speed of conduction from fastest to slowest?

A

Purkinje > atria > ventricles > AV nodes

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96
Q

What is the length of delay at the AV node and why is this important?

A

100 msec delay occurs at the AV node to allow for time for ventricular filling

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97
Q

What is the conduction pathway through the heart?

A

SA node to the atria to the AV node to the common bundle to the bundle branches to the purkinje fibers to the ventricles

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98
Q

What is the treatment for torsades de pointes?

A

magnesium sulfate

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99
Q

Name drugs that prolong the QT interval?

A 
Macrolides
chloroquine
haloperidol
risperidone
methadone
anti-HIV protease inhibitors
antiarrhythmics class  IA and III
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100
Q

A patient presents with congenital long QT syndrome and sensorineural deafness - what is the syndrome?

A

Jervell and Lange-Nielsen syndrome

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101
Q

Name the EKG: No discrete P waves in between irregularly spaced QRS complexes. can result in atrial stasis and lead to a stroke

A

Atrial fibrillation

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102
Q

What are some precipitating factors that can lead to atrial fibrillation?

A
  1. binge alcohol consumption (“holiday heart syndrome”)
  2. increased cardiac sympathetic tone
  3. pericarditis
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103
Q

A patient presents with atrial fibrillation - what determines the ventricular contraction here?

A

AV node refractory period

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104
Q

Name the EKG: A patient presents with a HR of 280bpm, EKG shows rapid succession of identical back to back atrial depolarization waves.

A

Atrial flutter

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105
Q

Name the EKG: Sawtooth appearance

A

Atrial flutter

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106
Q

What can be used for pharmacologic conversion to sinus rhythm for a pt with atrial flutter? for Rate control?

A

Class IA, IC or III anti-arrhythmics for conversion to sinus rhythm
Beta blocker or CCB for rate control

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107
Q

Name the EKG: A patient presents with a completely erratic rhythm with no identifiable waves. what is this and what do you do?

A

Ventricular fibrillation - this is fatal so you TX with immediate CPR and fibrillation

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108
Q

Name the EKG: PR interval is greater than 200 msec but the patient is asymptomatic

A

1st degree AV block

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109
Q

Name the EKG: A patient presents with a progressive lengthening of their PR interval until a beat is dropped, they are asymptomatic but have been taking a CCB.

A

2nd degree AV block - Mobitz type I - Wenckebach

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110
Q

What drugs can cause 2nd degree AV block - Mobitz type I - Wenckebach?

A

Anything that slows the signal through the AV node - digoxin, CCBs (verapamil>diltiazem), beta blockers, amiodarone, adenosine

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111
Q

Name the EKG: A patient presents with dropped beats that are not preceded by a change in the length of the PR interval - they are abrupt nonconducted P waves and it is a 2:1 block with 2 or more P waves to 1 QRS

A

2nd degree AV block - Mobitz type II

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112
Q

What is the concern with 2nd degree AV block - Mobitz type II and how do you treat it?

A

The concern is that it will develop into a 3rd degree block. Treated with a pacemaker often

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113
Q

Name the EKG: Atria and ventricles beat independently of each other. Atrial rate is faster than the ventricular rate.

A

3rd degree AV block

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114
Q

What can cause a 3rd degree AV block?

A

Lyme disease

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115
Q

How do you treat a 3rd degree AV block?

A

Pacemaker

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116
Q

what can be released from atrial myoctes in response to increased blood volume and atrial pressure?

A

Atrial natriuretic peptide

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117
Q

What does ANP result in ?

A

ANP causes generalized vascular relaxation (vasodilation) and decreased Na reabsorption at te medullary collecting tubules

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118
Q

What effect does ANP have at the kidneys?

A

Constricts efferent renal arterioles and dilates afferent arterioles (via cGMP) promoting diuresis and an escape from the aldosterone mechanism

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119
Q

If a patient has a premature ventricular contraction, what allows for this type of occurrence?

A

Usually due to microre-entry at the level of the purkinje fibers

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120
Q

Name the EKG: Shows delta waves

A

WPW

  • may lead to supraventricular tachycardia
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121
Q

What do you use to treat wolff-parkinson-white?

