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Cardiology > Nate extra, non DIT, FA cardio flash cards > Flashcards

Nate extra, non DIT, FA cardio flash cards

1
Q

Truncus arteriosus gives rise to

A

Ascending aorta and pulmonary artery

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2
Q

Bulbus cordis gives rise to

A

Smooth parts of the R. and L ventricle (outflow tract)

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3
Q

Primitive ventricle gives rise to

A

Trabeculated R and L ventricle

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4
Q

Primitive atria gives rise to

A

Trabeculated R and L atria

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5
Q

Right horn of sinus venosus (SV) gives rise to

A

Smooth part of R. atrium

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6
Q

Absorbed pulmonary veins give rise to

A

Smooth part of left atrium

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7
Q

Left horn of sinus venosus (SV) gives rise to

A

Coronary sinus

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8
Q

Right common cardinal vein and right anterior cardinal vein give rise to

A

SVC

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9
Q

What two structures fuse to form the aorticopulmonary septum? What embryologic tissue are they derived from?

A

The truncal and bulbar ridges (migrations of the neural crest)

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10
Q

What structure closes the interventricular foramen? What two tissues fuse to form this structure?

A

The interventricular foramen is closed by the membraneous inverventricular septum. It is formed via fusion of the dorsal aorticopulmonary septum and the ventral endocardial cushion tissue.

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11
Q

What causes a PFO?

A

Failure of the septum primum and secundum to fuse after birth

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12
Q

Fetal erythropoiesis occurs in which tissues? When?

A 
"Young liver synthesizes blood"
Yolk sac (week 3-10)
Liver (week 6- birth)
Spleen (week 15-30)
Bone marrow (week 22-adult)
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13
Q

Which bones have erythropoiesis occurring in them?

A

Ribs, skull, sternum, pelvis and vertebrae.

**Up until age 25, also have erythropoiesis occurring in the tibia and the femur also

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14
Q

What does fetal hemoglobin have higher affinity for oxygen than maternal hemoglobin?

A

The fetal gamma unit has lower affinity for 2,6 BPG and therefore higher affinity for oxygen than the mothers beta unit of hemoglobin

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15
Q

Are the umbilical vessels named according to the relation of flow to moms heart or the fetus’ heart? How many umbilical vein(s) and artery(ies) are there?

A

Named according the how flow relates to the fetal heart. Therefore, flow towards the fetal heart is a umbilical vein. There is one umbilical vein bring oxygenated blood to the fetal heart and there are two umbilical arteries bring deoxygenate blood away from the fetal heart and back towards the mother

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16
Q

During the late stages of exercise how is CO maintained?

A

By HR only b/c stroke volume plateaus. Excessively high HRs decrease CO b/c diastole is too short too completely fill the ventricles.

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17
Q

How do catecholamines increase heart contractility?

How do catecholamines increase HR?

A

They act on beta 1 receptors -> increasing cAMP via AC. PKA then increases the activity of the Ca++ pump on the SR. This allows more calcium to be released (Ca++ induced Ca++ release) via the ryanodine receptor thus increasing contractility.

Heart rate is increased via the same mechanism above, but specifically they increase the likelihood that funny channels controlling the phase 4 depolarization (diastolic depolarization) are to be open, thus increasing HR.

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18
Q

What is the equation for resistance in a blood vessel? What things can alter the viscosity?

A

R = (8 x viscosity x length) / (pi x r^4)
Viscosity depends mainly on hematocrit. Increased viscosity is seen in polycythemia, hyperproteinemic states (ie multiple myeloma) and hereditary spherocytosis, Viscosity is decreased in anemia.

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19
Q

In general, do left heart valves or right heart valves close first?

A

Left heart is under higher pressure so they tend to close first (mitral and aortic valves before tricuspid and pulmonic valves).

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20
Q

What is the physiological mechanism of a S3 heart sound? What pathological conditions it is seen in? When is it normal?

A

An S3 heart sound is due to rapid ventricular filling in early. It is associated with elevated filling pressures (mitral regurgitation, CHF, L -> R shunts (VSD, ASD, PDA)) and is also more common in DILATED hearts. Normal in pregnant women, young athletes and children.

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21
Q

What is the physiological mechanism of a S4 heart sound? What pathological conditions it is seen in? When is it normal?

A

S4 heart sounds are heard at end of diastole right before S1. They are caused by “atrial kick” against a stiff ventricle. They are associated with ventricular hypertrophy. Never normal.

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22
Q

What are the 5 parts of the Jugular Venous Pulse (JVP)? And what causes each?

