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Gen. Med > Test #2 Slide Questions > Flashcards

Test #2 Slide Questions Flashcards

1
Q

What is the leading cause of death in young athletes?

A

Sudden cardiac death (75% of all deaths)

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2
Q

True or false: Almost 50% of cases of SCD is due to hypertrophic cardiomyopathy.

A

True

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3
Q

What is the other name for HCM?

A

Idiopathic hypertrophic subaortic stenosis (IHSS)

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4
Q

What is the #1 cause of sudden death in athletes less than 35 years old?

A

Hypertrophic cardiomyopathy

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5
Q

What two anatomical findings are present with HCM?

A

Abnormal growth of the ventricular septum & abnormal cardiac muscle cells

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6
Q

What two possible fatal problems arise in individuals with HCM?

A

Outflow obstruction (the thicker septum blocks bloodflow) and arrhythmias (result in ventricular fibrililation)

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7
Q

How prevalent is HCM?

A

1 in every 500 people

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8
Q

True or false: HCM is not very genetic.

A

False…HCM is very genetic. Typically people with HCM have one of 3 specific genes. These genes could cause differing severities in how HCM presents. Some people may not have any problems with exercise, and to others exercise could be fatal.

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9
Q

What are the risk factors of HCM? (x5)

A
  • Prior cardiac arrest
  • FHx of sudden cardiac death due to HCM
  • Unexplained exertional syncope
  • Exertional hypotension
  • Extreme left ventricular hypertrophy (>30mm)
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10
Q

What are some HCM symptoms? (x3)

A
  • *Asymptomatic in most cases
  • chest pain, lightheadness, syncope (especially with exertion), however cardiac arrest (or sudden cardiac death) is often the first symptom
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11
Q

What is one major sign of a possible HCM?

A

Often there are no physical findings (during PPE) but a systolic murmur that increases with valsalva may raise suspicion.

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12
Q

How is HCM diagnoses?

A

For sure with an echocardiogram. It will show the left ventricle to be thicker than 12mm and asymmetrical.

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13
Q

What is the athletic heart?

A

A increase in left ventricular mass and volume as a result of adaptation to exercise. (Hypertrophy of the heart so to speak).

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14
Q

What is one major difference between an athletic heart and HCM?

A

While both hearts will have increased mass, HCM will have a decreased left ventricular volume and an athletic heart will have an increase in volume.

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15
Q

True or false: Murmurs are often heard in highly trained aerobic athletes.

A

True…30-50% of these athletes may present with a heart murmur.

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16
Q

What is the treatment for HCM? (x3)

A

-Hold out of all strenuous exercise, sometimes treat with medications, or a implantable cardiac defibrillator (ICD). Some may be allowed

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17
Q

True or false: Some people with HCM may be allowed to participate in sports.

A

True

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18
Q

What is ventricular fibrillation?

A

When the heart “quivers” instead of beating.

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19
Q

What is a defibrillator?

A

An implantable device that detects V-fib and give the person a shock to place them back into rhythm.

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20
Q

What happens in someones diagnosed with an anomalous coronary artery?

A

They are lacking a coronary artery, have a very small coronary artery, or one of the coronary arteries will take an unusual pathway.

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21
Q

What are the two main symptoms associated with an anomalous coronary artery?

A

Angina and sudden death.

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22
Q

What is the treatment for an anomalous coronary artery?

A

CABG (coronary artery bypass graft)

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23
Q

What is Marfan Syndrome?

A

A disorder of connective tissue in which fibrillin is abnormally produced. This results in the connective tissue to be more elastic than normal. It is caused by an autosomal dominant inheritance.

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24
Q

What is fibrillin?

A

Connective tissue that helps give structure to blood vessels

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25
Q

How does a person with Marfan Syndrome look? (x4)

A
  • Tall stature with a wingspan greater than their height
  • Arachnodactyly (really long fingers)
  • Pectus excavatum (depressed sternum into chest)
  • Scoliosis
26
Q

What may also be associated with Marfan Syndrome that may require an opthamologist?

