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USMLE: step 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

What does the truncus arteriosus become?

A
  1. Ascending aorta

2. Pulmonary artery

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2
Q

What does the bulbus cordis become?

A

Becomes the conus cordis with inturn becomes the smooth part of L/R ventricular outflow tracks

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3
Q

What does right / left horn of sinus venosus become?

A

Right: Smooth part of right atrium
Left: coronary sinus

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4
Q

What forms the SVC?

A

Right anterior cardinal vein and common cardinal vein

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5
Q

Where does the SVC drain?

A

Right side of heart

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6
Q

When does heart start beating?

A

4th week, think, “4 chambers” and also 4 limbs

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7
Q

What is dextrocardia?

A

When heart is located in right side of thorax

- Spleen and liver often commonly switched as well

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8
Q

What is kartagener syndrome?

A

Mutation in L to R dynein microtubule protein of cillia:

  1. Dextrocardia
  2. Infertility
  3. URIs
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9
Q

What is the septum primum?

A
  • Small piece of tissue to come down between L / R atria forming the ostium primum
  • Reaches down to fuse w/ endocardial cushion
  • Once it connects to cushion on bottom, top undergoes apoptosis forming ostium secundum
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10
Q

What happens when septum primum fuses with endocardial cushion?

A
  • Ostium secundum forms where septum primum was so R/L atria still have a communication
  • Septum secundum begins to come down to flap over it `
  • Septum 1 / 2 are now flapping next to each other with one coming from top and one from bottom
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11
Q

What is an ostium?

A

Synonym for foramen

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12
Q

What becomes the foramen ovale?

A

The foramen secundum

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13
Q

What is the goal in forming foramen ovale?

A
  • Creating a valve / flap to prevent blood flowing from left to right atrium
  • The septum primum at bottom is acting as valve with higher pressure in R atria allowing it to open
  • Blood can / and is wanted to flow R / L allowing oxygenated blood from mother to enter L atria
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14
Q

What happens to foramen ovale at birth?

A
  • Pressure in R atria drops dramatically as pulm circuit opens when baby breathes
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15
Q

What is the fossa ovalis?

A

Remnant of the foramen ovale once pulm circuit opens and the septum 1 / 2 push together and fibrose

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16
Q

What is an embolism on brain indicative of?

A

Patent foramen ovale allowing DVT to move from R to L atria and into brain
***Normally DVTs will embolize in lung

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17
Q

What is cause of paradoxic embolism in brain?

A

Patent foramen ovale

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18
Q

Does muscular part of ventricular septum form from top of bottom of chambers?

A

Left and right ventricular muscular walls meet medially at bottom pushing muscle up from bottom to top
- Interventricular foramen is left and will be close by membranous interventricular septum coming from top

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19
Q

What is membranous interventricular septum derived from?

A
  • Endocardial cushion
  • Comes from top to bottom to close ventricular foramen
  • **More likely to break as muscle is stronger
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20
Q

What causes transposition of great vessels?

A

Failure of AV septum to properly rotate is it descends

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21
Q

What is problem of great vessel transposition?

A
  • Aorta connected to RV

- Pulm A connected to LV

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22
Q

What is necessary for great vessel swapping to be viable?

A

One of the following allowing blood to mix:

  1. VSD
  2. ASD
  3. Patent ovale
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23
Q

Cause of tetralogy of fallot? What is seen?

A

Anterior and lateral displacement of of ventricular septum:

  1. Pulmonary stenosis
  2. Open VSD with R -> L shunt
  3. RVH
  4. Overriding aorta: sits over VSD
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24
Q

What is persistent truncus arteriosus?

A
  • No septum formed to separate pulm artery and aorta

- One vessel draining both ventricles

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25
Q

What forms valves?

A

Endocardial cushion tissue

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26
Q

What is an atretic valve?

A

Valve that does not form

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27
Q

Which side is tricuspid on?

A

RIght

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28
Q

What is an atretic tricuspid valve?

A
  • One that does not effectively separate Right A / V

- RV becomes extremely tiny and LV is huge

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29
Q

What is ebstein’s anomaly?

A
  • Problem with apoptosis of tricuspid = leaflets tethered to myocardium
  • Right ventricle becomes atrialized as it appears RA descends into RV
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30
Q

When does fetal erythropoiesis being?

A

Week 3 in the yolk sac

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31
Q

When and where is fetal blood made?

A 
"Young liver synthesizes blood"
Yolk sac 
Liver: week 6 - birth 
Spleen: 10 - 28 week 
Bones: week 18
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32
Q

What happens in beta thalassemia?

A

Hepatosplenomegaly because parts of body that synthesized blood in utero not begin to do so again

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33
Q

Why does fetal hemoglobin have higher O2 binding affinity?

A

Binds 2-3 BPG much less avidly

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34
Q

What is 2-3 BPG byproduct of? What does it do?

A
  • Glycolysis
  • Binds and stabilizes deoxy hgB decreasing O2 binding
  • This occurs to increase O2 delivery
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35
Q

Where is highest fetal O2 saturation?

A

Umbilical vein

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36
Q

Fate of blood in umbilical vein?

A

Portal circulation / vein: 1/3

Ductus venosus: other 2/3 bypasses liver

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37
Q

What does ductus venosus connect to?

A

IVC bypasses liver

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38
Q

What do the great vessels supply?

