Clinmed: Cardiology

Front 1

What is an atrial septal defect?

Back 1

congenital heart defect characterized by persistence of foramen ovale or atrial-septal defect resulting in abnormal blood flow between atria

Front 2

What is the cause of an ejection systolic murmur in anemia?

Back 2

anemia -> O2 carrying capacity of blood reduced -> CO increases to meet metabolic demands -> heart pumps harder and faster -> creating ejection systolic murmur

constricted garden hose analogy:
-slow water speed -> no sound
-fast water speed -> sound

Front 3

What is the clinical presentation and diagnostic workup of patent ductus arteriosus?

Back 3

CLINICAL PRESENTATION:
dependent on size of shunt and degree of pulmonary HTN
diaphoresis with feeding
failure to thrive
tachypnea
S2 narrowly split or paradoxically split (narrows on inspiration and widens on expiration)
continuous machinery murmur
begins shortly after S1, peaks at S2, passes through S2 into diastole, becomes a decrescendo murmur and fades before S1
maximal at 2nd left intercostal space
radiates into anterior lung fields
diastolic flow murmur at apex
bounding peripheral pulses
widened pulse pressure

DIAGNOSTIC WORKUP:
CXR
EKG
ECHO

Front 4

What is the ddx for ejection systolic murmur?

Back 4

anemia
pregnancy
excessive exercise

Front 5

What is patent ductus arteriosus?

Back 5

congenital heart defect characterized by persistence of ductus arteriosus resulting in abnormal blood flow between pulmonary artery and aorta

ductus arteriosus normally closes spontaneously at 3-5 days of age

Front 6

What is dextrocardia?

Back 6

congenital defect where heart is situated on RT side of body

Front 7

What is tetralogy of fellot?

Back 7

congenital heart defect characterized by:
1. narrowing of pulmonary valve
2. thickening of RT ventricular wall
3. displacement of aorta over ventricular-septal defect
4. ventricular-septal defect

Front 8

What is the clinical presentation and diagnostic workup of tetralogy of fellot?

Back 8

CLINICAL PRESENTATION:
easy fatigability
exertional dyspnea
cyanotic spells characterized by:
1. sudden onset of cyanosis or deepening of cyanosis
2. dyspnea
3. altered consciousness ranging from irritability to syncope
4. decrease or disappearance of systolic ejection murmur d/t complete obstruction of right ventricular outflow tract
squatting (though rare since often diagnosed at birth)
cyanosis
clubbing
palpable RV lift
rough systolic ejection murmur at left sternal border in 3rd ICS, radiates to back

DIAGNOSTIC WORKUP:
CBC → polycythemia 2° to chronic arterial desaturation
CXR
EKG
ECHO

Front 9

What is rheumatic fever?

Back 9

complication of strep throat or scarlet fever

Front 10

What is the etiology of rheumatic fever?

Back 10

strep throat
scarlet fever

uncommon in United States

Front 11

What is the clinical presentation of rheumatic fever?

Back 11

recent infection
fatigue
fever
erythema marginatum → erythematous rings mostly on trunk that disappear and reappear over weeks to months
subcutaneous nodules → small painless nodules on extensor surfaces
chorea → abrupt nonrhythmic involuntary movements and muscular weakness
carditis
polyarthritis

Front 12

What is the diagnostic workup of rheumatic fever?

Back 12

↑ ESR
↑ CRP
↑ ASO → repeat in 10-14 days if normal
↑ PR interval on EKG → repeat in 2 weeks and 2 months if abnormal

also order:
CBC
BC if febrile
throat culture
CXR
echocardiogram → repeat in 1 month if negative

Hint 12

Current
Harrisons

Front 13

What is the diagnostic (Jones) criteria of rheumatic fever?

Back 13

recent strep throat + 2 major criteria or 1 major and 2 minor criteria

Major:
erythema marginatum
subcutaneous nodules
pericarditis, myocarditis, or endocarditis
polyarthritis
chorea

Minor:
hx of rheumatic fever or rheumatic heart disease
fever
arthralgias
↑ ESR
↑ CRP
↑ ASO
↑ PR interval on EKG

Hint 13

Current EMED ch19

Front 14

What is the most common symptom of rheumatic fever?

Back 14

arthritis

Front 15

What is the management of rheumatic fever?

Back 15

1. for strep throat → benzathine penicillin G 1.2 million units IM single dose
2. if penicillin allegy → erythromycin 40mg/kg daily
3. for fever and arthritis → aspirin
4. if refractory to aspirin → corticosteroids
4. bed rest until afebrile and resting HR, ESR, and EKG normal
5. to prevent recurrence → benzanthine penicillin G 1.2 million units IM every 4 weeks
-if no carditis → continue until 21 y/p
-if carditis + no valvular damage → continue for 10 years
-if carditis + valvular damge → continue for 10 years or until 40y/o if high risk for reexsposure of strep throat (parent, teacher, medical professional, military personnel)

If chorea:
1. provide calming environment
2. medications only control symptoms but do not alter duration or outcome
3. carbamazepine → may not see effect for 2 weeks, continue for 2 weeks after symptoms subside

If HF:
see HF management

Hint 15

Current ch10

Front 16

Who is most commonly affected by rheumatic fever?

Back 16

children 5-15y/o

Hint 16

Current ch10

Front 17

What are the complications of rheumatic fever?

Back 17

1. CHF
2. rheumatic heart disease
3. myocardial involvement
4. arrhythmia
5. pericardial effusion
6. rheumatic pneumonitis

Hint 17

Current ch10

Front 18

True or false, increasing HR decreases cardiac output?

Back 18

true

Front 19

What are causes of increased HR?

Back 19

stress, anxiety, body temperature, hormones (thyroxine, epinephrine, norepinephrine), medications

Front 20

What is pulsus alternans?

Back 20

pulse with alternating strong and weak beats

Front 21

What is the ddx of pulsus alternans?

Back 21

LT-sided HF
LT ventricular failure
low ejection fraction
pericardial effusion
asthma

Front 22

*What is the etiology of endocarditis?

Back 22

1. community acquired:

2. hospital acquired:
UTI, catheter infection, or nosocomial wound → bacteremia → endocarditis

3. prosthetic valve infection

4. IV drug use

Front 23

*What is the clinical presentation of endocarditis?

Back 23

fever
murmur
osler's nodes
subungual hemorrhages

Front 24

What is the diagnostic workup of endocarditis?

Back 24

BC x 3
echocardiography

Hint 24

Current ch118

Front 25

*What is the management of endocarditis?

Back 25

1. antibiotic therapy → dependent on BC results

Front 26

What is the general ddx for chest pain?

Back 26

cardiac
pulmonary
musculoskeletal
esophageal/GI
anxiety

Front 27

What is another name for thromboangiitis obliterans?

Back 27

Buerger's disease

Hint 27

Current ch12

Front 28

What is thromboangiitis obliterans?

Back 28

disease characterized by blood vessel inflammation and thrombosis
often resulting in blood vessel obstruction of the hands or feet

Front 29

Who is most commonly affected by thromboangiitis obliterans?

Back 29

20-40 y/o male smokers

Hint 29

Current ch12

Front 30

What is the etiology of thromboangiitis obliterans?

Back 30

cause unknown

associated with smoking

Hint 30

Current ch12

Front 31

What are the complications of thromboangiitis obliterans?

Back 31

necrosis → amputation

Front 32

What is the management of thromboangiitis obliterans?

Back 32

1. stop smoking to prevent amputation
2. avoid cold temperatures to prevent reduced circulation

Front 33

Define dyspnea.

Back 33

SOB; subjective difficulty in breathing

Front 34

Define orthopnea.

Back 34

SOB lying down that is relieved when upright

Front 35

Define paroxysmal nocturnal dyspnea.

Back 35

sudden SOB upon waking

Front 36

Define rubor.

Back 36

red discoloration of skin

Front 37

Define pallor.

Back 37

pale skin

Front 38

Define cyanosis.

Back 38

bluish discoloration of skin

Front 39

Define diaphoresis.

Back 39

sweating

Front 40

Define syncope.

Back 40

fainting

Front 41

What is the etiology of secondary HTN?

Back 41

KIDNEY:
chronic kidney disease
renal vascular HTN/disease

ENDOCRINOPATHIES:
thyroid disease
parathyroid disease
Cushing syndrome
primary hyperaldosteronism
pheochromocytoma

DRUGS:
alcohol
NSAIDs
decongestants
corticosteroids
cocaine
methamphetamines

sleep apnea
aortic coarctation

Front 42

*What is the diagnostic workup of HTN?

Back 42

Hct
BMP
-glucose - diabetes screening
-BUN/CREAT - kidney disease?
-calcium - parathyroid disease
LIPID -
UA - glucose, protein?
EKG - LVH?

Front 43

What is the etiology of occlusive disease of the lower extremeties?

Back 43

atherosclerosis

associated with:
smoking
DM

Hint 43

Current ch12

Front 44

What is the clinical presentation of occlusive disease of the lower extremeties?

Back 44

intermittent claudication of calf → exacerbated by exercise, relieved by rest

dependent rubor of foot with blanching upon elevation

reduced skin temp
atrophic changes → hair loss, thinning of skin, muscle atrophy, ulcerations (think toes!)
decreased pulses

Hint 44

Current ch12

Front 45

Define natriuresis.

Back 45

excretion of sodium in urine

Front 46

Describe the renin-angiotensin-aldosterone system.

Back 46

Front 47

What is the etiology of an aortic aneurysm?

Back 47

result from abnormal production or degradation of structural components (elastin and collagen) of aorta

associated with:
genetic or developmental diseases
trauma → penetrating or non-penetrating chest trauma
infection → syphilis, TB
vasculitis → giant cell arteritis, Takayasu arteritis
spondyloarthrapathies
degenerative diseases → associated with atherosclerosis

Front 48

What is the clinical presentation of an aortic aneurysm?

Back 48

Thoracic:
often asymptomatic
chest pain
SOB
cough
dysphagia
hoarseness → due to stretching of recurrent laryngeal nerve

Abdominal:
often asymptomatic
palpable, pulsatile, nontender mass
if painful → impending rupture → surgical emergency!!!
pain may refer to chest, back, or scrotum

Hint 48

Harrisons ch242

Front 49

What is the diagnostic workup of an aortic aneurysm?

Back 49

Thoracic:
CXR → widening of mediatinal shadow, displacement or compression of trachea or left mainstem bronchus
CT

Abdominal:
CT or abdominal ultrasound

Hint 49

Hairrons ch242

Front 50

What is the initial management of an aortic aneurysm?

Back 50

Thoracic:
1. long-term B-blocker
2. if symptomatic, >5.5cm, or growing >1cm per year → surgery
3. if Marfan syndrome + >5cm → surgery
4. if asymptomatic → monitor with CT every 6-12 months

Abdominal:
1. if symptomatic, expanding, or >5.5.cm → surgery

Hint 50

Harrisons ch242

Front 51

What is an aortic aneurysm?

Back 51

pathological dilation of the aorta

Front 52

90% of abdominal aortic aneurysms are related to?

Back 52

atherosclerosis

Hint 52

Harrisons ch242

Front 53

Back 53

widening of aortic shadow → thoracic aortic aneurysm

Front 54

What is aortic dissection?

Back 54

spontaneous tear in intima (inner) layer of aorta

Hint 54

Current ch12

Front 55

What is the etiology of aortic dissection?

Back 55

spontaneous

associated with:
HTN (most common)
pregnancy
bicuspid aortic valve
coarcation
abnormalities of smooth muscle, collagen, and elastin

Hint 55

Current ch12

Front 56

What is the clinical presentation of aortic dissection?

Back 56

sudden severe persistent chest pain
radiation to back, neck, or abdomen
HTN
peripheral pulses diminished or unequal
possible diastolic murmur due to aortic regurgitation

Hint 56

Current ch12

Front 57

What is the diagnostic workup of aortic dissection?

Back 57

EKG → LVH from long-standing HTN common
CXR → widened superior mediastinum
*CT → chest and abdomen

Hint 57

Current ch12

Front 58

What is the intial treatment of aortic dissection?

Back 58

EMERGENCY!!!

1. if suspected aortic dissection → aggressively lower BP via B-blocker (start even before diagnostic complete)
2. if type A or complicated type B → emergency surgery

Hint 58

Current ch12

Front 59

What are 3 things you need to determine when talking about arrhythmias?

Back 59

1. narrow or wide QRS complex
2. regular or irregular
3. normal, bradycardia, or tachycardia

Front 60

What is the etiology of sinus arrhythmia?