A

Amiodarone or procainamide

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122
Q

What nerve and nucleus is used for the aortic arch receptors?

A

vagus nerve tot he solitary nucleus - responds to increased BP only

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123
Q

What nerve and nucleus is used for the carotid sinus receptors?

A

Glossopharyngeal nerve to solitary nucleus - responds to increased and decreased BP

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124
Q

What is the triad seen in a cushing reaction?

A
  1. hypertension
  2. bradycardia
  3. respiratory depression

this is increased intracranial pressure

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125
Q

What stimulates peripheral chemoreceptors?

A

decreased PO2 (<60), Increased PCO2, decreased pH of blood

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126
Q

What stimulates the central chemoreceptors?

A

Changes in pH and PCO2 of brain interstitial fluid which are influenced by arterial CO2

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127
Q

which organ receives the largest blood flow (100% of CO)?

A

Lung

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128
Q

What organ has the largest share of the systemic CO?

A

liver

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129
Q

Which organ has the highest blood flow per gram of tissue?

A

Kidney

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130
Q

What is normal pulmonary capillary wedge pressure?

A

<12 mmHg

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131
Q

What is PCWP a good approximation of?

A

Left atrial pressure

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132
Q

What is the relationship between PCWP and LV diastolic pressure in mitral stenosis?

A

PCWP > LV diastolic pressure

133
Q

What is the equation for net filtration pressure?

A

Pnet = (Pc - Pi) - (πc - πi)

134
Q

What is the equation for net fluid flow?

A

Net fluid flow = Kf [(Pc - Pi) - (πc - πi)]

135
Q

Describe Eisenmenger’s syndrome

A

Uncorrected VSD, ASD or PDA causes compensatory pulmonary vascular hypertrophy which results in progressive pulmonary hypertension. As pulmonary resistance increases the shunt reverses from L-to-R to R-to-L which causes late cyanosis, clubbing and polycythemia

136
Q

What is the cause of Tetralogy of Fallot and what mnecmonic helps you remember the findings?

A

Tetrology of fallot is caused by anterosuperior displacement of the infundibular septum.

Findings: PROV

  1. Pulmonary infundibular stenosis — MOST important determinant for prognosis
  2. RVH = boot
  3. Overriding aorta
  4. VSD
137
Q

what is the most important determinant for the prognosis in tetralogy of fallot?

A

Pulmonary infundibular stenosis

The pulmonary stenosis is what causes the VSD to be R to L instead of L to R which is why these kids get cyanotic

138
Q

An infant is born to a diabetic mom - what congenital heart disease are they most likely to have?

A

Transposition of the great vessels

139
Q

What is the cause of transposition of the great vessels

A

Failure of the aorticopulmonary septum to spiral

140
Q

what murmur can result from a coarctation of the aorta?

A

Aortic regurgitation

141
Q

What is the position of the coarctation in a patient with the infantile type of coarctation of the aorta?

A

Aortic stenosis proximal to the insertion of the ductus arteriosus

142
Q

What is associated with an infant born with coarctation of the aorta?

A

Turner syndrome

143
Q

What is the position of the coarctation in a patient with the adult type of coarctation of the aorta?

A

Stenosis is distal to ligamentum arteriosum

144
Q

What is associated with an adult with coarctation of the aorta?

A

bicuspid aortic valve

145
Q

What BP is considered hypertension?

A

greater than or equal to 140/90

146
Q

What is a xanthelasma?

A

Xanthoma of the eye

147
Q

What is a corneal arcus?

A

lipid deposit in the cornea

148
Q

Name the Arteriosclerosis: Medial calcific sclerosis

A

Monckeberg arteriosclerosis

149
Q

Name the Arteriosclerosis: Calcification in the media of the arteries - especially radial or ulnar.