A

The brain

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39
Q

What type of blood is in SVC in fetus? To where does it go

A
  • Very low oxygenation as it is returning blood from brain
  • Heads to RV or lungs
  • The rest is shunted across ductus arteriosus which is AFTER great vessels as we do not want low O2 blood going to brain
  • Allows deoxygenated blood to aorta then to veins and umbilical artery
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40
Q

What happens to DA when baby is separated from placenta?

A
  • High O2 in lungs = dilation

- Cutting cord = great decrease in PGE2 causing uterus and DA to contract

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41
Q

What is ligamentum arteriosum?

A

Remnant of ductus arteriosus

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42
Q

What drug closes PDA?

A
  • Want to inhibit COX to drop PGE

- INDOMETHACIN is drug of choice

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43
Q

What is allontos?

A
  • Outgrowth of yolk sac helping form umbilical vessels
  • Proximal portion drains urinary bladder and becomes urachus
  • Normally becomes median umbilical ligament
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44
Q

What do umbilical arteries become?

A

Medial umbilical ligament

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45
Q

What is median umbilical ligament derived from?

A

Urachus

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46
Q

What does umbilical vein become?

A

Ligamentum teres hepatis

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47
Q

What is fossa ovalis?

A

Remnant of foramen ovale

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48
Q

What is remnant of ductus arteriosus?

A

Ligamentum arteriosum

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49
Q

What loops the ligamentum arteriosum?

A

Left recurrent laryngeal nerve

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50
Q

What does PDA sounds like?

A

Pan systolic / diastolic machine like murmur

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51
Q

Infection associated with congenital PDA?

A

Rubella

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52
Q

What is a holosystolic murmur at left sternal border?

A

VSD

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53
Q

What does sorbitol dehydrogenase turn sorbitol into?

A

Fructose

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54
Q

What does RNA polymerase I, II, III do?

A

I: Ribosomal RNA, only in nucleolis
II: Messenger RNA
III: tRNA

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55
Q

Does a larger or smaller alveoli have higher pressure in it?

A

Smaller, causing air to flow into larger alveoli

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56
Q

What does surfactant do?

A

Decreases surface tension

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57
Q

What allows for an indirect inguinal hernia?

A

Patent processes vanginalis

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58
Q

What can patent process vanginalis lead to?

A
  1. Hydrocele

2. Indirect inguinal hernia

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59
Q

Type of hernia seen in kids?

A

Indirect inguinal

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60
Q

Difference between malingering and factitious disorder?

A

In malingering you are looking to gain something tangible, nothing other than attention is gained in factitious
*Goal is to assume sick role in factitious

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61
Q

What does the 12th rib overly?

A

Kidney

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62
Q

Treatment to prevent HIV transmission if woman is pregnant?

A

Antiretrovirals

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63
Q

What does V1 / 2 stimulation cause?

A

V1: vasoconstriction and PG release
V2: ADH response

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64
Q

What do the Various HPVs cause?

A

1 - 4: skin warts
6, 11: Condyloma accuminata
16, 18: Cancer

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65
Q

What drains the testes?

A

Para aortic nodes

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66
Q

What do the deep inguinal nodes drain?

A
  1. Glans penis
  2. Superficial nodes
  3. Posterior calf
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67
Q

What do superficial inguinal node drain?

A
  1. Scrotum

2. Nearly all cutaneous lymph from belly button to feet

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68
Q

Sign of chronic organ rejection?

A
  1. Vascular wall thickening q

2. Fibrosis

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69
Q

What are the causes of early cyanosis?

A

Right to left shunts “eaRLy”

  1. Truncus arteriosus
  2. Transposition of great vessels
  3. Tricuspid atresia
  4. Tetralogy of Fallot
  5. TAPVR
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70
Q

What is persistent truncus arteriosus? Other defect often associated?

A
  • Septum that divides ascending aorta and pulm artery did not develop
  • Caused by failure of neural crest cells
  • Blood from R/L V are mixing before leaving heart
  • *Almost always seen with VSD as the septum that would divide great vessels would also form membranous portion of ventricular septum
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71
Q

What is transposition of great vessels?

A
  • Aorta comes off RV
  • Pulm artery comes off LV
  • **Blood does not mix at all so another defect is necessary to make viable
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72
Q

What is tricuspid atresia? What is needed to make viable?

A
  • Little to no communication between RV/RA

* **ASD and VSD necessary for life

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73
Q

What is happening in tetralogy? Treatment?

A
  1. VSD
  2. Overriding aorta
  3. Pulmonary artery stenosis: forces blood through VSD which is where cyansosis comes from
  4. RVH
    ***Boot shaped heart seen on CXR
    Fix the VSD
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74
Q

What is boot shaped heart on CXR indicative of?

A

Tetralogy of Fallot

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75
Q

What is a tet spell?

A
  • Cyanosis seen in kid with tetralogy of fallot due to decreased O2 flow to brain
  • Fix by doing a squat to increase PVR which forces blood back through pulmonary circulation
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76
Q

What is a kid squatting indicative of?

A

Tetralogy of fallot

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77
Q

What is TAPVR?

A
  • Both R/L pulmonary vein drain to RA

- Should be going to LA so no oxygenated blood is making to body

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78
Q

What is Ebstein anomaly? Cause?

A
  • Often caused by Li
  • Tricuspid valve does not separate and is tethered down to RV wall causing extension into RA “Atrialization of RV”
  • Massive tricuspid regurg since valves can’t close
  • Right sided HF is main game
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79
Q

What is atrialization of RV indicative of?

A
  • Ebstein anomaly
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80
Q

What are the L -> R shunts in order of frequency?

