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203 Cards in this Set
- Front
- Back
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What artery supplies the SA and AV nodes (in the majority)?
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Right coronary artery (RCA)
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The posterior descending (PD) artery is supplied by (a) in 80% and (b) in 20%?
What does it supply? |
80% = RCA
20% = circumflex artery It supplies the inferior portion of the LV |
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Coronary artery occlusions occur mostly commonly in what artery?
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LAD
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Do coronary arteries fill during systole or diastole?
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Diastole
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What are symptoms of enlargement of the left atrium? Why?
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It is the most posterior part of the heart.
Enlargement causes dysphagia (compresses esophogeal nerve) and hoarseness (compression of recurrent laryngeal nerve...which is a branch of the vagus) |
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CO = ?
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SV x HR
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Mean arterial pressure = ?
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CO x TPR
(and) 2/3 diastolic + 1/3 systolic |
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Pulse pressure = ?
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systolic - diastolic
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What is the effect of HR on CO as HR increases?
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Initially, CO increases.
If HR is too high, diastolic filling is incomplete and CO falls (as in ventricular tachycardia) |
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What factors affect stroke volume?
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SV CAP
Contractility, Afterload, Preload |
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Contractility (and SV) increase with... (list of 4 things)
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1. catecholamines (which increase activity of Ca++ pump in SR)
2. increased IC Ca++ 3. decreased EC Ca++ 4. digitalis |
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Contractility (and SV) decrease with... (list of 5 things)
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1. B1 blockade (decreases cAMP)
2. heart failure 3. acidosis 4. hypoxia/hypercapnea 5. non-dihydropyrdine Ca++ channel blockers (verapimil) |
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Myocardial O2 demand is increased by?
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Increased...
-afterload -contractility -HR -heart size (wall tension) |
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Preload is determined by?
Afterload is determined by? |
Preload = ventricular EDV
Afterload = MAP (proportional to peripheral resistance) |
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What factors can increase preload?
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Exercise
Overtransfusion Sympathetics |
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What class of drugs are good at decreasing preload?
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venodilators (nitroglycerin)
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What class of drugs are good at decreasing afterload?
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vasodilators (hydralazine)
Mnemonic: remember the As: hydrAlAzine = decreased Afterload (Arterial) |
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Ejection fraction (EF) is an index of _______ ?
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ventricular contractility
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EF = ?
What should EF be above normally? |
EF = SV/EDV = (EDV-ESV) / EDV
Should be above 55% |
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Resistance is directly proportional to (a)?
...indirectly proportional to (b)? |
(a) viscosity
(b) radius^4 |
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Viscosity depends mostly on _____ ?
Given that, what states/diseases does viscosity increase? |
Hematocrit
polycythemia, hyperproteinemic states (multiple myeloma/Waldenstrom's), hereditary spherocytosis |
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What types of vessels account for most of TPR?
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arterioles
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What are the 5 phases of the cardiac cycle for the LV?
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1. isovolumetric contraction (between mitral closing and aortic opening)
2. systolic ejection (between aortic opening and closing) 3. isovolumetric relaxation (between aortic closing and mitral opening) 4. rapid filling (after mitral opens) 5. reduced filling (just before mitral closes) |
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What period of the cardiac cycle has the highest O2 consumption?
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isovolumetric contraction
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What is the cause of all 4 basic heart sounds?
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S1 = mitral/tricuspid closure
S2 = aortic/pulmonic closure S3 = rapid V filling (during early diastole) S4 = "atrial kick," high atrial pressure from ventricular hypertrophy (LA must push against still LV wall) |
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What do the "a" "c" and "c" waves of the JVP signify?
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a = atrial contraction
c = RV contraction (closed tricuspid bulges into atrium) v = increase RA pressure from filling against close tricuspid valve |
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What is S2 splitting? This normally increases during....
What is wide splitting, fixed splitting, and paradoxical splitting...and what disease causes each? |
S2 splitting = aortic valve closes before pulmonic; increases during inspiration
Wide = pulmonic stenosis, RBBB = just a bigger time delay Fixed = ASD = doesn't change with expiration/inspiration Paradoxical = aortic stenosis, LBBB = P closes before A |
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What organ receives the largest share of systemic CO?