Back 60

normal in children and young adults
enhancement of vagal tone → digoxin, morphine
early sick sinus syndrome

Hint 60

Current Cardiology ch20

Front 61

What is the management of sinus arrhythmia?

Back 61

benign → no treatment necessary

Hint 61

Current Cardiology ch20

Front 62

What is the etiology of pulmonary HTN?

Back 62

primary → idiopathic; associated with genetic factors
secondary →

most common in younger women

Front 63

What is the clinical presentation of pulmonary HTN?

Back 63

cyanosis
dyspnea
right ventricle heave
elevated JVP

Front 64

What is the diagnostic workup of pulmonary HTN?

Back 64

CXR → enlarged pulmonary arteries
echocardiography → often diagnostic

Front 65

What is normal pulmonary arterial pressure?

Back 65

~25/9 mmHg

Hint 65

http://tiny.cc/merckBP

Front 66

*What is the etiology of cor pulmonale?

Back 66

pulmonary disease → most commonly COPD
pulmonary HTN

Front 67

What is unstable angina?

Back 67

angina pectoris with at least one of the following features:
1. occurs at rest or with minimal exertion, usually lasting >10 min
2. severe and of new onset (within last 4-6 weeks)
3. increasingly becomes more severe, prolonged, or frequent

Front 68

What is stable angina pectoris?

Back 68

1. chest or arm discomfort
2. associated with physical exertion or stress
3. relieved by 5-10 min rest or sublingual nitroglycerin

Front 69

What is NSTEMI?

Back 69

presentation of unstable angina + elevated cardiac biomarkers indicating myocardial necrosis

Front 70

What are 3 sources of BP measurement error?

Back 70

clinician
equipment
technique

http://tiny.cc/bp124

Front 71

What are Korotkoff sounds?

Back 71

sounds heard when measuring BP

Front 72

Describe how to accurately measure BP.

Back 72

ensure patient hasn't recently ingested caffeine, eaten food, or smoked cigarettes
ensure patient doesn't have full bladder
explain procedure to reduce anxiety
allow patient to quietly rest for 5 minutes
position patient correctly: have patient sit with back supported, midpoint of arm at heart level, legs uncrossed, feet on floor
use proper cuff size: bladder length should encircle 80% of adult's arm or 100% of child's arm; width should encircle 40% of adult’s arm
position cuff correctly: do not measure over clothing, snug fit, 1in above antecubital space, middle of bladder over brachial artery
take BP in warm, quiet room
do not measure when patient talking
palpate radial pulse and pump cuff to estimate systolic BP, pulse will disappear at systolic BP
place bell of stethoscope over brachial artery
rapidly inflate cuff 30mmHg above estimated systolic BP
deflate cuff 2-3 mm/sec
when sounds audible, deflate cuff 2 mmHg/pulse beat
continue slow deflation for 10 mmHg after last Korotkoff sounds heard to detect auscultory gap
rapidly and completely deflate cuff
do not inflate/deflate too slowly or quickly
record phase I (systolic BP) and phase V sounds (diastolic BP), do not round
in children or when sounds are heard nearly to 0 in adults, record phase IV sounds (ex: 136/64/10)
wait ≥30 sec to repeat or measure opposite arm
average measurements if >1 BP taken

http://tiny.cc/bp124

Front 73

What are the phases of Korotkoff sounds?

Back 73

phase I: when sounds appear = systolic BP
phase II: clinically insignificant
phase III: clinically insignificant
phase IV: muffled sounds
phase V: when sounds disappear = diastolic BP

http://tiny.cc/bp124

Front 74

Is the stethoscope diaphragm more effective at transmitting low or high frequency sounds?

Back 74

high frequency

Front 75

What are examples of high frequency sounds?

Back 75

splitting of sounds
opening snaps
aortic diastolic murmurs

Front 76

Do you press lightly or firmly when using the stethoscope diaphragm?

Back 76

firmly

Front 77

Do you press lightly or firmly when using the stethoscope bell?

Back 77

lightly

Front 78

Is the stethoscope bell more effective at transmitting low or high frequency sounds?

Back 78

low frequency

Front 79

What are examples of low frequency sounds?

Back 79

bruits
diastolic murmur of mitral stenosis
3rd and 4th heart sounds

Front 80

Define precordium.

Back 80

chest area overlying heart

Hint 80

Mosbys p414

Front 81

Define dextrocardia.

Back 81

heart located on RT side of body in mirror image of normal LT-sided heart

Hint 81

Mosbys p414

Front 82

Define situs inversus.

Back 82

heart and stomach found on LT side of body and liver on RT side

Hint 82

Mosbys p414

Front 83

List the layers of the heart and their functions.

Back 83

pericardium → outermost layer; fibrous double-walled sac encasing and protecting heart
myocardium → middle layer; muscular layer providing pumping action
epicardium → innermost layer; lines heart chambers and valves

Hint 83

Mosbys p414

Front 84

What is the function of the atria?

Back 84

collecting of blood

Front 85

What is the function of the ventricles?

Back 85

pumping of blood

Front 86

Back 86

Front 87

List the pathway of blood starting from the body.

Back 87

veins returning CO2 → superior/inferior vena cava → RT atrium → tricuspid valve → RT ventricle → pulmonic valve → pulmonary trunk → LT/RT pulmonary arteries → lungs → exchanges CO2 for O2 → LT/RT pulmonary veins → RT atrium → mitral valve → RT ventricle → aortic valve → ascending aorta → aortic arch → descending aorta → arteries supplying O2

Front 88

Where is PMI normally seen?

Back 88

LT mid-clavicular line in 5th ICS while sitting

*if in more than 1 ICP or seen while supine → suggest problem

Front 89

Define systole.

Back 89

phase of cardiac cycle characterized by ventricular contraction and atrial filling

Front 90

Define diastole.

Back 90

phase of cardiac cycle characterized by atrial contraction and ventricular relaxation

Front 91

What equipment is needed for the cardiac exam?

Back 91

marking pen
cm ruler
stethoscope

Front 92

Describe the cardiac exam.

Back 92

1. inspect precordium
2. inspect PMI → use tangential light at level of chest
3. palpate PMI → assess for heaves/lifts
4. measure PMI to midsternal line
5. palpate for thrills
6. auscultate with diaphragm
7. auscultate with bell
8. ask patient to lean forward and exhale → auscultate with diaphragm over aortic valve
9. auscultate with bell over

Front 93

List signs of HF.

Back 93

crackles
hepatomegaly
peripheral edema

Hint 93

Mosbys p428

Front 94

Absent apical impulse + faint heart sounds may indicate?

Back 94

pleural effusion
pericardial effusion

Hint 94

Mosbys p429

Front 95

Apical impulse that is more forceful and widely distributed, fills systole, or inferolaterally displaced may indicate?

Back 95

increased cardiac output
LT ventricular hypertrophy

Hint 95

Mosbys p430

Front 96

A lift along the LT sternal border may indicate?

Back 96

RT ventricular hypertrophy

Hint 96

Mosbys p430

Front 97

Loss of apical impulse may indicate?

Back 97

overlying air or fluid → pneumothorax, pleural effusion, pericardial effusion
displacement of heart beneath sternum

Hint 97

Mosbys p430

Front 98

Displacement of apical impulse to right + no loss of thrust may indicate?

Back 98

dextrocardia
diaphragmatic hernia
distended stomach
pulmonary abnormality

Hint 98

Mosbys p430

Front 99

Define thrill.

Back 99

palpable murmur

Hint 99

Mosbys p431

Front 100

Thrill + systole + suprasternal notch and/or RT 2nd-3rd ICS suggests?

Back 100

aortic stenosis

Hint 100

Mosbys p431

Front 101

Thrill + systole + suprasternal notch and/or LT 2nd-3rd ICS suggests?

Back 101

pulmonic stenosis

Hint 101

Mosbys p431

Front 102

Janeway lesions indicate?

Back 102

bacterial endocarditis

Front 103

Define S1.

Back 103

first heart sound characterized by "lubb" sound caused by closing of tricuspid and mitral valves

Hint 103

Mosbys p419

Front 104

Which is normally silent, opening or closing of heart valves?

Back 104

opening

Hint 104

Mosbys p419

Front 105

Define S2.

Back 105

second heart sound characterized by "dubb" sound caused by closing of pulmonic and aortic valves

Hint 105

Mosbys p419

Front 106

What are the 2 parts of S2?

Back 106

A2 → closing of aortic valve
P2 → closing of pulmonic valve

Hint 106

Mosbys p419

Front 107

Define S3.

Back 107

occasional third heart sound caused by filling of ventricles during diastole

Hint 107

Mosbys p419

Front 108

Define S4.

Back 108

occasional fourth heart sound caused by atrial kick

Hint 108

Mosbys p419

Front 109

What grade murmur is a thrill?

Back 109

grade IV

Hint 109

Mosbys p431

Front 110

Thrill + systole + LT 4th ICS may indicate?

Back 110

ventricular septal defect

Hint 110

Mosbys p431

Front 111

Thrill + systole + apex may indicate?

Back 111

mitral regurgitation

Hint 111

Mosbys p431

Front 112

Thrill + systole + LT lower sternal border may indicate?

Back 112

tetralogy of fallot

Hint 112

Mosbys p431

Front 113

Thrill + systole + LT upper sternal border +/- radiation may indicate?

Back 113

patent ductus arteriosus

Hint 113

Mosbys p431

Front 114

List the 5 locations for auscultating the heart.

Back 114

RT 2nd ICS at sternal border → aortic valve
LT 2nd ICS at sternal border → pulmonic valve
LT 3rd ICS at sternal border → Erb's point
LT 4th ICS at sternal border → tricuspid valve
LT 5th ICS at midclavicular line → mitral valve (PMI)

Hint 114

Mosbys p433

Front 115

What can you do to figure out if thrill corresponds with systole or diastole?

Back 115

palpate carotid pulse which coincides with S1

Front 116

What is the etiology of a thrill based on timing and location?

Back 116

Front 117

Back 117

Front 118

How can you differentiate S1 from S2?

Back 118

period between S1 and S2 is twice as quick as period between S2 and S1

Front 119

Define thrombosis.

Back 119

formation of a blood clot

Front 120

Define infarction.

Back 120

vascular obstruction → tissue hypoxia → tissue necrosis

Front 121

Define hypoxia.

Back 121

inadequate O2 supply to body or tissue

Front 122

Define anoxia.

Back 122

complete O2 deprivation

Front 123

Define hypoxemia.

Back 123

abnormally low [blood O2]

Front 124

Define stroke volume.

Back 124

volume of blood pumped from one ventricle of the heart with each beat

Front 125

How do you calculate cardiac output?

Back 125

SV X HR = CO

Front 126

The jugular veins help you evaluate?

Back 126

RT side of heart

Front 127

List risk factors of varicose veins.

Back 127

women 4x > men
genetic predisposition → Irish or German descent, mother with varicosities
age → veins become less elastic as age
race → whites > blacks
sedentary lifestyle → allows blood to pool and veins to be compromised

Hint 127

Mosbys p467

Front 128

Describe the peripheral vascular exam.

Back 128

1. inspect for JVD
2. inspect upper extremity
-skin color
-hair distribution
-varicosities
-ulcerations
-cyanosis
-clubbing
3. palpate upper extremity
-temperature
-skin texture
-edema
-capillary refill
4. assess pulses bilaterally
-carotid
-brachial
-radial
-ulnar

5. assess pulses
-abdominal aorta
-femoral

6. inspect lower extremity
-skin color
-hair distribution
-varicosities
-ulcerations
-cyanosis
-clubbing
7. palpate lower extremity
-temperature
-skin texture
-edema
-capillary refill
8. assess pulses bilaterally
-popliteal
-dorsalis pedis
-posterior tibialis

Front 129

What are you assessing when palpating pulses for the peripheral vascular exam?

Back 129

rhythm
amplitude
symmetry

Front 130

How is the amplitude of pulses documented?

Back 130

on scale of 0 to 4:
0 = absent, not palpable
1 = diminished, barely palpable
2 = expected
3 = full, increased
4 = bounding

Hint 130

Mosbys p470

Front 131

Define tachycardia.

Back 131

HR > 100

Hint 131

Mosbys p470

Front 132

Define bradycardia.

Back 132

HR < 60

Hint 132

Mosbys p470

Front 133

Define pulsus paradoxus.

Back 133

arterial pulse amplitude decreases on inspiration

Hint 133

Mosbys p470

Front 134

What is the ddx for pulsus paradoxus?

Back 134

COPD
pericardial effusion
constrictive pericarditis

Hint 134

Mosbys p470

Front 135

Define pulsus alternans.