A

Monckeberg arteriosclerosis

150
Q

Name the Arteriosclerosis: Usually benign, “pipestem” arteries, does not obstruct blood flow and the intima is NOT involved. Commonly seen in elderly in the extremities

A

Monckeberg arteriosclerosis

151
Q

Name the Arteriosclerosis: Thickening of the small arteries in essential hypertension or diabetes mellitus

A

Hyaline Arteriolosclerosis

152
Q

Name the Arteriosclerosis: “onion skinning” in malignant hypertension

A

Hyperplastic Arteriolosclerosis

153
Q

Name the Arteriosclerosis: Fibrous plaques and atheromas form in the intima of the artiers

A

Atherosclerosis

154
Q

Name 4 modifiable risk factors for atherosclerosis

A
  1. smoking
    2, hypertension
  2. hyperlipidemia
  3. diabetes
155
Q

What are the locations for atherosclerosis?

A

Abdominal aorta > coronary artery > popliteal artery > carotid artery

156
Q

What is an abdominal aortic aneurysm associated with?

A

atherosclerosis

157
Q

What is the patient profile for abdominal aortic aneurysm?

A

hypertensive male smoker >50 yo

158
Q

What are the 3 associations with thoracic aortic aneurysm?

A
  1. hypertension
  2. cystic medial necrosis (marfan’s syndrome)
  3. tertiary syphilis
159
Q

what is commonly seen on CXR of a patient with an aortic dissenction?

A

Mediastinal widening

160
Q

With an aortic dissection, where is the blood ripping through and collecting?

A

Tunica media

161
Q

What is the classic presentation seen with an aortic dissection?

A

Tearing chest pain that radiates tot he back

162
Q

Describe a Stanford Type A aortic dissection?

A

Dissection involving the ascending aorta or aortic arch, regardless of how far down it goes — emergency surgery!

163
Q

Describe a Stanford Type B aortic dissection?

A

Descending aorta DISTAL to the left subclavian Artery — medical treatment for type B — beta blocker

164
Q

What will you see on EKG with a patient with stable angina?

A

ST depression

165
Q

What will you see on EKG with a patient with Prinzmeta’s angina?

A

ST elevation of EKG

166
Q

What will you see on EKG with a patient with unstable angina?

A

ST depression

167
Q

What stage of an MI: Dark mottling is present with coagulative necrosis, edema and wavy fibers

168
Q

What stage of an MI: Nothing seen on gross or light microscope

169
Q

What stage of an MI: Dark mottling with contraction bands from reperfusion injury

170
Q

What stage of an MI: beginning of neutrophil migration

171
Q

What stage of an MI: Hyperemia - red at the infarct. extensive coagulative necrosis with neutrophil migration

172
Q

What stage of an MI: Risk of fibrinous pericarditis

A

1-3 D

note that fibrinous pericarditis only occurs with a transmural infarct

173
Q

What stage of an MI: Risk of arrhythmia

174
Q

What stage of an MI: Risk of Arrhythmia, CHF exacerbation, cardiogenic shock

175
Q

What stage of an MI: Yellow-tan softening, macrophage infiltrate

176
Q

What stage of an MI: Granulation tissue at margins, hyperemic border

177
Q

What stage of an MI: Risk of free wall rupture leading to tampnade, papillary muscle rupture, ventricular aneurysm, or intervetnricular septa rupture

178
Q

What stage of an MI: Gray white scar

A

2 weeks to several months

179
Q

What stage of an MI: Risk of dressler’s syndrome

A

2 weeks to several months

180
Q

Name the type of infarct: Increased necrosis, causes ST elevation of EKG and Q waves

A

Transmural infarct - involves the entire wall

181
Q

Name the type of infarct: subendocardial especially vulnerable to ischemia, causes ST depression on EKG

A

Subendocardial infarcts - due to ischemic necrosis of <50% of ventricle wall

182
Q

Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI, patient may have a fever and elevated ESR

A

Dressler’s syndrome

183
Q

What type of hypertrophy is seen in dilated cardiomyopathy?

A

eccentric - sarcomeres added in series

184
Q

What is the most common type of cardiomyopathy?

185
Q

What are the possible causes of dilated cardiomyopathy?

