Mcphs Management And Manifestation Of Disease Test Five

Front 1

Pathological state in which the heart cannot pump blood efficiently enough to meet the metabolic needs of the body.

Back 1

Congestive Heart Failure

Front 2

What are the four governing factors of systolic function?

Back 2

Contractility, Preload, Afterload, Heart Rate

Front 3

What leads to decreased myocardial contractility?

Back 3

Loss of functional muscle (MI) or Diffuse deposits in the myocardium (amyloidosis, sarcoidosis, hemochromatosis)

Front 4

Increased preload (ie. in valve regurgitation) leads to?

Back 4

CHF

Front 5

This is end diastolic volume and resultant fiber length of the ventricle prior to onset of contraction?

Back 5

Preload

Front 6

Increased afterload (ie. in aortic stenosis or in severe HTN) leads to?

Back 6

CHF

Front 7

This is the forsce against which a ventricle that contracts that is contributed to by the vascular resistance especially of the arteries and by the physical characteristics (mass and viscosity) of the blood.

Back 7

Afterload

Front 8

This is stroke volume X heart rate?

Back 8

Cardiac Output

Front 9

To maintain arterial pressure and perfusion of vital organs the CV system responds to excessive hemodynamic burden or disturbance in myocardial contractility with the following three mechanisms.

Back 9

Frank starling mechanism
Myocardial hypertrophy
Activation of neurohumeral systems

Front 10

This is increased preload of dilation that helps to sustain cardiac performance by enhacing contractility.

Back 10

Frank Starling mechanism

Front 11

This happens to augment mass of contractile tissue in the heart?

Back 11

Myocardial hypertrophy

Front 12

This involves the following three things:
1. Release of norepi by adrenergic cardiac nerves leading to increased heart rate and increased myocardial activity
2. Renin angiotensin aldosterone system
3. Release of atrial naturitic peptide

Back 12

Activation of neurohumeral systems as an initial compensatory mechanism in CHF

Front 13

This is the ability of the heart to change its force of contraction and therefore stroke volume in response to changes invenous return.

Back 13

Frank Starling Law

Front 14

This occurs when the normally functioning heart cannot keep up with the dramatically increased demand for blood flow to one or more organs in the body e.g. in severe anemia, hyperthyroidism, AV fistula, Beriberi, Paget's disease.

Back 14

High output heart failure

Front 15

True or false, high output heart failure is not a common cause of CHF?

Back 15

True

Front 16

This occurs in ischemic heart disease, HTN, dilated cardiomyopathy, valvular and paricardial disease.

Back 16

Low output heart failure

Front 17

This is a B1 or thiamine deficiency, most cases are found in asia due to diets of white rice, or in alcoholic patients, patients who also undergo gastric bypass can suffer from this. This is associated with high output heart failure.

Back 17

Beriberi

Front 18

This condition happens when the right side of the heart loses its ability to pump blood efficiently.

Back 18

Right sided heart failure

Front 19

This condition occurs when the left side of the heart cannot pump enough blood to the body.

Back 19

Left sided heart failure

Front 20

What is the most common cause of RHF?

Back 20

LHF

Front 21

The principle abnormality is the inability to contract normally and expel sufficient blood.

Back 21

Systolic failure

Front 22

The principle abnormality is the inability to relax and fill normally (the heart).

Back 22

Diastolic failure

Front 23

How many classes are in the NY heart association classification?

Back 23

Four

Front 24

This is when patients have no limitations of activities, they suffer no symptoms from ordinary activities.

Back 24

Class I NYHA classification

Front 25

This is when patients have slight, mild limitation of activity, they are comfortable with rest or with mild exertion.

Back 25

Class II NYHA classification

Front 26

This is when patients have marked limitation of activty, they are comfortable only at rest.

Back 26

Class III NYHA classification

Front 27

This is when patients who should be at complete rest, confined to bed or chair, any physical activity brings on discomfort and Sx occur at rest.

Back 27

Class IV NYHA classification

Front 28

This is insufficiently sensitive to be useful in predicting outcomes or assessing results of Tx - needs to be based on individual patient. Helps in comparing groups of pts ie. in research studies.

Back 28

NYHA classification

Front 29

This tracks disease development and progression in heart patients?

Back 29

ACC/AHA staging system

Front 30

This is when a patient is at high risk for HF but without structural heart dz or Sx of HF; risk factors are HTN, DM, obesity and metabolic syndrome

Back 30

Stage A ACC/AHA staging system

Front 31

This is when a patient has a structural heart dz but without Sx and Sx of HF, possible Hx of MI, LVH, asymptomatic valvular heart dz, or low EF.

Back 31

Stage B ACC/AHA staging system

Front 32

This is when a patient has structural heart dz and prior or current Sx of HF.

Back 32

Stage C ACC/AHA staging system

Front 33

This is when a patient with refractory HF requries specialized intervention.

Back 33

Stage D ACC/AHA staging system

Front 34

These are all causes of what?
Arrhythmias, MI, PE, Sytemic HTN, Thyrotoxicosis, Pregnancy, Infection, Anemia, Rheumatic and other forms of myocarditis, Physical, dietary, fluid, environmental and emotional excesses, infective endocarditis.

Back 34

CHF

Front 35

What are the causes of primarily systolic failure CHF?

Back 35

CAD, HTN, Dilated cardiomyopathy - idiopathic, toxic (EtOH, doxorubicin), infection (viral parasitic and other)

Front 36

What are the causes of primarily diastolic CHF?

Back 36

HTN, Hypertrophic cardiomyopathy, Restrictic cardiomyopathy - amyloidosis, sarcoidosis, hemtochromatosis, Constrictive pericarditis, High output failure - chronic anemia, AV shunts, thyrotoxicosis

Front 37

What are four arrhythmias that show up with CHF?

Back 37

Tachyarrhythmias, A-V dissociation, Abnormal intraventricular conduction, Severe bradycardia

Front 38

This occurs in CHF, decreased filling time and as a result there is decreased cardiac output. Since increased heart rate increases myocardial oxygen demand, cardiac ischemia may be induced which may lead to decreased contractility.

Back 38

Tachyarrhythmias

Front 39

This occurs in CHF, results in loss of the atrial contribution to ventricular filling, therefore end diastolic volume is decreased with an associciated decrease in cardiac output.

Back 39

A-V dissociation

Front 40

This may cause a decrease in synchronicity of contraction with a decrease in myocardial performance. Optimal output requires coordinated impulse propegation and contraction.

Back 40

Abnormal intraventricular conduction

Front 41

This occurs in the absence oif increased stroke volume can seriously decrease cardiac output and thus precipitate CHF, increased stroke volume may not be possible if the patient has significant heart disease.

Back 41

Severe bradycardia in the absence of increased stroke volume

Front 42

These two things decrease LV function, and may precipitate CHF.

Back 42

MI and tissue death.

Front 43

Pt with this has an increased arterial pressure which may worse or cause LV failure.

Back 43

Pulmonary emoblism

Front 44

Rapid increases in arterial BP w/associated increases in peripheral resistance can increase afterload to an extent sufficient to produce heart failure.

Back 44

Systemic HTN

Front 45

Up to how many CHF diagnoses made in primary care setting may be wrong?

Back 45

50%

Front 46

What do you do for the lab workup in CHF?

Back 46

CBC (for e/o infection or anemia), increased BUN and creatinine, decreased Na, increased hepatic enzymes, BNP, TSH, cardiac enzymes, electrolytes K, Mg, and Ca

Front 47

This helpts distinguish CHF from other causes of acute dyspnea, helps monitor severity but can't distinguish between systolic and diastolic CHF, normal value is under 200.

Back 47

BNP - Brain Natriuretic Peptide

Front 48

These are not diagnostic for CHF?

Back 48

EKG

Front 49

EKG's do increase suspicion of CHF when what four things are seen?

Back 49

Previous MI, LV hypertrophy, Left bundle branch block, Tachyarrhythmia e.g rapid afib

Front 50

This evaluates the chamber dimensions of the heart, valve function, shunts, LVEF, Wall motion abnormalities (suggestive of CAD leading to catherterization/coronary angiography, or patchy myocarditis, LV hypertrophy, pericardial effusion, intracardiac thrombi, tumors and calcifications within heart valves.

Back 50

Echocardiogram

Front 51

This evaluates how well the heart is pumping. The amount of blood pumped out of a ventricle during each hear beat divided by the total amount of blood in the left ventricle.

Back 51

Ejection Fraction

Front 52

What is a normal EF (ejection fraction)?

Back 52

50-70%

Front 53

If you have an EF over 40% it means what?

Back 53

Mainly diastolic function

Front 54

If you have an EF under 40% it means what?

Back 54

Mainly systolic function

Front 55

What do you look for on the CXR in CHF?

Back 55

Cardiomegaly, Engorged pulm. vasculature, Pleural fluid R>L (better in upright or decubitus films), thickened fissure between upper and middle lobe, Kerley-B lines

Front 56

These are short, straight lines in the periphery of the lung lying approximately perpendicular to the pleural surface, caused by increased fluid in the interlobular septa.

Back 56

Kerley-B lines

Front 57

What are the goals of Tx in CHF?

Back 57

To correct underlying reversible causes, to relieve symptoms, and to prevent woresening of the condition. Tx remains empiric based on small studies and pathophysiologic dz.

Front 58

What are four things used to Tx systolic dysfunction?

Back 58

Diuretics, ACE inhibitor, Beta-Blocker, Digoxin

Front 59

With diuretic therapy for systolic dysfunction, what three diuretics are used?

Back 59

Loop diuretics (Furosemide - Lasix 20mg-80mg PO or IV up to TID)
Thiazides in mild to mod CHF
Metolazone (Zaroxolyn) in addition to furosemide

Front 60

What are thiings shat should be done when giving diuretics for systolic heart failure?

Back 60

Monitor BP (hypotension) renal fct (prerenal azotemia), electrolytes (natriuresis, kaliuresis), strict ins/outs, daily weights

Front 61

These causes dilation of arteriolar resistance vessels and venous capacitance vessels leads to decreased preload and afterload
Proven to decrease mortality in patients with CHF
Considered part of the initial Tx in addition to diuretic
Start low to prevent hypotension
Contraindicated in renal insufficiency (cr>3), hyperkalemia, hypotension, allergy

Back 61

ACE Inhibitors for CHF Tx

Front 62

What do you use in CHF Tx if patient is unable to tolerate ACE because of cough?

Back 62

Angiotensin II receptor blockers

Front 63

Until the mid 90's considered contraindicated, but it causes substantial increase in EF and decrease in LV size, decreased mortality and hospitalization rate.

Back 63

Beta-Blocker

Front 64

You should start these low in CHF Tx to prevent bradycardia.