Back 135

arterial pulse amplitude that alternates from beat to beat with weak and strong beats

Hint 135

Mosbys p470

Front 136

Pulsus alternans is associated with?

Back 136

LT ventricular HF

Hint 136

Mosbys p470

Front 137

What is the ddx for bounding pulse?

Back 137

exercise
atherosclerosis
aortic rigidity
patent ductus arteriosus
anemia
hyperthyroidism
fever
anxiety

Hint 137

Mosbys p470

Front 138

An irregular regular HR may indicate?

Back 138

sinus arrhythmia → increased HR on inspiration and decreased rate on expiration

Hint 138

Mosbys p470

Front 139

Asymmetrical pulses suggests?

Back 139

impaired circulation

Hint 139

Mosbys p470

Front 140

Diminished femoral pulse may indicate?

Back 140

aortic coarctation

Hint 140

Mosbys p470

Front 141

What is aortic coarctation?

Back 141

congenital condition characterized by narrowing of aorta where ductus arteriosus inserts

Front 142

When auscultating for bruits, what should you ask the patient to do?

Back 142

hold breath

Hint 142

Mosbys p472

Front 143

What are the 5 Ps of arterial occlusion?

Back 143

pain
paresthesias → if major artery occluded
pallor
pulselessness
paralysis → rarely

Hint 143

Mosbys p473

Front 144

Compartment syndrome is characterized by?

Back 144

pain
paresthesias
pallor
pulselessness
paralysis

Hint 144

Mosbys p473

Front 145

What is the ddx for carotid bruit?

Back 145

obstructive disease in carotid artery → athersclerosis, arteritis, fibromuscular hyperplasia
transmitted murmurs → aortic stenosis, severe aortic regurgitation, ruptured chordae tendinae of mitral valve
vigorous LT ventricular ejection → more common in children

Hint 145

Mosbys p472

Front 146

Define claudication.

Back 146

pain caused by muscle ischemia

Front 147

How do you differentiate pain due to vascular insufficiency and pain due to musculoskeletal disorders?

Back 147

Arterial:
onset during exercise
quickly relieved by rest
intensity increases with intensity and duration of exercise

Venous and Musculoskeletal:
onset during or several hours after exercise
relieved by rest but sometimes only after hours or days
greater variability than arterial pain in response to intensity and duration of exercise

Hint 147

Mosbys p473

Front 148

What is the range for normal BP?

Back 148

<120/80 mmHg

Hint 148

http://tiny.cc/jncvii

Front 149

What is the management for normal BP?

Back 149

encourage lifestyle modification:

1. ↑ fruit, vegetables, and low-fat dairy
2. ↓ sodium, fat, and alcohol → <2 drinks/day for men and <1 drink/day for women
3. get 30 minutes of aerobic exercise daily → brisk walking
4. obtain normal BMI → 18.5-24.9

Hint 149

http://tiny.cc/jncvii

Front 150

What is the BP range for pre-HTN?

Back 150

120/80-139/89 mmHg

Hint 150

http://tiny.cc/jncvii

Front 151

What is the managment for pre-HTN?

Back 151

1. encourage lifestyle modification
2. no drug therapy unless compelling indication → DM,
increased risk of coronary disease, post-MI, HF, chronic kidney disease

Hint 151

http://tiny.cc/jncvii

Front 152

What is the BP range for stage I HTN?

Back 152

140/90-159/99 mmHg

Hint 152

http://tiny.cc/jncvii

Front 153

What is the management for stage I HTN?

Back 153

1. encourage lifestyle modification
2. prescribe thiazide diuretic

Hint 153

http://tiny.cc/jncvii

Front 154

What is the BP range for stage II HTN?

Back 154

>160/100 mmHg

Hint 154

http://tiny.cc/jncvii

Front 155

What is the management for stage II HTN?

Back 155

1. encourage lifestyle modification
2. prescribe thiazide diuretic + either B-blocker, ACE inhibitor, ARB or CCB

Hint 155

http://tiny.cc/jncvii

Front 156

For BP management, what does "lifestyle modification" consist of?

Back 156

1. ↑ fruit, vegetables, and low-fat dairy
2. ↓ sodium, fat, and alcohol → <2 drinks/day for men and <1 drink/day for women
3. get 30 minutes of aerobic exercise daily → brisk walking
4. obtain normal BMI → 18.5-24.9

Hint 156

http://tiny.cc/jncvii

Front 157

For pre-HTN management, what qualifies as a "compelling indication" for drug therapy?

Back 157

DM
increased risk of coronary disease
post-MI
HF
chronic kidney disease

Hint 157

http://tiny.cc/jncvii

Front 158

Which is more common, essential HTN or secondary HTN?

Back 158

essential (95%)

Hint 158

Current

Front 159

What patient population is most commonly affected by isolated systolic HTN?

Back 159

elderly

Hint 159

Primary Care Medicine p130

Front 160

What is hypertensive urgency?

Back 160

severely elevated BP with NO signs of end-organ damage

Hint 160

EMED Current

Front 161

What is hypertensive emergency?

Back 161

severely elevated BP with signs of end-organ damage → mental status changes, cardiac ischemia, CHF, or acute renal failure

Hint 161

EMED Current

Front 162

What are the most important complications of HTN?

Back 162

coronary heart disease
stroke
HF
end-stage kidney disease

Hint 162

Current ch11

Front 163

What is the etiology of essential HTN?

Back 163

complex combination of genetic and environmental factors:

-sympathetic nervous system hyperactivity → young?
-abnormal cardiac or renal development → low birth weight?
-abnormal renin-angiotensin-aldosterone system
-abnormal natriuresis
-increased intracellular sodium and calcium
-polycythemia

-high salt intake
-low potassium intake
-high alcohol intake
-cigarette smoking
-obesity
-sleep apnea
-NSAIDs

Hint 163

Current ch11

Front 164

When should secondary HTN be suspected?

Back 164

1. presents at early age
2. presents >50y/o
3. HTN previously controlled but now refractory to treatment

Hint 164

Current ch11

Front 165

When does essential HTN usually present?

Back 165

25-55 y/o

Hint 165

Current ch11

Front 166

What are the risk factors of essential HTN?

Back 166

1. poor diet → low potassium, high sodium
2. sedentary lifestyle
3. alcohol
4. smoking
5. drugs → NSAIDs, decongestants, corticosteroids, oral contraceptives, cocaine, methamphetamines
6. obesity

Hint 166

Current ch11

Front 167

What is the full name for B-blockers?

Back 167

beta-adrenergic blocking agents

Front 168

List types of B-blockers.

Back 168

propranolol
atenolol
metoprolol

Front 169

What is the MOA of B-blockers?

Back 169

decrease activation of B1-adrenergic receptors on heart → decreasing cardiac output → decreasing BP

decrease renin → decreasing angiotensin II → decreasing aldosterone → decreasing Na+ and water retention → decreasing blood volume → decreasing cardiac output → decreasing BP

Hint 169

Pharmacology p220

Front 170

What B-receptors do propranolol, atenolol, and metoprolol effect?

Back 170

propranolol → decrease activation of B1 and B2
atenolol → decrease activation of B1
metoprolol → decrease activation of B1

Hint 170

Pharmacology p220

Front 171

What are the contraindications for propranolol?

Back 171

asthma → due to blockade of B2-mediated brochodilation

Hint 171

Pharmacology p220

Front 172

What are the indications for B-blockers?

Back 172

HTN in young white patients
HTN + concomitant diseases such as migraine HA, angina pectoris, previous MI, chronic HF, supraventricular tachyarrhythmia

Hint 172

Pharmacology p221

Front 173

What does ACE inhibitors stand for?

Back 173

angiotensin converting ezyme inhibitors

Front 174

List types of ACE inhibitors.

Back 174

lisinopril
captopril
benazepril
enalapril
quinapril

Front 175

What class of drugs end in -olol?

Back 175

B-blockers

Front 176

What class of drugs end in -pril?

Back 176

ACE inhibitors

Front 177

What is the MOA of ACE inhibitors?

Back 177

inhibit ACE → leading to decreased angiotenin II (and subsequent decreased vasoconstriciton) and increased bradykinin (and subsequent vasodilation)

ACE normally converts angiotensin I into angiotensin II leading to vasoconstriction
ACE also normally breaksdown bradykinin
bradykinin is a vasodilator

Hint 177

Pharmacology p222

Front 178

What are the indications for ACE inhibitors?

Back 178

HTN in young white patients
if used with diuretic → effect in black patients similar to white patients
post-MI
HF
diabetic neuropathy
albuminuria

Hint 178

Pharmacology p222

Front 179

What are the adverse effects of ACE inhibitors?

Back 179

dry cough
fever
rash
hyperkalemia
hypotension
angioedema or first-dose syncope → administer first dose under close observation of patient

Hint 179

Pharmacology p222

Front 180

What are the contraindications of ACE inhibitors?

Back 180

pregnancy
K supplementation
K-sparing diuretics

Hint 180

Pharmacology p222

Front 181

What class of drug ends in -artan?

Back 181

ARBs

Front 182

What does ARB stand for?

Back 182

angiotensin II receptor blockers

Front 183

List types of ARBs.

Back 183

losartan
valsartan

Front 184

What are the adverse effects of ARBs?

Back 184

similar to ACE inhibitors → fever, hypotension, skin rash, hyperkalemia
but compared to ACE inhibitors, risk of cough and angioedema significantly decreased

Hint 184

Pharmacology p223

Front 185

What are the indications for ARBs?

Back 185

alternative to ACE inhibitors
(i.e. if chronic cough)
HTN + diabetes → reduce nephrotoxicity of diabetes

Hint 185

Pharmacology p223

Front 186

What are the contraindications for ARBs?

Back 186

pregnancy

Hint 186

Pharmacology p223

Front 187

What is the treatment for ischemic heart disease?

Back 187

B-blocker
anti-platelet
smoking cessation
exercise
weight loss
treatment of diabetes and hyperlipidemias

if not well-controlled by B-blocker alone or B-blocker contraindicated → add or substitute CCB

if still not-well controlled → add nitrates

Hint 187

JNCVII

Front 188

What should be prescribed for HTN + HF?

Back 188

ACE inhibitor, B-blocker, and diuretic

if intolerant to ACE inhibitor → substitute ARB

if severe LT ventricular dysfunction → aldosterone anatagonist → spironolactone

Hint 188

JNCVII

Front 189

What is the BP goal for hypertensive diabetics?

Back 189

130/80 mmHg

Hint 189

JNCVII

Front 190

What should be prescribed for HTN + DM?

Back 190

thiazide diuretic, ACE inhibitor

B-blockers useful in combination
CCB useful in combination

Hint 190

JNCVII

Front 191

What is the BP goal for patients with HTN and chronic kidney disease?

Back 191

130/80 mmHg

Hint 191

JNCVII

Front 192

What should be prescribed for HTN + chronic kidney disease?

Back 192

ACE inhibitor or ARB + loop diuretic

Hint 192

JNCVII

Front 193

How do the effectiveness of B-blockers, ACE inhibitors, and ARBs compare in blacks and whites?

Back 193

monotherapy of B-blocker, ACE inhibitor or ARB less effective in blacks than whites

if combined with diuretic, these differences are abolished

ACE inhibitor less effective than either thiazide diuretic or CCB in blacks

Front 194

How do the adverse effects of ACE inhibitors compare in blacks and whites?

Back 194

risk of angioedema 3-4 times higher in blacks than whites

risk of cough higher in blacks than whites

Front 195

What are the adverse effects of B-blockers?

Back 195

CNS → fatigue, lethargy, insomnia, hallucinations
hypotension
bradycardia
sexual dysfunction → decreased libido or impotence

Hint 195

Pharmacology p221

Front 196

Discuss the approach to modifying treatment when antihypertensive agents adversely affect sexual function?

Back 196

to decrease risk of erectile dysfunction → encourage smoking cessasation, exercise, and weight loss

if erectile dysfunction occurs as a result of therapy → discontinue offending agent and prescribe a different one

Hint 196

JNCVII

Front 197

List types of CCBs.

Back 197

verapamil
diltiazem
nifedipine
amlodipine

Front 198

What are the indications for CCBs?

Back 198

verapamil → migraine HA, HTN, angina, supraventricular tachyarrhythmias

diltiazem → HTN, angina, supraventricular tachyarrhythmia

nifedipine and amlodipine → HTN, angina

overall useful in HTN with asthma, diabetes, angina or PVD

blacks respond well

Hint 198

Pharmacology p223

Front 199

What is the MOA of CCBs?

Back 199

block calcium channels → vasodilation of coronary vessels

Hint 199

Pharmacology p223

Front 200

What are the adverse effects of CCBs?