A

“At Carter’s crossing (X) vehicles yield”
a wave- atrial contraction
c wave- RV contraction (tricuspid bulges back into RA)
x descent- atrial relaxation, further ventricle contraction causes downward displacement of tricuspid b/c RV has ejected most of its blood
v wave- incr RA pressure d/t filling against closed tricuspid
y descent- rapid ventricular filling

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23
Q

What is the dicrotic notch? Why does it occur and what important function does it serve?

A

The dicrotic notch is a rebound in the aortic pressure after the aortic valve closes, while ventricular pressure continues to fall. It is due to the elastic property of the aorta. The wall of the aorta stretches during ventricular contraction and then this rebounding of the wall increases pressure in the aorta. It is important b/c it pushes blood back against the aortic valve and into the coronary arteries (remember: coronary arteries undergo DIASTOLIC FILLING).

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24
Q

What is normal splitting of the second heart sound?

A

Normally, the pulmonary valve will close slightly after the aortic valve. During inspiration, this split is widened. This happens because during inspiration decreased intrathoracic pressure pulls more blood into the right heart, thereby increase RV SV and increasing ejection time -> delayed closure of the pulmonic valve -> increased split.

**There is also an effect on the left heart during inspiration. Increased RV size pushes intenrventricular septum into the LV -> decreasing LV volume -> early aortic valve closure

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25
Q

What is wide splitting and when is it heard?

A

Wide splitting is an exagerration on normal splitting such that is seen regardless of breath). Occurs when there is delayed RV emptying (pulmonic stenosis, R bundle branch block)

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26
Q

What is fixed splitting and when does it occur?

A

Occurs with an ASD. L->R shunt which drastically increases R heart volumes and GREATLY delays pulmonic closure. Seen regardless of breath (basically an exaggeration of wide splitting)

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27
Q

What is paradoxical splitting and when does it occur?

A

Paradoxical splitting occurs when the aortic valve closes after the pulmonic valve. It occurs in conditions that delay LV emptying (aortic stenosis, L bundle branch block). How do we know the aortic valve is closing second? Just like before, inspiration will delay pulmonic valve closure. This will bring closure of aortic and pulmonic valves closure together, aka paradoxically eliminating the split. This doesn’t happen in other types of splits. Inspiration will either do nothing or widen the split.

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28
Q

What three heart murmurs have snaps or clicks?

A

Aortic stenosis has an ejection click in early systole.
Mitral stenosis has opening snap in early diastole
Mitral valve prolapse has a midsystolic click

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29
Q

In which position is auscultation of a PDA the loudest? When is a PDA murmur present in regard to heart sounds?

A

PDA is loudest when auscultated at the left infraclavicular area. It is a CONTINUOUS murmur, loudest near S2.

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30
Q

What are normal PR intervals and QRS complexes (how long)?

A

PR interval should be less than 200ms (one large box on EKG) and a narrow QRS complex (normal) should be less than 120ms (three small boxes on EKG).

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31
Q

What are the three EKG changes that could represent an MI?

A

ST elevation, pathological Q wave and T wave inversion

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32
Q

Where is the largest delay in the hearts conductions system?

A

AV node (100 ms) -> allows time for ventricular filling

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33
Q

What does a T wave tell you about electrolytes?

A

T wave is an indicator of potassium levels. A peaked T wave indicates high K+ and a flat T wave represents low K+

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34
Q

When is a U wave seen on an EKG?

A

Bradycardia or low potassium (think about a flattened T wave pushing K+ out and forming a new U wave)

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35
Q

A 12 year old boy has had multiple syncopal episodes and is deaf. What is the most likely cause?

A

Jervell and Lange-Nielson syndrome. This is an inherited (autosomal recessive) defect in potassium channels. This causes prolonged QT and syncope due to trigger Torsades. Tx- beta blocker and implantable defibrillator

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36
Q

What is the treatment of Torsades?

A

Push Mg2+

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37
Q

Common QT prolonging drugs

A

Macrolides (erythromycin), anti-malarial (chloroquine, methloquine), Haloperidol, risperidone, methadone, protease inhibitors, class Ia antiarrhythmics (procainamide, quinidine, disopyramid), class III antiarrhythmics (AIDS- amiodarone, ibutilide, dofetilide, sotalol)

38
Q

What is the characteristic finding of Wolff Parkinson White on EKG? How is WPW treated?

A

Delta waves (initial widening of the QRS complex d/t some early ventricular depolarization thru an accessory pathway). Tx- Procainamide or Amiodarone (not adenosine!!!)

39
Q

What are the characteristic EKG findings in Atrial fibrillation?

A

“Irregularly irregular” -> no discreet P waves and irregularly spaces RR intervals.

40
Q

What are the characteristic EKG findings in Atrial flutter?

A

“Saw tooth” pattern of flutter waves. These are excessive P waves. The RR interval is regular compared to A-fib.

41
Q

Briefly describe heart blocks type 1st, 2nd and 3rd degree.