Back 64

Beta-Blocker

Front 65

This is useful secondary to inotropic and vagotonic effect. It is beneficial in pt w/rapid afib, severe CHF, or EF <30%, can be added to diuretic and ACE inhibitor.

Back 65

Digoxin

Front 66

Decreased hospitalization rate and decreased worsening HF, but no improvement in mortality.

Back 66

Digoxin

Front 67

You have to give a decreased dose in elderly patients with renal insufficiency.

Back 67

Digoxin

Front 68

You have to check serum levels of this drug after 7-14 days of TX.

Back 68

Digoxin

Front 69

The Sx of this are anorexia, nausea, HA, blurred or yellow vision, confusion leading to tachycardia and ventricular fibrillation.

Back 69

Digoxin toxicity

Front 70

What predisposes patients to digoxin toxicity?

Back 70

Quinidine, Verapamil, decreased kalemia, decreased magnesemia

Front 71

What is the Tx for digoxin toxicity?

Back 71

Digoxin Fab (ovine)

Front 72

Tx for this is determined by underlying cause?

Back 72

Diastolic Dysfunction CHF

Front 73

If you have HTN as the underlying cause of diastolic dysfunction CHF what do you give for TX?

Back 73

CCB, ACEI, BB, Diuretics (careful since higher filling pressure may be needed to maintain cardiac output)

Front 74

If you have aortic stenosis as the underlying cause of diastolic dysfunction CHF what do you give for TX?

Back 74

Diuretics, Valve replacement

Front 75

If you have aortic regurgitation and mitral regurgitation as the underlying cause of diastolic dysfunction CHF what do you give for TX?

Back 75

ACEI to increase cardiac output and decrease pulmonary wedge pressure, together with diuretics.

Front 76

If you have mitral stenosis with decreased emptying of the LA as the underlying cause of diastolic dysfunction CHF what do you give for TX?

Back 76

Diuretics if Afib is present, give digitalis, verapamil and or BB, valve replacement or balloon valvuloplasty.

Front 77

What are the lifestyle modifications for helping with the TX of diastolic dysfunction CHF?

Back 77

Weight loss, fluid intake restrictions to less than 1.5L, sodium restrictions (<2g day), regular aerobic exercise tailored to the pt’s tolerance level, abstinence from EtOH, daily body weight (monitor for fluid retention)

Front 78

What is a sign of fluid retention?

Back 78

If the pts weight goes up five lbs over after a few days it can show signs of holding onto fluid.

Front 79

In which, diastolic or systolic dysfunction CHF, is morbidity and mortality 50% lower?

Back 79

Lower in diastolic dysfunction

Front 80

This is a multisystem disease resulting from an autoimmune reaction to infection with group A streptococci.

Back 80

Acute Rheumatic Fever

Front 81

Almost all manifestations of acute rheumatic fever resolve completely, except for what?

Back 81

Cardiac valvular damage (rheumatic heart disease) which may persist after the other features have disappeared.

Front 82

Up to what percentage of patients with ARF progress to RHD?

Back 82

Up to 60% of patients with ARF progress to RHD

Front 83

ARF is mainly a disease of children aged?

Back 83

5-14

Front 84

The prevalence of RHD peaks between what ages and is more common in what gender?

Back 84

RHD peaks between 25 and 40 years and is more common in females.

Front 85

ARF is exclusively caused by infection of the upper respiratory tract with any strain of what?

Back 85

Group A strep

Front 86

There is a latent period of how many weeks between the precipitating group A strep infection and the appearance of the clinical features of ARF?

Back 86

Three weeks

Front 87

What is the most common clinical presentation of ARF?

Back 87

Polyarthritis and fever

Front 88

What are four other clinical presentations, besides polyarthritis, of ARF?

Back 88

Carditis, Chorea, Erythema marginatum, Subcutaneous nodules

Front 89

What is the hallmark of heart involvement with ARF?

Back 89

Valvular damage from endocardial involvement

Front 90

What valve is almost always affected with ARF?

Back 90

Mitral valve

Front 91

Myocardial inflammation with ARF may lead to what in the EKG?

Back 91

P-R interval prolongation

Front 92

Pericardial involvement with ARF may lead to what?

Back 92

Pericarditis

Front 93

To qualify as a major manifestation this must have inflammation of more than one joint in ARF.

Back 93

Joint involvement

Front 94

ARF almost always affects what?

Back 94

Large joints and is symmetrical

Front 95

What do you give for joint involvement in ARF?

Back 95

Highly responsive to salicylates or other NSAIDS

Front 96

This commonly occurs in the absence of other manifestions in ARF, it follows a prolonged latent period after infection, particularly affects the head (causing characteristic darting movements of the tongue) and the upper limbs. May be generalized or restricted to one side of the body. Varies in severity from very mild to interfering ADLS, eventually resolves completely within six weeks.

Back 96

Sydenham’s chorea

Front 97

This is the classic rash of ARF, begins as pink macules that clear centrally, leaving a serpiginous, spreading edge, evanescent appearing and disappearing before the examiner’s eyes. Occurs usually on the trunk, sometimes on the limbs, but almost never on the face.

Back 97

Erythema marginatum

Front 98

This is a painless, small (0.5-2cm), mobile lump that is beneath the skin near tendons or overlying bony prominences, particularly of the hands, feet, elbows, occiput, and occasionally the vertebrae. This is associated with ARF.

Back 98

Subcutaneous nodules

Front 99

Apart from erythema marginatum, and subcutaneous nodules, what are other features of ARF?

Back 99

Fever occurs in most cases of ARF, Elevated acute phase reactants (CRP and ESR) are also present in most cases, mild leukocytosis is occasionally seen.

Front 100

What is essential in making the diagnoses of ARF

Back 100

Evidence of a preceding group A streptococcal infection

Front 101

Most cases of ARF do not have a what?

Back 101

Most cases off ARF do not have a positive throat culture or rapid antigen test, so serologic evidence is usually needed.

Front 102

What are the most common serologic tests associated with ARF?

Back 102

Anti-streptolysin O (ASO) and anti-DNase B (ADB) titers

Front 103

When you are making a diagnosis of ARF what do you need to do?

Back 103

There is no definitive test, Jones criteria refers to clinical features, major and minor criteria, To make the diagnosis group A streptococci PLUS 2 major criteria or 1 major and 2 minor criteria.

Front 104

What are the major criteria for diagnosing ARF?

Back 104

Carditis, Migratory polyarthritis, subcutaneous nodules, erythema marginatum, chorea

Front 105

What are the minor criteria for diagnosing ARF?

Back 105

Arthralgia, fever, elevated acute phase reactants, prolonged PR interval

Front 106

What are the three exceptions to the Jones criteria?

Back 106

Chorea is only manifestation, indolent carditis as only manifestation, and recurrent rheumatic fever.

Front 107

If ARF is untreated it last on average how long?

Back 107

12 weeks

Front 108

With treatment, patients with ARF are usually discharged from hospital within?

Back 108

1-2 weeks

Front 109

Echocardiography should be obtained in patients with what in ARF?

Back 109

Patients with cardiac findings

Front 110

With the exception of Tx of heart failure, which may be life saving, the Tx of ARF is what?

Back 110

Symptomatic

Front 111

To treat the precipitating group a strep infection what do you use?

Back 111

Penicillin is the drug of choice, erythromycin may be used if Pen allergy

Front 112

For Tx of arthritis, arthralgia, and fever, associated with ARF, what do you give?

Back 112

Salicylates and NSAIDS, Aspirin is the drug of choice

Front 113

Many clinicians treat cases of severe carditis, associated with ARF, with what?

Back 113

Glucocorticoids – Prednisone or prednisolone are recommended. IV methylprednisolone may be used in very severe carditis

Front 114

Medications do not alter the outcome of this. Milder cases can usually be managed by providing a calm environment.

Back 114

Chorea

Front 115

In patients with severe chorea, associated with ARF, what do you give?

Back 115

Carbamazepine or sodium valproate are preferred, or IV immunoglobulin

Front 116

In the follow up to ARF Tx what should be done?

Back 116

Inflammatory markers should be monitored every 1-2 weeks until they have normalized, echocardiogram after 1 month, if carditis is present pt should be informed of need for antibiotic prophylaxis against endocarditis for dental and surgical procedures.

Front 117

What should be done with patients who had ARF after they are TX

Back 117

Patients should be entered onto the local ARF registry and contact made with a PCP to ensure a plan for follow up and administration of secondary prophylaxis before the patient is discharged.

Front 118

What is the primary prevention of ARF?

Back 118

Tx of group A streptococcal pharyngitis

Front 119

What is the secondary prevention of ARF?

Back 119

Long term penicillin prophylaxis to prevent recurrences, Benzathine penicillin G delivered every four weeks or more frequently, also oral penicillin V can be given instead but less effective, if Pen allergy erythromycin can be given.

Front 120

What are two other things that are post-streptococcal syndromes that may be confused with rheumatic fever?

Back 120

Post streptococcal reactive arthritis
Pediatric Automimmune neuropsychiatric disorders associated with streptococcal infection.

Front 121

How do you differentiate Post Streptococcal Reactive Arthritis from RF?

Back 121

Small joint involvement that is often symmetric, A short latent period following strep infection, occasional causation by non group A hemolytic strep infection, slower responsiveness to salicylates, the absence of other features of ARF, PARTICULARLY CARDITIS.

Front 122

This is a term that links a range of tic disorders and obsessive compulsive symptoms with group A streptococcal infections.

Back 122

PANDAS

Front 123

This is infection or inflammation of the heart valves or the lining of the heart.

Back 123

Endocarditis

Front 124

This is endocarditis caused by any microorganism

Back 124

Infective endocarditis

Front 125

This most commonly involves heart valves (native or prosthetic). It may occur on the mural endocardium where it is damaged by aberrant jets of blood or foreign bodies. May occur on intracardiac devices themselves.

Back 125

Infective endocarditis

Front 126

This is a hectically febrile illness that rapidly damages cardiac structures, hematogenously seeds extracardiac sites, and, if untreated, progresses to death within weeks.

Back 126

Acute endocarditis

Front 127

What three pathogens are primarily responsible for acute endocarditis?

Back 127

Hemolytic streptococci, S. Aureus, Pneumococci

Front 128

This follows an indolent course, causes structural cardiac damage slowly, if at all, rarely metastasizes, gradually progressive unless complicated by a major embolic event or ruptured mycotic aneurysm.

Back 128

Subacute endocarditis

Front 129

What typically causes subacute endocarditis?

Back 129

Viridans streptococci, enterococci, HACEK group, Bartonella species.

Front 130

What are the predisposing factors for endocarditis?