A

VSD > ASD > PDA

*VSD most likely to close on own

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81
Q

Normal cause of VSD?

A
  • Endocardial cushion defect leading to failure of membranous portion of septum
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82
Q

What makes the ostium secundum? What causes senundum ASD?

A
  • Perforation in septum primum during development

- Septum secundum does not grow to cover ostium

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83
Q

Where does the DA connect?

A
  • Connects aortic arch distal to L subclavian
  • Is connecting the pulm artery and aorta
  • Allows blood to flow from RV to aortic arch while in womb to go to lower body
  • Foramen ovale is sending blood from R->L though great vessels to upper extremities
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84
Q

What happens in PDA?

A
  • Pulm vascular resistance has dropped so oxygenated blood from aorta is shunted back into lungs rather than rest of body
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85
Q

Continuous machine like murmur?

A

PDA

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86
Q

Presentation of PDA?

A
  • Machine like murmur
  • Upper extremities well perfused because great vessels are before PDA
  • However, when heads for descending, blood is shunted to lungs as lower resistance = lower extremity cyanosis
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87
Q

What is eisenmenger syndrome?

A
  • Reversal of L/R shunt to R/L shunt
  • Increase in pulmonary flow from L/R = vascular remodeling and pulm HTN = reversal of shunt as systemic is now lower pressure
  • **Late cyanosis as remodeling takes time
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88
Q

What does endothelin 1 do?

A
  1. Vasoconstric

2. Recruit vascular smooth muscle

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89
Q

How does clubbing occur?

A
  • Low O2 in blood
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90
Q

Associations with Coarctation of aorta?

A
  1. Turner syndrome

2. Bicuspid aorta

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91
Q

Presentation of coarctation?

A
  • BP in upper extremities > lower
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92
Q

Blood flow in coarctation?

A
  1. Narrowing of descending aorta pushes blood to Internal thoracic
  2. From thoracic to anterior intercostals, to posterior intercostals
  3. Posterior connects with aorta distal to coarctation = normal flow resumed
    * **Leads to characteristic notching under ribs
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93
Q

Where do intercostals run related to ribs?

A

Inferior

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94
Q

What is rib notching indicative of?

A

Coarctation of aorta

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95
Q

What is misplaced in tetralogy?

A

Infundibular septum

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96
Q

Presentation of fetal alcohol syndrome?

A
  1. Thin upper lip
  2. Small eye openings
  3. Smooth philtrum
  4. Short palpebral fissures
  5. VSD / ASD / PDA
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97
Q

Cardiac effects of Down syndrome?

A
  • Endocardial cushion defects as chromosome 21 codes for this area
  • Cushion = septum formation
  • Ostium primum ASD
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98
Q

CV problems in diabetic mother?

A
  • Transposition of great vessels
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99
Q

CV problem in marfans?

A
  1. Mitral valve prolapse
  2. Aortic regurg
  3. Aortic aneurism from weak walls
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100
Q

What does Li put the heart at risk or?

A

Ebstein’s anomaly

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101
Q

Heart association in turner’s?

A
  1. Bicuspid aorta

2. Coarctation

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102
Q

Cardiac anomaly in Williams syndrome?

A
  • Supravalvular aortic stenosis
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103
Q

What does mutation in 22q11 cause re. heart?

A
  1. Tetralogy
  2. Truncus arteriosus
    * *Problem with neural crest communication
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104
Q

What does BP need to be for HTN and urgency?

A

HTN: > 140
Urgency: > 180

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105
Q

Normal cause of secondary HTN?

A

RAAS activation:

  1. HYPERaldosteronism
  2. Decreased RBF
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106
Q

What is fibromuscular dysplasia?

A
  • Cause of secondary HTN in young women

- Fibrosis of tunica media leading to aneurysmal like dilatation of artery blocking renal blood flow

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107
Q

Tunica layers of vessels from in to out?

A
  1. Intima
  2. Media
  3. Externa
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108
Q

What is happening in papilledema?

A
  • Swelling of optic disk
  • Sign of hypertensive emergency
  • Caused by swelling = decrease drainage of CSF out of eye area
  • Increased pressure damages retinal A/V
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109
Q

What is vasa vasorum?

A

Small vessels providing outer layers of vessels with flow

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110
Q

What is corneal arcus?

A
  • Blue ring in cornea from deposition of cholesterol
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111
Q

Difference between arteriosclerosis and arteriolosclerosis?

A

Arteriolosclerosis: Extra LO means smaller vessels

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112
Q

When is hyaline arteriolosclerosis seen?

A
  1. HTN - high pressure pushes proteins in basement membrane damaging endothelium = collagen
  2. Diabetes mellitus - non enzymatic glycosylation = ROS
    - Damages endothelium via cytokines
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113
Q

When is onion skinning seen?

A

Extremely high BPs

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114
Q

What happens in monkeberg?

A
  • Idiopathic deposition of Ca

- Pipe stemming of arteries

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115
Q

Female risk factor for atherosclerosis?

A

> 50 yo: post menopause as estrogen was protective by increasing HDL

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116
Q

What does LDL do to vessels?

A
  • Attached to proteoglycans in vessel wall so attach
  • Become oxidized = ROS damaging endothelium
  • Endothelial cells express VCAM1 “Vascular cell adhesion molecule 1”
  • Also release MPC1 “Monocyte chemotactic protein 1”
  • **Combination of these 2 allow macs to enter vessel walls
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117
Q

What is VCAM1?