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liver
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What organ has the highest blow flow per gram of tissue?
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kidney
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What is unique about O2 extraction in the heart?
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Large AV O2 difference because O2 extraction is always 100%
increase O2 demand met by increased flow, not increased extraction |
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Why and from where is ANP released?
What is its physiologic effect? |
ANP is released from the atria in response to increased blood volume and atrial pressure
Causes generalized vascular relaxation. Constricts efferent renal arterioles and dilates afferents (cGMP mediated), promoting diuresis and contributing to the "escape from aldosterone" mechanism. |
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PCWP is a good approximation of what?
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Left atrial pressure
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Rank the speed of conduction:
ventricles, atria, AV node, Purkinje fibers |
Purkinje > atria > ventricles > AV node
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What causes wide splitting?
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Conditions that delay RV emptying
1. pulmonic stenosis 2. RBBB |
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What causes fixed splitting?
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ASD leads to R-->L shunt, and therefore increased flow through pulmonic valve and delayed closure of the valve regardless of breath.
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What causes paradoxical splitting?
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Seen in conditions that delay LV emptying
1. aortic stenosis 2. LBBB |
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What murmers are best heard in the aortic area?
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aortic stenosis
flow murmur aortic valve sclerosis |
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What murmers are best heard in the pulmonic area?
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pulmonic stenosis
flow murmur (e.g. atrial septal defect) |
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What murmers are best heard in the tricuspid area?
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Pansystolic
--tricuspid regurg --VSD Diastolic --tricuspid stenosis --ASD |
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What murmers are best heard in the mitral area?
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mitral regurg
mitral stenosis |
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What murmers are best heard at the left sternal border?
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Diastolic
--aortic regurg --pulmonic regurg Systolic --hypertrophic cardiomyopathy |
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Mitral regurgitation
sound, location, enchanced by, cause |
holosystolic, high-pitched "blowing murmur"
loudest at apex (toward axilla) enhanced by squatting, hand grip (increase TPR) or expiration (increase LA return) often caused by ischemic heart disease, valve prolapse, LV dilation, rheumatic fever |
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Tricuspid regurgitation
1. sounds like 2. area 3. enhanced by 4. due to |
1. holosystolic, high-pitched "blowing murmur" (just like mitral regurg)
2. loudest at tricuspid area, radiates to R sternal border 3. enhanced by inspiration (increases RA return) 4. due to RV dilation or endocarditis, rheumatic rever |
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1. holosystolic, high-pitched "blowing murmur" (just like mitral regurg)
2. loudest at tricuspid area, radiates to R sternal border 3. enhanced by inspiration (increases RA return) 4. due to RV dilation or endocarditis, rheumatic rever |
Tricuspid regurgitation
1. sounds like 2. area 3. enhanced by 4. due to |
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Aortic stenosis
1. sounds like 2. radiates to 3. pulses? 4. cause |
1. crescendo-decrescendo systolic ejection murmur following ejection click
2. radiates to carotids/apex 3. pulses weak compared to heart sounds 4. oftenage-related calcification |
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1. crescendo-decrescendo systolic ejection murmur following ejection click
2. radiates to carotids/apex 3. pulses weak compared to heart sounds 4. oftenage-related calcification |
Aortic stenosis
1. sounds like 2. radiates to 3. pulses? 4. cause |
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VSD murmer
1. sounds like 2. listen at? |
1. holosystolic, harsh-sounding murmur
2. loudest at tricuspid |
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1. holosystolic, harsh-sounding murmur
2. loudest at tricuspid |
VSD murmer
1. sounds like 2. listen at? |
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Mitral prolapse
1. sounds like 2. loudest at? 3. clinical considerations? 4. enhanced by? |
1. late systolic crescendo murmur with midsystolic click