Back 130

Congenital heart disease, chronic rheumatic heart disease, degenerative valve disease, prosthetic valves, intracardiac devices, IV drug use, health care associated infection.

Front 131

This is from IV catheter infections, nosocomial wound and urinary tract infections, chronic invasive procedures such as hemodialysis, transvenous pacemaker lead – and/or implanted defibrillator associated endocarditis.

Back 131

Health Care-Associated Native Valve Endocarditis

Front 132

This can come from the oral cavity, skin and upper respiratory tract are the respective primary portals for viridans streptococci, staphylococci, and HACEK organisms, streptococcus bovis from the GI tract, enterococci enter the bloodstream from the genitourinary tract.

Back 132

Community acquired native valve endocarditis

Front 133

What organisms are a part of the HACEK organisms?

Back 133

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella

Front 134

This is generally the result of an intraoperative or postoperative complication, coagulase negative staphylococcus, S. Aureus, facultative gram negative bacilli, diphtheroids, and fungi.

Back 134

Prosthetic valve endocarditis arising within 2 months of valve surgery.

Front 135

Pathogens are similar to those in community acquired native valve endocarditis.

Back 135

Prosthetic valve endocarditis arising over 12 months after surgery.

Front 136

This is commonly caused by E. aureus, many of which are MRSA, when involving the tricuspid valve. Left sided infections have a more varied etiology and involve abnormal valves, often involving Pseudomonas aeruginosa and Candida species, with sporadic cases involving bascillus, lactobacillus, and corynebacterium species.

Back 136

IV Drug Use associated with endocarditis

Front 137

This is more common among injection drug users than among patients who do not inject drugs.

Back 137

Polymicrobial endocarditis

Front 138

This accounts for 5 to 15% of endocarditis cases, may be due to prior antibiotic exposure, may be due to fastidious organisms.

Back 138

Culture negative endocarditis

Front 139

Endothelial injury causes aberrant flow and allows either direct infection by virulent organisms or the development of an uninfected platelet fibrin thrombus – a condition called what?

Back 139

Nonbacterial thrombotic endocarditis (NBTE)

Front 140

The nonbacterial thrombotic endocarditis subsequently serves as a site of what?

Back 140

Serves as a site of bacterial attachment during transient bacteremia

Front 141

Fibrin deposition combines with platelet aggregation to generate an infected what?

Back 141

Vegetation

Front 142

In the absence of host defenses, organisms enmeshed in the growing platelet fibrin vegetation proliferate to form what?

Back 142

Dense microcolonies

Front 143

The pathophysiologic consequences and clinical manifestations of endocarditis arise from?

Back 143

Damage to intracardiac structures, embolization of vegetation fragments, leading to infection or infarction of remote tissues, hematogenous infection of sites during bacteremia, tissue injurly due to the deposition of circulating immune complexes or immune responses to deposited bacterial antigens, constitutional symptoms probably result from cytokines.

Front 144

What are the clinical manifestations of endocarditis?

Back 144

Fever, chills, sweats, anorexia, weight loss, malaise, myalgias, arthralgias, back pain, heart murmur, aterial emboli, spenomegaly, clubbing, neurologic manifestations, peripheral manifestations, Petechiae

Front 145

What are the peripheral manifestations of endocarditis?

Back 145

Osler’s nodes, subungal hemorrhages, janeway lesions, Roth’s spots

Front 146

What are the lab manifestations with endocarditis?

Back 146

Anemia, leukocytosis, microscopic hematuria, elevated erythrocyte sedimentation rate, elevated C-reactive protein level, rheumatoid factor, circulating immune complexes, decreased serum complement

Front 147

In patients with subacute endocarditis, fever is typically what?

Back 147

Low grade and rarely exceeds 103 F

Front 148

In patients with acute endocarditis, fever is typically what?

Back 148

Temperatures of 103-104 F are often noted

Front 149

Fever may be blunted or absent in patients who are what?

Back 149

Elderly or severely debilitated or who have marked cardiac or renal failure.

Front 150

What are the cardiac manifestations of endocarditis?

Back 150

Heart murmurs, heart failure, heart block, abscess, MI

Front 151

If you see heart murmurs with endocarditis it means?

Back 151

Usually indicative of the predisposing cardiac pathology, valvular damage and ruptured chordae may result in new regurgitant murmurs. If involving a normal valve, heard on presentation in only 30-45% of patients but ultimately detected in 85%.

Front 152

If you see heart failure with endocarditis it means?

Back 152

Develops in 30-40% of patients, usually a consequence of valvular dysfunction but occasionally is due to endocarditis associated myocarditis or an intracardiac fistula.

Front 153

This is usually from extension of infection into paravalvular tissue adjacent to the aortic valve. Occasionally from abscess near mitral valve.

Back 153

Heart block in endocarditis.

Front 154

This happens from extension of infection beyond valve leaflets into adjacent annular or myocardial tissue, which in turn may cause fistulae with new murmurs. May extend into pericardium, causing pericarditis.

Back 154

Abscess in endocarditis

Front 155

This can occur from emboli to coronary artery.

Back 155

MI in endocarditis.

Front 156

What are five non cardiac manifestations in endocarditis?

Back 156

Embolic events, septic embolization, neurologic symptoms, musculoskeletal symptoms, renal complications, splenic abscess, mycotic aneurysms.

Front 157

These are often seen with infarction, may involve extremities, spleen, kidneys, bowel or brain, associated with non cardiac manifestations of endocarditis.

Back 157

Embolic events

Front 158

These are common with S. Aureus, vegetation over 10mm in diameter and those located on the mitral valve are the most likely to embolize, tricuspid involvement may cause septic pulmonary emboli, associated with non cardiac manifestation of endocarditis.

Back 158

Septic embolization

Front 159

These are most often resulting from embolic strokes, other complications include aseptic or purulent meningitis, microabscesses in brain and meninges, intracranial hemorrhage due to hemorrhagic infarcts or ruptured mycotic aneurysms, seizures, and encephalopathy, associated with non cardiac manifestation of endocarditis.

Back 159

Neurologic symptoms

Front 160

Inflammatory arthritis and back pain, must be distinguished from local metastatic infection, associated with non cardiac manifestation of endocarditis.

Back 160

Musculoskeletal symptom

Front 161

Embolic renal infarcts cause flank pain and hematuria, glomerulonephritis, from immune complex deposition on the glomerular basement membrane, associated with non cardiac manifestation of endocarditis.

Back 161

Renal complications

Front 162

Half of these cases involve the cerebral arteries, extracerebral aneurysms present as local pain, a mass, local ischemia or bleeding, associated with non cardiac manifestation of endocarditis.

Back 162

Mycotic aneurysms

Front 163

What are the peripheral manifestations associated with endocarditis?

Back 163

Petechiae, Osler’s Nodes, Janeway Lesions, Roth Spots

Front 164

These are peripheral manifestations associated with endocarditis that show up on the palate, conjunctiva, or beneath the fingernails. They can also show up as splinter hemorrhages – Linear reddish brown lesions of the nailbed.

Back 164

Petechiae

Front 165

These are tender violaceous raised lesions on the finger pads, toes or feet that are associated with peripheral manifestation in endocarditis.

Back 165

Osler’s Nodes

Front 166

These are macular erythematous, blanching, non painful lesions on the palms or soles of the feet, associated with peripheral manifestation in endocarditis.

Back 166

Janeway Lesions

Front 167

These are exudative lesions in the retina, associated with peripheral manifestation in endocarditis.

Back 167

Roth Spots

Front 168

What are the specific predisposing conditions for endocarditis? 4 of them.

Back 168

Early onset prosthetic valve endocarditis, late onset prosthetic valve endocarditis, IV drug use, health care associated endocarditis.

Front 169

This lacks peripheral vascular manifestations, and typical symptoms, may be obscured by comorbidity associated with recent surgery. It is a specific predisposing condition for endocarditis.

Back 169

Early-onset prosthetic valve endocarditis

Front 170

This presents with typical clinical features, and It is a specific predisposing condition for endocarditis.

Back 170

Late-onset prosthetic valve endocarditis

Front 171

This is seen in almost 50% of endocarditis, infection is limited to the tricuspid valve, these patients present with fever, faint or no murmur, and prominent pulmonary findings. It is a specific predisposing condition for endocarditis.

Back 171

IV Drug Use

Front 172

This arises after recent hospitalization, or it is a direct consequence of long term indwelling devices. It is a specific predisposing condition for endocarditis.

Back 172

Health care associated endocarditis

Front 173

This is established with certainty only when vegetations obtained at cardiac surgery, at autopsy, or from an artery (an embolus) are examined histologically and microbiologically.

Back 173

Diagnosis of infective endocarditis.

Front 174

This has highly sensitive and specific diagnostic schema for endocarditis.

Back 174

Duke Criteria

Front 175

If you have two major criteria, one major and three minor criteria, or five minor criteria allows a clinical diagnosis of what?

Back 175

Definite endocarditis

Front 176

Alternative diagnosis is established, symptoms resolve and do not recur with 4 days of antibiotic therapy, surgery or autopsy after four days of antimicrobial therapy yields no histologic evidence of endocarditis.

Back 176

Rejected endocarditis

Front 177

Illnesses not classified as definite endocarditis or rejected, one major and one minor criterion or three minor criteria.

Back 177

Possible endocarditis.

Front 178

Positive blood culture – typical microorganisms for infective endocarditis from two separate blood cultures, persistently positive blood culture, blood cultures drawn 12 hours apart or all of three or a majority of four or more separate blood cultures. Single positive blood culture for Coxiella burnetii or antibody titer of >1:800

Back 178

Major Duke Criteria

Front 179

Evidence of endocardial involvement – positive echocardiogram, intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted material, or abscess, or new partial dehiscence of prosthetic valve, or new valvular regurgitation.

Back 179

Major Duke Criteria

Front 180

What are the five minor Duke criteria

Back 180

1.Predisposing heart condition or IV drug use, 2. Fever 38C/100.4 F, 3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, janeway lesions, 4. immunologic phenomona: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor, 5. Microbiologic evidence: Positive blood culture not meeting major criterion or serologic evidence.

Front 181

In the absence of prior antibiotic therapy, three blood culture sets separated from each other by at least 1 hour, should be obtained from different venipuncture sites over how many hours to help diagnose endocarditis?









I

Back 181

24 hours

Front 182

If cultures remain negative after 48-72 hours, how many additional blood culture sets should be obtained to diagnose endocarditis?

Back 182

Two or three.

Front 183

This cannot image smaller vegetations, may be technically inadequate in some patients, and is not adequate for evaluating prosthetic valves or detecting intracardiac complications in endocarditis.

