5/5/2022

Department of Family and

Preventive Medicine
Physician Assistant Program
CORONARY ARTERY DISEASE (CAD)
ETIOLOGY
Review of Common
Cardiovascular Disorders • Ischemia = inadequate O2 supply for
metabolic demand of cardiac muscle
– Coronary artery atherosclerosis (MCC)
– Coronary artery spasm: idiopathic, cocaine
– ↑ myocardium O2 needs: exercise, LVH
– Congenital abnormalities of coronary arteries
– Coronary artery thrombosis

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Risk Factors for Atherosclerosis CAD CLINICAL MANIFESTATIONS

• Tobacco abuse • Often asymptomatic
• High plasma LDL ( > 100 ) • If symptomatic - Pain is most common
– Character = heaviness, squeezing, pressure,
• Low plasma HDL ( < 40 ) smothering, crushing
• Diabetes Mellitus glucose intolerance – May (or may not) radiate to arm (L or R), jaw, neck,
interscapular
• Hypertension – Relieved by rest
• Sedentary lifestyle – Precipitated by emotion or exertion
– Location usually substernal, may be epigastric in
• Male relative with IHD <age 55; female <65 inferior ischemia (RCA)
– Avg age at first MI is 64.9 yrs for men and 72.3 yrs for women – ↑ in frequency is of concern

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All chest pain is not CAD!

CAD CLINICAL MANIFESTATIONS
• Chest pain differential dx
– Pericarditis
– Pulmonary embolism • Variant Angina (Prinzmetal’s or atypical), caused
– Pneumonia by arterial spasm; often occurs at rest or may
– Esophageal ds wake patient from sleep

• Noncardiac chest pain may coexist in pt with CAD • Asymptomatic (silent ischemia) especially in DM

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CAD CLINICAL MANIFESTATIONS CAD Dx: The ECG

• Look for changes consistent with old MI. Is
CAD already present?
• Accompanying sx • ECG changes consistent with ischemia
– N&V (especially in – repolarization abnormalities
inferior ischemia), – T wave or ST segment changes (depressed,
diaphoresis, “fist” elevated, flipped)
(Levene’s) sign, dyspnea
– Intraventricular conduction disturbances
• Physical exam often nl – Widened QRS including new BBB
• High Index of Suspicion • ~50% of people with CAD have nl resting ECG

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Coronary Arteriography
CAD Dx: Stress Testing
Gold Standard for Dx
Most commonly used diagnostic tests for CAD
• 12 lead ECG recording during exercise
– 0.2 depression of ST segment lasting greater than 0.08 Invasive, $$$$
seconds (ST flat or downsloping)
– 15% false + (especially in those with low probability)
Visualizes
– 15% false negatives locations of
• Adenosine, dobutamine, persantine stress test if can’t coronary
exercise artery
• Radionuclide (Thallium scanning)
occlusions
• blood testing not really helpful
– ↑ lipids suggestive but not diagnostic

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CAD MANAGEMENT CAD DRUG THERAPY

PRIMARY PREVENTION IS BEST!
Effects
Secondary Prevention • systemic venodilation (↓ preload and O2
needs) = ↓ demand
• Reduce risk factors
• coronary artery dilation (@ high doses) →
– Diet, exercise and drugs to ↓ cholesterol ? Nitrates ↑ blood flow = ↑ supply
– Stop tobacco
– Treat HTN, DM Downside
– Exercise and Obesity • Flushing, headache
• Patient education • REBOUND = worse ischemia after
cessation

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CAD DRUG THERAPY CAD DRUG THERAPY

Effects Calcium Channel Blockers
• Negative inotrope and chronotrope
→↓ O2 demand (especially during Effects Downside
exercise) • coronary artery dilation All can → hypotension
Beta Blockers Downside • ↓ myocardial O2 demand • Nifedipine
• – flushing, edema
• fatigue and depression ↓ contractility
– worsening angina
• erectile dysfunction • ↓ arterial blood pressure
• Diltiazem and Verapamil
• bradycardia • DOC for variant angina
– CONSTIPATION!
• heart failure – AV conduction block
• bronchospasm – worsening heart failure
• hypoglycemia
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CAD DRUG THERAPY

CAD DRUG THERAPY
• Effects
Effects – inhibit HMG CoA reductase
Aspirin – inhibits platelet aggregation
Statins (rate-limiting step in cholesterol
synthesis)→↓LDL, ↑HDL,
↓TGs
Downside
– GI upset/bleeding
– allergy
• Downside
• assoc with nasal polyps and asthma – myopathy
– ↑ transaminases

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COMPLICATIONS OF CAD

ACUTE CORONARY SYNDROMES

▪ Myocardial infarction (ACS)
▪ CHF Unstable angina
▪ Arrhythmias NSTEMI
STEMI
750,000 MIs per year in the US--116,000 die

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Acute Coronary Syndrome Dx of ACS

Unstable Angina Myocardial Infarction
NSTEMI STEMI
• Risks for ACS the same as for CAD plus: Typical Crescendo, rest or Prolonged, severe crushing
– cocaine abuse Symptoms new onset squeezing, substernal chest pain + radiation
pressing substernal
– hypercoagulability (e.g.polycythemia,
chest pain or
nephrotic synd, protein C or S deficiency) “tightness” + radiation
– embolic disease Biomarkers No elevation Elevated
– collagen vascular diseases Troponin,
CK-MB
Initial EKG ST depression and/or ST depression ST
T wave inversion and/or T wave elevation;
inversion permanent Q
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MI diagnosis criteria ACS SIGNS AND SYMPTOMS

▪ ↑ troponin or CK-MB (biochemical markers of • Early AM common (circadian BP surge)
myocardial necrosis) with >1 of the following: • Pain is MC presenting complaint
– ischemic symptoms – similar to CAD - longer duration and more severe
– pathologic Q waves on the ECG (STEMI) – more N&V, diaphoresis, anxiety or weakness
– + radiation to arm, jaw, shoulder
– ST segment elevation (STEMI) or depression
– usually > 30 minutes
(NSTEMI) (ECG changes indicative of ischemia)
– if > 15 min despite 2 NTG SL separated by 5 min,
– coronary artery intervention (e.g., coronary suspect MI
angioplasty) OR – 15 - 20% of MIs are painless, especially in DM
▪ Pathologic changes of acute MI • May have sudden onset SOB due to CHF
Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of
Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000;36(3):959–969 • Weakness may be only symptom, especially in
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ACS PHYSICAL EXAM ACS PHYSICAL EXAM

• ¼ of patients with anterior MI have ↑HR and/or HTN bc

of SNS hyperactivity • If pulmonary edema (CHF) present
• ½ of patients with inferior MI have ↓HR and/or BP bc of – increased work of breathing
PSNS hyperactivity – frothy sputum
• Look for S3 or S4, may have rales if in CHF – gasping respirations
• Pericardial friction rub (inflammation) transient during – dyspnea
recovery • MR murmur may be heard if damage
• May have ↑ temp (to 38o) (inflammation, not infection) to papillary muscle
• Acral cyanosis, if in shock • Ectopy common
• Impaired mentation if poor CNS perfusion
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ACS EKG STEMI (transmural)

• STEMI (transmural)
1 = Normal
– ECG changes occur in local area of the infarct 2 = ST elevation
– “Typical” STEMI ECG changes - ST elevation of at 3 = T wave inversion
starting, Q beginning to
least 1mm in 2 contiguous leads deepen
• 1st “convex” ST elevation and tall T waves 4 = Q very deep, ST
• 2nd T wave inversion in hours to days returning to nl
5 = Q very deep, ST back
• then permanent Q waves ( > 40 msec) to nl
6 = ST, T back to nl,
Q wave permanent

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ACS - THE EKG

ACS EKG Changes
Anatomic Leads with Coronary
• NSTEMI (subendocardial) Site changes Artery
– ST segment depression and /or T wave inversion Inferior II, III, AVF RCA
Anteroseptal V1, V2 LAD
Anteroapical V3, V4 Distal LAD
Lateral I, AVL, V5, V6 LCx
Posterior V1, V2, V3-4 (look for RCA
st depressions*)

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Biomarker Evaluation
ACS Biomarker Evaluation
• Cardiac-specific Troponin • CK-MB distinguishes cardiac tissue from
– Higher specificity, sensitivity than CK-MB other sources of CK
– Elevated in several hours – skeletal muscle [MM-CK]
– In acute events, subsequent death is directly – brain [BB-CK]
proportional to ↑ in troponin, even if MB-CK is nl • Infarct size relates to total CK-MB
– Good for late diagnosis of prolonged episodes of
• LDH, AST will be elevated– not used for dx
chest pain (elevation lasts weeks; CPK up only 24
to 48 hours) anymore but need to know so don’t go
looking for liver ds when CMP results (done
on everybody in ER)
Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of
Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000;36(3):959–969
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ACS MANAGEMENT (THIS IS OLD NEWS)

Biomarkers in MI
• Morphine 2 - 4 mg IV (AVOID in hypotension or
Troponin need for serial examinations)
Rise in 3 - 4 hrs • Oxygen (ONLY to maintain SpO2 = 90%;
Peak at 18 hrs needless supplemental O2 causes HARM)
Lasts 10 - 14 days • Nitrates SL and/or IV (AVOID in inferior/R MI,
Creatinine kinase (CK or CPK) hypotension, preload dependence)
Isoenzyme MB >2.5% of total • Aspirin (all good, go ahead)
Rise in 3 - 8 hrs • Chewed, 162-325 mg, not enteric-coated
Peak in 24 hrs
Back to nl in 48 - 73 hrs
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Rx of NSTEMI Rx of STEMI

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Contraindications for fibrinolytics Post-ACS COMPLICATIONS

• Prior intracranial • Active bleeding or bleeding •P • Pericarditis
hemorrhage diathesis (not menses)
• Known cerebral vascular • Head/face trauma within 3 mo •F • Failure
lesion
• Known malignant
• Intracranial/intraspinal surgery •A • Arrhythmia/ Aneurysm
within 2 mo
intracranial neoplasm • Severe uncontrolled HTN •R • Rupture
• Ischemic CVA within 3
mo
• For streptokinase, prior
treatment within 6 mo
•T • Thromboembolism
• Septal Perforation
• Suspect aorta dissection •S
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Department of Family and

Preventive Medicine
Physician Assistant Program

Review of Common
Cardiovascular Disorders
Part 2
Heart Failure

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Heart Failure stats* Heart Failure

Diastolic dysfunction HFpEF
• ~5.7 million adults in the United States have HF
• Heart is unable to fill enough blood to pump
• 1/9 deaths included heart failure as contributing cause
• EF by echo is OK; NOT a problem of contractility
• ~ 1/2 die within 5 yrs of dx
• may have cardiac muscle dysfunction due to
– Infiltrative ds: amyloidosis, fibrosis, hemochromatosis
– LVH
• Heart failure costs the US ~ $30.7 billion/yr-- includes
cost of health care svcs, meds, and missed days of work. – HCM
– pericardial disease
*Per CDC data 6/2016
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Heart Failure CLINICAL MANIFESTATIONS

Systolic dysfunction HFrEF
• Heart unable to pump blood needed by tissues • DOE, PND,
• Cardiac muscle dysfunction due to orthopnea, rales
– Ischemic heart ds., prior MI, HTN • Weight loss/gain,
– Toxins poor appetite
• EtOH
• S3, MR murmur,
• adriamycin
– Infections
displaced PMI, ↑ HR
• viral (ECHO, coxsackie) • JVD, HJR, pedal
• Chaga’s ds (Trypanosoma cruzi) edema, ascites
– Abn cardiac valves
– Anemia, thyroid disease, peripartum
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CLINICAL MANIFESTATIONS HF Diagnosis

• H&P
• Abn CXR • Labs:
– cardiomegaly – BNP/nt-Pro BNP
– pulmonary edema – Hyponatremia
– ↑ BUN, creatinine
• ↓ mentation
• Echocardiography
• ↓ urination (poor
renal perfusion) – ↓ ejection fraction
– Doppler abnormalities for diastolic dysfunction

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Treatment Treatment
• Correct underlying cause • Reduce cardiac work
– anemia, arrhythmia, HTN, infection, thyroid – ↓ physical activity
disease, alcohol abuse, etc.
– ↓ afterload -- makes each beat more effective
• ACE inhibitors (enalapril, lisinopril, etc.)
• ↓ excess fluid • ARBs (losartan, candesartan, etc.)
– ↓ sodium intake • ARNI
– loop diuretics (furosemide, bumetanide, – ARB + inhibitor of neprilysin (enzyme that degrades
torsemide) natriuretic peptides, vasoactive peptides)
– Valsartan/sacubitril (Entresto)
– Spironolactone (shown to decrease mortality)
– ACE inhibitors
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Treatment Stages in the development of HF and recommended

Rx by stage

• ↓ excess catecholamine
– Β blockade
• Coreg (carvedilol), metoprolol
• Ivabradine
– Inhibits SA node, slows HR; more time to fill
• ↑ contractility
– Digitalis not used much now but historically
important
• Cardiac rehab
Clyde W. Yancy et al.
Emory University Physician Assistant Copyright © American Heart Association, Inc.
Circulation.
2013;128:e240-e327
Program All rights reserved.

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Guideline-directed mgmt and therapy of Stage C, D HFrEF

Cardiomyopathy
ISCHEMIC
DILATED
RESTRICTIVE
HYPERTROPHIC

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Dilated Cardiomyopathy Restrictive Cardiomyopathy

• Systolic dysfunction
same as CHF • Etiologies
– Amyloidosis
• Etiologies
– Hemochromatosis
– EtOh
– Scleroderma
– Peripartum
– Sarcoidosis
– Viral
– Chemotherapy
(esp. doxorubicin)
– Muscular dystrophy

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Restrictive Cardiomyopathy Restrictive Cardiomyopathy

• Diagnosis
• Pathogenesis
– Echo = normal sized heart with normal motion,
– Diastolic dysfunction = inability of the LV to fill → “speckled” appearance
↓ preload
– PYP technetium scan for amyloidosis
– Cardiac bx is gold standard but $$$ and invasive
• Clinical manifestations • Treatment
– Like RHF – treat basic ds if possible
• JVD, HJR, pedal edema
– maintain adequate fluid to maximize preload

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Hypertrophic Cardiomyopathy Hypertrophic Cardiomyopathy

• Etiology
• Synonyms – congenital autosomal dominant
– IHSS
– HOCM • Pathogenesis
– ASH – Diastolic + systolic dysfunction = inability of the
heart to fill + obstruction to outflow (↑ afterload)

HCM Normal LV
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HCM Clinical manifestations HCM Diagnosis

– Arrhythmias esp v-fib → syncope, sudden death – Echo
– Dyspnea • thick LV especially septum
– Angina (↑muscle needs ↑O2) • systolic anterior motion of the mitral valve and
– Cresc-dec systolic murmur @LLSB (if outflow may have mitral regurgitation (if outflow
obstruction present) that ↑ with Valsalva and obstruction present)
standing, ↓ with squatting
– S4
– May be asymptomatic!
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HCM Diagnosis HCM Treatment

• Β blockers, CCBs • AVOID
EKG
– ↓ myocardial O2 – digoxin
• LVH
demand
• tall R in V4,5,6 – diuretics
• Deep S in V1,2,3
– ↓ ectopy
– vasodilators
• LAE – ↓ outflow obstruction
– + inotropes/
• Wide biphasic P
by ↑ LV filling
chronotropes
mitrale • Pacemaker/ICD – strenuous
• arrhythmias • Myomectomy exercise
• Genetic counseling
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INFECTIVE ENDOCARDITIS
Native Heart Valve

• Bacterial etiology 60 – 80% have

Endocarditis underlying pathology
– Staph aureus > epi
– Strep viridans – rheumatic valvular ds
– Enterococcus – congenital heart ds
– Males > females – degenerative hrt ds
– Most: age > 50; not – calcific AS
common in children – fistulas

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Endocarditis in IV Drug Users Endocarditis in Prosthetic Valves

• Etiology
– > 50% S. Aureus • Any intravascular ▪ Incidence = 1 – 2% in yr 1
– streptococci and enterococci ~ 15% prosthesis predisposes post-op, then 1% per yr
– fungus (Candida) ~ 10% for endocarditis ▪ Early post-op
– G- bacilli ~ 10% – Sutures / Valves ▪ think contamination
before/during: Staph
• Multiple organisms common – Pacers (wires)
▪ Late onset after
• Young males common – Stents surgery
• Tricuspid valve >50% • Usually males > 60 yo ▪ think sources of
transient bacteremia: S
• Septic pulmonary emboli with tricuspid infection viridans
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Endocarditis S&S / Diagnosis Endocarditis Osler nodes

Subungual
SIGNS & SYMPTOMS petechiae
DIAGNOSIS
(splinter
• Fever • Strong index of hemorrhages)
• Murmur (new/changing) suspicion
• Splenomegaly ~ 30% • + blood cultures
• Embolic events in ~30% • TTE helpful, NOT Roth spots
• Roth spots, Janeway diagnostic (retinal
lesions, Osler’s nodes
• TEE diagnostic hemorrhages)
Janeway
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Endocarditis Treatment Endocarditis Complications

• Eradication of organisms from vegetations
• Valve destruction
– Culture and sensitivities • Renal disease
– may see acute CHF
– Appropriate antibiotic regimens – glomerulonephritis
• Embolic phenomena
• May need to replace valve if – emboli
– CVA
– Appropriate therapy not possible (e.g. resistant – abscess
– Brain abscess
organisms, pt has drug allergies)
• Conduction defects • Sepsis
– + cultures despite therapy
• Myocardial abscess • DEATH
– Valve destruction
– Fungal etiology
Endocarditis
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For dental, upper resp tract, infected skin and

Endocarditis prophylaxis musculoskeletal

• Guidelines from the AHA for abx prophy of

IE updated in 2007
– Somewhat controversial bc prophylaxis now
recommended for fewer pts
– Dental procedures involving manipulation of
gingival tissue, periapical region of teeth or
perforation of oral mucosa
– Abx solely for IE prophylaxis NOT
recommended for GI or GU procedures
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PERICARDITIS Etiology
• ETIOLOGIC
• CLINICAL CLASSIFICATION
CLASSIFICATION – Infectious: TB, viral,
Pericarditis – Acute pericarditis (<6 wks) fungus, bacterial
– Subacute pericarditis (6 – Noninfectious:
wks to 6 months) sarcoid, idiopathic,
etc.
– Chronic pericarditis (>6
months) – Hypersensitivity or
Autoimmune: SLE,
scleroderma, drug-
induced, post-MI
(Dressler’s)
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PERICARDITIS Clinical Manifestations PERICARDITIS ECG Changes

• PAIN Changes result of subepicardial inflammation
– often severe • ST segment elevations in two or three limb leads and
– left precordial, sometimes radiation to back many chest leads (“global” or “diffuse”)
– relieved by sitting up and leaning forward • Rare QRS changes, if any
– often pleuritic, sharp • ST segment returns to nl after a few days, then T
wave inversion may occur
• PERICARDIAL FRICTION RUB
– most specific physical sign (but not sensitive)
– scratching or grating
– positional
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Pericarditis

PERICARDITIS Dx

No specific tests for idiopathic pericarditis

Dx is one of exclusion and suspicion

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PERICARDITIS
PERICARDITIS Management Acute Complications
Depends on etiology
• No specific therapy
• Bed rest until pain and fever subsides
• Pericardial effusion
• Anti-inflammatory agents
– soft heart sounds, echo,
– ASA, NSAIDS, rarely steroids
EKG with ↓ voltage
• Surgery rarely needed (except constrictive pericarditis)
• Cardiac tamponade (may
• Monitor for complications
be fatal if not treated)
– may have EM dissociation