A

Idiopathic mostly or ABCCCD-HP

chronic Alcohol abuse
wet Beriberi
Coxsackie B virus myocarditis
chronic Cocaine use
Chaga's disease
Doxorubicin toxicity
Hemochromatosis 
peripartum cardiomyopathy
186
Q

A patient presents with an S3 heart sound, a balloon appearance on chest X ray and a dilated heart on US - whats the DX?

A

dilated cardiomyopathy

187
Q

What are the treatments for dilated cardiomyopathy?

A

Sodium restriction, ACE inhibitors, diuretics, digoxin, heart transplant

188
Q

Which cardiomyopathy (ies) have systolic dysfunction?

A

Dilated cardiomyopathy

189
Q

Which cardiomyopathy (ies) have diastolic dysfunction?

A

Hypertrophic cardiomyopathy and restrictive cardiomyopathy

190
Q

A patient presents with a systolic murmur and syncopal episodes, they have hypertrophic cardiomyopathy - what is causing the above mentioned symptoms?

A

The hypertrophied interventricular septum is “too close” to the mitral valve leaflet leading to outflow tract obstruction

191
Q

What familial autosomal dominant mutation can cause hypertrophic cardiomyopathy?

A

A mutation in the Beta-myosin heavy chain

192
Q

What is hypertrophic cardiomyopathy associated with?

A

Friedrich’s ataxia

193
Q

A patient presents with a normal sized heart, the presence of an S4 sound, apical impulse that is large and diffuse and a systolic murmur - what is the cause?

A

Hypertrophic cardiomyopathy

194
Q

What type of hypertrophy is seen in hypertrophic cardiomyopathy?

A

Asymmetric concentric hypertrophy - sarcomeres are added in parallel

195
Q

What are the possible treatments for a patient with hypertrophic cardiomyopathy?

A

Beta blockers, non-dihydropyridine CCBs like verapamil

196
Q

What are the possible causes of Restrictive/obliterative cardiomyopathy?

A

LEASH

Loffler's syndrome
Endocardial fibroelastosis
Amyloidosis
Sarcoidosis
Hemochromatosis (though this is more commonly causing dilated cardiomyopathy)
197
Q

A child presents with a thick fibroelastic tissue in their endocardium and they have restrictive cardiomyopathy - what is this?

A

Endocardial fibroelastosis

198
Q

What would cause an ISOLATED right heart failure?

A

Cor pulmonale

199
Q

What symptoms are seen in left heart failure?

A

Pulmonary edema, paroxysmal nocturnal dyspnea (hemosiderin laden macrophages in the lungs)
orthopnea (shortness of breath when supine)

200
Q

What symptoms are seen in right heart failure?

A

Hepatomegaly (nutmeg liver)
Peripheral edema
Jugular venous distension

201
Q

What is a difference between infective and non-infective endocarditis?

A

Infective endocarditis tends to have vegetations on only one side of the valve
non-infective endocarditis tends to have vegetations on BOTH sides of the valve

202
Q

What are the findings in a patient with bacterial endocarditis?

A 
"FROM JANE"
Fever
Roth spots
Osler's nodes
Murmur 
Janeway lesions (on palms or soles)
Anemia
Nail bed hemorrhages 
Emboli
203
Q

What bug causes acute bacterial endocarditis and what do the vegetations look like?

A

Staph aureus, large vegetations on previously normal valves

has a rapid onset

204
Q

What bug causes subacute bacterial endocarditis and what do the vegetations look like?

A

Viridans strep, smaller vegetations on abnormal valves

- this is why you do Ab prophylaxis before dental procedures

205
Q

What valve is commonly involved in bacterial endocarditis caused by IVDA?

A

Tricuspid valve

206
Q

What valve is most commonly involved in bacterial endocarditis?

A

mitral valve

207
Q

What bug should you think of when a patient with colorectal cancer gets bacterial endocarditis?

A

Strep bovis

208
Q

What bug should you think when a patient with prosthetic valves gets bacterial endocarditis?

A

Staph epidermidis

209
Q

A biopsy is done of a heart and Aschoff bodies are seen in the myocardium with Anitschkow cells - what did they die from?

A

Rheumatic fever

210
Q

What criteria do you use to diagnose rheumatic fever?