Back 183

Transthoracic echocardiography

Front 184

This is significantly more sensitive than TTE, and is the optimal method for the diagnosis of prosthetic endocarditis or the detection of myocardial abscess, valve perforation, or intracardiac fistulae.

Back 184

Transesophageal echocardiography

Front 185

f you have a negative transesophageal echocardiography when endocarditis is likely, what does it mean?

Back 185

does not exclude the diagnosis but rather warrants repetition of the study in 7–10 days.

Front 186

What should not be administered initially to hemodynamically stable patients with subacute endocarditis, especially those who have received antibiotics within the preceding 2 weeks.

Back 186

Empirical antimicrobial therapy

Front 187

Patients with acute endocarditis or with deteriorating hemodynamics who may require urgent surgery should be treated empirically after?

Back 187

Three sets of blood cultures are obtained.

Front 188

It is difficult to eradicate bacteria from vegetations because?

Back 188

this site is relatively deficient in host defenses and because non-growing, metabolically inactive bacteria are less easily killed by antibiotics.

Front 189

To cure endocarditis, all bacteria in the vegetation must be killed; therefore, therapy must be?

Back 189

bactericidal and prolonged. Generally given parenterally.

Front 190

The minimum inhibitory concentration (MIC) of penicillin for the causative isolate must be determined with this.

Back 190

Streptococcal Endocarditis

Front 191

Killing requires the synergistic interaction of a cell wall–active antibiotic and an aminoglycoside
Enterococci causing endocarditis must be tested for high-level resistance to streptomycin and gentamicin, -lactamase production, and susceptibility to penicillin and ampicillin

Back 191

Enterococcal Endocarditis

Front 192

Regimen is based on the presence or absence of a prosthetic valve or foreign device, the native valve(s) involved, and the resistance of the isolate to penicillin and methicillin

Back 192

Staphylococcal Endocarditis

Front 193

What patients with endocarditis are able to complete threapy as outpatients?

Back 193

If the patient is fully compliant and have sterile blood cultures, are afebrile during therapy, and have no clinical or echocardiographic findings that suggest an impending complication they may complete therapy outpatients.

Front 194

What three things should be done when monitoring antimicrobial therapy in endocarditis?

Back 194

Serum concentrations of aminoglycosides and vancomycin
Blood tests to detect renal, hepatic, and hematologic toxicity
Blood cultures should be repeated daily until sterile, rechecked if there is recurrent fever and performed again 4-6 weeks after therapy to document cure.

Front 195

People who have endocarditis and also have congesitive heart failure, perivalvular infection, uncontrolled infection, S. aureus endocarditis or patients that need preventntion of systemic emboli may need?

Back 195

Intracardiac surgery

Front 196

What factors adversely affect the outcome of endocarditis?

Back 196

Older age, severe comorbid conditions, delayed diagnosis, involvement of prosthetic valves or the aortic valve, an invasive or antibiotic resistant pathogen, intracardiac complications, major neurologic complications.

Front 197

This has been recommended by the American Heart Association in conjunction with selected procedures considered to entail a risk for bacgeremia and endocarditis.

Back 197

Antibiotic prophylaxis

Front 198

What procedures require prophylaxis when a patient has had endocarditis?

Back 198

All dental procedures that involve manipulation of the gingival tissue or the periapical region of the teeth or perforation of the oral mucosa, respiratory tract procedures that involve incision of the respiratory mucosa, Procedures on infected skin, skin structure, or musculoskeletal tissue.

Front 199

Prophylaxis for patients who have had endocarditis is not required for what?

Back 199

Gastrointestinal tract procedures, genitourinary tract procedures, routine dental anesthetic injections through noninfected tissue, dental radiographs, placement of removable prosthodontic or orthodontic appliances, adjustment of orthodontic appliances, placement of orthodontic brackets, shedding of deciduous teeth, bleeding from trauma to the lips or oral mucosa.

Front 200

What are the high risk cardiac lesions for which endocarditis prophylaxis is advised before dental procedures?

Back 200

Prosthetic heart valves, prior endocarditis, unrepaired cyanotic congenital heart disease, for six months following complete repair of a congenital heart defect, incompletely repaired congenital heart disease with residual defects adjacent to prosthetic material, valvulopathy devloping after cardiac transplantation.

Front 201

What is the standard oral regimen for prophylaxis of endocarditis in adults with high risk cardiac lesions?

Back 201

Amoxicillin 2 grams 1 hour before procedure

Front 202

What is the Rx for pts unable to take oral medications, but need prophylaxis of endocarditis in adults with high risk cardiac lesions?

Back 202

Ampicillin 2 grams IV or IM wihtin one hour of procedure

Front 203

What is the ABX regimen for prophylaxix of endocarditis in adults with high risk lesions if someone has a penicillin allergy?

Back 203

Clarithromycin or azithromycin, cephaxalin, clindamycin

Front 204

What is the ABX refimen for prophylaxis of endocarditis in adults with high risk cardiac lesions if the patient has a penicillin allergy and is unable to take PO meds?

Back 204

Cefazolin or ceftriaxone, or clindamycin

Front 205

Heart “grows” from outside of pericardial cavity into cavity
Three layers result what are they?

Back 205

Fibrous pericardium and Serous pericardium

Front 206

This is the outermost layer, fibrous, rigid, and adhered to surround surfaces?

Back 206

Fibrous pericardium

Front 207

This is made up of two layers of pericardium.

Back 207

Serous pericardium
A. Parietal pericardium – closely attached to the fibrous pericardium
B. Visceral pericardium – adherent to the outer surface of the myocardium

Front 208

The intent of this is to allow free movement of the heart throughout the cardiac cycle. It also limits distention of the cardiac chambers and works to increase the heart’s efficiency.

Back 208

the pericardial space and the fluid that fills it

Front 209

This is thin, clear, straw colored fluid, normally void of cells

Back 209

Pericardial fluid

Front 210

This is inflammation of the pericardium.

Back 210

Pericarditis

Front 211

This is when there is an increase in pericardial fluid.

Back 211

Pericardial fluid

Front 212

This is an increase in pericardial fluid that interferes with proper filling of the ventricles.

Back 212

Cardiac tamponade

Front 213

This is surgical perforation of the pericardium for the purpose of draining the pericardial space and obtaining pericardial fluid for analysis.

Back 213

Pericardiocentesis

Front 214

What is the most common form of pericarditis observed?

Back 214

Acute pericarditis

Front 215

This has less than six weeks since symptom onset, it is classified as infectious, non-infectious, idiopathic, and as post cardiac injury.

Back 215

Acute pericarditis

Front 216

This is when there is 6 weeks to 6 months of symptoms and is known as effusive-constrictive pericarditis.

Back 216

Subacute pericarditis

Front 217

This is when there has been symptoms over six months in pericarditis.

Back 217

Chronic constrictive pericarditis

Front 218

What are the top three causes of acute pericarditis?

Back 218

Neoplastic, Autoimmune and Viral - adenovirus, enterovirus, cytomegalovirus, influenza virus, hepatitis B virus and herpes simplex virus.

Front 219

A patient with the following symptoms shows the cardinal manifestations of what?Chest pain, pericardial friction rub, characteristic ECG changes, Pericardial effusion +/- cardiac tamponade, Paradoxical pulse

Back 219

Acute pericarditis

Front 220

Chest pain that is steady, severe, constricting, retrosternal, radiating to the neck, arms and left shoulder, OFTEN RELIEF WITH SITTING UP, LEANING FORWARD, BUT WORSE WITH LYING SUPINE, can be pleuritic - aggrivated by inspiration, cough, change in body position.

Back 220

Acute pericarditis chest pain

Front 221

Chest pain in acute pericarditis can look like what two things?

Back 221

AMI or STEMI

Front 222

This is audible in up to 85% of patients, one, two, or three components, high pitched, rasping, scratching, or grating sounds, heard best along Lower Left Sternal Border with diaphragm, Accentuate with patient sitting upright, leaning forward, end expiration.

Back 222

Pericardial Friction Rub

Front 223

What is seen in stage one of acute pericarditis ECG changes?

Back 223

Stage 1: widespread ST elevation with ST depressions in aVr and or V1

Front 224

What is seen in stage two of acute pericarditis ECG changes?

Back 224

Days later return of ST segments to baseline

Front 225

What is seen in stage three of acute pericarditis ECG changes?

Back 225

Days later T wave inversion

Front 226

What is seen in stage four of acute pericarditis ECG changes?

Back 226

Weeks later return to baseline

Front 227

What is the Tx ofr acute pericarditis?

Back 227

Rule out MI, Anti-inflammatories - Aspirin, Ibuprofen, Selective COX-2 inhibitors, Colchicine. Steroids, ABX - if bacterial cause, Discontinue anticoagulant therapy - may lead to hemopericardium

Front 228

On x-ray, usually obvious widening of cardiac silhouette. But what else can cause this finding? à enlarged heart (from CHF for example) So how do you tell the difference between say CHF and Acute pericarditis?

Back 228

On physical exam of two patients, both with enlarged silhouette on chest xray, the one with reduced or muffled heart sounds will likely have pericardial effusion.
the one with normal or louder than normal heart sounds will have cardiomegaly

Front 229

This is when there is accumulation of fluid in the pericardial space, an inflammatory response or bleeding, causes enlargement of cardiac silhouette on chest X-Ray (Water Bottle configuration) and Ewart's sign

Back 229

Acute pericarditis: Pericardial Effusion

Front 230

This is when the base of the left lung is compressed by pericardial fluid causing dullness, increased fremitus, and egophony beneath angle of left scapula. Associated with acute pericarditis: pericardial effusion.

Back 230

Ewart's sign

Front 231

How do you diagnose an effusion in acute pericarditis?

Back 231

Transthoracic echo is gold standard

Front 232

This is an echo-free space between posterior pericardium and left ventricular epicardium.

Back 232

Small effusion <100mL

Front 233

This is an echo-free space between anterior right ventricle and anterior pericardium.

Back 233

Large effusion >500mL

Front 234

This is the accumulation of fluid in the pericardial space in a quantity sufficient to cause serious obstruction to the inflow or blood to the ventricles.

Back 234

Acute pericarditis: Cardiac Tamponade

Front 235

To help distinguish from heart failure, remember the hallmark findings of tamponade that aren’t found with heart failure, including:

Back 235

-Reduced QRS amplitude
-Electrical alternans

Front 236

In general, a rapid accumulation of a small amount of fluid (<200 mL) can produce?

Back 236

Cardiac Tamponade

Front 237

A slow progressive accumulate of a large amount of fluid (>2000 mL) may not produce tamponade because?

Back 237

The pericardium has had time to distend appropriately to accommodate the excess fluid and pressure.