Back 200

verapamil → constipation

nifedipine and amlodipine → fatigue, dizziness, HA, hypotension

Hint 200

Pharmacology p223

Front 201

What are the contraindications for verapamil?

Back 201

CHF
AV block

Hint 201

Pharmacology p223

Front 202

What class of drugs ends in -zosin?

Back 202

alpha-blockers

Front 203

Lists types of alpha blockers.

Back 203

doxazosin
prazosin
terazosin

Front 204

What is the MOA of alpha blockers?

Back 204

block alpha 1 adrenergic receptors → decreasing peripheral vascular resistance and lowering BP by relaxation of arterial and venous smooth muscle

Front 205

What are the indications for prazosin?

Back 205

mild-to-moderate HTN
prescribed in combination with propranolol or a diuretic

Hint 205

Pharmacology p225

Front 206

What are the adverse effects of prazosin?

Back 206

reflex tachycardia
first-dose syncope

Hint 206

Pharmacology p225

Front 207

What are the indications for alpha-blockers?

Back 207

seldom used to treat HTN

Hint 207

Pharmacology p225

Front 208

List central alpha agonists.

Back 208

clonidine
guanabenz
methyldopa

Front 209

What are the indications for clonidine?

Back 209

HTN refractory to treatment with 2 or more drugs

useful in HTN + renal disease → does not decrease renal blood flow or glomerular filtration

Hint 209

Pharmacology p225

Front 210

What are the adverse effects of clonidine?

Back 210

sedation
drying of nasal mucosa

rebound HTN if withdrawn → so withdraw slowly

Hint 210

Pharmacology p226

Front 211

What are the indications for methyldopa?

Back 211

HTN + renal insufficiency

Hint 211

Pharmacology p226

Front 212

What type of drug is hydralazine?

Back 212

vasodilator → acting primarily on arteries and arterioles → decreasing peripheral resistance → reflex increase in HR and cardiac output

Hint 212

Pharmacology p226

Front 213

What are the indications for hydralazine?

Back 213

moderately severe HTN → prescribe with B-blocker (to balance reflex tachycardia) and loop diuretic (to decrease sodium retention)

pregnancy-induced HTN

Hint 213

Pharmacology p226

Front 214

What are the adverse effects of hydralazine?

Back 214

HA, nausea, sweating, tachycarida, arrhythmia, angina

Hint 214

Pharmacology p226

Front 215

What are the indications for minoxidil?

Back 215

severe to malignant HTN refractory to other drugs → prescribe with B-blocker (to balance reflex tachycardia) and loop diuretic (to decrease sodium retention)

Hint 215

Pharmacology p226

Front 216

What are the adverse effects of minoxidil?

Back 216

sodium and water retention volume overload, edema, and CHF

Hint 216

Pharmacology p226

Front 217

What does NCEP stand for?

Back 217

National Cholesterol Education Program

Hint 217

http://tiny.cc/ncep

Front 218

What is the goal of NCEP?

Back 218

"The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percent of Americans with high blood cholesterol."

Hint 218

http://tiny.cc/ncep

Front 219

What are the NCEP guidelines for 1° prevention screening in adults?

Back 219

fasting lipid profile (total cholesterol, LDL, HDL, triglycerides) for all adults >20 y/o every 5 years

Hint 219

http://tiny.cc/ncep1

Front 220

What are the ranges for optimal, borderline, and high total cholesterol?

Back 220

Hint 220

National Heart, Lung & Blood Institute - http://tiny.cc/ncep
NCEP Guidelines - http://tiny.cc/ncep1
Lab Tests Online - http://tiny.cc/lipid

Front 221

What are the ranges for optimal, near optimal, borderline high, high, and very high LDL cholesterol?

Back 221

Hint 221

National Heart, Lung & Blood Institute - http://tiny.cc/ncep
NCEP Guidelines - http://tiny.cc/ncep1
Lab Tests Online - http://tiny.cc/lipid

Front 222

If a patient does not fast for a lipid profile, which tests are valid and what are the indications for ordering a follow-up lipid profile?

Back 222

only total cholesterol and HDL are valid
order a follow-up lipid profile if total cholesterol >200 mg/dL or HDL <40 mg/dL

Hint 222

http://tiny.cc/ncep1

Front 223

List risk factors for atherosclerosis.

Back 223

1. >45y/o for men and >55y/o for women
2. FH of early heart disease
3. poor diet → high in saturated fat, trans fat, sodium, and sugar
4. lack of exercise
5. smoking
6. overweight or obesity
7. HTN
8. hyperlipidemia
9. DM

Hint 223

http://tiny.cc/nhlbi-atherosclerosis

Front 224

What is familial hypercholesterolemia?

Back 224

lipid disorder characterized by defective or absent cell-surface receptors for LDL resulting in unregulated synthesis of LDL

if heterozygous for this disorder → LDL concentrations are 2x normal; presents in 3rd-4th decade

if homozygous for this disorder → LDL concentrations 8x normal; presents in childhood

HMG CoA reductase inhibitors and bile-acid sequestrants not effective in treating this disorder

Hint 224

Current p1123

Front 225

What is familial hyperchylomicronemia?

Back 225

lipid disorder characterized by an abnormality in lipoprotein lipase

lipoprotein lipase normally enables peripheral tissues to take up triglyceride from VLDL particles and chylomicrons

Hint 225

Current p1123

Front 226

What is the clinical presentation and diagnostic workup of familial hyperchylomicronemia?

Back 226

presents in childhood with recurrent hepatosplenomegaly and pancreatitis

LIPID panel → hypertriglyceridemia

Hint 226

Current p1123

Front 227

Do modest amounts of alcohol (1-2 ounces) increase or decrease HDL cholesterol?

Back 227

increase

Hint 227

Current p1130

Front 228

What is the normal range for triglycerides?

Back 228

<150 mg/dL

Hint 228

Current p1133

Front 229

High triglycerides increases the risk for what condition?

Back 229

pancreatitis

Hint 229

Current p1133

Front 230

What is the management of hypertriglyceridemia?

Back 230

1. goal → TRIG <150 mg/dL; reduce risk of cardiovascular disease and pancreatitis
2. secondary causes → ask about alcohol, oral contraceptives, diuretics; BMP for chronic kidney disease; A1C for DM; obesity
2. dietary modification → restrict total calories; avoid alcohol, simple sugars, refined starches, and saturated/trans fats
3. exercise
4. if TRIG >500 mg/dL + refractory to dietary modification → prescribe triglyceride-lowering drug → fibric acid derivative, niacin, or HMG CoA reductase inhibitor

Hint 230

Current p1133

Front 231

What are the ranges for borderline high, high, and very high triglycerides?

Back 231

borderline high: 150-199 mg/dL
high: 200-499 mg/dL
very high: ≥500 mg/dL

Hint 231

http://tiny.cc/lipid

Front 232

True or false, in a LIPID profile, if TRIG is too high, LDL cannot be calculated?

Back 232

true
LDL cannot be calculated if TRIG >400

Front 233

What should you order to determine LDL, if LDL cannot be calculated because TRIG is >400?

Back 233

LDL direct

Front 234

What is the management for elevated LDL?

Back 234

1. goal → LDL <100; reduce risk of cardiovascular disease
2. secondary causes of total cholesterol → ask about alcohol/meds; order CMP, A1C, TSH
obstructive liver disease
chronic liver disease
nephrotic syndrome
DM
hypothyroidism
Cushing's syndrome
alcohol
oral contraceptives
corticosteroids
diuretics (short-term effects)
B-blockers (short-term effects)
2. diet therapy → reduce total fat to 25-30% of calories, reduce saturated fat to <7% of calories, reduce cholestrol to <200mg/d, eat more fruits, vegetables, and fiber, could try mediterranean diet

3. prevention/risk factor modification
-exercise 30 minutes per day
-lose weight
-reduce alcohol
-stop smoking
-control HTN
-control DM

Front 235

List 2° causes of hypercholesterolemia.

Back 235

obstructive liver disease
chronic liver disease
nephrotic syndrome
DM
hypothyroidism
Cushing's syndrome
alcohol
oral contraceptives
corticosteroids
diuretics (short-term effects)
B-blockers (short-term effects)

Hint 235

Current ch28

Front 236

List 2° causes of decreased HDL.

Back 236

sedentary lifestyle
obesity
B-blockers (short-term effects)

Hint 236

Current ch28

Front 237

List 2° causes of hypertriglyceridemia.

Back 237

obesity
chronic kidney disease
DM
alcohol
oral contraceptives
diuretics (short-term effects)

Hint 237

Current ch28

Front 238

List possible systolic murmurs.

Back 238

aortic or pulmonic stenosis
mitral or tricuspid regurgitation

Front 239

Describe systole and diastole.

Back 239

mitral and tricuspid valves close (S1)
aortic and pulmonic valves open
ventricles eject blood
aortic and pulmonic valves close (S2)
mitral and triscuspid valves open
ventricles fill with flood

Front 240

List possible diastolic murmurs.

Back 240

mitral or tricuspid stenosis
aortic or pulmonic regurgitation

Front 241

What is another name for aortic stenosis?

Back 241

systolic ejection murmur

Front 242

Describe the murmur of aortic stenosis.

Back 242

occurs between S1 and S2 → crescendo-decrescendo
S2 → paradoxically split, soft, or absent (since only pulmonic valve slamming shut)

Front 243

What is the clinical presentation of aortic stenosis?

Back 243

syncope, angina, LT ventricular HF → all present on exertion

harsh murmur between S1 and S2
crescendo-decrescendo
S2 paradoxically split, soft, or absent
best heard at RT 2nd ICS
radiation to carotid arteries

parvus et tardus → weakened and delayed carotid pulse

Front 244

What is the etiology of aortic stenosis?

Back 244

congenital biscuspid aortic valve → presents in middle/old age
degenerative aortic stenosis

Front 245

What are the HDL CHOLESTEROL ranges for increased risk, average risk, and less than average risk for coronary heart disease?

Back 245

increased: <40 mg/dL for men or <50 mg/dL for women
average: 40-50 mg/dL for men and 50-59 mg/dL for women
less than average: ≥60 for both men and women

Hint 245

http://tiny.cc/lipid

Front 246

What is the management of aortic stenosis?

Back 246

surgery for all symptomatic patients with aortic stenosis

Front 247

When is a lipid profile ordered?

Back 247

to determine risk of coronary artery disease

Hint 247

http://tiny.cc/lipid

Front 248

What is the prevention of aortic stenosis?

Back 248

risk factors same as atherosclerosis

Front 249

When is HS-CRP ordered?

Back 249

cardiac risk assessment

Hint 249

http://tiny.cc/hscrp

Front 250

What is the etiology of aortic regurgitation?

Back 250

congential biscupsid valve
HTN
endocarditis
aortic root dilation → syphilis, Marfan's syndrome, aortic dissection
ankylosing spondylitis
reactive arthritis

Front 251

Where is CRP synthesized and then secreted?

Back 251

liver then secreted into bloodstream

Hint 251

http://tiny.cc/hscrp

Front 252

What is the clinical presentation of aortic regurgitation?

Back 252

fatigue, exertional dyspnea, chest pain or LT ventricular HF

diastolic murmur
occurs between S2 and S1
best heard along LT sternal border

wide pulse pressure (i.e. distance between systolic and diastolic pressure widened since diastolic pressure cannot be maintained)

bounding pulse
-Corrigan's pulse → carotids
-Musset sign → head bobs with pulse
-Quinke pulse → nailbed capillary pulsations

Front 253

Which is more sensitive, CRP or HS-CRP?

Back 253

HS-CRP
more accurately detects lower concentrations of CRP

Hint 253

http://tiny.cc/hscrp

Front 254

Describe the murmur of aortic regurgitation.

Back 254

occurs between S2 and S1 during diastole
descrescendo
best heard along left sternal border

Front 255

What does an elevated CRP indicate?

Back 255

non-specific inflammation

Hint 255

http://tiny.cc/hscrp

Front 256

What is the management of aortic regurgitation?

Back 256

surgery

Front 257

What is the difference b/w CRP and HS-CRP?

Back 257

CRP detects elevated levels of CRP in patients w/ inflammation or infection

HS-CRP distinguishes b/w low normal and high normal levels of CRP in patients who are otherwise healthy

Hint 257

http://tiny.cc/hscrp

Front 258

What is the prevention of aortic regurgitation?

Back 258

reduce risk factors for HTN

Front 259

Should HS-CRP be ordered to determine cardiac risk in a patient w/ chronic inflammation?

Back 259

no
HS-CRP only meaningful in patients who are otherwise healthy

Hint 259

http://tiny.cc/hscrp1

Front 260

What is the etiology of mitral stenosis?