A

“Vascular cell adhesion molecule 1”

- Produced by endothelial cells in response to LDL damage

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118
Q

What recruits smooth muscle in atherosclerosis?

A
  • Macs production of PDGF moves muscle from media to intima

- Fibroblast GF tells fibroblasts to deposit as well

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119
Q

Where is greatest risk for AAA and why?

A
  • Below renal bifurcation as vessel here has no vaso vasorum
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120
Q

Presentation of aortic aneurism?

A
  1. Pulsatile mass

2 Low BP: from bleeding

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121
Q

Risk factors for thoracic aortic aneurism?

A
  1. HTN
  2. Marfan’s
  3. Ehlers Danlos
  4. Tertiary syphilis: enter vaso vasorum leading to inflammation
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122
Q

What is cystic medial degeneration?

A
  • Degeneration of elastin and vascular smooth muscle in media = tissue replaced with cysts
  • Cause of thoracic aneurysm
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123
Q

What do deceleration injuries often cause?

A

Thoracic aneurysm

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124
Q

What is aortic isthmus?

A

Transition zone between ascending and descending aorta at most risk for rupture

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125
Q

Last thing to tear before aortic rupture?

A

Adventitia

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126
Q

What is happening in aortic dissection? Presentation?

A
  • Intimal tear allowing blood flow into media
    Presents with:
    1. Sudden onset, tearing chest pain radiation to back
    2. Unequal BP in arms: compression of left subclavian but not right
    3. Tamponade blood around heart
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127
Q

What is “Sudden onset tearing chest pain radiation to back” indicative of?

A

Aortic dissection

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128
Q

Type A or B dissection more dangerous?

A

A, which is Ascending and unstable with risk of tamponade

129
Q

What is stable angina?

A
  • Chronic, fixed stenosis of vessel causing angina in times of increased demand
  • Only impact SUBendocardial layer
  • Resolves with rest
  • ST depression seen
130
Q

What is prinzmetal angina?

A
  • TRANSMURAL ischemia from vasospasm = ST elevation
131
Q

Things that can cause prinzmetal?

A
  1. Triptans
  2. Tobacco
  3. Cocaine
132
Q

Treatment of prinzmetal?

A
  1. Remove triggers
  2. Ca blocker to stop spasm
  3. Nitrate: dilation
133
Q

Does unstable angina improve with rest?

134
Q

What is chronic ischemic heart disease?

A
  • Chronic ischemic events = fibrosis

- Leads to HF

135
Q

What causes ST elevation?

A

Transmural ischemia

136
Q

What causes ST depression?

A

Subendocardial depression

137
Q

What does the right coronary supply?

A

SA / AV nodes

138
Q

Why does MI pain radiate to arm?

A

Both areas use same dorsal root ganglia in C7 - T5 distribution

139
Q

What is seen and risk in 0-4 hours post MI?

A 
Seen: nothing
Risk:
1. Arrhythmia
2. HF
3. Cardiogenic shock 
*Anaerobic metabolism = decrease ATP = malfunctioning Na/Kase and K accumulation in extracellular = arrhythmia
140
Q

What is seen and risk in 4-24 hours post MI?

A 
Seen:
1. Early coag necrosis
2. Release of cellular debris 
3. Edema / hemorrhage 
4 PMNs
5. Reperfusion
Complications:
1. Arrhythmia
2. HF
3. Cardiogenic shock
141
Q

What is seen and risk in 3-14 days post MI?

A 
Seen:
1. Macs
2. Granulation tissue at borders 
Risk:
1. Free wall rupture
2. Mitral regurge 
3. Septal rupture 
4. LV pseudoaneurysm
142
Q

What does tetrazolium stain do?

A

Bind LDH spilled by necrotic cells in MI to visualize it

143
Q

What is seen and risk in > 2 weeks post MI?

A 
Seen:
1. Scar
Risk:
1. Dressler syndrome
2. HF
3. Arrhythmias
4. True ventricular aneurysm
144
Q

What is seen and risk in 1-3 days post MI?

A 
Seen: 
1. Extensive coagulative necrosis
2. Acute inflammation with neutrophils
Risk:
1. Postinfarction  Fibrinous pericarditis
145
Q

What does infarct of LAD lead to

A

Rupture of septum and VSD

146
Q

Vessel feeding papillary muscle?

A

Posterior descending

147
Q

What is pseudoaneurysm?

A

Aneurysm at high risk for rupture because it only has 1 layer instead of 3

148
Q

What is dressler syndrome?

A

Macs are eating cardiac tissue and accidently present to T cell causing immune system to attack heart
- Seen > 2 weeks post MI

149
Q

What is ischemia?

A

Decreased blood flow to a tissue

150
Q

Do cells die in stable angina?

A

No, this is reversible injury

151
Q

What is hallmark of reversible injury?

A

Cellular swelling

152
Q

% stenosis required for angina?

153
Q

How long does pain in stable angina last?

A

> 20 minutes: after this irreversible cell death

154
Q

Hall mark of subendocardial ischemia?

A
  • ST depression, this is what occurs in stable angina
155
Q

Is unstable angina complete or incomplete occlusion?

A

Incomplete

156
Q

Unstable angina ST elevation or depression?

A

Depression: both stable and unstable are depressed

157
Q

What infarcts in LAD MI?

A

Anterior LV and anterior portion of ventricular septum

158
Q

What infarcts in Right coronary artery MI?

A

Posterior LV and posterior portion of ventricular septum

159
Q

Most sensitive and specific marker of MI?