Front 238

What can slow onset cardiac tamponade in pericardial effusion resemble?

Back 238

Dyspnea, orthopnea, hepatic engorgement = Heart Failure

Front 239

What are the diagnostic criteria for acute pericarditis: cardiac tamponade?

Back 239

Beck's Triad - Hypotension, Soft or absent heart sounds, Jugular venous distension
Paradoxical Pulse

Front 240

What is a greater than normal (10 mmHg) inspiratory decline in systolic arterial pressure?

Back 240

Paradoxical pulse

Front 241

What do you do immediately to confirm the suspicion of tamponade?

Back 241

Echocardiogram

Front 242

What is the Tx ofr cardiac tamponade in acute pericarditis?

Back 242

Pericardiocentesis

Front 243

This is the surgical removal of pericardial fluid.

Back 243

Pericardiocentesis

Front 244

How do you perform a pericardiocentesis?

Back 244

Echo guided insertion of needle into pericardial space - subxiphoid approach, 5th or 6th left intercostal space, insertion of catheter for drainage, fluid drained and collected, analyzed for cells, and cultures obtained, drain left in place until drainage ceases.

Front 245

This occurs after resolution of acute pericarditis, particularly in patients with tuberculosis origin, but many other causes such as post radiation/cancers breast, lung, lymphoma, Trauma, Cardiac Surgery, Autoimmune Dz, Chronic renal failure with uremia.

Back 245

Chronic Constrictive Pericarditis

Front 246

Everything in chronic constrictive pericarditis results in what?

Back 246

Results in deposition of granulation tissue in pericardium

Front 247

Impaired diastolic function due to restricted filling, poor forward flow: weakness and fatigue, Fluid retention: Weight gain, increased abdominal girth, abdominal discomfort and edema, Kussmaul's sign, and congestive hepatomegaly are all seen with what?

Back 247

Chronic Constrictive Pericarditis

Front 248

What is an elevation of the neck veins during inspiration?

Back 248

Kussmaul's sign

Front 249

This is impaired hepatic function and possibly jaundice, ascites (looks like cirrhosis)

Back 249

Congestive hepatomegaly

Front 250

What is seen on the ECG, CXR, Echo and CT or MRI with chronic constrictive pericarditis?

Back 250

ECG: Low voltage of QRS, diffuse T wave flattening or inversion
CXR: Usually normal silhouette
Echo: Pericardial thickening
CT or MRI: Pericardial thickening and calcifications

Front 251

What is the TX for chronic constrictive pericarditis?

Back 251

Pericardial resection

Front 252

Pericardial resection entails?

Back 252

Removing about as much as possible of the pericardium. It is the only definitive treatment of CCP Operative mortality is 5-10% and increases with severity, so early treatment is key.

Front 253

What are the most common aortic aneurysms?

Back 253

Infrarenal aortic aneurysms are most common.

Front 254

What is the male to female ration of those who have infrarenal abdominal aortic aneurysms?

Back 254

4:1 male:female

Front 255

What are significant comorbidities for aortic aneurysm?

Back 255

HTN, COPD, CAD

Front 256

An abdominal aortic aneurysm is ?

Back 256

Over 50% increase in normal aortic diameter

Front 257

AAA has associated vascular diseases such as?

Back 257

CAD, HTN, DM, Hyperlipidemia, Tobacco, COPD, CVD +/- stroke, claudication, visceral and renovascular occlusive disease

Front 258

What is an independent risk factor for mortality in AAA?

Back 258

Chronic renal insufficiency

Front 259

90-95% of proximal neck anatomy is what in AAA?

Back 259

Infrarenal

Front 260

What is the primary etiology with AAA?

Back 260

Degenerative 80%, Dissection 15%

Front 261

What age should a first degree relative of someone with AAA be screened?

Back 261

45-50

Front 262

What are the pathogenic - genetic causes of AAA?

Back 262

Enzyme deficiencies, Connective tissue disorders

Front 263

This is when AAA is due to lysl oxidase deficiency

Back 263

collagen and elastin cross linking.

Enzyme deficiencies - pathogenesis of AAA genetic

Front 264

What are the two particular connective tissue disorders associated with genetic pathogenesis of AAA?

Back 264

Marfan Syndrome - abnormal fibrillin, Structural component of elastin, Ehlers-Danlos (type IV) - Abnormal type III collagen

Front 265

When you have predilection for formation in distal aorta, Gradual tapering - less elastin, more collagen, - devoid of vasa vasorum, Reflected pressure waves from the peripheral arterial tree increases mural tension in the infrarenal aorta.

Back 265

Pathogenesis of AAA - Mechanical

Front 266

Degenerative aneurysms often coexist with?

Back 266

Generalized atherosclerosis, therefore are referred to as: atherosclerotic aneurysms.

Front 267

Focal intimal thickening encroaches on lumen leading to?

Back 267

Consequent compensatory arterial dilation

Front 268

In AAA there is a loss of normal arterial architecture due to what?

Back 268

Media thins underneath the plaque in atherosclerosis

Front 269

Aortic structural integrity and stability are dependent upon what two things?

Back 269

Media: Musculoelastic fascicles and Adventitia: Collagen

Front 270

When you have degredation of the media and adventitia this leads to what?

Back 270

Aneurysmal dilation - decrease quantity of elastin, increased activity of elastase, increased collagenase activity, decrease in the concentration of protease inhibitors.

Front 271

What diagnostic methods are used to find AAA?

Back 271

Physical exam, X-Ray, Aortography, US, CT Scan, MRI/MRA

Front 272

In the physical exam, the aorta must be?

Back 272

5cm to be palpated, prominent aortic pulsation experienced

Front 273

In X-ray with AAA you will see?

Back 273

A fine rim of calcification

Front 274

With ultrasound in AAA you will see?

Back 274

Initial evaluation of pulsatile mass or F/U accurate to 3mm

Front 275

What is an excellent technique to image the abdominal aorta and its branches?

Back 275

CT angiogram / Spiral CT

Front 276

What are the indications for an aortography in AAA?

Back 276

Renovascular HTN, unexplained impaired renal function, symptoms of visceral angina, iliofemoral occlusive disease, horseshoe or pelvic kidney, prior colectomy.

Front 277

When determining operative risk for repairing AAA, what are the independent risk factors for mortality?

Back 277

– CRI (creat >1.8)
– CHF
– CAD (ischemia on EKG)
– COPD
– Elderly

Front 278

When should AAA be treated?

Back 278

When long term risk of AAA related death exceeds risk of repair plus risk of death following repair.

Front 279

How is risk of AAA related death predicted?

Back 279

AAA size (diameter) has been the only reliable indicator of rupture and death.

Front 280

What are the four instances that AAA is a surgical emergency?

Back 280

When they are symptomatic patients showing Rupture - 50% immediate mortality, over 75% overall mortality, Aortoenteric fistula, Aortocaval fistula, Vague abdominal pain - constant or throbbing, epigastric radiating to the back

Front 281

What constitutes a rapid progressive enlargement of an AAA?

Back 281

Enlarging over .5 cm/yr

Front 282

What are the reasons why treat an aortic aneurysm?

Back 282

Thrombosis, embolization - blue toe syndrome, Fistulization - enteric, caval, Local compression, Atypical/Morphologic - False, mycotic, penetrating ulcer, saccular, inflammatory, Symptomatic - Pain, rupture.

Front 283

What is involved with open repair of an AAA?

Back 283

Direct exposure - transabdominal retroperitoneal, Proximal and distal control, ligation of branches, Prosthetic graft sutured to normal artery.

Front 284

This is when a device is inserted from remote site, passed intraluminally under radiologic guidance, secured by expandable stent attachment system, used to fix AAA.

Back 284

Endovascular AAA repair

Front 285

What are the anatomic criteria for endovascular AAA repair candidacy?

Back 285

Infrarenal neck, Aortic bifurcation, Iliac arteries and access vessels

Front 286

This is an intimal tear allowing blood to separate the intimal and medial layers of the aorta.

Back 286

Aortic dissection, acute is within 2 weeks of onset, chronic is over 2 weeks.

Front 287

What is no an associated risk factor for aortic dissection?

Back 287

Atherosclerosis

Front 288

50% of dissections in women under 40 occur during?

Back 288

Pregnancy

Front 289

What is the primary associated risk factors for aortic dissection?

Back 289

Hypertension and Connective Tissue Disorders

Front 290

What is the clinical presentation of aortic dissection?

Back 290

Chest Pain – “Worst pain ever”
Death
Stroke
Cardiac Tamponade
Lower extremity ischemia
Syncope
Renal Failure
Mesenteric Ischemia
Spinal Cord Ischemia
Voice Hoarseness

Front 291

What is seen in the CXR with aortic dissection?

Back 291

– Widening of mediastinum
– Low sensitivity, low specificity

Front 292

What is seen with the aortography with aortic dissection?

Back 292

– False lumen visualized 87%*
– Intimal flap in 70%*
– Intimal tear/entry site 56%*

Front 293

What imaging study has excellent sensitivity/specificity for aortic dissection?

Back 293

MRI

Front 294

What is seen with CT in aortic dissection?

Back 294

– Excellent sensitivity/specificity
– Excellent detail resolution
– Limitation: sensitivity slightly decreased at ascending aorta
– False lumen larger than true lumen 90% of time*

Front 295

What is the TX for type A aortic dissection?

Back 295

– Ascending arch replacement +/- valve repair/replacement
– Mortality increases 1% per hour*
– 60% in-hospital mortality with medical management**

Front 296

What is the TX for type B aortic dissection?

Back 296

– Uncomplicated: no end organ ischemia, meaning no malperfusion
• medical therapy with emphasis on decreasing blood pressure
– Intravenous B-blocker
– Intravenous arterial dilator

– Complicated: end organ ischemia, meaning malperfusion
• Surgery with graft replacement
• Endovascular Therapy

Front 297

One of the most challenging vascular problems Time is of the essence Patients often in generally poor health Questions remain as to optimal therapy - surgical vs. percutaneous Many will require a combination of modalities Multi-disciplinary involvement important Successful outcomes dependent upon experienced team

Back 297

Acute limb ischemia

Front 298

Acute limb Ischemia comes from embolism, what are the cardiac sources?

Back 298

• Atrial Fibrillation
• Myocardial infarction
• Prosthetic valves
• Atrial myxomas
• Endocarditis
• Rheumatic heart disease
• In-situ thrombosis
• Bypass graft occlusion
• Aortic dissection

Front 299

Acute limb Ischemia comes from embolism, what are the non cardiac sources?

Back 299

• Atherosclerotic disease of proximal vessels
• Mural thrombus of aortoiliac, femoral, popliteal aneursyms
• Tumor emboli
• Paradoxical embolus

Front 300

When acute limb ischemia is assocaited with Low flow state what are the two etiological factors?