Back 260

pregnancy
congenital
rheumatic fever
endocarditis

Front 261

What is the clinical presentation of mitral stenosis?

Back 261

exertional dyspnea, orthpnea, and PND
pulmonary HTN
RT HF
Afib

Front 262

Describe the murmur of mitral stenosis.

Back 262

diastolic murmur
occurs between S2 and S1
opening snap (more severe the earlier the snap)
apical rumble
best heard at apex in LT lateral ducubitus position

Front 263

What is the management of mitral stenosis?

Back 263

if Afib → warfarin
if mild-to-moderate + planning on pregnancy → surgery
othewise surgery depends on symptoms and severity

Front 264

When do initial elevation, peak elevation, and normalization occur for MYGB, CK, CKMB, and TROP?

Back 264

Front 265

What is the etiology of mitral regurgitation?

Back 265

ventricular dilation
mitral valve prolapse
rheumatic fever
endocarditis
ischemic heart disease

Front 266

List procedures used in diagnosis of cardiac disorders.

Back 266

CXR
CT of heart
MRI with gadolinium contrast
resting EKG
stress EKG
ambulatory EKG (Holter/event monitoring
transthoracic ECHO
transesophageal ECHO
stress ECHO
doppler US of extremities
MUGA scan
scintigraphy with thallium scan
angiography
cardiac catheterization

Front 267

What is the clinical presentation of mitral regurgitation?

Back 267

if acute → no LT atrial dilation, but pulmonary congestion
if chronic → LT atrial dilation, fatigue, dyspnea

systolic murmur
occurs between S1 and S2
pansystolic
possible S3
best heard at apex radiating into axilla

can lead to Afib

Front 268

Describe the murmur of mitral regurgitation.

Back 268

systolic murmur
occurs between S1 and S2
pansystolic
associated with S3 if large regurgant volume
best heard at apex radiating into axilla

Front 269

What is the management of mitral regurgitation?

Back 269

surgery

Front 270

Describe the murmur of mitral valve prolapse.

Back 270

systolic murmur
pansystolic or late-systolic
single or multiple mid-systolic clicks

Front 271

What is the clinical presentation of mitral valve prolapse?

Back 271

usually asymptomatic
fatigue, dyspnea, palpitations, chest pain
systolic murmur
pansystolic or late-systolic
single or multiple mid-systolic clicks

skeletal changes → straight back, pectus, scoliosis
hyperreflexes

Front 272

What is the etiology of mitral valve prolaspe?

Back 272

common in thin females

dilated aortic root
Marfan's syndrome

Front 273

What is the management of mitral vavle prolapse?

Back 273

mitral valve repair
B-blocker if arrhythmia

Front 274

Describe the murmur of tricuspid stenosis.

Back 274

diastolic murmur
rumble mimicking mitral stenosis
louder with inspiration
best heard at LT lower sternal border

Hint 274

Current ch10

Front 275

What is the etiology of tricuspid stenosis?

Back 275

rheumatic fever (less common in U.S.)
carcinoid disease
iatrogenic → tricuspid valve repair or replacement

more common in women

Hint 275

Current ch10

Front 276

What is the clinical presentation of tricuspid stenosis?

Back 276

diastolic murmur
rumble mimicking mitral stenosis
louder with inspiration
best heard at LT lower sternal border

may lead to RT HF → elevated JVP (giant a wave), hepatomegaly, ascities, dependent edema

Hint 276

Current ch10

Front 277

What is the management of tricuspid stenosis?

Back 277

1. diuretic for edema → torsemide if gut edema → better abosorbed than furosemide
2. aldosterone inhibitor if hepatomegaly or ascites
3. surgery → bioprosthetic valve replacement

Hint 277

Current ch10

Front 278

Describe the murmur of tricuspid regurgitation.

Back 278

systolic murmur
pansystolic
increases with inspiration
possible S3
best heard at LT parasternal border

Front 279

What is the etiology of tricuspid regurgitation?

Back 279

pulmonary or cardiac disease, especially if pulmonary HTN present

Front 280

What is the clinical presentation of tricuspid regurgitation?

Back 280

systolic murmur
pansystolic
increases with inspiration
possible S3
best heard at LT parasternal border

systolic c-v wave in JVP
symptoms of RT HF → hepatomegaly, ascites, peripheral edema
cyanosis

Front 281

What is the management of tricuspid regurgitation?

Back 281

1. treat edema → torsemide, aldosterone inhibitor
2. treat underlying problem → LT heart disease, pulmonary HTN etc.
3. surgery → bioprosthetic valve replacement if also need to replace mitral valve

Front 282

What is dilated cardiomyopathy?

Back 282

condition characterized by LV dilation + systolic dysfunction (EF <50%)

Hint 282

Current ch10

Front 283

What is the etiology of dilated cardiomyopathy?

Back 283

often idiopathic
genetic diseases
postpartum
myocarditis
endocrinopathies
alcoholism
doxirubicin
major catecholamine discharge

most common in black men

Hint 283

Current ch10

Front 284

What is the clinical presentation of dilated cardiomyopathy?

Back 284

gradual signs of left ventricular HF or bi-ventricular HF: dyspnea
crackles
cardiomegaly
S3 gallop rhythm
↑ JVP
peripheral edema
ascites

Hint 284

Current ch10

Front 285

What is the diagnostic workup of dilated cardiomyopathy?

Back 285

EKG → ST-T changes, conduction abnormalities, ventricular ectopy
CXR → cardiomegaly, pulmonary edema
echocardiogram → LV dilation and dysfunction

Hint 285

Current ch10

Front 286

What is the initial management of dilated cardiomyopathy?

Back 286

1. refer to cardiologist
2. standard CHF therapy
2. restrict sodium
3. no alcohol

Hint 286

Current ch10

Front 287

What is the most common cardiomyopathy?

Back 287

dilated cardiomyopathy (25%)

Hint 287

Current ch10

Front 288

List 4 common types of cardiomyopathy.

Back 288

dilated
hypertrophic
restrictive
Tako-Tsubo

Hint 288

Current ch10

Front 289

What is hypertrophic cardiomyopathy?

Back 289

condition characterized by LVH + diastolic dysfunction

Front 290

What is the etiology of hypertrophic cardiomyopathy?

Back 290

hereditary

Hint 290

Current ch10

Front 291

What is the clinical presentation of hypertrophic cardiomyopathy?

Back 291

dyspnea
chest pain
postexertional syncope
↑ diastolic pressure
pulsus bisferiens
sustained PMI
S4

Hint 291

Current ch10

Front 292

What is the diagnostic workup of hypertrophic cardiomyopathy?

Back 292

EKG → LVH, exaggerated Q waves
CXR → mild cardiomegaly
echocardiogram → LVH, diastolic dysfunction

Hint 292

Current ch10

Front 293

What is the initial management of hypertrophic cardiomyopathy?

Back 293

1. B-blockers → slows HR → assisting in diastolic filling of stiff LV
2. refer to cardiologist if syncope, difficulty controlling symptoms, or high risk (FH of sudden death, marked hypertrophy, BP fails to increase with exercise)

Hint 293

Current ch10

Front 294

Compare dilated, hypertrophic, and restrictive cardiomyopathies.

Back 294

dilated → ventricles dilated
hypertrophic → ventricles thickened
restrictive → ventricles stiffened

Hint 294

Current ch10

Front 295

Define pulsus bisferiens.

Back 295

when palpating pulse, double peak can be appreciated (striking twice)

Front 296

What is the ddx for pulsus bisferiens?

Back 296

aortic stenosis + aortic insufficiency
aortic insufficiency
hypertrophic cardiomyopathy

Front 297

What are the complications of hypertrophic cardiomyopathy?

Back 297

sudden death
often due to post-exertional arrhythmia
often in young athletes

Front 298

What is the etiology of angina pectoris?

Back 298

usually atherosclerotic heart disease
congenital anomolies
arteritis
dissection
emboli
severe myocardial hypertrophy
severe aortic stenosis or regurgitation
hyperthyroidism
anemia
paroxysmal tachycardias

Front 299

What is the clinical presentation of angina pectoris?

Back 299

precordial chest pain
precipitated by exertion or stress
relieved by rest or nitrates
usually <3 minutes; possibly 15-20 minutes if caused by meal or anger
if >30 min → think ustable angina, MI, etc!!

Front 300

What is the diagnostic workup of angina pectoris?

Back 300

CPP
EKG
scintigraphy

Front 301

What is the most common cause of angina pectoris?

Back 301

atherosclerotic heart disease

Front 302

Symptomatic aortic stenosis is a contraindication for EKG stress testing, true or false?

Back 302

true

Front 303

Which is more common, left HF or right HF?

Back 303

left HF

Front 304

What is the Functional Classification of Heart Disease?

Back 304

classification system used for patients with heart disease to quantify and monitor symptoms associated with rest/activity

Front 305

Describe the components of the Functional Classification of Heart Disease.

Back 305

Front 306

What is class I of the Functional Classification of Heart Disease?

Back 306

no limitation of physical activity → ordinary physical activity does not cause undue fatigue, dyspnea, or anginal pain

Hint 306

Current

Front 307

What is class II of the Functional Classification of Heart Disease?

Back 307

slight limitation of physical activity → ordinary physical activity causes symptoms

Hint 307

Current

Front 308

What is class III of the Functional Classification of Heart Disease?

Back 308

marked limitation of physical activity → ordinary physical activity causes symptoms

Hint 308

Current

Front 309

What is class IV of the Functional Classification of Heart Disease?

Back 309

unable to engage in physical activity w/out discomfort → symptoms may be present at rest

Hint 309

Current

Front 310

When monitoring patients with heart disease, it is best to document SPECIFIC activities that cause symptoms, true or false?

Back 310

true → grocery shopping, vacuuming, climbing stairs, etc.

Hint 310

Current

Front 311

What is the clinical presentation of left HF vs. right HF?

Back 311

Left HF: think lungs!!!
fatigue
exertional dyspnea
orthopnea
PND
cough
crackles
pulmonary edema
gallop
cardiomegaly


Right HF: think body!!!
elevated JVD and JVP
dependent peripheral edema
hepatomegaly
ascites

Hint 311

Current ch10

Front 312

Why do orthopnea and PND occur in heart failure?

Back 312

when lying down, blood reaches the heart more easily than when standing which increases the heart's workload → if heart failure present, the heart can't compensate appropriately → blood backs up into lungs → SOB

Hint 312

Clinical Pathology p3

Front 313

Define preload.

Back 313

pressure that fills ventricles during diastole

Hint 313

Clinical Pathology p3

Front 314

Define afterload.

Back 314

resistance that heart faces during systole

Hint 314

Clinical Pathology p3

Front 315

What are the 2 goals for treatment of HF?

Back 315

HF causes ↓ forward flow and ↑ backup of flow, so goals are:

1. ↑ forward flow by increasing cardiac output
↑ force of ventricular contraction → inotropes
↓ rate of ventricular contraction → B-blockers
2. ↓ backup of flow by decreasing heart's workload
↓ intravascular volume → decrease preload → diuretics
dilate arteries → decrease afterload → vasodilators

Hint 315

Clinical Pathology p3

Front 316

What is the clinical use of inotropes in HF?

Back 316

↑ force of ventricular contraction → increasing cardiac output → increasing foward flow and decreasing backup of flow

Hint 316

Clinical Pathology p4

Front 317

What is the clinical use of beta-blockers in HF?

Back 317

↓ rate of ventricular contraction → allowing for more filling time → increasing cardiac output → increasing foward flow and decreasing backup of flow

Hint 317

Clinical Pathology p4

Front 318

What is the clinical use of diuretics in HF?

Back 318

↓ intravascular volume → decrease preload → decrease heart's workload → decrease backup of flow

Hint 318

Clinical Pathology p4

Front 319

What is the clinical use of vasodilators in HF?

Back 319

dilate arteries → decrease afterload → decrease heart's workload → decrease backup of flow

Hint 319

Clinical Pathology p4

Front 320

Describe the renin-angiotensin-aldosterone system in relation to HF.

Back 320

HF → decreased blood flow to kidneys → kidney releases renin → renin converts angiotensinogen to angiotensin I → ACE converts angiotensin I to angiotensin II → angiotensin II causes vasoconstriction + release of aldosterone from adrenals → aldosterone causes ↑ sodium (and water) reabsorption → increased BP

Hint 320

Clinical Pathology p5

Front 321

What is the MOA of ACE inhibitors?

