Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med Comprehensive > Cardio Diseases > Flashcards

Cardio Diseases Flashcards

1
Q

clinical presentation of stable angina

A

onset during activity or stress
located substernal or left chest with radiation to L upper extremity
lasts <3 min -15 min
tightness, squeezing, pressure (not pain)
worsened with activity, stress
releived by rest and nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

PE findings of stable angina

A 
HTN or hypotension
Apical systolic murmur
Levine's sign
Hyperlipidemia
RF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What diagnostis studies do you order for stable angina?

A

CBC, thyroid fn, hsCRP, ECG, ETT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do you diagnose CAD?

A 
Gold standard: cardiac catheterization
ETT
Echo stress test
nuclear stress test
coronary CT angiogram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What will ETT show for stable angina?

A

inversion of T waves and typical or atypical chest pain (low intermediate or high on Duke)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is accelerating angina?

A

change in typical symptoms, greater severity and onset with less physical exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical presentation of coronary vasospasm

A

Looks like STEMI
Typical anginal sx
Sx occur AT REST not w/ exercise
Circadian pattern → sx frequently occur in early morning hours
Significant clamping down of vessel and responds readily to nitro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RF of coronary vasospasm

A

RF: smoking, cocaine use, hyperventilation, provacative agents (histamine, serotonin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a specific clinical finding for Atrial septal defect?

A

Wide split S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where can you hear murmur for atrial septal defect?

A

Left upper sternal border because volume overload to the pulmonic region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 4 basic mechanisms of heart failure pathophysiology?

A
  1. Increased Blood Volume (Excessive Preload)
  2. Increased Resistance to Blood Flow (Excessive Afterload)
  3. Decreased contractility 4. Decreased Filling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What occurs with increased afterload?

A

CHF, HTN, aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What occurs with decreased afterload?

A

mitral regurgitation, VSD< AV fistula, septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you classift heart failure?

A

I - No sx
II – Sx with ordinary activity
III – Sx with slight activity
IV – Sx at rest

A – Risk factors but normal heart and no sx
B – Asymptomatic structural heart disease
C – Symptomatic structural heart disease
D – Decompensated heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Who is considered stage A heart failure?

A 
AT RISK
Hypertension
Known atherosclerotic disease
Diabetes
Metabolic syndrome
Cardiotoxin exposure
Familial history of cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Who is considered stage B?

A 
Prior MI
Decreased LV EF
Diastolic Dysfunction
LVH
Asymptomatic Valvular Disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are symptoms of right sided heart congestion?

A

GI discomfort, edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are symptoms of left sided heart congestion?

A

orthopnea, immediate dyspnea, fatigue, trouble concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is elevated JVP a sign of?

A

elevated intravascular volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does dehydration present?

A

skin cool and dry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does volume overload present?

A

skin is wet and warm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does CHF present?

A 
skin is wet and cool, Fatigue
Altered Activity
Chest congestion
Edema
SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are precipitants of heart failure?

A

calcium channel blockers, beta blockers, NSAIDS, infection, anemia, worsening HTN, dietary indiscretion, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the mechanism of action of AVNRT?

A

Reentry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the mechanism of shock?

A

reduced O2 delivery and tissue perfusion, increased O2 consumption or inadequate O2 utilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the signs and symptoms of shock?

A 
↓CO
↓SVR
tachycardia
Dyspnea
Restlessness
Diaphoresis
Metabolic acidosis
Hypotension
Ogliuria
cool, clammy skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is a key feature of distributive shock?

A

Decrease systemic vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What makes you highly suspicious of shock?

A

hypotension, tachycardia, oliguria, AMS, tachypnea, cool, clammy, cyanotic skin, metabolic acidosis, hyperlactatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a PE finding that makes you suspicious of shock in younger patients?

A

tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are mechanisms of arrhythmias?

A

abnormal impulse formation (automaticity or triggered activity) and/or impulse conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What has late afterdepolarizations?

A

digitalis toxicity

32
Q

What has early afterdepolarizations

A

long QT syndrome

33
Q

What happens to HR with conduction block?