Back 300

– Cardiogenic shock
– Systemic sepsis

Front 301

When acute limb ischemia is assocaited with Drugs what are the two types of drugs often seen?

Back 301

– Cocaine
– Vasopressors

Front 302

When acute limb ischemia is associated with Vasculitides

Back 302

– Takyasu’s arteritis

Front 303

What involving the knee can be a part of acute limb ischemia?

Back 303

Popliteal entrapment

Front 304

What Hypercoagulable states can be a part of acute limb ischemia?

Back 304

– Protein C/S deficiency, malignancy

Front 305

When Trauma is involved in acute limb ischemia what is seen?

Back 305

– Supracondylar humerus fracture
– Posterior knee dislocation
– High velocity penetrating injury
– Iatrogenic (endovascular, a-lines)

Front 306

Factor - Embolism Fill in the rest. . .

Often Detected -

Source -

Claudication -

Physical Findings -

Back 306

Embolism - Factor
Often detected – Afib
Atherosclerotic lesion - Source
Often not present - Claudication
Normal contralateral pulses - Physical Findings - Minimal atherosclerosis, sharp cutoff, few collaterals Angiogram

Front 307

Factor - Thrombosis - Fill in the blanks. . .

Often detected

Source

Claudication

Physical Findings

Back 307

Thrombosis - Factor
No discrete - Source
Frequently present - Claudication
Contralateral evidence of PVD
Physical Findings - Diffuse atherosclerotic disease, tapered and irregular cutoff, collaterals Angiogram

Front 308

This is associated with a history of claudication - may be absent in 40% of patients.

Back 308

Acute arterial thrombosis

Front 309

This usually arises with no history of claudication.

Back 309

Acute arterial embolism - emboli usually occur in the setting of atrial fib, 80% AF, 10% prior MI, 10% other aneurysms

Front 310

Why does it matter to know the difference between embolism and thrombus?

Back 310

Can affect decision on first line therapy, pts subjected to balloon embolectomy in setting of acute arterial thrombosis have a particularly poor outcome.

Front 311

What are the six P's assocaited with acute limb ischemia?

Back 311

• Pain
• Paresthesia
• Paralysis
• Pallor
• Pulselessness
• Poikilothermia

Front 312

This is usually the first symptom with acute limb ischemia.

Back 312

Pain

Front 313

This is a sign of progressive ischemia, loss of proprioception and light sensation early.

Back 313

Paresthesia

Front 314

Reflects ischemic myopathy, intrinsic muscles of the foot, flexors/extensors of lower leg, indicative of need ofr emergent revascularization.

Back 314

Paralysis

Front 315

White, waxy leg in absence of collateral circ.
– In arterial thrombosis, this may gradually improve due to collaterals
• May have mottling
– Fixed cyanosis
• Capillary thrombosis and rupture
• Terminal ischemia

Back 315

Pallor

Front 316

This is an absolute prerequisite for acute limb ischemia diagnosis.

Back 316

Pulselessness

Front 317

Intact pulses in contralateral leg suggests?

Back 317

Embolic etiology

Front 318

Absent pulses in contralateral leg supports?

Back 318

Diffuse PAD and thrombosis

Front 319

What are exceptions to pulselessness?

Back 319

Venous gangrene and blue toe syndrome

Front 320

This is coolness compared to contralateral limb, both cool in aortic occlusion.

Back 320

Poikilothermia

Front 321

If you have Acute painful, cold leg, but no neuro deficit, and audible pedal arterial doppler signals what does this mean?



What is involved with category IIa and IIb of the rutherford scale?

Back 321

• Category I. Viable, on the rutherford scale. Often acute thrombosis of chronic atherosclerotic artery or previous bypass graft
• Time for angiographic assessment
• Institution of lytic therapy may be possible and beneficial
• Anticoagulation while awaiting urgent angiography
• Operative balloon thrombo-embolectomy alone unlikely to successfully treat arterial thrombosis or stenosed artery or graft

Front 322

What is involved with category IIa and IIb of the rutherford scale?

Back 322

– IIA: minimal sensory loss, no muscle weakness
• Time for angiography with CLOSE SURVEILLANCE of limb
– IIB: Greater sensory and motor dysfunction
• Immediate revascularization indicated

Further Class II information
• Acute pallor, no prior claudication history, palpable contralateral pulses, AFIB
• Embolism diagnosis most likely
• But in many cases, differentiating etiology challenging
• Debate: Does angiography waste valuable time, or provide beneficial information??

Front 323

What class of the rutherford scale follows this criteria?
– Cold cyanotic limb, calf muscle rigidity
– Patients often systemically very ill
• Severe comorbidities, nonambulatory
– Primary amputation may be appropriate

Back 323

Class III Rutherford Irreversible

Front 324

Initial bolus followed by continuous infusion
– Decrease thrombus propagation
OPTIONS
Angiography
Thrombolytic therapy, endovascular revascularization
Percutaneous Mechanical thrombectomy
Open surgical intervention

Back 324

Heparin Therapy and options associated

Front 325

What are the guides to TX in acute limb ischemia?

Back 325

Site and extent of occlusion
– Embolus versus thrombus
– Native artery versus bypass graft
– Duration of ischemia
– Patient co-morbidities
– Contraindications to thrombolysis or surgery

Front 326

What are the advantages of the cath lab in ALI?

Back 326

– Angiographic capabilities
• Roadmap anatomy
– Therapeutic possibilities
• Thrombolytic infusion
• Percutaneous mechanical thrombectomy
• Subsequent endovascular treatment of exposed underlying lesion

Front 327

What are the disadvantages of the cath lab in ALI?

Back 327

– “Time-factor”: clinical situation may not allow for time required for restoration of adequate arterial flow with lysis
– Endovascular therapy may not allow complete revascularization
– Need for continuing surveillance of limb, with need to re-image at any time if clinical deterioration

Front 328

Establish inflow
Balloon embolectomy catheters passed up iliac
If inadequate inflow, intraop agram may identify chronic lesion treatable by additional endovascular or surgical means
– Establish outflow
Balloon catheters for PFA, SFA, tibial embolectomy
Over the wire balloons under fluoro aid in thrombus retrieval
– Completion angiogram

Back 328

Embolectomy via CFA exploration

Front 329

Use of open surgical procedures in ALI has been shown to have high rates of?

Back 329

Peri-op morbidity and mortality
– Rates of amputation and death up to 25% each

Front 330

Thrombolysis is attractive in Tx ALI because?

Back 330

– Restoring patency, unmasking culprit lesion, allowing non-surgical Tx in some cases
– Latest devices/adjunct for thrombolysis may enhance, accelerate lytic results

Front 331

What are the criticisms for using thrombolysis in ALI TX?

Back 331

• Timing: slow rate of thrombus dissolution in some clinical situations
• Clinical ischemic time may not allow for lysis
• May require repeated imaging to assess progress
• Potential for distal embolism during lysis
• Risk of re-thrombosis
• Hemorrhagic risks

Front 332

What are the absolute contraindications for using thrombolysis to TX ALI?

Back 332

• Absolute
– CVA within past 3 months
– Active bleeding diathesis
– Recent GI bleeding
– Neurosurgery or head trauma within past 3 months

Front 333

What are the relative contraindications to using thrombolysis to TX ALI?

Back 333

– Major non-vascular surgery or trauma within 10 days
– Uncontrolled HTN
– Intracranial tumor
– Recent eye surgery
– Puncture of non-compressible vessel

Front 334

What are the minor contraindications for using thrombolysis to TX ALI?

Back 334

– Hepatic failure with coagulopathy
– Bacterial endocarditis
– Pregnancy
– Diabetic hemorrhagic retinopathy

Front 335

Often insufficient as stand-alone therapy

• grafts have a 2 year patency rate of 79% if underlying lesion is uncovered v. 9.8% if not

• Even if a subsequent bypass is needed, it may allow surgical bypass in more elective setting

Back 335

Thrombolysis in TX of ALI

Front 336

Signs/symptoms
– Weakness on toe extension and foot dorsiflexion
– Pain on passive toe flexion, foot plantar flexion
– Hypesthesia in dorsal first web space
– Anterior compartment tense

Back 336

Anterior Compartment Syndrome, ALI post revascularization

Front 337

Signs/symptoms
– Weakness of toe flexion and foot inversion
– Pain on passive toe extension, foot eversion
– Hypesthesia plantar aspect foot and toes
– Tense deep post. Compartment
• Between tibia and Achilles tendon

Back 337

Deep posterior compartment syndrome ALI Post revascularization

Front 338

If you have compartment syndrome, what can be done to alleviate it?

Back 338

4 compartment fasciotamy

Front 339

• One of the most complex decision pathways in vascular disease
• Treatment must be based upon severity of ischemia, rather than cause
• Time permitting, an arteriogram can add helpful diagnostic and anatomic information, and can be therapeutic
– should be considered in all appropriate patients
• Team approach can lead to improved outcomes
– Restoration of perfusion can require both catheter-directed and surgical techniques

Back 339

Acute Limb Ischemia Summary

Front 340

• Systemic panarteritis of the medium & large arteries
• Chronic inflammation
• Also known as Temporal Arteritis, temporal artery is most commonly involved
• Etiology is unknown
• Frequently associated with Polymyalgia Rheumatica, ½ of pts with Giant cell arteritis also have PMR
• Over the age of 50, peak age is 60-80 years old
• Twice as common in women & more common in whites than African Americans

Back 340

Giant Cell Arteritis

Front 341

What are the signs of Giant Cell Arteritis?

Back 341

• Localized HA or scalp pain

• Temporal artery tenderness or decreased temporal artery pulse

• Visual Sx (amaurosis fugax or visual loss)

• Jaw claudication—pain in the jaw with movement such as eating or talking, throat pain, fever

Front 342

Any patient over age 50 with fever of unknown origin, normal WBC & very high ESR…..must r/o?

Back 342

Giant Cell Arteritis even if no HA or other signs & symptoms

Front 343

The most important reason to Dx & Tx giant cell arteritis is to prevent?

Back 343

Blindness

Front 344

What Is the hallmark of possible blindness with giant cell arteritis?

Back 344

The hallmark is elevation of acute phase reactants, which is an acute inflammatory response, such as ESR & CRP. ESR is typically over 50, but a lower ESR doesn’t r/o the Dx

Front 345

What do you do to diagnose giant cell arteritis?

Back 345

Unilateral temporal artery bx (side that is Sx, tender or inflamed) within 1-2 weeks of initiating prednisone.

Front 346

What length must you get In the temporal biopsy to adequately diagnose giant cell arteritis?