A

JONES criteria need 2 major + 1 minor

Joints - migratory polyarthritis
Heart - pancarditis
Nodules - subcutaneous nodules
Erythema marginatum
Sydenham chorea
211
Q

What causes rheumatic fever?

A

Recent infection with group A Beta hemolytic strep - you get molecular mimicry because the bacterial M protein resembles human tissue

212
Q

What valve lesions are seen in acute vs chronic rheumatic fever?

A

Acute rheumatic fever - mitral regurgitation

Chronic rheumatic fever - mitral stenosis

213
Q

What type of hypersensitivity is rheumatic fever?

A

Type II HS - making antibodies to the M protein

214
Q

A patient presents with the signs and symptoms of acute pericarditis but they also have a positive kussmaul sign - what is a kussmaul sign and what is the DX?

A

Kussmaul sign is a JVD with inspiration. They have chronic pericarditis

215
Q

A patient presents with sharp pain that is aggravated with inspiration and relieved by sitting up and leaning forward. They also have a friction rub. What is the DX?

A

Acute pericarditis

216
Q

What EKG findings can be seen with acute pericarditis?

A

Widespread ST segment elevation and/or PR depression

217
Q

Name the acute pericarditis: Caused by dressler’s syndrome, uremia, radiation. Presents with a loud friction rub

A

Fibrinous acute pericarditis

218
Q

Name the acute pericarditis: Viral pericarditis that often resolves spontaneously or noninfectious inflammatory diseases ( RA or SLE)

A

Serous acute pericarditis

219
Q

Name the acute pericarditis: Usually caused by bacterial infections - rare now with antibiotics

A

Suppurative/purulent acute pericarditis

220
Q

Name the acute pericarditis: due to TB or melanoma

A

Hemorrhagic acute pericarditis

221
Q

What triad is seen with pericardial tamponade?

A

Muffled heart sounds
Increased jugular venous pressure
profound hypertension

222
Q

What is pulsus paradoxus?

A

decrease in amplitude of systolic blood pressure by greater than or equal to 10 mm Hg during inspiration.

223
Q

Where is pulsus paradoxus seen?

A

severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup
- whenever there’s an exaggerated inspiration

224
Q

A patient presents with equilibration of diastolic pressures in all 4 chambers and electrical alterans on EKG - what’s the diagnosis?

A

Cardiac tamponade

225
Q

What is seen in syphilitic heart disease?

A

Tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of the vessel wall and dilation of the aorta and valve ring.

226
Q

In what disease may you see calcification of the aortic root and ascending arch leading to a tree bark appearance of the aorta?

A

Syphilitic heart disease

227
Q

What’s the most common primary cardiac tumor in adults?

228
Q

Where does a myxoma most commonly occur?

229
Q

What is the most common heart tumor overall?

A

Metastasis from melanoma, lymphoma

230
Q

What is commonly seen in a patient with a myxoma?

A

syncopal episodes due to blockage of the mitral valve

231
Q

What is the most frequent primary cardiac tumor in children?

A

Rhabdomyoma

232
Q

What are Rhabdomyomas associated with in children?

A

Tuberous sclerosis

233
Q

When is a kussmaul sign most commonly seen?

A

with a constrictive pericarditis

234
Q

what is the name of decreased blood flow to the skin due to arteriolar vasopasm in response to cold temperature or emotional stress?

A

Raynaud’s phenomenon

235
Q

How do you distinguish between Raynaud syndrome and Raynaud disease?

A

Raynaud Syndrome is Secondary to a disease

Raynaud Disease is iDiopathic

236
Q

what condition is associated with temporal giant cell arteritis?

A

Polymyalgia rheumatica

237
Q

A 35 year old Asian female presents with a lack of pulses in her upper body, fever, nigh sweats, arthritis, mylagias, skin nodules and ocular disturbances - what does she have?

A

Takayasu’s arteritis

238
Q

What is the pathology seen in Takayasu arteritis?

A

Granulomatous thickening of the aortic arch and proximal vessels

239
Q

Is temporal giant cell arteritis associated with granulomatous inflammation?