A

1st degree- consistently prolonged PR interval. usually asymptomatic

2nd degree type 1 (Wenckebach)- “Warning” -> progressive prolonging or PR interval until QRS is dropped. Also usually asymptomatic.

2nd degree type 2- No longer any change in PR interval. Simply non-conducted P waves that drop beats. Often 2:1 (2 P waves per QRS). Tx- pacemaker

3rd degree- Ventricular contraction independent of atrial contraction. Atrial rate > Ventricular rate. No correspondance b/w P-waves and QRS complexes. Still have a narrow QRS. Tx- pacemaker

42
Q

Which bacteria can cause heart block?

A

Borrelia burgdorferi (lymes disease)

43
Q

When is ANP released and what does it do?

A

ANP can be thought of as opposing aldosterone. Atria sense excess stretch and release ANP. ANP vasodilates vasculature and causes decreases sodium reabsorption in the medullary collecting duct. It also constricts the efferent arteriole and dilates the afferent arteriole (cGMP mediated) promoting diuresis.

ANP contributes to the “escape from aldosterone” mechanism.

44
Q

What do baroreceptors in the aortic arch sense and what nerve transmits their signal? How does the amount of stretch affect firing of that nerve?

A

The aortic arch only senses increased pressure. The vagus nerve transmits signals to the solitary nucleus of the medulla. Amount of stretch correlates to amount of baroreceptor firing -> aortic only sense increased stretch so there will be increased firing -> increased parasympathetic output/ decreased sympathetic output.

45
Q

What do baroreceptors in the carotid body sense and what nerve transmits their signal? How does the amount of stretch affect firing of that nerve?

A

The carotid body senses increased pressure AND decreased pressure. The hypoglossal nerve (CN IX) transmits signals to the solitary nucleus of the medulla.

Amount of stretch correlates to amount of baroreceptor firing:

1) if carotid body senses increased stretch so there will be increased firing -> increased parasympathetic output/ decreased sympathetic output.
2) if carotid body senses increased stretch so there will be decreased firing -> decreased parasympathetic output/ increased sympathetic output.

46
Q 
What are the pressures in the following structures:
RA-
RV-
Pulmonary artery-
LA-
LV-
Aorta-
A

RA- <12
LV- 130/10
Aorta- 130/90

47
Q

What is used to sense pulmonary capillary wedge pressure and what does the PCWP estimate?

A

The Swan-Ganz catheter measures the PCWP. This catheter gets wedged into one of the branches of the pulmonary artery, a blood inflates and the pressure PAST the ballon is measured. Essentially tells you if there is congestion in the left heart and what the pressure of the LA is. PCWP should be <12.

PCWP estimates LA pressure.

48
Q

What causes the Cushing reaction and what is the triad?

A

Increased intracranial pressure-> constricts arterioles -> ischemia leads to increased CO2 which is sense by central chemorecpetors -> increased sympathetic response -> hypertension leads to increased pressure -> baroreceptor response of bradycardia and respiratory depression.

Triad = hypertension, bradycardia, and respiratory depression.

49
Q

Which organ receives the highest cardiac output?

A

The lungs, DUH!

50
Q

Which organ has the highest O2 extraction %?

A

The heart

51
Q

Which organ receives the largest share of systemic cardiac output?

A

the liver

52
Q

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

A

The kidney

53
Q

What is unique about autoregulation of blood flow in the lungs?

A

It is the only tissue where hypoxia causes vasoconstriction because in the lung perfusion must match ventilation.

54
Q

What are the 4 things that happen in the teratology of fallot?

A 
PROVe
Pulmonary trunk stenosis
RVH
Overriding aorta
VSD
55
Q

What would most likely give you excercise intolerance and cyanosis in lower extremities only in a child.

A

This is PDA. The PDA is initially L->R shunt, but then reverses and causes deoxygenated blood to lower extremities. Infantile coarctation of the aorta does NOT cause cyanosis. Look for weak femoral pulses.

56
Q

What congenital cardiac defect is associated with 22q11 deletion syndrome?

A

The TRUNC FALLS from 22 to 11

Truncus arteriosus and tetraology of Fallot

57
Q

What congenital cardiac defect is associated with down syndrome?

A

Endocardial cushion defect -> ASD, VSD, AVSD

58
Q

What congenital cardiac defect is associated with congenital rubella?

A

Septal defects, PDA, Pulmonary artery stenosis

59
Q

What congenital cardiac defect is associated with Turner syndrome

A

Coarctation of the aorta (preductal)

60
Q

What congenital cardiac defect is associated with Marfan’s

A

Aortic insufficiency and dissection

61
Q

What congenital cardiac defect is associated with maternal diabetes

A

Transposition of the great vessels

62
Q

What is Monckeberg arterioloscerosis and where does it occur?