A

Troponin I

  • Rises in 2 - 4 hours
  • Peaks in 24
  • Returns to normal in 1 week
160
Q

Use of CKMB?

A

Good at detecting new MIs

  • Peaks in 24
  • Rises in 4
  • Back to normal in 72
  • ***As such you can tell if new MI after 3 days whereas with troponin it stays elevated for 10 days
161
Q

What is contraction band necrosis?

A
  • From Ca entering necrotic cells via reperfusion causing them to contract
162
Q

Hallmarks of coagulative necrosis?

A
  1. Pyknosis
  2. Kereoexis
  3. Karyolysis
163
Q

When is yellow pallor seen in MI?

A

Entire inflammatory phase of PMNs and macs:

- 1 - 7 days

164
Q

When are fibrinous pericarditis, chest pain, and friction rub seen?

A
  • Days 1 - 3 as PMNs are mediating this
165
Q

What is cardiac tamponade?

A

When fluid gets between heart and pericardium (fibrous sac surrounding heart)
- Can be from LV rupture that occurs when mac each necrotic debris in days 4 - 7

166
Q

What feeds papillary muscles?

A

Right coronary artery

167
Q

What is hallmark of granulation tissue?

A
  1. Plump fibroblasts
  2. Collage
  3. Blood vessels
168
Q

What type of collagen is present in scar?

169
Q

Normal cause of sudden cardiac death?

A
  1. Fatal ventricular arrhythmia
170
Q

Which cardiomyopathies lead to left sided heart failure?

A
  1. Dilated

2. Restrictive

171
Q

Signs of left sided heart failure?

A
  1. Pulmonary edema
  2. Dyspnea
  3. Paroxysmal nocturnal dyspnea
  4. Orthopnea
  5. Crackles
172
Q

What are heart failure cells?

A

Hemosiderin laden macrophages
- From left sided heart failure when engorged capillaries rupture and blood pools in lung, macs eat them and become that color

173
Q

Systemic consequences of left sided heart failure?

A
  1. Decreased forward perfusion

2. Causes RAAS activation

174
Q

Most common cause of right sided heart failure?

A
  1. Left sided heart failure
  2. Left to right shunt
  3. Chronic lung disease = cor pulmonale
175
Q

Signs of right sided heart failure?

A
  1. JVD
  2. HSM
  3. Dependant pitting edema
  4. Cirrhosis / nutmeg liver
176
Q

Most common fetal heart defect and what is its association?

A

VSD associated with fetal alcohol syndrome

177
Q

Heart sound in ASD? Why?

A

Spit S2: extra volume on right side = delayed closure pulmonic valve

178
Q

Heart defect in rubella?

179
Q

What does the DA do?

A

Connect aorta to pulmonary artery after the great vessels

180
Q

What is cyanosis in lower extremities later in life indicative of?

181
Q

Where is coarctation in infantine form?

A
  • Distal to arch, proximal to PDA
  • Lower extremity cyanosis: Coaractation makes area distal to it lower pressure allowing blood from PDA to move to lower pressure area and head to lower exctremities as is distal to arch
  • Often seen in turners
182
Q

How does adult coarctation present?

A
  • Malformation distal to arch proximal to PDA
  • Blood forced up great vessels = HTN in upper extremities
  • HYPOtension and low pulse in lower extremities
183
Q

Association of adult coarctation?

A

Bicuspid aortic valves

184
Q

Markers of Group A strep infection?

A
  1. Anti ASO titers

2. Anti DNAse B titers

185
Q

What is the JONES criteria?

A 
Joints: migratory polyarthritis
O - Pancarditis 
Nodules in skin 
Erythema migratosums
Sydenham's chorea
186
Q

Valves involved in rheumatic fever?

A
  1. Mitral - always and first

2. Aortic - rarely

187
Q

What are aschoff bodies and when are they seen?

A
  • Fibrinoid material and macrophages seen in cardiac tissue in rheumatic fever myocarditis
  • Anitschkow cells in middle - histiocytes with slender wavy nuclei
188
Q

When are Anitschkow cells seen?

A

Rheumatic fever myocarditis

189
Q

Most common cause of death during acute phase rheumatic fever?

A

Myocarditis

190
Q

How does pericarditis present?

A

Friction rub - seen in RF

191
Q

What is happening to valves in RF?

A

Mitral: thickening of chordae tendinae and cusps
Aortic: Fusion of commisures

192
Q

When is fusion of aortic commissures seen?

193
Q

What distinguishes wear and tear aortic stenosis from that seen in RF?

A

RF will also have mitral valve issues and aortic valve will show fusion of commissures
- Normal aortic stenosis will not have these issues

194
Q

What is systolic click with crescendo decrescendo murmur indicative of?

A
  • Aortic stenosis: crescendo is from blood rushing out then dying down as blood finally forces valve open
195
Q

Impact of aortic stenosis on left ventricle?

A

CONCENTRIC hypertrophy

196
Q

When is blood flowing in aortic regurg? Causes?

A

During diastole:

  1. Most often caused by aortic root dilatation
  2. Aortic aneurysm
  3. Valvular damage from IE
197
Q

What is early blowing diastolic murmur indicative of?

A

Aortic regurg

198
Q

Presentation of aortic regurg?

A

“Hyperdynamic circulation”

  1. Bobbing head
  2. Bounding pulses
  3. Pulsatile nail beds
  4. Early blowing diastolic murmur
199
Q

What happens to LV in aortic regurg?