A

Yes, it’s focal granulomatous inflammation

240
Q

which medium vessel vasculitis involves the renal and visceral vessels but NOT the lungs?

A

Polyarteritis nodosa

241
Q

What is a possible association with polyarteritis nodosa?

A

Hepatitis B or C or Hairy cell leukemia

242
Q

Name the vasculitis: Immune complex mediated transmural inflammation of the arterial wall with fibrinoid necrosis. Shows many aneurysms and constrictions on arteriogram

A

Polyarteritis nodosa

243
Q

Name the vasculitis: Treated by smoking cessation

A

Buerger’s disease (thromboangiitis obliterans)

244
Q

Name the vasculitis: segmental thrombosing vasculitis with intermittent claudications that may lead to gangrene, autoamputation of the digits and superficial nodular phlebitis. They may also present with Raynaud’s phenomenon

A

Buerger’s disease (thromboangiitis obliterans)

245
Q

Name the vasculitis: A 2 year old Asian child presents with fever cervical lymphadenitis, conjunctival injection, changes in the lips/oral mucosa (“strawberry tongue”), hand-foot erythema, and desquamating rash

A

Kawasaki disease

246
Q

Name the vasculitis: Necrotizing vasculitis with a fever for at least 5 days and 4/5 of CRASH (Conjunctivitis, Rash, Adenopathy, Strawberry tongue, Hands and feet)

A

Kawasaki disease

247
Q

Name the vasculitis: Necrotizing vasculitis commonly involving the lung, kidnes, and skin with pauci-immune glomerulonephritis and palpable purpura

A

Microscopic polyangiitis

248
Q

Name the vasculitis: NO granulomas, p-ANCA positive

A

Microscopic polyangiitis

249
Q

Name the vasculitis: A patient has focal necrotizing vasculitis, necrotizing noncaseating granulomas in the lung and upper airway and necrotizing glomerulonephritis

A

Wegener’s granulomatosis

250
Q

Name the vasculitis: c-ANCA positive with a saddle nose

A

Wegener’s granulomatosis

251
Q

Name the vasculitis: Patient with painful mucosal ulcers and hematuria, hemoptysis and rapidly progressive (crescentic) glomerulonephritis

A

Wegener’s granulomatosis

252
Q

Name the vasculitis: A patient has asthma, sinusitis, palpable purpura and peripheral neuropathy. They are also p-ANCA positive

A

Churg-Strauss syndrome

253
Q

Name the vasculitis: Granulomatous, necrotizing vasculitis with eosinophilia

A

Churg-Strauss syndrome

254
Q

Name the vasculitis: most common childhood systemic vasculitis - often follows and Upper respiratory infection

A

Henoch-Schonlein purpura

255
Q

Name the vasculitis: a kid presents with palpable purpura on the butt and legs, arthralgia, and abdominal pain

A

Henoch shonlein purpura

256
Q

Name the vasculitis: Vasculitis secondary to IgA complex deposition

A

Henoch Schonlein purpura

- this is a type 3 HS

257
Q

Name the tumor: Benign capillary hemangioma of infancy. Appears in first few weeks of life, it grows rapidly but regresses spontaneously as a kid

A

Strawberry hemagioma

258
Q

Name the tumor: Benign capillary hemangioma of the elderly. does not regress and the frequency increases with age

A

Cherry hemangioma

259
Q

Name the tumor: Polypoid capillary hemagioma that can ulcerate and bleed. Associated with trauma and pregnancy

A

Pyogenic granuloma

260
Q

Name the tumor: cavernous lymphangioma of the neck. Associated with turner syndrome

A

Cystic hygroma

261
Q

Name the tumor: Benign, painful, red-blue tumor under the fingernails. Arises from modified smooth muscle cells of the glomus body

A

Glomus tumor

262
Q

Name the tumor: Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaken for Kaposi’s sarcoma

A

Bacillary angiomatosis

263
Q

Name the tumor: Rare blood vessel malignancy typically occurring in the head, neck and breast areas. Associated with patients receiving prior radiation therapy, aggressive and difficult to treat

A

Angiosarcoma

264
Q

Name the tumor: Lymphatic malignancy associated with persistent lemphedema

A

Lymphangiosarcoma

265
Q

Name the tumor: Endothelial malignancy most commonly of the skin, but also mouth, GI tract and respiratory tract. Associated with HHV-8 and HIV

A

Kaposi’s sarcoma

  • this is often mistaken for bacillary angiomatosis
266
Q

A patient has a port wine stain in the ophthalmic division of CN V what is the disease and what else is seen?