Back 346

3-5 cm In length because the disease Is segmental

Front 347

A positive biopsy of giant cell arteritis shows what?

Back 347

Inflammatory changes with an Infiltration of lymphocytes, histiocytes, plasma cells and giant cells.

Front 348

The results of a temporal artery bx remain positive for as long as __________ after Initiating treatment with prednisone. Never delay tx a patient with prednisone because of fear of the bx not showing Inflammation because of starting steroids.

Back 348

4 weeks

Front 349

When a pt has Sx suggestive of temporal arteritis, they are immediately started on?

Back 349

• prednisone 60 mg QD before a bx is even obtained, Continue prednisone 60 mg QD for 1-2 months then start tapering the dose when the symptoms have resolved.
• Start taking one aspirin a day

Front 350

What is the role of ESR when TX giant cell arteritis?

Back 350

• Use the ESR to adjust the steroid dose.

• As the ESR decreases, the disease activity is diminishing and you can decrease the steroid dose.

• Discontinue the prednisone when the ESR reaches normal range

Front 351

What is the prognosis of giant cell arteritis?

Back 351

• Blindness rarely occurs when the ESR is in the normal range.
• With prompt treatment, the prognosis is very good & Sx start to resolve over several days to months.
• Visual Sx are usually permanent.
• The average duration of treatment is usually 2 years.
• Morbidity from steroid treatment is often worse than the underlying disease.

Front 352

What is a presentation of Arterial peripheral vascular disease?

Back 352

Atherosclerosis

Front 353

What are three Venous presentations of peripheral vascular disease?

Back 353

Varicose Veins
Thrombophlebitis
Chronic Venous Insufficiency

Front 354

What race is more at risk of facing peripheral vascular disease?

Back 354

African American

Front 355

A disorder caused by atherosclerosis that limits blood flow to the limbs.

Back 355

Peripheral Arterial Disease (PAD)

Front 356

A symptom of PAD characterized by pain, aching, or fatigue in working skeletal muscles. It arises when there is insufficient blood flow to meet the metabolic demands in leg muscles of ambulating patients.

Back 356

Intermittent Claudication (IC)

Front 357

What are the systemic manifestations of atherosclerosis?

Back 357

• TIA or Ischemic Stroke
• MI or Unstable Angina
• Renovascular Hypertension
• Intestinal Ischemia
• Erectile Dysfunction
• Intermittent Claudication
• Critical Limb Ischemia, rest pain, gangrene, ulcers, amputation

Front 358

What are some of the features associated with the underlying causes of PAD?

Back 358

• Characterized by lipid deposits in intima of large and medium-sized arteries
• Associated with fibrosis/calcification
• Invariably a systemic condition
• Clinical recognition varies in individuals

Front 359

The hallmark of atherosclerosis is?

Back 359

atherosclerotic plaque

Front 360

Plaque is most commonly at?

Back 360

bifurcations or bends
– Local stress flow
– Turbulent blood flow
– Stasis of blood

Front 361

What are the modifiable risk factors of atherosclerosis?

Back 361

• Smoking
• Hypertension
• Diabetes
• Hyperlipidemia
• Obesity
• Hyperhomocysteinemia

Front 362

What are the nonmodifiable risk factors of atherosclerosis?

Back 362

Age, Sex, Genetics

Front 363

What do the following represent as a risk factor for atherosclerosis?
• Accelerates atherosclerosis 200%–400%
• Risk of coronary artery ischemic events increases 2–4 times
• Results in 4 times risk of stroke
• PAD develops a decade earlier than nondiabetics
• CV risk equivalent to 3 non-diabetic risk factors

Back 363

Diaebetes Mellitus

Front 364

The single most important risk factor for developing PAD
• PAD progresses faster and cuts longevity of revascularization procedures
• Increases the rate of limb amputation
• Significantly decreases patient survival

Back 364

Smoking

Front 365

This has a synergistic effect, dramatically raising risk when combined with any other risk factor.

Back 365

Smoking

Front 366

This is associated with
– Metabolic abnormalities stemming from reduced blood flow and O2 delivery
– Significant reduction (50%) in muscle fibers compared with controls
– Smaller type I and II muscle fibers with greater arterial ischemia
– Hyperplastic mitochondria and demyelination of nerve fibers

Back 366

Intermittent claudication

Front 367

Intermittent claudication is 2 to 4 times more common among persons with?

Back 367

Diabetes

Front 368

What Is the ADA/AHA Standardized approach to PAD?

Back 368

• Annual history for exercise-induced leg pain in all diabetic patients
• Annual palpation of leg pulses for all adult patients with diabetes
• ABI should be performed for insulin-dependent diabetic patients >35 years of age, or patients with ³20 years’ duration of diabetes

Front 369

How do you diagnose and assess the severity of peripheral vascular disease?

Back 369

Vascular history, physical examination, ankle brachial index measurement, noninvasive vascular laboratory tests.

Front 370

What are the symptoms to describe a functional description of Intermittent claudication?

Back 370

• Symptoms
– Exertional aching pain, cramping, tightness, fatigue
– Occur in muscle groups, not joints (buttocks, hips, legs, calves)
– Are reproducible from one day to the next on similar terrain
– Resolves completely with 2-5 minutes of rest

Front 371

When you are doing the arterial physical exam for PAD in the lower extremities you do what?

Back 371

• Auscultate abdomen for bruits
• Palpate for abdominal aortic aneurysm
• Palpate femoral, popliteal, posterior tibial, and dorsalis pedis pulses
• Inspect feet for ulcers, fissures, calluses
– Evaluate overall foot skin care

Front 372

Type of ulcer located on feet, toes and heel, pale foot , dependent rubor, yellow, brown or black color, ulcer appears punched out.

Back 372

Arterial (ischemic)

Front 373

Type of ulcer located at pressure points on bottom of feet, callous surrounding a punched out ulcer, color varies depending on circulation

Back 373

Neuropathic (diabetic)

Front 374

Type of ulcer below the knee and medially, base of ulcer is red, lots of drainage, irregular borders, venous stasis skin discoloration, shiny smooth skin, leg edema

Back 374

Venous ulcer

Front 375

What are the non-invasive vascular tests?

Back 375

• ABI measurements
• Pulse-volume recordings
• Segmental pressure measurements
• Duplex ultrasonography
• Treadmill exercise Noninvasive Vascular Tests

Front 376

Ankle sytolic pressure/Brachial artery systolic pressure =

Back 376

ABI

Front 377

Both ankle and brachial systolic pressures should be taken using a what?

Back 377

Hand held doppler

Front 378

For ABI is 95% sensitive and 99% specific for?

Back 378

PAD

Front 379

ABI
0.90–1.30
0.70–0.89
0.40–0.69
less than or equal to 0.40
>1.30

Back 379

Interpretation
Normal
Mild
Moderate
Severe
Noncompressible vessels

Front 380

What are ofur indications for referral ofr vascular specialty care?

Back 380

Lifestyle-disabling claudication (refractory to exercise or pharmacotherapy), Rest pain, Ischemic ulcers, gangrene

Front 381

What are the two medications used to Tx intermittent claudication?

Back 381

Pentoxifylline and Cilostazol

Front 382

What is a new medication for the Tx of PAD that reduces ischemic events, but doesn't improve claudication symptoms?

Back 382

Clopidogrel (Plavix)

Front 383

What new medication for patients with PAD doesn’t reduce ischemic events, but it does improve claudication symptoms?

Back 383

Cilostazol

Front 384

Patients with intermittent claudication have systemic atherosclerosis and are at increased risk for?

Back 384

MI and stroke

Front 385

What are the major lipid risk factors in PAD?

Back 385

– Elevated LDL-C
– Elevated triglyceride level
– Low HDL-C

Front 386

What are the four indications for revascularization for intermittent claudication?

Back 386

• Lifestyle-limiting symptoms
• Continued disability despite appropriate nonsurgical management
• Technically feasible revascularization
options exist
• Expectation of favorable risk/benefit ratio

Front 387

What are the goals with limb revascularization?

Back 387

• Relieve limb-threatening ischemia
• Treat claudication (after other measures)

Front 388

What are the indications for surgical intervention in PAD/PVD?

Back 388

• Gangrene
• Non-healing ulcers
• Ischemic rest pain
• Claudication causing lifestyle deterioration refractory to pharmacologic intervention and behavioral modification

Front 389

Ache, pain, numbness of arch of foot/toes with leg elevation, Most uncomfortable at night while resting in bed, Interferes with sleep, Relief with dependent positioning of limb

Back 389

Ischemic rest pain

Front 390

Found distally at ends of toes, over bony prominences on feet
• Dry, devitalized, black
• Intense pain

Back 390

Ischemic ulceration

Front 391

Endovascular techniques for the TX of PAD includee what four things?

Back 391

PTA
Atherectomy
Stents
Thrombolytic therapy

Front 392

Provides an anatomic assessment or a map for revascularization
• Not indicated in the routine diagnostic evaluation of patients with symptomatic PAD, except if claudication is disabling.
• absolutely indicated in patients who have critical limb ischemia, a condition characterized by ischemic pain at rest or tissue loss.
• If the patient is being considered for a revascularization procedure.

Back 392

Arteriography

Front 393

These are all manifestations of atherosclerois. Because of the generalized nature of atherosclerosis, the three disorders frequently occur together, but they may not be symptomatic.

Back 393

PAD, CAD, CVD

Front 394

• Smoking cessation
• Lipid control
– LDL-C, £ 100 mg/dL
– Raise HDL-C
– Lower triglycerides
• BP control
– Use ACE inhibitors
• Diabetes control
– HbA1C £ 7.0%
• Antiplatelet therapy
– ASA, clopidogrel
• Achieving ideal body weight
• Exercise

Back 394

Factors that may improve atherosclerosis

Front 395

When reevaluating a patient in follow up care for PAD 90 days after initation of therapeutic program what should you do?

Back 395

– Assess symptomatic status of limb
– Reassess atherosclerotic risk factor intervention and antiplatelet therapy
– Review compliance with home exercise therapy
– Consider pharmacologic therapy for nonresponders
– Continue monitoring every 90 days until patient improves
– Thereafter, monitor every 6 months

Front 396

• Involves the deep veins of the leg or arm.

• Can cause life threatening emboli to the lungs, venous dysfunction, and chronic swelling.

Back 396

Deep Venous Thrombosis

Front 397

This describes 3 factors that are critically important in the development of venous thrombosis:

Back 397

Rudolf Virchow (Virchow’s Triad)

Front 398

What makes up Rudolf Virchow (Virchow’s Triad)?

Back 398

• (1) venous stasis
• (2) activation of blood coagulation
• (3) vein damage.