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PERICARDITIS
Chronic Complications

• Constrictive pericarditis
– after healing
– scarring → ↓ventricular
Rheumatic Fever
motion/filling
– calcification in ~ 50%
– long term sequelae look
like cirrhosis, RHF

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Major Minor Evidence

RHEUMATIC FEVER Etiology Jones Criteria Criteria for Grp A
Infection
Criteria Carditis Fever (+) throat
culture or
rapid strep
• After Group A strep infection, MC throat or skin Dx requires test
• Not all Group A strep causes RF 2 major OR Polyarthritis Arthralgia

• Autoimmune reaction, NOT continued infection 1 major + 2 Chorea ↑ESR and ↑/rising strep
Ab titer
+ CRP
• Ages 5 - 15 years MC minor criteria Erythema Previous RH Recent scarlet
AND evidence Marginatum fever or RHD fever
Subcutaneous
for Group A nodules < 2 cm
attached to
strep infection tendon or fascia -
nontender
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RHEUMATIC FEVER
Complications, Treatment, Prevention
• Rheumatic heart disease is the main complication
• MC sequela is mitral stenosis, #2 is aortic stenosis
• Early dx and treatment of Group A strep
infections
• Prevent recurrence after 1o attack
• AHA no longer recommends prophylaxis for pts
Erythema marginatum with hx of rheumatic valvular heart ds during
procedures with transient bacteremia
Subcutaneous nodule
Rheumatic Fever 2003
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ARTERIAL OCCLUSIVE DISEASE OF

AORTA AND LOWER EXTREMITIES

• MCC = ATHEROSCLEROSIS
– Progressive narrowing and occlusion of artery due to
perivascular inflammation and plaques in the media
Arterial and Venous Vascular Diseases – Superficial femoral, popliteal are MC sites → calf pain
– Distal aorta, bifurcation into iliacs are next MC → thigh
and buttocks pain

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Arterial Occlusive Disease Arterial Occlusive Disease

Clinical Manifestations Clinical Manifestations
• Intermittent claudication, relieved with rest
– calf muscles, thighs, buttocks • Dependent rubor, foot
– “weakness” in legs when walking pallor on elevation
– impotence, buttock fatigue during sex • Cool, pulseless, cyanotic
– pain at rest is bad sign extremities
• Bruits over aorta or iliacs • Ankle Brachial Index <0.9
• ↓ femoral or distal pulses
• Atrophic changes mostly with fem-pop
– hair loss, thin skin, muscle atrophy, nail dystrophy
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Arterial Occlusive
Disease Complications Arterial Occlusive Disease Diagnosis
• Labs
Limb or digit loss – ↑ cholesterol suggestive

Many pts have • Radiological Imaging

coexisting cardiac – duplex arterial ultrasound
or carotid ds – MRI or CT helpful (aorto-iliac disease)
– aortography with distal vessel runoff useful in
preop planning

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Arterial Occlusive Disease

Acute Embolism/Thrombosis Signs and Sx
Prevention
• Pulseless
• Smoking cessation
• Paresthesia
• Normalize serum cholesterol
• Pallor • ASA, Plavix
• Pain
• Paralysis

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Arterial Occlusive Disease AORTIC

Management ANEURYSMS
• Percutaneous • Arterial stenting
transluminal angioplasty • Laser angioplasty 90% are
(PTCA) • Surgery abdominal
• Thromboendarterectomy – arterial grafting
• Drugs – endoprosthesis
– Pletal = cilostazol • Conservative care
– Plavix = clopidogrel – Specified walking
– Trental = pentoxifylline programs
– ASA
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Aortic Aneurysms
Etiology
Clinical Manifestations
• Most AAA are asymptomatic
– sonography done for other purposes (e.g. GB)
• Atherosclerosis = MCC • Less common – discovery of popliteal aneurysm leads to AAA ( >50%)
– Usual risk factors – vasculitis, • Symptomatic
– Narrowing and thromboangiitis
obliterans – mild to severe mid-abdominal or back pain
occlusion of the artery
(Beurger’s disease) – pulsating abdominal mass on physical exam
• weakening of arterial
wall due to loss of – Fibrodysplasia – may see distal arterial thrombotic manifestations
elastin and collagen – Syphilis • cholesterol shower
with aneurysm • digital arterial occlusion
formation – Radiation arteritis
– may see arterial occlusive symptoms
• claudication
– Rupture can cause death before hospital arrival
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Aortic Aneurysms Dx Aortic Aneurysms Dx