Back 321

decrease conversion of angiotensin I to angiotensin II → preventing vasoconstriction and aldosterone release → preventing sodium/water retention → preventing ↑ BP → preventing back up of fluid

Hint 321

Clinical Pathology p5

Front 322

What is the MOA of ARBs?

Back 322

block angiotensin II receptors → preventing vasoconstriction and aldosterone release → preventing sodium/water retention → preventing ↑ BP → preventing back up of fluid

Hint 322

Clinical Pathology p5

Front 323

What does the ACE in ACE inhibitors stand for?

Back 323

angiotensin converting enzyme inhibitors

Front 324

What drugs should be avoided in HF?

Back 324

alcohol, NSAIDs, CCB, some anti-arrhythmic drugs

Hint 324

Pharmacology 187

Front 325

List 5 ACE inhibitors.

Back 325

lisinopril
captopril
benazepril
enalapril
quinapril

Front 326

What are the indications for ACE inhibitors?

Back 326

all stages of left HF
post-MI

Hint 326

Pharmacology p189

Front 327

What is the patient education for ACE inhibitors?

Back 327

1. take on empty stomach → otherwise food may decrease absorption

Hint 327

Pharmacology p189

Front 328

What are the adverse effects of ACE inhibitors?

Back 328

postural hypotension, renal insufficiency, hyperkalemia, angioedema, peristent dry COUGH

Hint 328

Pharmacology p189

Front 329

What type of medication may cause an adverse effect of a persistent dry cough?

Back 329

ACE inhibitors

Hint 329

Pharmacology p189

Front 330

What is the MOA of digoxin?

Back 330

1. inhibits Na+/K+ exchange by Na+/K+ ATPase
2. intracellular [Na+] increases
3. Na+ concentration gradient decreases disrupting the Na+/Ca2+ exchanger
4. less Ca2+ is pumped into the extracellular space
5. more Ca2+ remains intracellularly causing ↑ force of ventricular contraction

Hint 330

Pharmacology p191

Front 331

What are the indications for digoxin?

Back 331

severe LT ventricular systolic dysfunction after initiation of ACE inhibitor and diuretic therapy

HF with atrial fibrillation

*not indicated for diastolic dysfunction or RT venticular HF

Hint 331

Pharmacology p192

Front 332

What are the adverse effects of digoxin?

Back 332

digoxin toxicity
→ digoxin has narrow therapeutic window and long half-life (36 hours)
→ mainly eliminated by kidneys so renal failure can lead to toxicity
→ hypokalemia enhances toxicity so give K+ supplementation or K-sparing diuretic
→ arrhythmia → usually due to hypokalemia
→ nausea and vomiting
→ fatigue, HA, confusion, vision changes

Hint 332

Pharmacology p193

Front 333

What are the drug interactions for digoxin?

Back 333

quinidine
verapamil
amiodarone

cause digoxin intoxication by displacing digoxin from protein-binding sites and by competing with digoxin for renal excretion

Hint 333

Pharmacology p193

Front 334

What is the patient education for digoxin?

Back 334

requires periodic blood draw to monitor digoxin and potassium levels

Front 335

What are the contraindications for digoxin?

Back 335

hypersensitivity to digoxin
history of toxicity
ventricular tachycardia
ventricular fibrillation
constrictive pericarditis
amyloid disease
Wolff-Parkinson-White syndrome + Afib

Hint 335

Drug Handbook p444

Front 336

List 4 inotropes.

Back 336

digoxin
dobutamine
dopamine
epinephrine

Front 337

What are the indications for dobutamine?

Back 337

acute HF

Front 338

What are the contraindications for dobutamine?

Back 338

hypersensitivity to dobutamine
idiopathic hypertrophic subarotic stenosis

Hint 338

Drug Handbook p470

Front 339

What is the MOA for dobutamine?

Back 339

stimulates B1 adrenergic receptors → increase intracellular [cAMP] → activation of protein kinase → phosphorylation of slow Ca2+ channels → increase in intracellular [Ca2+] → increase in force of ventricular contraction

Hint 339

Pharmacology p194

Front 340

What are the adverse effects of doputamine?

Back 340

↑ HR and BP (but occasionally hypotension)
increased ventricular ectopy
premature ventricular beats

Front 341

What is class of drug is spironolactone?

Back 341

potassium-sparing diuretic

Front 342

What is the MOA of spironolactone?

Back 342

anatgonist of aldosterone → preventing sodium (and water retention), myocardial hypertrophy, and hypokalemia

Hint 342

Pharmacology p195

Front 343

What is the patient education for spironolactone?

Back 343

do not take K+ supplements

Hint 343

Pharmacology p195

Front 344

What are the adverse effects of spironolactone?

Back 344

GI → gastritis, peptic ulcer
endocrine → gynecomastia, menstrual irregularities, ↓ lidibo
CNS → fatigue, confusion

Hint 344

Pharmacology p195

Front 345

S3 heard in context of HF suggests?

Back 345

dilated heart/systolic dysfunction

Hint 345

Pathophysiology p8

Front 346

S4 heard in context of HF suggests?

Back 346

hypertrophic heart/diastolic dysfuction

Hint 346

Pathophysiology p8

Front 347

What are the MOA, indications, contraindications, adverse effects, and drug interactions of dopamine?

Back 347

MOA → stimulate dopaminergic and beta-adrenergic receptors

indications → adjunctive therapy in treatment of shock (including cardiac decompensation) that persists after adequate fluid replacement

contraindications → hypersensitivity, pheochromocytoma, ventricular fibrillation

adverse effects → palpitations, angina, hypotension, tachycardia, vasoconstriction, ectopic beats, dyspnea, nausea, vomiting, HA

drug interactions →

Hint 347

Drug Handbook p480

Front 348

What are the MOA, indications, contraindications, adverse effects, and drug interactions of epinephrine?

Back 348

think EPI PEN!!!

MOA → stimulates alpha and beta receptors → vasoconstriction → increase in force of ventricular contraction

indications → cardiac arrest, bronchospasm (asthma, anaphylaxis), nasal congestion, viral croup, decrease superficial hemorrhage

contraindications → none to epi pen in life threatening situation

adverse effects →

drug interactions →

Hint 348

Drug Handbook p526

Front 349

What is the clinical presentation of rheumatic fever?

Back 349

recent infection
fatigue
fever
erythema marginatum → erythematous rings mostly on trunk that disappear and reappear over weeks to months
subcutaneous nodules → small painless nodules on extensor surfaces
chorea → abrupt nonrhythmic involuntary movements and muscular weakness
carditis
polyarthritis

Front 350

What is the most common symptom of rheumatic fever?

Back 350

arthritis

Front 351

What is pericarditis?

Back 351

inflammation of the pericardium

Front 352

What is the etiology of pericarditis?

Back 352

infection → cocksackieviruses, echoviruses
inflammation in lung or myocardium
post MI
post cardiac surgery
hemopericardium
uremia
autoimmune disease → RA, SLE
neoplasm → lung, breast, renal cell carcinoma, Hodgkin disease, lymphoma
drug toxicity → penicillins, clozapine, minoxidil
radiation

Hint 352

Current ch10

Front 353

What is the diagnostic workup of pericarditis?

Back 353

↑ elevated ESR
EKG → diffuse ST segment elevation, often PR depression, sometimes T wave inversion
CXR → often normal, possible cardiac enlargement if fluid present, R/O extracardiac disease

Hint 353

Current ch10

Front 354

What is the most common cause of pericarditis?

Back 354

viral infection

usually cocksackieviruses and echoviruses

sometimes influenza, varicella, mumps, EBV, hepatitis, or HIV

rarely TB or bacterial → pneumococci from lung infection or borrelia burgdorferi from lyme disease

Hint 354

Current ch10

Front 355

Describe the EKG often found in pericarditis.

Back 355

diffuse ST segment elevation
possible PR segment depression

Hint 355

Current ch10

Front 356

Back 356

pericardial effusion

Hint 356

Current ch10

Front 357

What are the characteristics of a pericardial friction rub?

Back 357

high frequency → use diaphragm
scratching, grating, squeaking sound
3 components → 1 systolic sound between S1 and S2 + 1 diastolic sound during early diastole + 1 diastolic sound during late diastole
loudest at lower left sternal border, during inspiration
sometimes better detected during forced expiration while leaning forward

Back 358

pericardial friction rub

Front 359

What is the management for pericarditis?

Back 359

1. if viral → symptomatic treatment
-aspirin 650mg every 3-4 hours or indomethacin
-if unresponsive → corticosteroids x 2 weeks
-may recur or be complicated by cardiac tamponade
2. if post-MI or cardiac surgery → symptomatic treatment
-aspirin 650mg every 3-4 hours x 2-4 weeks
-if severe → corticosteroids
-to prevent recurrences → colchicine x few months

Hint 359

Current ch10

Front 360

What is rheumatic heart disease?

Back 360

condition characterized by damaged heart valves due to rheumatic fever

Front 361

What is the management of rheumatic fever?

Back 361

1. for strep throat → benzathine penicillin G 1.2 million units IM single dose
2. if penicillin allegy → erythromycin 40mg/kg daily
3. for fever and arthritis → aspirin
4. if refractory to aspirin → corticosteroids
4. bed rest until afebrile and resting HR, ESR, and EKG normal
5. to prevent recurrence → benzanthine penicillin G 1.2 million units IM every 4 weeks
-if no carditis → continue until 21 y/p
-if carditis + no valvular damage → continue for 10 years
-if carditis + valvular damge → continue for 10 years or until 40y/o if high risk for reexsposure of strep throat (parent, teacher, medical professional, military personnel)

If chorea:
1. provide calming environment
2. medications only control symptoms but do not alter duration or outcome
3. carbamazepine → may not see effect for 2 weeks, continue for 2 weeks after symptoms subside

If HF:
see HF management

Hint 361

Current ch10

Front 362

Who is most commonly affected by rheumatic fever?

Back 362

children 5-15y/o

Hint 362

Current ch10

Front 363

What is the clinical presentation of rheumatic heart disease?

Back 363

history of rheumatic fever → may be single attack or repeated attacks

damage to valve cusps, commissures, and chordae tendineae → stenosis and/or insufficiency

50-60% → mitral valve
20% → mitral and aortic valves
10% → mitral and/or aortic + tricupsid valves

Hint 363

Current ch10

Front 364

What valve is most commonly affected in rheumatic heart disease?

Back 364

mitral valve

Hint 364

Current ch10

Front 365

What are the complications of rheumatic heart disease?

Back 365

endocarditis

Front 366

What is the clinical presentation of pericarditis?

Back 366

fever
dyspnea
anterior pleuritic chest pain → worse when supine, relieved when upright
may radiate to neck, shoulders, back, or epigastrium
pericardial friction rub

Front 367

What is superficial thrombophlebitis?

Back 367

inflammation of a superficial vein due to a blood clot

Hint 367

Current ch12

Front 368

What is the etiology of superficial thrombophlebitis?

Back 368

spontaneous → pregnancy, postpartum, varicose veins, thromboangitis obliterans
trauma → blow, irritating solution from IV
hypercoaguable states → factor V leiden, protein S deficiency, protein C deficiency, antithrombin III deficiency
abdominal cancer → pancreatic carcinoma → systemic hypercoaguability
oral contraceptives
iatrogenic → IV, PICC

20% associated with occult DVT

Hint 368

Current ch12

Front 369

What is the most common cause of superficial thrombophlebitis?

Back 369

IV or PICC lines

Hint 369

Current ch12

Front 370

What is the clinical presentation of superficial thrombophlebitis?

Back 370

localized dull pain
redness, warmth, induration, and tenderness along a superficial vein (usually great saphenous vein) or at recent IV site

inflammation clears in 1-2 weeks but firm cord may persist

Hint 370

Current ch12

Front 371

What is the most common site of superficial thrombophlebitis?

Back 371

great saphenous vein

Hint 371

Current ch12

Front 372

Back 372

superficial thrombophlebitis

Front 373

What is the management of superficial thrombophlebitis?

Back 373

1. if localized → NSAIDs, local heat
2. if extensive or near superficial-deep vein junction → ligation and division of vein
3. broad-spectrum antibiotics to prevent septic phlebitis

If septic phlebitis develops:
1. may be indicated by fever/chills or positive culture
2. continue antibiotics x 7-10 days
3. heparin
4. possible excision of vein

Hint 373

Current ch12

Front 374

What is the patient education for superficial thrombophlebitis caused by varicose veins?

Back 374

often recurrent

Hint 374

Current ch12

Front 375

What is the prognosis of superficial thrombophlebitis and septic phlebitis?

Back 375

superficial thrombophlebitis → generally benign and brief

septic phlebitis → 20% mortality rate

Hint 375

Current ch12

Front 376

What are the complications of superficial thrombophlebitis?