A

Lens dislocation (the tissue that holds the lens gets more elastic and stretchy)

27
Q

What is the main problem with Marfan syndrome?

A

Aortic aneurysms that may lead to aortic dissection (the tissue giving structure to the aorta gets stretchy and forms bubbles-aneurysm-which grow and eventually may pop).

28
Q

What two sports may be at greater risk for Marfan syndrome?

A

*Sports that require height and wingspan such as basketball and volleyball

29
Q

How is Marfan Syndrome diagnosed?

A

Echocardiogram and a slit lamp eye exam (for lens dislocation)

30
Q

How is Marfan Syndrome managed if an aneurysm is present?

A

Watched closely by cardiologist, prohibited from all sports, and aortic graft

31
Q

How is Marfan syndrome managed if an aneurysm is not present?

A

Annual echo, and low level cardiovascular stress sports (to avoid raising blood pressure) such as gold or walking

32
Q

If no aneurysm is diagnosed with Marfan syndrome, what types of sport activity or exercise is safe for them to do?

A

Golf.bowling, or walking for exercise (just trying to avoid raising blood pressure)

33
Q

What is the #1 cause of sudden death in Italy? What is its prevalence in the US?

A

Arrhythmogenic right ventricular dysplasia (ARVD); 5% of athletes (but may cause up to 20% of all sudden deaths in US)

34
Q

What is Arrhythmogenic Right Ventricular Dysplasia (ARVD)characterized by?

A

Fatty replacement of myocardium of the right ventricle, making the heart electrically unstable, and thus leading to arrhythmias

35
Q

What are the signs and symptoms of Arrhythmogenic Right Ventricular Dysplasia (ARVD)? (x3)

A
  • palpitations
  • syncope or presyncope
  • sudden death
36
Q

How do you diagnose Arrhythmogenic Right Ventricular Dysplasia (ARVD)? What is the best test to do so?

A

EKG abnormalities, echocardiogram, cardiac MRI (MRI is the best test)

37
Q

What is the management of Arrhythmogenic Right Ventricular Dysplasia (ARVD) if diagnosed? (x4)

A

No strenuous exercise, medications, ablation, or ICD

38
Q

What happens in a coarctation of the aorta? How does it present?

A

A congenital defect that creates a “bridge” (pinch) at the end of the aortic arch that decreases blood flow to the lower extremities. Pts present top heavy (large upper body and skinny lower body)

39
Q

What is commotio cordis?

A

Cardiac arrest caused by blunt trauma to the chest occurring during the T-wave of the heart electric cycle. By striking during this wave, it sends the heart into ventricular fibrillation

40
Q

Why would commotio cordis be more likely to occur in younger populations (under 16)?

A

Their bones (i.e. sternum) are more pliable and able to bend to absorb the impact. This causes the bones to squeeze the heart

41
Q

What are the three sports most likely to see commotio cordis? What is the prognosis of this disease?

A

Baseball, softball, and hockey

Low rate of rescue (7 reported survivors)

42
Q

What is the difference between a screening evaluation and a symptomatic evaluation for prevention of SCD?

A

Screening- more for prevention or in general

Symptomatic- after symptoms/episodes have occured

43
Q

What are the important personal history questions to ask during a SCD prevention screening? (x7)

A 
Syncope or near syncope
Chest pain
Palpitations
PMHx of heart problems
Past heart testing
More tired or SOB than peers
Unexplained seizure
44
Q

What are the important family history questions to ask during a SCD prevention screening? (x4)

A

Death from heart problem (unexpected/sudden death under the age of 49)
Drowning, car accident, SIDS
Other heart problems, pacemaker, ICD
Unexplained fainting, seizure, or near drowning

45
Q

What are two big key signs of a potential sudden cardiac arrest? What is a potential problem for rescuers dealing with SCA?