A

bradycardia

34
Q

What happens to HR with reentry?

A

tachycardia

35
Q

What is a specific finding for atrial septal defect?

A

fixed split S2

36
Q

Epidemiology of atrial septal defect

A

MC 10% of all congenital Heart disease

37
Q

Pathophys of atrial septal defect

A

Septum should close at birth but doesn’t fully and allows blood fo flow from LA to RA

38
Q

Clinical presentation of atrial septal defect

A

Usually asymptomatic

If larger-fatigue, DOE, wide fixed S2 split, mid systolic, LUSB murmur, recurrent LRTI

39
Q

How to diagnose atrial septal defect

A

Echo-Doppler study to demonstrate shunt
Cardiac cath-to measur O2 saturation (will be higher in RA than expected)
Bubble study

40
Q

Epidemiology of ventricular septal defect

A

MC than ASD but many will heal on own

41
Q

Pathophys of ventricular septal defect

A

Abnormal opening in interventricular septum
Small shunt-small Defect, less left to right shunt
Large shunt-large defect, low Pulm resistance

42
Q

Clinical presentation of ventricular septal defect

A

Asymptomatic if small
Heart failure if large defect
tachypnes, poor feeding, failure to thrive, frequent LRTI
If reversed shunt-dyspnea and cyanosis
harsh holosystolic murmur along LSB (smaller defects are louder), systolic thrill, mid diastolic murmur

43
Q

Diagnosis of ventricular septal defect

A 
Echo to confirm
Cardiac cath (unnecessary but will confirm step up in O2 from RA TO RV)
44
Q

Pathophys of pulmonic stenosis

A

Obstruction of flow across pulmonic valve due to abnormal development of valve or pulmonic artery

45
Q

Clinical presentation of pulmonic stenosis

A

Usually asymptomatic
DOE, exercise intolerance, r sided heart failure sx
Prominent JV a wave
RV heave and thrill
Widely split Sw and sour P2
Crescendo-decrescendo systolic murmur at LSB

46
Q

Diagnosis of pulmonic stenosis

A

Look at transvalvular gradient (if high need intervention)
Echo to confirm and assess pressure gradient
Mild <50 mmHg
Mod 50-80
Severe >80

47
Q

Pathophys of Patent Ductus Arteriosus

A

Ductus Fisk’s to close after birth resulting in persistent connection btwn pulmonary artery and aorta

48
Q

Clinical presentation of Patent Ductus Arteriosus

A

Small asymptomatic
larger looks like heart failure
Left to right shunt CHF, A fib in L atrial dilatation, continuous machine like murmur best at L subclavian region
Eisenmenger syndrome lower extremity cyanosis and clubbing

49
Q

Diagnosis of Patent Ductus Arteriosus

A

Echo can deter PDA, determine flow

50
Q

Pathophys of Coarctation of Aorta

A

Place aorta becomes narrowed→LVH

51
Q

Clinical presentation of Coarctation of Aorta

A

Firm bounding pulse in UE and diminished pulse in LE
Femoral pulses are weak or delayed
Preductal has differential cyanosis
Most cases are asx-postductal

52
Q

Diagnosis of Coarctation of Aorta

A

Echo: gradient change from high to low across the lesion

CXR-lower rib notching

53
Q

Epidemiology of Tetralogy of Fallot

A

MC form of cyanotic heart disease after infancy

Toddler

54
Q

Pathophys of Tetralogy of Fallot

A

Hole in intraventricular septum where AV and PV connect that causes mixing of blood in the aorta
Also mimics pulmonic stenosis (outflow tract is messed up)

55
Q

Clinical presentation of Tetralogy of Fallot

A

RVH & pulm stenosis

DOE
Mod cyanosis-clubbing of fingers and toes
Systolic ej murmur at LUSB

Spells: following exertion, feeding, crying→irritability, cyanosis, hyperventilation, syncope, convulsion→ squat relieves