Front 399

• The end result is early thrombus interaction with the endothelium.
• Stimulates local cytokine production
• Leukocytes adhere to the endothelium
• Over time, thrombus development begins with the infiltration of inflammatory cells into the clot.

Back 399

Results of Virchow's Triad

Front 400

What is one of the highest risk factors for venous thrombosis?

Back 400

Antithrombin deficiency

Front 401

What are the risk factors for DVT?

Back 401

• Prior history of DVT
• Age 30-80
• Venous stasis/immobilized patients
• Malignancy due to abnormal coagulation
• Post surgery
• Patients taking HRT…estrogen or birth control pills
• Pregnant women
• Smoking

Front 402

What are the symptoms of DVT?

Back 402

• Are due to obstruction of venous drainage
• Pain
• Tenderness
• Unilateral leg swelling
• Warmth
• Erythema
• Palpable cord
• Pain with dorsiflexion of foot (Homan’s Sign)

Front 403

True or False, DVT can not be diagnosed or excluded based on clinical findings.

Back 403

True

Front 404

Describe the correlation between DVT and Cellulitis?

Back 404

• Severe venous congestion produces a clinical appearance that can be indistinguishable from that of cellulitis.
• Patients with a warm, swollen, tender leg should be evaluated for both cellulitis and DVT because patients with DVT often develop a secondary cellulitis.
• Patients with primary cellulitis often develop a secondary DVT.
• Superficial thrombophlebitis is often associated with a clinically inapparent DVT.

Front 405

What is the study of choice to diagnose DVT?

Back 405

Ultrasound

Front 406

In the lab analysis for DVT this test shows degradation products of fibrin and plasmin. This is a sign of positive clot formation.

Back 406

D-Dimer

Front 407

What are the hypercoagulable studies performed in the lab analysis of DVT?

Back 407

• Hypercoagulable Studies
– Antithrombinn deficiency
– Protein C deficiency
– Protein S deficiency
– Factor V Leiden
– Hyperhomocysteinemia
– Anticardiolipin Antibodies

Front 408

How do you prevent DVT?

Back 408

• Compression
• Anticoagulation
– Subcutaneous heparin
– Early prophylaxis is associated with a significant reduction in post op thrombosis
– Greatest effect if initiated within 8 hours of surgery
– Continue for 7-10 days after surgery

Front 409

What is the medical TX of DVT?

Back 409

Anticoagulation, Thrombolysis, Vena Caval Filters

Front 410

What is the mainstay of medical therapy for DVT?

Back 410

Anticoagulation
• The mainstay of medical therapy.
– Continuous IV heparin until systemic anticoagulation is achieved (in patient)
– Low molecular weight heparin as QD or bid subcutaneous injection (out patient)
• Rapid anticoagulation in first 24 hours of Dx to prevent recurrent venous thrombosis during first 3 months from 25% to 5%.

Front 411

This is used for Long term anticoagulation
• Vitamin K antagonist
• Interrupts the production of Vitamin K–dependent coagulation factor production by the liver.
• The effect is delayed by 72 hours until the existing circulating coagulation factors are cleared.
• During this period, heparin anticoagulation is important to prevent worsening thrombosis.
• INR maintained between 2.0 to 3.0

Back 411

Warfarin

Front 412

The first episode venous thrombosis or thrombotic event due to a transient reversible risk factor should be treated for at least?

Back 412

Three months

Front 413

First episode Idiopathic venous thrombosis, Tx length should be?

Back 413

6-12 months

Front 414

This Is recommended for patients with recurrent episodes of venous thrombosis regardless of the cause.

Back 414

Indefinite therapy

Front 415

Long-term therapy with LMWH has been shown to be as effective as warfarin in the treatment of venous thrombosis, except in those patients with?

Back 415

A concurrent malignancy

Front 416

What are the contraindications to warfarin TX?

Back 416

• Hemorrhagic stroke
• Active bleeding
• Intracranial Neoplasm
• Malignant hypertension
• Recent major surgery
• Recent significant trauma
• Severe thrombocytopenia
• Pregnancy

Front 417

This is a TX for DVT that does the following things:
• Catheter based reduction of the thrombus with intrathrombus injection of plasminogen.
• Preserves valve function
• It accelerates the body’s own natural thrombolytic pathway.

Back 417

Thrombolysis

Front 418

This was developed to trap emboli and minimize venous stasis in DVT.

Back 418

IVC Filter

Front 419

Deep venous thrombosis, with or without pulmonary embolism, in patients with contraindications for anticoagulation, is the most common indication for an?

Back 419

IVC Filter

Front 420

What are the indications for an IVC filter?

Back 420

• DVT or PE with contraindication for anticoagulation
• Recurrent thromboembolism while on anticoagulation
• Anticoagulation complications requiring termination of therapy
• Large, free-floating iliofemoral thrombus in high-risk patients
• Enlarging iliofemoral thrombus while on anticoagulation
• Chronic PE in patient with pulmonary hypertension and cor pulmonale
• Patient with significant fall risk

Front 421

Progression of DVT and PE can occur despite full therapeutic anticoagulation in?

Back 421

13% of patients

Front 422

This develops as venous thrombi break off from their location of origin and travel through the right heart and into the pulmonary artery, causing a ventilation perfusion defect and cardiac strain.

Back 422

Pulmonary Embolism

Front 423

What Is the relationship between DVT and CVI?

Back 423

• Venous thrombosis causes an injury to the endothelial layer initiating inflammation that leads to vein wall fibrosis.
• Decreased vein wall contractility and valve dysfunction causes chronic venous insufficiency.
• The increase in venous pressure causes symptoms of varicose veins, lower extremity edema, and venous ulceration.

Front 424

normal veins that have dilated under the influence of increased venous pressure

Back 424

Varicose veins and Spider veins

Front 425

This is the result of venous insufficiency due to valve incompetence in the deep or superficial veins.

Back 425

Elevated venous pressure

Front 426

These are the undesirable pathways by whichh venous blood refluxes back into the congested extremity.

Back 426

Varicose veins

Front 427

Prevalance of venous insufficiency

Back 427

– Telangiectasias : 80% in men and 85% in women
– Varicose veins : 40% in men and 16% of women
– Ankle edema : 7% in men and 16% in women
– Venous ulcers : 1%

Front 428

What are the risk factors for venous insufficiency?

Back 428

– Caucasian
– older age
– female
– obesity
– pregnancy
– prolonged standing
– taller height

Front 429

What are the symptoms of varicose veins?

Back 429

• leg heaviness
• exercise intolerance
• pain or tenderness along the course of a vein
• pruritus
• burning sensations
• restless legs
• night cramps
• edema
• skin changes
• paresthesias

Front 430

Pain caused by this often improves with walking or by elevating the legs in contrast to the pain of arterial insufficiency, whichh is worse with ambulation and elevation.

Back 430

Venous insufficiency

Front 431

Pain and other symptoms associated with venous insufficiency may worsen with what?

Back 431

Menstrual cycle, pregnancy, and in response to exogenous hormonal therapy (oral contraceptives)

Front 432

How many stages are associated in rating venous insufficiency?

Back 432

0-6, 6 being the worst

Front 433

What is the goal of using imaging studies with venous insufficiency?

Back 433

To identify and map all areas of acute or chronic obstruction and all areas of reflux within the deep and superficial venous systems.

Front 434

What is the standard imaging used for venous insufficiency?

Back 434

Color-flow duplex ultrasonography

Front 435

Imaging study for venous insufficiency:
• Most specific & most sensitive for pelvis and legs where other imaging can’t reach.

• Can detect nonvascular causes off leg pain and edema.

Back 435

MRI

Front 436

• Invasive
• Infuses radiographic contrast material into the veins.
• Good for difficult cases
• Nearly 15% of patients undergoing this for detection of deep venous thrombosis (DVT) develop new thrombosis after contrast associated with this.

Back 436

Venography

Front 437

These must not be removed or sclerosed in regards to venous insufficiency.

Back 437

Hemodynamically helpful varices

Front 438

Superficial varicosities are the inevitable result of high-pressure flow into a normally low-pressure system.

Back 438

If there's NO deep system obstruction

Front 439

What type of varicosities are hemodynamically harmful?

Back 439

Varicosities carrying retrograde flow

Front 440

What are the nonsurgical txs for venous insufficiency?

Back 440

Compression, sclerotherapy, laster therapy

Front 441

What are the surgical txs for venous insufficiency?

Back 441

Endovenous laser therapy, radiofrequency ablation, phlebectomy

Front 442

What are the grade levels ofr compression stockings?

Back 442

Grade 1-VI with Six being the most compression

Front 443

What are the tips and tricks with compression stockings?

Back 443

Put them on in the morning, wear them as part of your work "uniform, take them off at night, replace stockings every 3-6 months

Front 444

• A sclerosing substance is injected into the vein to produce endothelial destruction which causes a fibrotic cord and eventually reabsorption of all vascular tissue layers.
• Local treatment of the superficial varicosities of venous insufficiency is unsuccessful if the underlying areas of reflux have not been found and treated.

Back 444

Sclerotherapy

Front 445

• Effective for tiny surface spider veins (those found on the face).
• Not useful as primary therapy for treatment of spider veins of the lower extremity.
• More painful
• High variability of light absorption in the skin

Back 445

External Laser Therapy

Front 446

• Thermal ablation technique that uses a laser fiber inside the vein.
• Under ultrasound guidance, local anesthetic is injected around the vessel separating it from its fascial sheath.

Back 446

Endovenous Laser Therapy

Front 447

• New thermal ablation technique that uses a special catheter placed inside the vein.
• Thermal sensors record the temperature within the vessel.
• Energy is delivered until the tissue temperature is sufficient to ensure endothelial ablation.

Back 447

Radiofrequency Ablation

Front 448

• Allows removal of short segments of vein through tiny incisions along the length of the vein.

• A day procedure

Back 448

Phlebectomy

Front 449

• Occurs in the gaiter distribution
• Ferritin and ferric oxide deposition

• Treatments
– Compression stockings
– Evaluate and treat the GSV/LSV

Back 449

Pigmentation

Front 450

• Delayed tissue healing

• Treatments
– Compression stockings
– Unna boot
– Evaluate and treat the GSV/LSV

Back 450

Ulceration

Front 451

• Contents
– Zinc oxide
– Calamine
– Glycerin
• Covered with Ace bandage
• Changed weekly
• Don’t use on patients with arterial disease

Back 451

Unna Boot

Front 452

What are the chronic venous disease Key Points

Back 452

• Different patient population
• Distinguish venous vs. arterial ulcers
• Compression stockings for relief
• Appropriate treatment
• Compression stockings for prevention

Beware of patients with PAD and CVI

Front 453

Back 453