A
  1. LV dilation

2. ECCENTRIC hypertrophy: involves one aspect of ventricle

200
Q

What is midsystolic click indicative of?

A

MV prolapse

201
Q

What heart sound does MV prolapse make?

A

Midsystolic click

202
Q

What does papillary muscle rupture lead to?

A
  • Mitral regurg

- Often seen post MI

203
Q

What is holosystolic blowing murmur usually indicative of? When is it louder?

A

MV regurg

- Louder on squatting and expiration

204
Q

Sound of MV regurg?

A

Holosystolic blowing murmur louder when exhaling / squatting

205
Q

Whey is mitral regurg louder on expiration?

A
  • Expiration = more blood in LA increasing backwards pressure
206
Q

Difference in effect of active / chronic RF on valve?

A

Acute: regurg
Chronic: Stenosis

207
Q

Sound of mitral stenosis?

A

Opening snap followed by diastolic rumble

208
Q

What is following sound indicative of:

Opening snap followed by diastolic rumble

A

Mitral stenosis

209
Q

Sequelae of mitral stenosis?

A
  1. Pulm congestion / HTN

2. A fib: from stretching of atrium = abnormal wall movement an thrombi

210
Q

What is endocarditis usually impacting?

A
  • Inflammation of the endocardium that lines cardiac valves

- Usually caused by bacterial infection

211
Q

Most common cause of endocarditis? Tell me more about it?

A

Strep viridans

  • Low virulence - Infects previously damaged valves
  • Small vegetation that do not destroy valves
212
Q

Pathogenesis of strep v. ?

A
  • Damage endocardial surface develops thrombotic vegetations of platelets and fibrin
  • Transient bacteremia = bacteria being caught in these vegetations
213
Q

Most common cause of endocarditis in IV drug abuse? Characteristics?

A

S. Aureus

  • High virulence
  • Non damaged valves
  • Large vegetations destroying valves
  • Likes tricuspid as coming from circulation
214
Q

Bug in endocarditis of prosthetic valves?

A

S. Epidermidis

215
Q

Bug in endocarditis of colorectal carcinoma?

216
Q

What is next step if ptn has endocarditis with S bovis?

A

Check for colorectal carcinoma

217
Q

What causes endocarditis with negative blood cultures?

A 
"Hacek Group"
Haemophilus 
Actinobacillus 
Cardiobacterium 
Eikenella
Kingella
218
Q

Signs of endocarditis?

A
  1. Fever
  2. Murmur
  3. Janeway lesions - non tender
  4. Osler’s nodes - Painful
  5. Anemia of chronic disease
  6. Splinter hemorrhages in nail bed
219
Q

What does hepcidin do?

A
  • Released by liver in disease states to trap iron
  • Ferritin will be high
  • TIBC will be how
220
Q

What is libman sacks endocarditis?

A
  • Sterile vegetations from lupus
  • *Vegetations on both sides of cardiac valve
  • Mitral regurg
221
Q

What happens in dilated cardiomyopathy?

A
  • Massive dilation of all heart chambers
  • Leads to systolic dysfunction and BIventricular HF
  • Mitral / tricuspid regurg and arrhythmia
222
Q

Causes of dilated cardiomyopathy?

A
  1. Coxsackievirus
  2. Alcohol
  3. Cocaine
  4. Doxorubicin
  5. Pregnancy
223
Q

Cause of hypertrophic cardiomyopathy?

A

Autosomal dominant mutations in sarcomere proteins

224
Q

Features of hypertrophic cardiomyopathy?

A
  1. Decreased CO: heart so tight can’t be filled
  2. Sudden death from arrhythmias - young athletes
  3. Syncope with exercise
225
Q

How does hypertrophic cardiomyopathy appear on imaging?

A

Myofiber hypertrophy with disarray

226
Q

What is happening in restrictive cardiomyopathy?

A
  • Decreased compliance of ventricular endocardium

- Restricts filling during diastole

227
Q

Causes of restrictive myocardiopathy?

A
  1. Amyloid
  2. Sarcoid
  3. Hemochromatosis
  4. Endocardial fibroelastosis in kids
  5. Loeffler syndrome
228
Q

What is Loeffler syndrome?

A

Eosinophilic infiltrate into wall of heart = fibrosis = restrictive cardiomyopathy

229
Q

Presentation of restrictive cardiomyopathy?

A
  1. Low voltage EKG

2. Diminished QRS

230
Q

What is the following indicative of:

  1. Low voltage EKG
  2. Diminished QRS
A

Restrictive cardiomyopathy

231
Q

What does myxoma look like? Presentation?

A
  • Benign mesenchymal proliferation
  • Abundant ground substance
  • Causes syncope from mitral valve obstruction
232
Q

When is rhabdomyoma seen in heart?

A
  • Usually in ventricle of child

- Associated with tuberous sclerosis

233
Q

Most common tumor in heart?

A

Metastasis usually to pericardium

234
Q

When does acute rejection occur? What is seen?

A

1 - 4 weeks post transplant

  • Dense infiltrate of macs and T cells
  • Result of host T cell sensitivity to donor MHC
235
Q

What is cause of tetralogy of fallot?

A
  • Deviation of infundibular septum due to abnormal neural crest cell migration
236
Q

Which heart chamber lays over esophagus?

237
Q

What vessel is posterior to esophagus?

A

Descending thoracic aorta

238
Q

What is pulsus paradoxus? What does it indicated?

A
  • Fall of systolic > 10 on inspiration

- Indicates cardiac tempanonde

239
Q

Triad of signs indicative of cardiac tamponade?