56
Q

Epidemiology of Transposition of the Great Vessels

A

Rare but MC causes of neonatal cyanosis

Will only make it to birth if ductus arterosis in tact

57
Q

Pathophys of Transposition of the Great Vessels

A

Aorta arises off RV outflow tract and PA arises out of LA

Two closed loops-circulating deoxy blood throughout body and oxy blood through lungs

58
Q

Clinical presentation of Transposition of the Great Vessels

A

Blue baby

Extremely hypoxic

59
Q

Epidemiology and RF of Coronary Artery Disease

A

MC males

RF: inc age, diabetes II, smoking, physical inactivity, emotional stress, low intake of fruits and veggies, alcohol

60
Q

Pathophys of Coronary Artery Disease

A

Development of atherosclerotic plaques over long term
stable plaque vs nonstable
75% can no longer compensate

61
Q

Clinical presentation of Coronary Artery Disease

A

Asymptomatic
Angina
MI

62
Q

Epidemiology and RF of Stable Angina

A

At younger ages 45-64 Mc black women
>65 all
RF: DM, smoking

63
Q

Clinical presentation of Stable Angina

A 
Onset during activity
substernal or L chest
Lasts <3 to 15 min
Tightness, squeezing, burning, pressure, gas but not typically pain 
Worsened with activity, emotional stress and heavy meal
Relieved with rest and nitroglycerin
Levine’s sign
Hyoerlipidemia (xanthelosma)
Hypertension or hypotension
systolic murmur (mitral regurg)
64
Q

Prognosis of Stable Angina

A

Usually benign
CABG improves lifespan
PCI does not improve lifespan

Severity: number of diseased vessels, location, LV function, arrhythmias, accelerating angina, Duke Treadmill score

65
Q

RF of Coronary Vasospasm or Variant Angina

A

RF: smoking, cocaine use, hyperventilation, provacative agents (histamine, serotonin)

66
Q

Pathophys of Coronary Vasospasm or Variant Angina

A

vasospastic disorder that occurs in some patients

67
Q

Clinical presentation of Coronary Vasospasm or Variant Angina

A

Looks like STEMI
Typical anginal sx
Sx occur AT REST not w/ exercise
Circadian pattern → sx frequently occur in early morning hours
Significant clamping down of vessel and responds readily to nitro

68
Q

Diagnosis of Coronary Vasospasm or Variant Angina

A

Check cardiac biomarkers (troponin, CK, CK-MB)

12 lead EKG

69
Q

Pathophy of Unstable Angina & NSTEMI

A

Detachment of stable clot of plaque

partial obstruction by emboli, clot or spasm

70
Q

Clinical presentation of Unstable Angina & NSTEMI

A 
Sx of MI at rest
Dyspnea, nausea, diaphoresis, syncope
Hx of stable angina
S3 or S4, transient mitral regurg murmur, arrhythmias
1st clinical presentation of CAD
71
Q

Diagnosis of Unstable Angina & NSTEMI

A 
ECG-may show T wave inversion or ST depression
Labs
UA: no cardiac biomarkers
NSTEMI: does have release of biomarkers
Non-invasive stress test
72
Q

Epidemiology of Acute Myocardial Infarction

A

Males, older, smokers, diabetes, HTN, and obestiy, alcohol

73
Q

Pathophys of Acute Myocardial Infarction

A

Rise and fall in troponin or CKMB of myocardial necrosis biomarkers due to occlusive thrombosis

74
Q

Clinical presentation of Acute Myocardial Infarction

A

Look sick, sudden onset chest pain, substernal or L chest with radaiton to L upper extremity, continuous duration, dull pressure, aching pain, nothing makes better but anything makes it worse, severity close to 10
Pale, sweaty, agitated, restless, ↕BP or pulse, JVP, rales, pulm congestion, soft S1, pericardail friction rub (MI several days ago)

75
Q

Diagnosis of Acute Myocardial Infarction

A

ECG changes: ST elevation (>1 mm limb leads, >2mm precordail leads in 2 or more contiguous leads) or depression, pathologic Q waves
Cardiac biomarkers: CKMB, MB index, troponin I
CXR: failure or dissection

Clin Med Comprehensive (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions