Pitcher- CV and PV

Question 1

A 28 y/o female seen in the ED with chest pain that worsens with deep breathing and is quite uncomfortable lying down. She reports a dry cough the last 4 days, have a 2 and 5 y/o at home and is a social worker in a teen homeless and suicide prevention center. She is on an oral contraceptive and states her grandfather had a stroke from poorly controlled hypertension last year.

Answer 1

key factors: oral contraceptives–> hypercoagulable state

close to tachycardia

What could lead to pericarditis? pneumonia, for example.

Order troponin, d-dimer

amount and color of sputum could be useful; high volume - bacterial,

CBC with left shift might represent baterial

Question 2

What are we looking for in peripheral pulses?

Answer 2

How they feel, if you can feel them, and how symmetric they are help in diagnosis

Pulses: superficial temporal artery, facial artery, common carotid artery, brachial artery, radial, femoral, popliteal, posterior tibial, dorsalis pedis

Question 3

Inspection/Palpation

Answer 3

Supine with head/chest elevated 30 degrees, inspect and palpate precordium for thrills, significant changes in pulse amplitude. If amplitude is elevated, this is felt as a heave. A thrill feels like a vibration and is from a valve problem.

Question 4

Auscultation

Answer 4

Supine, head up 30 degrees to accentuate sounds best
Use diaphram and bell (with light pressure)
Always identify S1 and S2

Question 5

different places to hear special things

Answer 5

leaning forward– accentuates aortic murmurs and pericarditis

left lateral decubitus- accentuates mitral murmurs

Question 6

Murmur

Answer 6

Defined as turbulence across a valve causing sound.
Can be High, Medium or Low pitch
Blowing, Harsh, Musical, Rumble
Occur in systole, diastole or both
Any of 4 valves in either or both phases
Can vary in intensity
May be increased or caused by changes in velocity of flow across normal valves, ie, exercise or hyperthyroidism.
Low viscosity blood causes murmurs at normal velocity with normal valves, ie, anemia

Question 7

Bruit

Answer 7

Similar noise from turbulence within an artery outside the heart itself.

Typically lower pitch and softer

Usually best heard with the bell (do not press hard)

Question 8

Grading Murmurs

Answer 8

1/6 Very faint
2/6 Quiet, but can easily be heard if in quiet room
3/6 Moderately loud
4/6 Loud, with palpable thrill
5/6 Very Loud, Thrill, can be heard with stethoscope partially off chest
6/6 Very Loud, Thrill, can be heard with stethoscope
OFF the chest

Question 9

Murmurs or Bruits– common and less common causes

Answer 9

Benign or Innocent:  Stills
	typically infants
Valvular problems
	papillary muscle tear or rupture
	chordae tendoneae rupture
	congenital malformation
	fibrosis annulus or leaflet (infection)
Patent ductus (Aorta-Pulm A)
Septal defects  ASD,  VSD
Artery stenosis

less common causes:

Tetralogy of Fallot: Pulmonic Stenosis + VSD + Aorta overriding VSD + RVH
Abdominal Aneurysm
Hyperthyroid state
Obstructive Hypertrophic Cardiomyopathy (IHSS)

Question 10

Heart Sounds

Answer 10

S1 : Mitral and Tricuspid closures. Signals onset of systole
S2: Aortic and Pulmonic closures. Signals onset of diastole

Question 11

Anything that causes a separation in the closure of paired valves is called

Answer 11

a split heart sound

Split S1: may be normal variant or abnormal from RBBB or PVC (premature ventricular contraction)

Probably normal if heard LSB

If both split, or consider RBBB and premature ventricular beats (PVC)

Changing the conduction characteristics changes contraction timing , changing valve closure timing: bundle branch blocks
Abnormal valve characteristics also can change closure times: prolonged in stenosis
Split S2 can vary with respiration, Split S1 does not.
LSB = left sternal border RBBB right bundle branch block

Question 12

Split S2

Answer 12

Split S2: may be normal variant increasing with inspiration, decreasing with expiration or abnormal in pulmonic stenosis or RBBB again

So to be more certain, listen at pulmonic area and have patient take a deep breath and hold it, split should change in normal variant.

Question 13

S1, S2, S3, S4

Answer 13

S1 and S2 are normal valvular sounds caused by the closure of matching valves during normal heartbeat.
“Lup Dup”

S3 and S4 are NON-valvular sounds occurring in diastole caused by some form of non-compliance of a ventricle
Indicates possible pathology

Question 14

S3

Answer 14

S3
	Early Diastole, closely follows 
		S2
	Best at apex in left lateral decubitus
	May be normal up to age 30 yr	
	“Kentucky”
Pathology (etiology still uncertain)
	Occurs at the ** transition of rapid to slow ventricular filling as the ventricular wall reaches the extent of diastolic excursion of the muscle that is inadequate to accommodate the inflow of blood.  This causes a reverberation defined as an S3.  Most common: LV myocardial damage (CHF, MI) causing systolic dysfunction from dilated cardiomyopathy.  Due to sudden limitation of normal ventricular relaxation during filling stage in diastole.***

Often present in hemodynamically significant chronic mitral regurgitation
Over fills LA = more blood flow back into LV
An important early finding in heart failure due to a dilated myocardium (more often systolic failure)
Early detection (BNP, Pro-BNP, doppler echocardiogram) allows treatment that might improve prognosis for asymptomatic patients

Question 15

S4

Answer 15

Just before S1, very late diastole just after atrial contraction
Best at apex in left lat decubitus
Caused by *** vibration of LV from the atrial kick trying to pump the last of the blood in but instead hitting poorly compliant ventricular wall.
Low pitch. Quieter. Best with bell. “Tennessee”.

Pathology (etiology still uncertain)
Aortic/pulmonic stenosis , HTN (elevated afterload) , wall damage from MI from remodeling or tissue death cause *** thickening of ventricular walls from a higher work load, and some stiffening. This also leads to non-compliance of the ventricle as the atria pump the last of the blood from the chamber to the ventricle.

Decreased ventricular distensibility 
Hypertension
Aortic valve stenosis
Pulmonic valve stenosis
Hypertrophic cardiomyopathy

First 3 result in muscle hypertrophy due to increased work load. Hypertrophic cardiomyopathy is a genetic disorder.

Question 16

Gallop” Rhythm technically refers to

Answer 16

either pattern of 
S1…S2S3
Or
S4S1…S2
Or
S4S1…S2S3

Question 17

Ejection Click

Answer 17

An ejection click is a sound occurring at the moment of maximal pressure with sudden tensing of a valve root.

Question 18

Aortic Ejection Click:

Answer 18

Early systolic: at onset of left ventricular ejection, aortic root suddenly stretched. (Second right interspace)

Pathology:
Dilated aneurysm of aortic root, coarctation of aorta, HTN all can dilate aorta and change the root dimensions.
Aortic valve stenosis, and aortic regurgitation also can change the dynamic of the aortic root.
Anything that can cause over working of the root of the aortic valve can over-distend it and cause click.

Question 19

Aortic Stenosis:

Answer 19

Systolic crescendo-decrescendo pattern,
medium pitch, typically harsh
Transmits sound to carotid arteries.
Pathology: Rheumatic disease (progressive fusion), congenital bicuspid valve, calcification of valve.
Symptoms: None until severe, then dyspnea on exertion, angina and syncope. Left ventricular enlargement can occur, creating hypertrophic, poorly compliant muscle and an S4

Question 20

Aortic Regurgitation

Answer 20

“Austin-Flint” murmur associated (mitral diastolic flow murmur)
Early diastolic, high pitch blowing decrescendo murmur from initial high pressure back flow through a more narrow orifice
What position can enhance the sound?-
Dilates the left ventricle (S3!) and can cause high pulse pressure and brisk carotid pulse
Pathology:
Rheumatic disease, congenital bicuspid valve, endocarditis (Strep, Staph, Haemophilius..)

Question 21

Pulmonic Ejection Click

Answer 21

Pulmonic Ejection Click:
Sudden root tensioning. Very early systole.
(Second left interspace)
Pathology:
Pulmonary HTN, aneurysm dilating the root
Pulmonary valve stenosis or regurgitation can alter stress on root of valve causing click.

Question 22

Pulmonary Stenosis:

Answer 22

Systolic crescendo-decrescendo murmur when severe enough to hear, 2nd left interspace more harsh as severity worsens = pulmonic post
Most are asymptomatic and if mild, usually will not progress. If more severe, progressive stenosis occurs.

Symptoms:
Include exertional dyspnea, chest pain, syncope. Can dilate the right ventricle , thicken muscle, causing right heart failure symptoms, including poor muscle compliance creating an S4

Etiology: Usually congenital, rarely associated with carcinoid tumor. Infrequently affected by rheumatic fever or infective endocarditis. Most pathology is from pulmonary hypertension dilating the artery affecting the valvular ring for either stenosis or regurgitation.

Question 23

Pulmonary Regurgitation

Answer 23

Graham Steell Murmur occurs
with increased pulmonary artery pressure causing higher
velocity regurgitant flow.
Identical to aortic regurgitation, not as loud.
Identify best by which post it is most clear. Softer diastolic decrescendo

Pathology:
Anything that causes pulmonary HTN: mitral stenosis, LV failure, obstructive sleep apnea, emphysema, idiopathic pulmonary hypertension

Question 24

Tricuspid Valve Stenosis:

Answer 24

Diastolic low pitch rumble, best heard with bell, with inspiration
Opening snap may be heard over tricuspid area.
Distinguished from mitral stenosis by location and that it is accentuated by inspiration, increasing heart filling dynamics.
Pathology:
Rheumatic valvular disease, congenital heart disease, carcinoid tumor.
Impeding right ventricular filling increases central venous pressure.
Symptoms of decreased cardiac output since blood not able to get into the cardiac/pulmonary system effectively
Physical: look for elevated JVP; RA enlargement

Question 25

Tricuspid Valve Regurgitation:

Answer 25

Early to holosystolic at left sternal border. Better with diaphragm High pitch, blowing Will NOT radiate to left axilla (regurg points right; mitral can radiate) Inspiration increases RV filling, accentuating the murmur Pathology: Ebstein congenital anomaly is a very thin valve structure predisposing to failure. “Incidental” findings are common reading on echocardiography. Severe failure can enlarge right atrium increasing risk for arrhythmia.

Question 26

Mitral Valve Stenosis

Answer 26

Mitral Valve Opening Snap: occurs in diastole When stenotic mitral leaflets are tethered at the orofice but still mobile, as left ventricular emptying lowers intraventricular pressure below the left atrium, they snap into the LV space momentarily before atrial blood flows in. Mitral Valve Stenosis: Diastolic murmur, can be with opening snap Can result in pulmonary hypertension, JVD( elevated JVP) and LA and eventually RV hypertrophy Snap and stenosis almost always from rheumatic heart disease: Mitral valve most often affected

Question 27

Mitral Valve Prolapse

Answer 27

“Click and Murmur” Leaflet prolapse=click mitral regurge=murmur Mid to late (non-ejection) systolic click at apex may or may not be followed by a murmur High pitch, short murmur = Mitral insufficiency Accentuated: Valsalva (lowers atrial volume) Standing Diminishes: Release of Valsalva (increased atrial volume) Squatting Momentary increase in forward flow of blood return reduces prolapse capability therefore lowering murmur*** Approximately 2.4% incidence, evenly distributed men and women, can be inherited, at risk for endocarditis, often without a murmur. Most cases idiopathic Severe regurgitation may dilate left atrium increasing risk for various arrhythmias, both atrial and ventricular. Most asymptomatic, but if more severe can show dyspnea, non-anginal chest pain, pre/syncope, palpitations and anxiety Very uncommonly associated with CHF and sudden death.

Question 28

Mitral Valve Regurgitation

Answer 28

Holosystolic (pansystolic) murmur Loud, High Pitch, best at Apex Can radiate to the left axilla Endocarditis, Rheumatic dz Post MI papillary mm rupture Heart failure, pulmonary HTN, atrial fibrillation

Question 29

Hypertrophic Obstructive Cardiomyopathy

Answer 29

May also see IHSS: Idiopathic Hypertrophic Subaortic Stenosis Mutations in cardiac sarcomere signal Hypertrophy of the left ventricle and the interventricular septum Must consider in FMH of sudden cardiac death, especially among athletes. Symptoms identical to aortic stenosis: exercise induced dyspnea, angina or syncope. ***

Question 30

What do we hear in HOCM?

Answer 30

Systolic ejection murmur; best along left sternal border and apex; often with accentuated PMI Murmur is INTENSIFIED by standing from a squat, or a Valsalva maneuver Resting Echocardiography is the study of choice Important to look for on sports physicals even without hearing initial murmur due to sudden death potential with exertion if missed due to arrhythmias and ischemia Asymptomatic incidence not well known.

Question 31

The Murmur of IHSS is the only systolic ejection murmur that

Answer 31

increases in intensity during Valsalva (or standing) Left ventricular volume falls, stroke volume falls, walls collapse in, narrows the exit passageway = intensified murmur

Question 32

Maneuvers to alter murmur

Answer 32

Valsalva: Take a deep breath and “push like you’re having a baby” 2. Squatting from a standing position 3. Standing from a seat or squatting position Few reliable changes in heart sounds

Question 33

Squatting

Answer 33

momentarily increases volume from more venous return and increases arterial blood pressure (afterload); Typically increases the murmur of mitral regurgitation and Lessens IHSS/obstructive cardiomyopathy murmur Due to enhanced left ventricular pressure from the increased afterload.

Question 34

Standing from squat

Answer 34

momentarily decreases volume and therefore right ventricular filling. (less physiologic effect on afterload) Not so much volume in LA to prevent back flow therefore Increases mitral prolapse sound Increases out flow obstruction without the blood pressure to hold space open: Increasing IHSS/obstructive cardiomyopathy murmur

Question 35

Valsalva

Answer 35

Strain against closed glottis supine Venous return to LA reduced LV volume falls = Stroke volume falls Arterial pressure falls This increases IHSS and can decrease aortic stenosis Same results with standing may be expected, but less reliable changes with valvular pathology.

Question 36

Patent Ductus Arteriosis (PDA)

Answer 36

Ductus Arteriosis is a fistula existing between aorta and pulmonary artery during fetal development to bypass fluid filled lungs directly until birth. Persistent patency after birth causes continuous murmur through all of systole and most of diastole. Best left 2nd interspace, may have thrill. Often machine like in quality and can radiate to the back. May hear quietly the first 1-2 days after birth, but should resolve quickly.

Question 37

Innocent murmurs

Answer 37

are often systolic ejection murmurs, can radiate to the back and persist after PDA closes. The majority of these are from a benign pulmonary branch stenosis. Still’s murmur is an innocent murmur thought to be vibrations of the pulmonic valve leaflets, typically 2/6 systolic ejection murmur. The vast majority of these resolve by 6 months of age. No innocent murmur would be a likely cause of distress on an exam. Loud (grade 3 or higher), harsh and pan-systolic murmurs indicate more of a pathologic murmur that needs investigation.

Question 38

Bruit

Answer 38

A bruit is equivalent to a murmur in a peripheral vessel from narrowing sufficient to cause turbulent flow. Often heard best with bell applied lightly. Can be heard with the diaphragm: Thyroid, Carotid, Abdominal, Femoral arteries From atherosclerosis, congenital stenosis or aneurysm. Thyroid from increased blood flow in the thyroid with Graves disease, best with bell

Question 39

Pericarditis:

Answer 39

Fluid in the sac Pathology: Infection of pericardium, MI, metastasis to pericardium, post cardiac surgery. Often associated with recent respiratory viral infection. CP worsens with breathing or cough and they are most comfortable leaning forward Best diagnosed with classic symptoms of pleuritic chest pain and friction rub. EKG typically most helpful in diagnosis, echocardiogram can confirm effusion and should be used if cardiac tamponade is suspected.

Question 40

Pericardial knock:

Answer 40

diastolic knock heard widely over precordium in constrictive pericarditis. Blood coming in to fill RV,LV chambers finds smaller chambers, stops abruptly and vibrates the walls.

Question 41

Rub:

Answer 41

noise from the two inflamed pericardial surfaces rubbing together when beating. Damp leather shammy. Scratchy, raspy, squeaky. More in systole, can be in diastole. Lean forward to accentuate Triphasic: Atrial systole, ventricular systole, ventricular diastole

Question 42

You found a murmur or bruit, now what?

Answer 42

``` Diagnostics: Finish your exam Include periphery: third spacing? Doppler ultrasound to define bruit Echocardiogram done with doppler to define murmurs TTE (transthoracic) or TEE (transesophageal) ``` Treatment Observation only: no to minor symptoms, mild defect Treat risk factors: Smoking, hyperlipidemia, HTN ?oxygen +/- CPAP Medication: Beta Blockers, ACE, ARB, Peripheral vasodilators (Ca+ Channel Blockers) Surgical: Valve replacement or repair Stent Endarterectomy

Question 43

Peripheral Arterial Disease

Answer 43

``` Intermittent Claudication Carotid Artery Stenosis Aneurysm Raynaud Disease or Phenomenon Vasculitis Hypertension (Just FYI) ``` Asymptomatic or atypical leg pain in 90% of patients with PAD. Only 10% have classic claudication symptoms of lower extremity

Question 44

Inflammation to Atherosclerosis

Answer 44

This is occurring in the endothelium, the vessel wall itself, and is the cause of vascular issues that result in stenosis, plaque, aneurysm. Small, dense LDL is worst, infiltrates vessel wall, causes oxidative/inflammatory response leading to plaque (atherosclerosis)

Question 45

Intermittent Claudication

Answer 45

A (not fully) occlusive arterial disease of the limbs ***Symptoms characterized by pain, tension and weakness of a limb when walking which intensifies with continued walking, resolving only when activity stops.*** Also seen in compression of the cauda equina (also called Charcot Syndrome), not vascular occlusion Most commonly seen in the legs bilaterally (what is the other common bilateral leg pain issue?)

Question 46

causes of intermittent claudication

Answer 46

Caused by ischemia in the peripheral tissue. Results from the balance of oxygen delivery and lactate removal favoring anaerobic metabolism If truly unilateral more likely thrombotic or entrapment Important factors/history to consider include Aortic Stenosis: poor perfusion Anemia: lowered O2 capacity Polycythemia: acts like a traffic jam Atherosclerosis: local stenosis Volume status: ability to circulate good in, waste out Cardiac exam, listen for bruits, examine skin/conjunctiva for pallor and tenting.

Question 47

intermittent claudication: common predisposing factors, symptoms, PE

Answer 47

Common predisposing factors include diabetes, smoking, other known atherosclerotic disorders (CAD, carotid stenosis, renal artery stenosis), HTN, hyperlipidemia. Seen most commonly in elderly males Symptoms occur distal the site of stenosis or occlusion: Activity induced pain, positional pain (elevated), rest pain, poorly healing wounds. LE Physical exam: Poor pedal pulses, ulcerations, palor, cool, shiny and hairless skin, bruit may be heard. Diabetes, smoking, hypertension and hyperlipidemia are a deadly combination and should always make you think of high vascular disease potential (MI, angina, CVA, PAD = peripheral artery disease) don’t forget the smaller arteries to organs that won’t hurt too, like the kidney.

Question 48

ABI

Answer 48

ankle pressure over arm pressure The lower the ABI number, the worse the PAD Diagnose ankle pressure by inflating the cuff above the ankle until the DP pulse stops, then deflating noting the pressure when the pulse returns. Example: Arm BP (brachial) 135/90 Ankle BP 85 palp 85/135=.63=moderate PAD likely

Question 49

intermittent claudication dx and treatment

Answer 49

diagnosis: Typically by history and exam Segmental blood pressure measurements good non-invasive tools. Ankle/Brachial BP ratio <0.9 (ABI) seals diagnosis. Contrast angiography gold standard for targeting surgical intervention Treatment Meticulous foot care Smoking cessation!! Lower lipids Walk! But not through pain Cilostazol (Pletal) and Pentoxifylline (Trental) can offer limited help Revascularization procedures Some treatment offered to decrease risk for other events, not primarily to help PAD.

Question 50

Carotid Artery Stenosis risk factors

Answer 50

``` Older male Hypertension, Diabetes Smoking , Hyperlipidemia Heart Disease Prevention is Key! Exam Palpation of pulses Listen for bruit with bell Events Stroke, TIA, Amaurosis Fugax (transient blindness) Effect of low cerebral oxygen? ```

Question 51

carotid artery stenosis diagnostics

Answer 51

Bruit does not predict extent of underlying stenosis Doppler Ultrasound, and if +: MRA or CT angiography 100 % accurate Treatment Endarterectomy if >69% occluded, soon after CVA if this occurred, only in patients with >5yrs life expectancy. Elective endarterectomy >50% stenosis Stents Risk factor management Aspirin prophylaxis: 81 to 325mg daily if not contraindicated Asymptomatic bruit approaching 8% in age >75 yr , accompanying 3 fold increase in CVA and ischemic heart disease Avoid angiography if possible to avoid 1% risk of non fatal stroke from procedure, but it is the most diagnostic. Risk factors begin to look familiar. If there is heart artery problems, the same mechanisms causing this cause peripheral artery issues as well.

Question 52

Aneurysm

Answer 52

Dilation of a segment of a blood vessel True aneurysm involves all three layers of vessel wall and can dissect Pseudoaneurysm is a dilation or hematoma that may or may not involve layers of the vessel wall which is contained and does not dissect Due to weakening of the wall from atherosclerosis, hypertension, vasculitis (inflammation)and infection. Risk factors include smoking, known atherosclerosis, hypertension, hyperlipidemia, diabetes sound familiar? Most asymptomatic and found incidentally on xray or ultrasound done for other reasons; 5-10% incidence men age 65-80 yr Painful only when expanding or leaking Thrombi CAN form and embolize

Question 53

aneurysm risk factors

Answer 53

Vessel disease, no matter where it is found, has common risk factors. Important in history, catch it early to avoid major disease later controlling the factors that are controllable pseudoaneurysm Cecil page 556 Treatment is elective grafting, emergent if needed Something weakens the wall and it begins to leak into itself to start things off

Question 54

Thoracic Aneurysm

Answer 54

Involve ascending, arch and distal aorta Pain from sudden dilation, compression of adjacent organs or dissection Ascending aneurysm can cause aortic regurgitation by distorting the ring Descending aneurysms are frequently silent, discovered incidentally on CXR

Question 55

Abdominal Aortic Aneurysm (AAA)

Answer 55

75% are distal to renal arteries Uncommon < age 60 yr Major risk is male, increasing age and smoking. Typically asymptomatic Risk of rupture high if over 5 cm diameter mortality 80% even if reach hospital Exam Palpate for pulsatile mass, just above umbilicus. Palpate diameter. Poor reliability if obese, moderate at best. Listen for bruit with bell If present, bedside US or CT angiography will confirm; contrast CT preferred if they present non-emergently US found to underestimate size of aorta by an average of .95 cm. American college of radiology recommends CT, with “contrast may help better delineate the (pulsitile) mass

Question 56

Femoral Artery Aneurysm

Answer 56

Not uncommon, can rupture. | Feel for pulsatile mass and listen for bruit

Question 57

Aneurysm Treatment

Answer 57

Elective graft strongly preferred! Mortality >50% if rupture occurs. Use Beta Blockers to reduce shear stress unless hypotensive already

Question 58

(Mrs.) Raynaud

Answer 58

Paroxysmal constriction/dilation of small arteries/arterioles Constriction producing palor, followed by dilation and initial filling of deoxygenated blood in capillaries producing cyanotic color. Release of spasm flushes system causing warmth and hyperemia Often intensely painful, 15-60 minutes in classic cycle. Raynaud Disease is not associated with other problems Raynaud Phenomenon is associated with other disorders such as ***scleroderma (90%), lupus, peripheral neuritis, polyarteritis Etiology unknown, 2x more common in women Commonly stress and cold induced, associated with use of vibrating tools (construction) Notable 26% incidence in people with migraine

Question 59

Raynaud treatment

Answer 59

Avoid or stop smoking Avoid cold temperatures Avoid beta blockers: they block vasodilation receptors leaving vasospastic receptors in sympathetic system unchecked = potential for necrosis Manage stressors Calcium Channel Blockers as vasodilators may be helpful

Question 60

Vasculitis

Answer 60

General term characterizing inflammation and damage to vessels, often the lumen, causing stenosis and ischemia to the involved tissue. It can be localized to a single organ, ie skin, or generalized. Etiology largely believed to be circulating immune complex mediated. Signs and symptoms involved depend on the site affected. Large Vessel: Takayasu Aortitis: Aorta and major branches, “pulseless disease”. Etiology often unknown Medium Vessel: Polyarteritis Nodosa or Wegener’s Granulomatosis; May be associated with infections/post-infectious insult or circulating immune complex Small Vessel: Henoch-Schonlein Purpura: A palpable purpura abdomen and legs, children more than adults; most often associated with immune complex

Question 61

Polyarteritis Nodosa

Answer 61

Multisystem necrotizing vasculitis of primarily medium arteries (=arteritis). Inflammation thickens vessel wall causing stenosis , ischemia and possibly infarct to distal tissues. Inflammation also weakens the wall predisposing to aneurysm formation . Thrombosis can also occur. Incidence no more than 30 per million people, estimates vary.

Question 62

Polyarteritis nodosa symptoms/ signs

Answer 62

Fatigue, weakness, fever, wt loss, headache, abdominal or other tissue pain occur. Invariably an elevated ESR is seen, often with elevated neutrophilic WBC count. *** Biopsy confirms diagnosis. Steroids and immune modulating agents to treat