A
  1. JVD
  2. Muffled heart sounds
  3. HYPOtension
240
Q

What is hibernating myocardium?

A
  • Reduced myocardial metabolism and function due to chronic state of ischemia
  • Normal function can return when reperfused
241
Q

How long after infarct will ATP levels drop to levels preventing contraction?

A

60 seconds

- Due to cessation of aerobic glycolysis and start of anaerobic

242
Q

After how long is myocardial ischemia irreversible?

A

30 Minuts, function will return if perfusion restored but there will be a lag

243
Q

Impact of adenosine on vessels?

A

Vasodilator - as ATP runs out and is broken down, it will help to keep blood flowing

244
Q

What is the following indicative of:

  • Narrow QRS
  • Absent B
  • Irregularly irregular intervals
A

A-Fib: AV node controls rate of ventricular contraction

245
Q

What controls rate of ventricular contraction in A fib?

246
Q

What does myxomatous degeneration with pooling of proteoglycans in media indicate?

A

Cystic medial degeneration that can cause Aortic aneurysm

- Often seen in marfans

247
Q

What is clubbing and cyanosis in distal extremities indicative of?

A

PDA - PDA is delivering oxygenated blood distal to left subclavian which is providing it to the lower extremities

248
Q

What causes cells to swell during ischemia?

A

Increased intracellular [Na/Ca] due to failure of pumps from lack of ATP

249
Q

Facial features of downs?

A
  1. Flat face
  2. Protruding tongue
  3. Small ears
  4. Epicanthal folds
  5. Upslanting palpebral fissures
250
Q

What is composition of amyloid found in atrai?

A

Missfolded beta pleated sheets of ANP

251
Q

What sounds would decreased compliance of hypertrophic atrial myocardium make?

252
Q

Describe the marfanoid habitus?

A
  1. Problem with eye lense
  2. Increased arm:height
  3. Breast bone abnormalities
  4. Hypermobile joints
  5. Scoliosis
  6. Long fingers
  7. Flat feet
  8. Tall and slender
  9. Decreased upper:lower body
253
Q

Mutation in marfans?

A
  • Mutation in glycoprotein fibrillin 1
254
Q

Heart disease in marfan’s?

A
  1. Mitral valve prolapse

2. Cystic medial degeneration of aorta = aortic disection which is most common cause of death

255
Q

Effects of ANP?

A
  1. Vasodilation
  2. Diuresis
  3. Natriuresis
    * Dilates afferent, inhibits aldosterone, inhibits renin and Na resorption
256
Q

Causes of CONcentric LV hypertrophy?

A

Increased wall thickness:

  1. HTN
  2. Aortic stenosis
257
Q

Causes of ECCentric LV hypertrophy?

A

Increased cavity size:

  1. Volume overload
  2. Aortic / mitral regurg
  3. MI
  4. Dilated cardiomyopathy
258
Q

What is holosystolic murmur at left sternal border that increases with hand grip?

259
Q

Do nitro and morphine reduce MI mortality?

A

No, only provide symptomatic relief

260
Q

What happens in dilated cardiomyopathy?

A
  • Myocyte damage leading to decreased systolic function
  • This increases wall tension
  • **Heart responds by adding sarcomeres in series
261
Q

When are sarcomeres added in series?

A

Dilated cardiomyopathy

262
Q

Causes of dilated cardiomyopathy?

A
  1. Alcohol: acetaldehyde is toxic
  2. Wet beriberi: Lack of B1, thiamine
  3. Coxsackie B
  4. T cruzi
  5. Cocaine: mitchondrial damage
  6. Doxorubicin: Intercalates DNA
  7. Hemochromatosis
  8. Pregnancy
263
Q

What does cytochrome C do?

A
  • Activate caspases = apoptosis
264
Q

What heart sound heard in dilated cardiomyopathy?

265
Q

2 people hypertrophic cardiomyopathy usually seen in?

A
  1. Young athlete

2. Friedreich’s ataxia

266
Q

Genetics of hypertrophic cardiomyopathy? What is happening?

A
  • AD mutation in beta myosin heavy chain leading to haphazardly arranged sarcomeres
  • Inflammation leads to fibroblast deposition of collagen
  • Sarcomeres added in PARALLEL = concentric thickening
  • Causes diastolic dysfunction as ventricle is not compliant
267
Q

When are sarcomeres added in parallel?

A

Hypertrophic cardiomyopathy

268
Q

Heart sound heard in hypertrophic cardiomyopathy?

269
Q

What happens in restrictive cardiomyopathy?

A
  • Infiltration of myocardium restricts filling
270
Q

Causes of restrictive cardiomyopathy?

A
  1. Endocardial Fibroelastosis
  2. Loeffler
  3. Sarcoid / Amyloid
  4. Hemochromatosis
  5. Radiation
271
Q

What happens to heart in Loeffler syndrome?

A

Eosinophils release MBP on heart = necrosis and fibrosis of heart

272
Q

Genetics of friedreich’s ataxia?

A

GAA repeat in frataxin gene

273
Q

What is problem in diastolic heart failure?

A
  • Stiff ventricle / decreased compliance
274
Q

What are orthopnea and paroxysmal nocturnal dyspnea signs of?

A

Left sided HF

275
Q

What causes acute endocarditis and what are virulence factors?

A

S. Aureus

  1. Hyaluronidase: damages valves
  2. Leukocidin: creates pores in myocytes
276
Q

Signs of bacterial endocarditis?