2. loudest at S2 3. usually benign, can predispose to infective endocarditis 4. enhanced by squatting, hand grip (increase TPR) |
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1. late systolic crescendo murmur with midsystolic click
2. loudest at S2 3. usually benign, can predispose to infective endocarditis 4. enhanced by squatting, hand grip (increase TPR) |
Mitral prolapse
1. sounds like 2. loudest at? 3. clinical considerations? 4. enhanced by? |
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Aortic regurgitation
1. sounds like 2. associated clinical features 3. causes? 4. what decreases intensity of murmur? |
1. immediate high-pitched "blowing" diastolic murmur
2. wide pulse pressure when chronic, often present with bounding pulses/head bobbing 3. aortic root dilation, bicuspid aortic valve, rheumatic fever 4. vasodilators decrease intensity of murmur |
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1. immediate high-pitched "blowing" diastolic murmur
2. wide pulse pressure when chronic, often present with bounding pulses/head bobbing 3. aortic root dilation, bicuspid aortic valve, rheumatic fever 4. vasodilators decrease intensity of murmur |
Aortic regurgitation
1. sounds like 2. associated clinical features 3. causes? 4. what decreases intensity of murmur? |
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Mitral stenosis
1. sounds like 2. cause 3. chronicity causes? 4. enhanced by? |
1. delayed (after opening snap) rumbling late diastolic murmur
2. secondary to rheumatic fever 3. if chronic, can lead to LA dilation 4. enhaced by expiration |
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1. delayed (after opening snap) rumbling late diastolic murmur
2. secondary to rheumatic fever 3. if chronic, can lead to LA dilation 4. enhaced by expiration |
Mitral stenosis
1. sounds like 2. cause 3. chronicity causes? 4. enhanced by? |
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PDA murmur
1. sounds like 2. loudest at? 3. cause |
1. continuous machine-like murmur
2. loudest at S2 3. often due to congenital rubella or prematurity |
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1. continuous machine-like murmur
2. loudest at S2 3. often due to congenital rubella or prematurity |
PDA murmur
1. sounds like 2. loudest at? 3. cause |
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What is the response to hypoxia in the pulmonary vasculature vs. other organs.
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Pulm vasculature = hypoxia causes vasoconstriction to ensure that only well-ventilated areas are perfused
Other organs = hypoxia causes vasodilation |
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What is the most common cause of early cyanosis?
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Tetrology of Fallot
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What are the five Ts?
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Right-to-left shunts
1. Tetrology of Fallot 2. Transposition of the great vessels 3. Truncus arteriosus 4. Tricuspid atresia 5. TAPVR (Total anomalous pulmonary venous return) |
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What is a persistent truncus arteriosus?
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Failure of truncus arteriosus to divide into pulmonary trunk and aorta
R-to-L shunt |
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What is tricuspid atresia?
What is necessary for viability? |
Abscence of tricuspid valve, hypoplastic RV
requires both ASD and VSD for viability |
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What is the most common congenital cardiac anomaly?
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VSD
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What are the three main causes of L-->R shunts?
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1. VSD
2. ASD 3. PDA |
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What is Eisenmenger's syndrome?
What is the clinical presentation? |
--uncorrected VSD, ASD, or PDA causes compensatory vascular hypertrophy
--leads to progressive pulmonary hypertension --as pulmonary resistance increases, shunt reverses to R-->L...which causes late cyanosis --leads to clubbing and polycythemia |
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What is the Tetrology of Fallot?
What is the most important determinant for prognosis? |
PROVe
-Pulmonary stenosis (most important determinant for prognosis) -RVH -Overriding aorta (overrides the VSD) -VSD |
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What is the pathophysiology of Tetralogy of Fallot?
Cause? |
1. early cyanosis = caused by R-to-L shunt across VSD from high pressure caused by stenotic pulm valve
2. caused by anterosuperior displacement of infundibular septum |
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What do patients with Tetrology of Fallot accomadate?
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Pts learn to squat to improve symtpoms
--compression of femoral arteries increases TPR, which decreases shunt --directs more blood from RV to lungs |
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What causes transposition of the great arteries?