Back 376

cellulitis
gangrene
septic phlebitis
DVT
PE

Front 377

What is the prevention of superficial thrombophlebitis?

Back 377

1. monitor IV lines daily
2. remove IV if inflammation develops to prevent septic phlebitis and thrombotic complications
3. avoid remaining still for long periods of time

Hint 377

Current ch12

Front 378

What does PICC line stand for?

Back 378

peripherally inserted central catheter

Hint 378

Current ch12

Front 379

What is chronic venous insufficiency?

Back 379

disorder characterized by limited venous return to heart caused by malfunctioning valves → scarred valves or dilated vein prevents valve closure → blood pools → pressure increases → causing edema and skin changes

Hint 379

Current ch12

Front 380

What is the etiology of chronic venous insufficiency?

Back 380

leg trauma
DVT
varicose veins
arteriovenous fistula
neoplastic obstruction

Hint 380

Current ch12

Front 381

What is the clinical presentation of chronic venous insufficiency?

Back 381

lower extremities:
dull aching
itching
pitting edema
liposclerosis
brown skin discoloration around ankles
ulcers around ankles
secondary varicosities

Hint 381

Current ch12

Front 382

What causes the brown skin discoloration seen in chronic venous insufficiency?

Back 382

blood leaks out of blood vessels → hemoglobin broken down into hemosiderin → hemosiderin permanently deposited in dermal macrophages

Hint 382

Current ch12

Front 383

Back 383

chronic venous insufficiency

Front 384

Back 384

chronic venous insufficiency

Front 385

What is the management of chronic venous insufficiency?

Back 385

1. compression stockings worn from mid foot to just below knee
2. elevate legs intermittently during day
3. elevate legs above heart with pillows at night
4. avoid long periods of sitting/standing
5. if refractory to above → pneumatic compression of leg

If ulceration:
1. control edema
2. apply compression or semi-rigid gauze boot and change every 2-3 days

Hint 385

Current ch12

Front 386

What is the prevention of chronic venous insufficiency?

Back 386

aggressive management of DVT
compressive stockings for varicose veins

Hint 386

Current ch12

Front 387

What is the etiology of varicose veins?

Back 387

usually hereditary
pregnancy
prolonged standing
heavy lifting
superficial thrombophlebitis with deep vein complications
arteriovenous fistula → diagnose by presence of bruit
obstruction due to neoplasm

vein dilation causes malfunctioning of valves → blood pools

Hint 387

Current ch12

Front 388

What is the clinical presentation of varicose veins?

Back 388

asymptomatic or aching pain exacerbated by standing
dilated tortuous superficial veins in lower extremities
often great saphenous vein, sometimes small saphenous vein
secondary varicosities

Hint 388

Current ch12

Front 389

What is the management of varicose veins?

Back 389

1. compression stockings
2. intermittent elevation of legs
3. sclerotherapy
4. surgery

Hint 389

Current ch12

Front 390

Who is most commonly affected by varicose veins?

Back 390

women following pregnancy

Hint 390

Current ch12

Front 391

What is the prevention of varicose veins?

Back 391

wear compression stockings during pregnancy

Hint 391

Current ch12

Front 392

Back 392

varicose veins

Front 393

Why is surgical removal of varicose veins often not helpful?

Back 393

removal of one vein just puts more pressure on adjacent veins creating more varicose veins

Front 394

What are diuretics?

Back 394

medications that increase urine flow

Hint 394

Pharmacology p261

Front 395

What are the classes of diuretics?

Back 395

carbonic anhydrase inhibitors
osmotic diuretics
loop diuretics
thiazide diuretics
potassium-sparing diuretics

Front 396

List classes of diuretics in order of most effective to least effective.

Back 396

loop diuretics < thiazide diuretics < potassium sparing diuretics

Hint 396

Pharmacology p261

Front 397

List types of carbonic anhydrase inhibitors.

Back 397

acetazolamide

Front 398

What is the MOA for carbonic anhydrase inhibitors (acetazolamide)?

Back 398

inhibition of HCO3- reabsorption in proximal convoluted tubule

Hint 398

Pharmacology p261

Front 399

What are the indications for acetazolamide?

Back 399

prophylaxis for mountain sickness
↓ intraocular pressure of open-angle glaucoma

Hint 399

Pharmacology p272

Front 400

What are the contraindications for acetazolamide?

Back 400

hepatic cirrhosis

Hint 400

Pharmacology p272

Front 401

What are the adverse effects of acetazolamide?

Back 401

hypokalemia
metabolic acidosis
renal stone formation
drowsiness
paresthesia

Hint 401

Pharmacology p272

Front 402

List types of osmotic diuretics.

Back 402

mannitol

Front 403

What is the MOA for osmotic diuretics?

Back 403

cause increased water secretion (not increased Na+ excretion like other diuretics)

Hint 403

Pharmacology p272

Front 404

What are the indications for mannitol?

Back 404

maintain urine flow following:
increased ICP due to shock
acute renal failure due to shock
drug toxicity
trauma

prevents kidneys from failing

Hint 404

Pharmacology p272

Front 405

What are the adverse effects of mannitol?

Back 405

extracellular water expansion and dehydration
hypo and hypernatremia

Hint 405

Pharmacology p272

Front 406

List types of loop diuretics.

Back 406

furosemide
torsemide
bumetanide
ethacrynic acid

Front 407

What is the MOA for loop diuretics?

Back 407

inhibition of Na+/K+/2Cl- cotransport in ascending loop of Henle → retention of Na+, Cl-, and water in tubule

Hint 407

Pharmacology p261

Front 408

What are the indications for loop diuretics?

Back 408

acute pulmonary edema due to HF
hypercalcemia
hyperkalemia

Hint 408

Pharmacology p269

Front 409

What are the adverse effects of loop diuretics?

Back 409

ototoxicity → especially ethacrynic acid
hypokalemia
hypomagnesemia
hyperuricemia → furosemide and ethacrynic acid
hypotension

Hint 409

Pharmacology p269

Front 410

List types of thiazide diuretics.

Back 410

hydrochlorathiazide
chlorothiazide
metolazone

Front 411

Describe chlorothiazide.

Back 411

thiazide diuretic
MOA → inhibits Na+/Cl cotransporter in ascending loop of Henle
indications → mild-to-moderate HTN; adjunctive therapy for edema
contraindications → renal failure

Hint 411

Drug Handbook p308

Front 412

What is the MOA for thiazide diuretics?

Back 412

inhibition of Na+/Cl- cotransporter in distal convoluted tubule → retention of water in tubule

Hint 412

Pharmacology p261

Front 413

What are the indications for thiazide diuretics?

Back 413

HTN
mild-to-moderate HF (if thiazide fails → prescribe loop diuretic)
hypercalciuria
diabetes insipidus

Hint 413

Pharmacology p267

Front 414

What are the adverse effects of thiazide diuretics?

Back 414

hypokalemia
hyperuricemia

hyponatremia
hypomagnesemia
hypercalcemia
hyperglycemia
volume depletion → hypotension
hyperlipidemia
hypersensitivity

Hint 414

Pharmacology p267

Front 415

List the thiazide diuretics from most effective to least effective?

Back 415

metolazone < hydrochlorothiazide < chlorothiazide

Hint 415

Pharmacology p265

Front 416

How does the strength of metolazone compare to the other thiazide diuretics?

Back 416

more potent
causes Na+ excretion even in advanced renal failure

Hint 416

Pharmacology p268

Front 417

List types of potassium sparing diuretics.

Back 417

spironolactone
triamterene
amiloride hydrochloride

Front 418

What is the MOA for potassium-sparing diuretics?

Back 418

occurs in collecting duct and tubule

spironolactone → aldosterone agonist → inhibits aldosterone-mediated Na+ resorption/K+ secretion
triamterene and amiloride → block Na+ channels

Hint 418

Pharmacology p261

Front 419

What are the indications for spironolactone?

Back 419

adjunctive therapy to prevent hypokalemia
severe HF
hepatic cirrhosis
secondary hyperaldosteronism

Hint 419

Pharmacology p270

Front 420

What are the adverse effects of spironolactone?

Back 420

GI upset → nausea, peptic ulcer
gynecomastia
menstrual irregularities
hyperkalemia → lethargy, mental confusion

Hint 420

Pharmacology p270

Front 421

What are the indications for triamterene and amiloride hydrochloride?

Back 421

adjunctive therapy to prevent hypokalemia

Hint 421

Pharmacology p271

Front 422

What are the adverse effects of triamterene?

Back 422

leg cramps
hyperkalemia
hyperuricemia
↑ BUN

Hint 422

Pharmacology p271

Front 423

What is the effect of adrenergic stimulation on heart, lungs, and blood vessels?

Back 423

heart → increase HR, contractility, and conduction velocity
lungs → bronchiole dilation (relaxing smooth muscle)
blood vessels → vasoconstriction in skin and mucous membranes; dilation to liver and skeletal muscle

Front 424

What is the effect of cholinergic stimulation on heart, lungs, and blood vessels?

Back 424

heart → decreases HR, contractility, and conduction velocity
lungs → bronchiolar constriction, increase in mucus secretion
blood vessels → vasodilation

Front 425

What class of drug is epinephrine?

Back 425

catecholamine → adrenergic receptor agonist

Hint 425

Pharmacology p71

Front 426

What are the indications for epinephrine?

Back 426

1. cardiac arrest
2. brochoconstriction → acute asthma, anaphylactic shock
3. glaucoma
4. anesthetics
3.

Hint 426

Pharmacology p71

Front 427

*What are the adverse effects of epinephrine, norepinephrine, and isoproterenol?

Back 427

adverse effects → CNS disturbances (HA, tremor, tension, anxiety, fear), cardiac arrhythmia, pulmonary edema, cerebral hemorrhage

NE also causes blanching and skin sloughing at site of injection due to extreme vasoconstriction

Hint 427

Pharmacology p71

Front 428

What are the clinical uses of norepinephrine?

Back 428

shock → NE causes vasoconstriction → increase in vascular resistance → increase BP

*though metaraminol preferred b/c it does not reduce blood flow to kidneys

Hint 428

Pharmacology p74

Front 429

What class of drug is norepinephrine?

Back 429

catecholamine → adrenergic agonist

Front 430

What are the adverse effects, contraindications, and toxicities of norepinephrine?

Back 430

same as epinephrine + blanching and skin sloughing along injected vein (due to extreme vasoconstriction)

Hint 430

Pharmacology p75

Front 431

What class of drug is isoproterenol?

Back 431

synthetic catecholamine → B1- and B2-adrenergic receptor agonist

Hint 431

Pharmacology p75

Front 432

What are the clinical use of isoproterenol?

Back 432

1. stimulation of heart in emergency situations
2. rarely used as brochodilator in asthma

Hint 432

Pharmacology p75

Front 433

What class of drug is phenylephrine?

Back 433

synthetic noncatecholamine → primarily binds alpha1 receptors
causes vasoconstriciton → raising BP
no effect on heart

Hint 433

Pharmacology p77

Front 434

What is the clinical use of phenylephrine?

Back 434

nasal decogestant
increase BP
terminate supraventricular tachycardia

Hint 434

Pharmacology p77

Front 435

What are the adverse effects of phenylephrine?

Back 435

hypertensive HA
cardiac irregularities

Hint 435

Pharmacology p77

Front 436

What class of drug is ephedrine?

Back 436

noncatecholamine → mixed action adrenergic agonist

Hint 436

Pharmacology p79

Front 437

What are the clinical uses of ephedrine?

Back 437

raise BP
treat asthma via bronchodilation
nasal decongestant

Hint 437

Pharmacology p79

Front 438

What class of drug is ephedrine?

Back 438

noncatecholamine → mixed action adrenergic agonist

Hint 438

Pharmacology p79

Front 439

What are the clinical uses of ephedrine?

Back 439

raise BP
treat asthma via bronchodilation
nasal decongestant

Hint 439

Pharmacology p79

Front 440

What is the MOA and clinical use of B-blockers?

Back 440

MOA → B-adrenergic agonists → diminsh phase 4 depolarization → depressing automaticity, prolonging AV conduction, and decreasing HR and contractility
clinical use → atrial flutter, atrial fibrillation, AV-nodal reentrant tachycardia, prevention of ventricular arrhythmia following MI

Front 441

What is the MOA and clinical use of digoxin?

Back 441

MOA → cardiac glycoside → shortens refractory period in atrial and ventricular myocardial cells while prolonging refractory period and decreasing conduction velocity in AV node

clinical use → atrial flutter, atrial fibrillation, paroxysmal supraventricular tachycardia, HF

*digoxin toxicity → can lead to ventricular fibrillation

Front 442

What is the MOA and clinical use of CCBs?