A
  1. Osler nodes - Ouch ouch
  2. Janeway’s lesions
  3. Roth spots
  4. New onset murmur
  5. Anemia of chronic disease
277
Q

Which valve does S aureus like to infect?

A
  • Tricuspid: introduced to stream from IVDs
278
Q

What causes subacute endocarditis?

A

Strep Viridans

- Needs a previously infected valve to cause damage

279
Q

What are vegetations on both sides of valves indicative of?

A

SLE - libman sachs endocarditis

280
Q

What is pain on inspiration that is relieved by sitting up and leaning forward indicative of?

A

Acute pericarditis

281
Q

What is cardiac tamponade?

A

Pathologic compression of heart chambers by fluid in pericardial space

282
Q

Presentation of cardiac tamponade?

A
  1. HYPOtension from decreased filling
  2. Distended neck veins
  3. Distant heart sounds: blocked by thick layer of fluid
  4. Pulsus paradoxus
283
Q

Major fear in giant cell arteritis?

A

Blindness from involvement of ophthalmic artery

- Need to give steroids immediately to prevent this

284
Q

What do 50% of persons with giant cell arteritis have?

A

Polymyalgia rheumatica

285
Q

Disease associated with polyarteritis nodosa?

286
Q

Vessels commonly impacted by polyarteritis nodosa?

A
  1. Renal - can activate RAAS
  2. Hepatic
  3. Splanchnic - Sharp abdominal pain
287
Q

Presentation kawasakis?

A
  1. Red tongue
  2. Desquamating rash on hands and feet
  3. MI
  4. Swollen eyes / lips
288
Q

Another name for granulomatosis with polyangiitis?

A

Wegener’s

289
Q

What is involved in wegener’s?

A
  1. Kidneys
  2. Lungs
  3. Nasopharynx
290
Q

How does microscopic polyangiitis differ from wegener’s?

A
  • No granulomas, no nasal involvement

* **Palpable purpura are seen

291
Q

Staining in wegener’s / microscopic?

A

Wegener’s: C-ANCA

Polyangiitis: P-ANCA

292
Q

What is seen in Churg strauss?

A
  1. IgE
  2. Eosinophils
  3. Allergic rhinitis
  4. Asthma
  5. Neuropathy: wrist drop / foot drop
293
Q

What is perivascular foci of collagen and giant cells indicative of?

A

Rheumatic fever

294
Q

When is free wall likely to rupture in MI and what is presentation?

A

5 - 14 days:

  1. Tamponade
  2. JVD
  3. Distant heart sounds
  4. HYPOtension / shock
295
Q

When is IV septum likely to rupture and how does present?

A

3 - 5 days:

  1. New holosystolic murmur
  2. Stepped up O2 level between LV and RV
296
Q

When will papillary muscle rupture and presentation?

A

3 - 5 days

  1. Acute pulmonary edema
  2. Severe mitral regurg
297
Q

When does RV fail in MI and presentation?

A

Acute

  1. Kussmaul sign
  2. Hypotension with clear lungs
298
Q

Cardiac defect in turner’s?

A
  1. Bicuspid aorta

2. Coarcted aorta

299
Q

Cardiac defect in tuberous sclerosis?

A

Rhabdomyoma

300
Q

Cardiac defect in marfan?

A

Cystic medial necrosis:

  1. Aortic dissection
  2. Aortic aneurysm
  3. Mitral valve prolapse
301
Q

Cardiac abnormality in digeorge?

A

Tetralogy of fallot

302
Q

What would prevent diphtheria infection?

A

IgG against circulating protein capsule

303
Q

Sequelae of aortic regurg?

A
  1. LV EDV increases
  2. Eccentric hypertrophy
  3. Hypertrophy increased chamber size and stroke volume
304
Q

What does ST elevation in 1/AVL indicate?

A

Left circumflex MI

305
Q

What does ST in V1-4 and V1-2 indicate?

A

V1-4: LAD infarct

V1-2: Distal LAD infarct

306
Q

What does ST in V1-6, I, and AVL indicate?

A

Left main coronary occlusion

307
Q

What does ST in II, III, AVF indicated?

A

Right coronary occlusion

308
Q

What is supine HYPOtension syndrome?

A
  • From baby pressing against SVC giving mom HYPOtension when laying down
309
Q

What does pulmonary capillary wedge pressure approximate?

A

Left atrial pressure

310
Q

Cardiac tissue velocity from Fast to slow?

A 
"Park At Ventura Avenue"
Purkinje
Atrial 
Ventricular 
AV node
311
Q

What is wide and fixed splitting of S2 indicative of?

312
Q

What is S3 indicative of and where is it best heard?

A

LV failure heard best with bell over apex in left lateral decubitus position

313
Q

Measurements seen in diastolic HF?

A
  1. Increased LVEDP
  2. Normal LVEDV
  3. Normal EF
314
Q

First step in atherosclerosis?

A

Endothelial injury

315
Q

What causes coronary sinus dilation?

A

Elevated right heart pressure from pulmonary HTN

316
Q

Cause of pulsus paradoxus other than pericardial disease?

A
  1. Asthma

2. COPD

317
Q

Presentation of osler weber rendu syndrome?

A
  1. Nosebleeds

2. Mucosal telangiectasias

318
Q

What heart abnormality can berry aneurysms be associated with?

A

Coarctation of aorta

319
Q

What is cause of platelet rich non bacterial thrombi to mitral valve?

A

Malignancy

USMLE: step 1 (15 decks)

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