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Failure of the aorticopulmonary septum to spiral
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What is the difference between infantile type and adult type coarctation of the aorta?
What is each associated with? |
INfantile: IN close to heart
ADult: Distal to Ductus Infantile= proximal to insertion of ductus arteriosis (associated with Turner syndrome) Adult = distal to ligamentum arteriosum (associated with notching of ribs, HTN in UE, weak pulses in LE --can result in aortic regurg --most commonly associated with bicuspid aortic valve |
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What defect is associated with 22q11 syndromes?
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Truncus arteriosis
Tetrology of Fallot |
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What defects are associated with Down syndrome?
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ASD, VSD, AV septal defect
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What defects are associated with congenital rubella?
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Septal defects, PDA, pulm artery stenosis
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What defect is associated with Turner syndrome?
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Coarcation of the aorta (preductal)
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What defect is associated with Marfan's syndrome?
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aortic insufficiency (late complication)
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What defect is associated with an infant of a diabetic mother?
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Transposition of the great vessels
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Hypertension
1. Defined as 2. Risk factors 3. Breakdown of epidemiology/causes 4. Predisposes to? |
1. BP > 140/90
2. age, obesity, diabetes, smoking, genetics, black>white>asian 3. 90% essential; 10% mostly due to renal disease 4. atherosclerosis, LV hypertrophy, stroke, CHF, renal failure, retinopathy, aortic dissection, getting all your shit fucked up |
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What are four signs of hyperlipidemia?
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1. Atheromas = plaques in vessel walls
2. Xanthomas = plaques/nodules of lipid-laden histiocytes in skin (esp eyelids) 3. Tendinous xanthoma = lipid deposit in tendon (esp Achilles) 4. Corneal arcus = lipid deposit in cornia, non-specific |
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What is Monckeberg arteriosclerosis?
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Calcification in media of arteries, esp radial or ulnar
usually benign, pipestem arteries Does not obstruct blood flow...intima not involved |
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What is arteriolosclerosis?
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Hyaline thickening of small arteries in essential HTN, diabetes mellitus
hyperplastic "onion skinning" in malignant HTN |
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What is atherosclerosis?
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Fibrous plaques and atheromas in intima of large and medium muscular arteries
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What are risk factors for atherosclerosis?
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smoking, HTN, diabetes mellitus, hyperlipidemia, FH
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What is the progression of atherosclerosis, starting at endothelial cell dysfunction?
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Macrophage and LDL accumulation
Foam cell formation Fatty streaks SM cell migration (involves PDGF and TGF-B) Fibrous plaque Complex atheromas |
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What factors are involved in SM cell migration in atherosclerosis?
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PDGF and TGF-B
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What are the common locations for atherosclerosis to develop, in order of likelihood?
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abdominal aorta > coronary artery > popliteal artery > carotid artery
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Aortic dissection
1. What is it? 2. Associated with? 3. presenting symptoms... 4. diagnostic test? |
1. Longitudinal intraluminal tear --> creating a false lumen
2. associated with HTN, cystic medial necrosis (part of Marfan's) 3. Tearing chest pain radiating to back 4. CXR shows mediastinal widening |
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1. Longitudinal intraluminal tear --> creating a false lumen
2. associated with HTN, cystic medial necrosis (part of Marfan's) 3. Tearing chest pain radiating to back 4. CXR shows mediastinal widening |
Aortic dissection
1. What is it? 2. Associated with? 3. presenting symptoms... 4. diagnostic test? |
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What are the 4 possible manifestations for ischemic heart disease?
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1. Angina
2. MI 3. Sudden cardiac death 4. Chronic ischemia heart disease |
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What % narrowing defines angina?
What are the three types, how do they present, and what are their associated ECG findings? |
CAD narrowing >75%
1. Stable = secondary to athero, ST depression on ECG (retrosternal chest pain with exertion) 2. Prinzmetal's variant = occurs at rest secondary to coronary artery spasm, ST elevation on ECG 3. Unstable/crescendo = thrombosis, but no necrosis; ST depression of ECG (worsening chest pain at rest or with minimal exertion) |
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What is the definition of sudden cardiac death?