A

1) involuntary movements or seizure-like activity (20-30% of cases)
2) occasional breathing or agonal gasping
- inaccurate rescuer assessment of pulse or respiration, or that it is too time-consuming

46
Q

In dealing with sudden cardiac arrest, what is the time in which you want to do CPR and use the AED? What is the survival rate within this time frame? What is the survival rate outside of this time frame?

A

3-5 of the collapse

  • 41-74% survival within time frame
  • less than 5% survival with no AED or CPR
47
Q

What are the 8 steps to Emergency Prepardness for a sudden cardiac arrest event?

A

1) Chain of Survival
2) Establishing an EAP
3) Access to early defibrilition
4) Emergency communication
5) Emergency personnel
6) emergency equipment
7) Emergency transportations
8) Practice and review of the EAP

48
Q

What is the other name for Coronary Artery Disease (CAD)? What is it?

A

“Atherosclerotic heart disease”

-there is a decrease in oxygen delivery to the heart because of a blockage in a coronary artery(ies)…this is the #1 killer in the developed nations and 1 out of 3 people will develop it

49
Q

What are the two conditions included in CAD?

A

Angina pectoris and myocardial infarction

50
Q

Describe the pathogenesis of CAD.

A

A normal artery has damage to its intima (lining of the vessel) and a fatty streak penetrates the smooth muscle wall. Then a build-up of fibrous plaque builds up and eventually leads to occulusion or ruptures of the plaque. This can result in blockage or a clot

51
Q

Describe the pathophysiology of CAD.

A

Decreased blood flow is going to the heart muscle —> hypoxia —–> damage to heart muscle (if not corrected quickly)

52
Q

What are the major risk factors for CAD? Which are modifiable and which are nonmodifiable?

A
  • Cigarette smoking (modifiable)
  • elevated serum cholesterol (modifiable)
  • hypertension (modifiable)
  • diabetes mellitus (modifiable)
  • physical inactivity (modifiable)
  • age (nonmodifiable)
  • male (nonmodifiable)
  • family history (nonmodifiable)
  • race (nonmodifiable) (white men are more likely to have sudden death while black men are more likely to have heart disease)
53
Q

What are other contributing factors to CAD (besides modifiable and nonmodifiable risk factors)?

A

Obesity, response to stress, personality, hormonal status, and elevated triglycerides

54
Q

What is Syndrome X (Metabolix syndroms)?

A

Four factors that increase a person’s risk for heart disease, stroke, and diabetes. These include: obesity, insulin resistance, high blood cholesterol, and high blood pressure

55
Q

What is angina pectoris?

A

Ischemia of the heart muscle due to an imbalance between cardiac workload and oxygen supply (in general chest pain due to CAD)

56
Q

What are the symptoms for angina pectoris?

A

Retrosternal chest pressure that worsens with exercise but gets better with rest, that may radiateto the L arm, neck or back. Often mistaken for heartburn

57
Q

What is a acute myocardial infarction?

A

The oxygen supply to needs ratio is imbalanced and lasts long enough to cause injury to the myocardium. This may occur with gradual stenosis or a sudden plaque rupture

58
Q

What are the symptoms of an acute MI?

A

Chest pain (often similar to angina) but may or may not be more intense
Associated with:
-dyspnea, diaphoresis, nausea, lightheadedness, and pallor
**These symptoms will NOT resolve with rest or nitroglycerin

59
Q

What are the signs of an acute MI?

A

Hand over chest, tachycardia, bradycardia, tachypnea, and hypotension

60
Q

What are the three cardiac isoenzymes that are released in response to damage to the cardiac muscle cells? What is their importance during a cardiac episode?

A
  • Myoglobin
  • Troponin I
  • Creatine kinase MB
  • *Because they are released when there is damage to the heart, they may be a useful indicator of a MI if the EKG wasn’t abnormal
61
Q

What occurs during a cardiac catheterization?

A

Dye is injected to visualize an artery (or blockage of an artery) and a scope is inserted up through the femoral artery

Gen. Med (13 decks)

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