Radiology
• plain films may
show calcification
Lab Evaluation
of aneurysm wall
• suprarenal AAA may cause renal dysfunction
• US is noninvasive,
• bleeding may cause anemia can help follow
progression
• MRI or CT helpful
• aortography
helpful for preop
planning
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Aortic Aneurysms Complications Aortic Aneurysms

Management
• Rupture and death
• Operative complications 1 - 8% mortality • Elective surgery • Ruptured AAA
– CVA
when AAA is 5-6 cm – treat for shock
– MI depending on co-morbid risk – STAT surgery consult
• ↓ Renal blood flow factors
• Bleeding – Grafting
• Intestinal ischemia – Endoprosthesis

• Graft-enteric fistula with GI bleeding

• Infection
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Giant cell arteritis Giant cell arteritis

• Sx
• Most often affects temporal arteries • Dx – HA/tenderness
• Often associated with polymyalgia rheumatica – ↑ ESR – Jaw pain
• Cause unknown – Temporal artery biopsy – Visual
• Treatment disturbance/blindness
• Epidemiology
– High dose corticosteroids – Fever, fatigue, wt loss
– Women > men
• start before confirming dx – Myalgia
– Elderly age group (>70 yo)
• ↑ risk of aortic
– Highest risk in people of Scandinavian origin
aneurysm, stroke
Emory University Physician Assistant Emory University Physician Assistant
Program Program

101 102

17
 5/5/2022

Polyarteritis nodosa Varicose veins/

Inflammatory vasculitis of medium-size arteries Venous insufficiency
• Segmental necrotizing lesions • Varicose veins = Torturous, enlarged veins
• →stenoses, aneurysms, infarction, • Venous insufficiency = incompetent
hemorrhage, thromboses
valves so blood does not adequately
• MC affects renal, GI, nervous
systems flow back to heart → edema
• Assoc with hepatitis B, C • Often cosmetic concern only
• Dx by bx or angiography • May → pain, ulcers, thrombophlebitis
• ↑ ESR, CRP • MC in lower extremities bc of
• Rx = steroids, pressure from standing
immunosuppresion
Emory University Physician Assistant Emory University Physician Assistant
Program Program

103 104

Varicose veins/ Varicose veins/

Venous insufficiency Venous insufficiency
• Risk factors • Prevention/treatment • Treatment
– ↑ Age – Weight loss – ↓ salt diet (↓ fluid
– Walking retention)
– Family history
– Keep legs elevated – Compression hose
– Female gender, and ↑ with OCPs or HRT
– Don’t sit with legs crossed – Sclerotherapy
– Pregnancy
– Avoid long periods of – Vein stripping
– Obesity
sitting/standing surgery
– Standing/sitting upright long periods of time
– No tight clothing at/below – Laser surgery
• Dx waist
– Doppler ultrasound – No high heels
Emory University Physician Assistant Emory University Physician Assistant
Program Program

105 106

Arteriovenous malformation Arteriovenous malformation

• May occur anywhere, but MC in brain
• Tangled arteries and veins with no capillary bed in • May cause HA, seizures
btwn • Most serious complication is bleeding
• Estimated detection rate in US general population (hemorrhagic CVA)
is 1.4/100,000/yr • Dx
• Estimated 300,000 Americans have AVMs – CT angiography or MR angiography
– 12% have symptoms

Emory University Physician Assistant Emory University Physician Assistant

Program Program

107 108

18
 5/5/2022

Arteriovenous malformation
• Treatment
– endovascular embolization
– neurosurgery
– Radiosurgery/gamma knife

Emory University Physician Assistant

Program

109

19