A

Sturge-Weber disease - describing a nevus flammeus

This is a congenital vascular disorder that affects capillary sized blood vessels. they can also have ipsilateral leptomaningeal angiomatosis, seizures and early onset glaucoma

267
Q

What drug is first line therapy for hypertension in pregnancy?

A

Hydralazine with methyldopa

268
Q

what is the number 1 drug used to treat lamignant hypertension?

A

Nitroprusside

269
Q

How does hydralazine work?

A

Increasing cGMP leading to smooth muscle relaxation , vasodilates arteries

270
Q

What is a side effect of using nitroprusside?

A

Can cause cyanide toxicity

271
Q

What is Fenoldopam?

A

A drug to treat malignant hypertension

272
Q

How does Fenoldopam work?

A

Dopamine D1 receptor agonist - causes coronary, peripheral , renal and splanchnic vasodilation
leads to decreased BP and increased natriuresis

273
Q

Which lipid lowering agent inhibits the conversion of HMG-CoA to mevalonate, a cholesterol precursor?

274
Q

How do statins work?

A

They inhibit HMG-CoA reductase

275
Q

Which lipid lowering agent is a competitive inhibitr of mevalonate production?

276
Q

Which lipid lowering agent has hepatotoxicity and rhabdomyolysis as side effects and can lead to myoglobinemia?

277
Q

Which lipid lowering agent work to mostly decreased LDL?

278
Q

Which lipid lowering agent inhibits lipolysis in adipose tissue?

279
Q

Which lipid lowering agent is the DOC for increasing HDL levels?

280
Q

Which lipid lowering agent reduces hepatic VLDL secretion into the circulation?

281
Q

Which lipid lowering agent can cause a red, flushed face and how do you stop this?

A

Niacin

You can administer aspirin 30 min before or it will go away on its own with prolonged use

282
Q

Which lipid lowering agent can cause hyperglycemia, acanthosis nigricans and hyperuricemia which can exacerbate gout?

283
Q

Which lipid lowering agent binds to clostridium difficile toxin?

A

Cholestyramine

284
Q

Which lipid lowering agent prevents intestinal reabsorption of bile acids and so the liver must use cholesterol in order to make more?

A

Bile acid resins

285
Q

Which lipid lowering agent do patients hate because it tastes bad and causes GI discomfort?

A

Bile acid resins

286
Q

Which lipid lowering agent can decrease absorption of fat soluble vitamins?

A

Bile acid resins

287
Q

Which lipid lowering agent Can lead to cholesterol gallstones?

A

Bile acid resins

288
Q

Name 3 types of bile acid resins

A

Cholestyramine, colestipol, colesevelam

289
Q

Which lipid lowering agent prevents cholesterol absorption at the small intestine brush border?

290
Q

Which lipid lowering agent rarely causes increased LFTs but can cause diarrhea?

291
Q

Which lipid lowering agent mostly lowers triglycerides?

292
Q

Which lipid lowering agent upregulates lipoprotein lipase leading to increased triglyceride clearance?

293
Q

Which lipid lowering agent can caused myositis, hepatotoxicity and cholesterol gallstones?

294
Q

Which two drugs should you not use in combination because they both cause hepatotoxicity?

A

Statins and fibrates

295
Q

Name 4 types of fibrates

A

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

296
Q

What drugs can be used for Chronic CHF and are shown to improve survival?

A

ACE inhibitors
ARBs
Aldosterone antagonists
certain beta blockers - metoprolol, cervedilol, bisoprolol

297
Q

What drugs can be used for chronic CHF symptoms but are NOT shown to improve survival?

A

diuretics esp loops - furosemide
digoxin
vasodilators like hydralazine or nitrates

298
Q

What drugs should you use for Acute decompensated CHF?