A

Calcification of the MEDIA. Monckeburg dont CURR. Coronaries, ulnar, renal, radial arteries. Monckeburg does NOT effect blood flow.

63
Q

What is the initiator of atherosclerosis? What is the earliest lesion seen in atherosclerosis?

A

Endothelial dysfunction. Fatty streak in the INTIMA

64
Q

What is the most common post MI complication in the first few days?

A

Arrhythmia

65
Q

When do you get rupture of the myocardium after and MI and what can it result in?

A

Days 3-7. Cardiac tamponade (free wall rupture), mitral regurgitation (papillary muscle rupture), VSD (septal rupture)

66
Q

What leads would you see Q waves in with an anterior wall infarct? What vessel?

A

V1-V4. LAD

67
Q

What leads would you see Q waves in with an anterolateral wall infarct? What vessel?

A

V1-V6. LCX

68
Q

What leads would you see Q waves in with an anteroseptal defect? What vessel?

A

V1-V2. LAD

69
Q

What leads would you see Q waves in with a lateral wall infarct? What vessel?

A

V6, I, aVL. LCX

70
Q

What leads would you see Q waves in with an inferior wall infarct? What vessel?

A

II, III, aVF

71
Q

After an MI, when is an aneurysm most likely to form? Complications?

A

One week post MI. Decreased CO, arrhythmias, thrombus/ embolus

72
Q

When would you most likely to get fibrinous pericarditis after an MI?

A

Days 1-3

73
Q

Unilateral headache and jaw pain (jaw claudication) in an elderly patient

A

Temporal (giant cell) arteritis. Can also cause blindness and joint pain (polymyalgia rheumatica). Must have elevated ESR. 1 year high dose corticosteroids.

74
Q

Young asian female, weak upper extremity pulses, B symptoms, incr ESR

A

Takayasu’s arteritis (granulomatous thickening of the aortic arch and proximal great vessels.

75
Q

34 year old man w/ purple spots on skin, headache, abdominal pain and Hep B, proteinuria. Diagnosis?

A

Polyarteritis nodosa

76
Q

What are the 6 important points about Kawaski disease?

A

1) Asian child
2) Hand and foot erythema/ peeling skin (handle bars and pegs of a kawaski motorcycle)
3) Oral -> (red cracked lips, strawberry tongue)
4) Cervical lymphadenitis
5) Coronary aneurysm-> rupture and MI
6) ASPIRIN and IVIG = Tx

77
Q

30 year old smoker with finger pain and Reynauds phenomenon

A

Buerger’s disease (thromboangitis obliterans)

78
Q

Lung disease, kidney disease, palpable purpura, p-ANCA, no granulomas

A

Microscopic polyangitis. Tx- cyclophosphamide and corticosteroids

79
Q

Necrotizing vasculits, necrotizing GRANULOMAS in lung and upper airway, necrotizing glomerulonephritis

A

Wegener’s granulonatosis: hempotysis, perforated nasal septum, chronic sinusitis, otitis media, hematuria, red cell casts, +c-ANCA, Tx- cyclophosphamide and corticosteroids.

80
Q

Chrug-Strauss unique things

A

Asthma, eosinophilia, elevated IgE, p-ANCA, Granulomas

81
Q

5 things to know about Henoch-Schonlein

A

1) Child with palpable purpura on legs/ buttocks
2) recent URI
3) Arthralgia (joint pain)- commonly in the knee
4) Abdominal pain
5) IgA nephropathy

82
Q

Red lesion that can ulcerate and bleed. Associated with trauma and pregnancy

A

Pyogenic granuloma

83
Q

Hemangioma (red/pink) appears in the first few weeks of life and spontaneously regresses

A

Strawberry hemangioma

84
Q

Red mole on elderly person

A

Cherry hemangioma -> benign. Does NOT regress.

85
Q

Cavernous lymphangioma of the NECK

A

Cystic hygroma. A/w Turner syndrome

86
Q

Skin papule in AIDS patient caused by Bartonella henselae

A

Bacillary angiomatosis

87
Q

Blood vessel malignancy of the head, neck, breast area and liver. A/w aresenic, vinyl chloride and thorotrast/ radiation therapy.

A

Angiosarcoma

88
Q

lymphatic malignancy causing chronic lymphedema (ie post-radical mastectomy)

A

Lymphangiosarcoma

89
Q

Endothelial malignancy of the skin mostly (but also mouth, GI tract and respiratory tract). AIDS paitents

A

Kaposi’s sarcoma -> a/w HHV-8 and HIV

90
Q

Purple face discoloration, mental retardation, glaucomas, seizures

A

Sturge-Weber disease (port wine stain)

Cardiology (4 decks)

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