Back 442

MOA →
clinical use → atrial flutter, atrial fibrillation, supraventricular tachycardia, HTN, angina

Front 443

What is the MOA and clinical use of quinidine?

Back 443

MOA → Na+ channel blocker → binds to Na+ channels → prevents Na+ influx → slows phase 0 depolarization in ventricular muscle fibers

clinical use → atrial, junctional, and ventricular tachyarrhythmias; maintain sinus rhythm following cardioversion of atrial flutter or a-fib; prevent frequent ventricular tachycardia

Front 444

What is the MOA and clinical use of lidocaine?

Back 444

MOA → Na+ channel blocker → shortens phase 3 repolarization and decreases duration of AP
clinical use → ventricular arrhythmias arising during myocardial ischemia

Front 445

What should be prescribed for atrial fibrillation?

Back 445

first line → B-blocker
second line → CCBs, digoxin

if ≥1 risk factor for stroke → long-term warfarin with INR 2.0-3.0

Front 446

List 2 Na+ channel blockers.

Back 446

lidocaine
quinidine

Front 447

What is lidocaine?

Back 447

Na+ channel blocker used to treat ventricular arrhythmias often associated with MI

Front 448

What is quinidine?

Back 448

Na+ channel blocker used to treat atrial, junctional, or ventricular arrhythmias

Front 449

List arrhytmias treated by B-blockers, CCBs, digoxin, quinidine, and lidocaine.

Back 449

BBs:
-atrial flutter
-atrial fibrillation
-supraventricular tachycardia
-ventricular tachycardia

CCBs:
-atrial flutter
-atrial fibrillation
-paroxysmal supraventricular tachycardia

DIGOXIN:
-atrial flutter
-atrial fibrillation
-paroxysmal supraventricular tachycardia

QUINIDINE:
prevention of atrial, junctional, and ventricular arrhythmias
-atrial fibrillation
-paroxysmal supraventricular tachycardia
-premature atrial contraction
-ventricular tachycardia
-premature ventricular contraction
-following cardioversion for atrial flutter or fibrillation

LIDOCAINE:
-ventricular arrhythmias (often due to MI)

Front 450

What is the clinical use of nitroglycerin and isosorbide dinitrate for angina and how does it effect myocardial O2 demand?

Back 450

clinical use → stable angina, prinzmetals

MOA → vasodilator
1. dilation of large veins → decreased venous return → decreased preload → decreased work of heart → decreased myocaridal O2 demand
2. dilation of coronary arteries → increased blood supply to myocardium

Front 451

What is nitroglycerin?

Back 451

vasodilator

Front 452

List nitrates.

Back 452

nitroglycerin
isosorbide dinitrate

Front 453

What is isosorbide dinitrate?

Back 453

vasodilator

Front 454

What is the clinical use of ranozaline and how does it effect myocardial O2 demand?

Back 454

clinical use → chronic angina
*does not relieve acute angina

MOA →

Front 455

What type of nitrate should be given for prompt relief of ongoing stable angina attack?

Back 455

sublingual nitroglycerin

Hint 455

Pharmacology p210

Front 456

What are the routes of administration, onset, and duration of nitroglycerine and isosorbide dinitrate?

Back 456

NITROGLYCERIN:
1. sublingual tablet or spray
-onset → 2 min
-duration → 25 min

2. transdermal patch
-onset → 30 min
-duration → 8-14 hrs

3. oral sustained release tablet
-onset → 35 min
-duration → 4-8 hrs

ISOSORBIDE DINITRATE:
1. sublingual
-onset → 5 min
-duration → 1 hr

2. oral slow-release tablet
-onset → 30 min
-duration → 8 hrs

Hint 456

Pharmacology p211

Front 457

What should you prescribe for newly diagnosed stable angina?

Back 457

nitroglycerin or isosorbide dinitrate sublingual tablet or spray

take if angina attack
can also take before activities that may precipitate angina attack

Hint 457

Current ch10

Front 458

What are the adverse effects of nitrates?

Back 458

HA!!!
facial flushing
postural hypotension
tachycardia

Hint 458

Pharmacology p211

Front 459

Discuss tolerance to nitrates.

Back 459

tolerance develops rapidly where blood vessels become desensitized to vasodilation

TO AVOID TOLERANCE:
-schedule daily 8-12 hr nitrate-free interval to restore sensitivity
-remove transdermal patch at night
-if prinzmetal's angina → remove transdermal patch in afternoon since angina worsens early in morning

Hint 459

Pharmacology p211

Front 460

Nitrates are contraindicated if taking what drug?

Back 460

sildenafil (Viagra) → potentiates action of nitrates → may cause extreme hypotension

*can prescribe ranolazine instead

Hint 460

Pharmacology p211

Front 461

List drugs for treatment of angina.

Back 461

acute → nitrates

chronic →
-first line → B-blockers, ranozaline
-third line → CCBs

Front 462

What is the clinical use of pentoxifylline (Trental)?

Back 462

MOA → reduces blood viscosity
clinical use → symptomatic treatment of intermittent claudication due to chronic occlusive arterial disease of limbs

Hint 462

Drug Handbook p1173

Front 463

What is the pharmological treatment following MI?

Back 463

1. immediate chewable aspirin → 162mg or 325mg
2. if aspirin allergy → clopridogrel 300mg or 600mg
3. if STEMI → aspirin + clopridogrel
4. if STEMI (not NSTEMI) → thrombolytic therapy or coronary angioplasty
5. thrombolytic therapy → streptokinase or tissue plasminogen activator
6. continued aspirin 81mg and heparin
7. long term → aspirin 81mg, clopridogrel or both

Front 464

What does HMG COA reductase inhibitors stand for?

Back 464

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors

Hint 464

Pharmacology p253

Front 465

What is the common name for HMG COA reductase inhibitors?

Back 465

statins

Hint 465

Pharmacology p253

Front 466

What are the indications for prescribing HMG COA reductase inhibitors?

Back 466

1. elevated LDL
2. hyperlipidemias
*not familial hypercholesterolemia

Hint 466

Pharmacology p253

Front 467

What are the first-line agents for elevated LDL?

Back 467

HMG COA reductase inhibitors

Hint 467

Pharmacology p253

Front 468

HMG COA reductase inhibitors are effective in patients who are homozygous for familial hypercholesterolemia, true or false?

Back 468

false → since these patients lack LDL receptors

Hint 468

Pharmacology p253

Front 469

What is the MOA for HMG COA reductase inhibitors?

Back 469

inhibition of HMG COA reductase → decreased cholesterol synthesis → decreased [intracellular cholesterol] →
1. increased LDL receptor synthesis→ increased number of LDL receptors → increased internalization of LDL → decreased plasma cholesterol
2. decreased VLDL secretion → decreased plasma cholesterol

Hint 469

Pharmacology p253

Front 470

What are the contraindications of HMG COA reducatse inhibitors?

Back 470

adolescents
pregnancy
breast-feeding
renal insufficiency

Hint 470

Pharmacology p255

Front 471

What are the adverse effects of HMG COA reductase inhibitors?

Back 471

1. liver failure → monitor LFTs
2. myopathy and rhabdomyolysis → usually associated with renal insufficiency or drug interaction → monitor CK

Hint 471

Pharmacology p255

Front 472

What is rhabdomyolysis?

Back 472

disintegration of muscle

Hint 472

Pharmacology p255

Front 473

What are the drug interactions for HMG COA reductase inhibitors?

Back 473

increase in warfarin → monitor INR

Hint 473

Pharmacology p255

Front 474

What is the patient education for HMG COA reductase inhibitors?

Back 474

1. do not take if pregnant or breast-feeding
2. must periodically get blood drawn to monitor LFTs and CK
3. if taking warfarin → must periodically get blood drawn to monitor INR

Hint 474

Pharmacology p255

Front 475

What are other names for niacin?

Back 475

nicotinic acid
vitamin B3

Hint 475

Pharmacology p255

Front 476

What are the indications for niacin?

Back 476

1. decreased HDL
2. increased LDL
3. hypercholesterolemias
4. familial hyperlipidemias

Hint 476

Pharmacology p255

Front 477

What is the most effective agent for increasing HDL levels?

Back 477

niacin

Hint 477

Pharmacology p255

Front 478

What is the MOA of niacin?

Back 478

inhibition of lipolysis in adipose tissue → decreased plasma levels of cholesterol and triglycerides

Hint 478

Pharmacology p255

Front 479

What are the adverse effects of niacin?

Back 479

*cutaneous flush
*pruritus
nausea and abdominal pain
hyperuricemia and gout → niacin inhibits uric acid secretion
impaired glucose tolerance
hepatotoxicity

Hint 479

Pharmacology p255

Front 480

What are the drug interactions of niacin?

Back 480

alcohol → may increase cutaneous flushing
gout meds → allopurinol, probenecid, sulfinpyrazone
DM meds

Front 481

What is the patient education for niacin?

Back 481

if experience cutaneous flushing:
1. usually lasts 15-30min
2. may be accompanied by pruritus, especially in clothing-covered areas
3. take 300mg aspirin 30min before niacin to reduce flushing
4. flushing is usually self-limited after several weeks of a consistent dose

Hint 481

Pharmacology p256

Front 482

Which HMG COA reductase inhibitors are most effective at decreasing LDL, increasing HDL, and decreasing triglycerides?

Back 482

decreasing LDL → atorvastatin, rosuvastatin
increasing HDL → pravastatin, simvastatin
decreasing triglycerides → atorvastatin

Hint 482

Pharmacology p255

Front 483

List HMG COA reductase inhibitors in order of most effective to least effective at reducing LDL.

Back 483

atorvastatin = rosuvastatin > pravastatin = simvastatin > lovastatin = fluvastatin

Hint 483

Pharmacology p255

Front 484

Name 5 HMG COA reductase inhibitors.

Back 484

atorvastatin
simvastatin
pravastatin
lovastatin
fluvastatin

Front 485

Name 2 bile-acid sequestering agents

Back 485

cholestyramine
colestipol

Front 486

What are the indications for prescribing bile-acid sequestering agents?

Back 486

1. elevated LDL
*though not as effective as statins

Hint 486

Pharmacology p257

Front 487

What is the MOA of bile-acid sequestering agents?

Back 487

bind negatively charged bile acids and bile salts in small intestine → complex secreted in feces → preventing bile acids from returning to liver → lowering [bile acid] → causing hepatocytes to increase conversion of cholesterol to bile acids → decreasing[intracellular cholesterol] → increasing LDL uptake into cell → decreasing plasma LDL

Hint 487

Pharmacology p257

Front 488

List the categories of drugs used to treat elevated LDL, decreased HDL, and elevated TRIG in order of most effective to least effective.

Back 488

elevated LDL → HMG CoA reductase inhibitors > bile acid sequestrants > niacin > fibrates
decreased HDL → niacin > fibrates > HMG CoA reductase inhibitors > bile acid sequestrants
elevated TRIG → fibrates > niacin > HMG CoA reductase inhibitors > bile acid sequestrants

Hint 488

Pharmacology p259

Front 489

List statins and how they effect LDL, HDL, and TRIG.

Back 489

lovastatin → decreases LDL, increases HDL
pravastatin → decreases LDL and TRIG
fluvastatin, simvastatin, and atorvastatin → decreases LDL and TRIG, increases HDL

Front 490

Which is the cheapest statin?

Back 490

lovastatin (but also least potent)

Front 491

MI:

Back 491

-sudden prolonged (>30 min) anterior chest discomfort; often describe as “gas” or pressure
-worsening
-occurs at rest or with minimal exertion
-diaphoresis
-anxiety
-SOB
-soft heart sounds may indicate LV dysfunction
-S4 is common
-S3 is less common and indicates significant LV dysfunction
-mitral regurgitation murmur may indicate papillary muscle dysfunction or rupture
-cyanosis, cold temp, weak peripheral pulses, abnormal cap refill indicate low cardiac output
-ST segment elevation with MI, Q waves, mean axis deviation, poor R wave progression
-ST segment depression with angina or subendocardial MI
-inverted T waves with ischemia
-give aspirin 162 or 325mg
-if present <12 hours with STEMI, reperfusion therapy either via percutaneous coronary intervention or via thrombolytic therapy

Front 492

AORTIC DISSECTION:

Back 492

-sudden searing chest pain
-radiation to neck, back, or abdomen
-HTN
-diminished or unequal pulse in extremities
-LVH common
-mediastinal widening on CXR
-lower BP to 100-120 with B-blocker
-CT
-surgical intervention if involving arch of aorta