A

“NO LIP”

Nitrates
Oxygen
Loop diuretics
Inotropic drugs like dobutamine or phosphodiesterase inhibitors
Positioning
299
Q

What are the classes for antiarrhythmics?

A 
"No Bad Boy Keeps Clean"
Class I: Na channel blockers
Class II: Beta Blockers
Class III: K+ channel blockers
Class IV - Ca 2+ channel blockers
300
Q

what drugs are included in Class IA antiarrhythmics?

A

“Double Quarter Pounder”

Disopyramide, Quinidine, Procainamide (IV)

301
Q

Which Class IA antiarrhythmics can cause lupus like syndrome?

A

Procainamide

302
Q

what drugs are included in Class IB antiarrhythmics?

A

“Mayo Lettuce Tomato”

Mexiletine, Lidocaine, Tocainide

303
Q

What drug should be used in WPW syndrome?

A

Procainamide

304
Q

Which class of drugs increase the QT interval, affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia?

A

Class IA antiarrhythmics

305
Q

what drugs are included in Class IC antiarrhythmics?

A

“Fries Please”

Flecainde, Propafenone

306
Q

What class of drugs are useful in acute ventricular arrhythmias (especially post MI) and in digitalis induced arrhythmias?

307
Q

what drugs are included in Class II antiarrhythmics?

A

Beta blockers like Metoprolol, propranolol, esmolol, atenolol or timolol

308
Q

How do Class II antiarrhythmics work?

A

Decreases the SA and AV nodal activity by decreasing cAMP and decreasing calcium currents

309
Q

Which slope do Class II antiarrhythmics decrease?

A

Slope of phase 4

310
Q

When are class II antiarrhythmics useful?

A

ventricular tachycardia, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

311
Q

Which beta blocker can cause dyslipidemia as a toxicity?

A

Metoprolol

312
Q

Which beta blocker can exacerbate vasospasm in Prinzmeta’s angina?

A

Propanolol

313
Q

How should you treat beta blocker overdose?

A

With glucagon

314
Q

what drugs are included in Class III antiarrhythmics?

A

K+ channel blockers - “AIDS”
Amiodarone
Ibutilide, Dofetilide, Sotalol

315
Q

which antiarrhythmic has class I, II, III, and IV effects because it alters the lipid membrane?

A

Amiodarone

316
Q

What should you check when using amiodarone?

A

PFTs, LFTs, TFTs

amiodarone can cause pulmonary fibrosis, hepatotoxicity, hypo/er thyroidism, corneal deposits, skin deposits resulting in photodermatitis, neurologic effects, constipation and cardiovascular effects

317
Q

What phase do class III antiarrhythmics work at?

318
Q

what drugs are included in Class IV antiarrhythmics?

A

Nondihydropyridine CCBs - verapamil, diltiazem

319
Q

Where do Class IV antiarrhythmics work?

A

they decreased the slope of phase 0

320
Q

what is the mechanism of Class IV antiarrhythmics?

A

Decrease conduction velocity, increase the effective refractory period, increase the PR interval

321
Q

what is the use of Class IV antiarrhythmics?

A

used in prevention of nodal arrhythmias like SVT

322
Q

what is the toxicity of Class IV antiarrhythmics?

A

Constipation, flushing, edema, CV effects

323
Q

When can Mg2+ be an effective treatment?

A

in Torsades de pointes and digoxin toxicity

324
Q

What is the MOA of adenosine?

A

increases K+ out of cells leading to hyperpolarizing the cell and decreased calcium influx

325
Q

What is the drug of choice in diagnosing/abolishing supraventricular tachycardia?

A

Adenosine

very short acting (15s)

326
Q

What are the SE of adenosine?

A

flushing, hypotension, chest pain

327
Q

What can block the affects of adenosine?

A

Theophylline and caffeine

328
Q

What is Atropine used to treat?

A

Sinus bradycardia

329
Q

What are the findings in a patient with ASD?

A

Loud S1 and wide, fixed split S2

First aid Chs Part 1 (8 decks)

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