Most common cause? |
death from cardiac causes within 1 hour of symptom onset
most commonly due to lethal arrhythmia (V-fib, etc) |
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2-4 hours after an acute MI, what can be seen on light microscopy?
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Nothing...no visible change
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When are contraction bands seen after an MI?
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12-24 hours
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When is early coagulative necrosis seen after an MI?
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after 4 hours
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When, after an MI, do you see release of contents of necrotic cells into bloodstream and beginning of neutrophil emigration?
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1st day
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2-4 days after an MI, what can be seen on a tissue sample?
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Tissue around infarct shows acute inflammation
Dilated vessels (hyperemia) Neutrophil emigration Extensive coagulation necrosis |
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At what point after an MI do you see the hyperemic border and central yellow-brown softening? When is it maximally yellow and soft?
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5-10 days. Maximally soft/yellow by day 10.
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What are the major risks 5-10days after an MI? Why?
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Risk for free wall rupture, tamponade, papillary muscle rupture, interventricular septal rupture
(macrophages have degraded important structural components) |
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What happens 7 weeks after an MI? Risk of...?
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Recanalized artery and gray-white scar tissue
Risk of ventricular aneurysm |
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What is the gold standard for diagnosing MI in the first 6 hours?
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ECG
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What is the usefulness in diagnosing MI of...
1. Cardiac troponin I 2. CK-MB 3. AST What are you looking for? |
1. Cardiac troponin I = rises after 4 hours, elevated for 7-10 days, more specific than others
2. CK-MB = mostly in cardiac muscle, but also released from skeletal; useful in diagnosing reinfarction on top of acute MI 3. AST = nonspecific, found in cardiac/liver/skeletal muscle cells |
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What ECG changes are seen in transmural vs subendocardial infarct?
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Transmural = ST elevation, pathologic Q waves
Subendocardial = ST depression |
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Where is the MI if Q waves are in leads V1-V4?
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Anterior wall (LAD)
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Where is the MI if Q waves are in leads V1-V2?
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Anteroseptal (LAD)
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Where is the MI if Q waves are in leads V4-V6?
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Anterolateral (LCX)
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Where is the MI if Q waves are in leads I, aVL?
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Lateral wall (LCX)
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Where is the MI if Q waves are in leads II, III, aVF?
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Inferior wall (RCA)
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What is Dressler's syndrome?
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Autoimmune phenomenon resulting in fibrinous pericarditis
(several weeks post-MI) |
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How many days post-MI might you find postinfarction fibrinous pericarditis and a friction rub?
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3-5 days post-MI
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What is the most common cardiomyopathy?
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Dilated (congestive) cardiomyopathy
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What are the etiologies of dilated cardiomyopathy?
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A-B-CCC-D
Alcohol abuse wet Beriberi Coxsackie B virus myocarditis Cocaine use (chronic) Chagas' disease Doxorubicin toxicity Others: hemochromatosis, peripartum cardiomyopathy |
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What are the clinical findings for dilated cardiomyopathy?
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S3, dilated heart on US, balloon appearance on CXR
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What are the clinical findings for hypertrophic cardiomyopathy?
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normal-sized heart, S4, apical impulses, systolic murmur
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How do you treat a hypertrophic cardiomyopathy?
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B-blocker or non-dihydro Ca-channel blocker (e.g. verapamil)
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What is the pathophysiology of hypertrophic cardiomyopathy? What does this cause clinically?
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hypertrophied IV septum "too close" to mitral leaflet --> outflow tract obstruction
This results in a systolic murmer and syncopal episodes |
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Which cardiomyopathy is associated with Friedreich's ataxia?
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hypertrophic cardiomyopathy
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What is the etiology of hypertrophic cardiomyopathy?
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50% of cases are familial, autosomal dominant
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What are the major causes of restrictive cardiomyopathy?
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sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler's syndrome, and hemochromotosis
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What is Loffler's syndrome, and what is it associated with?
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endomyocardial fibrosis with a prominent eosinophilic infiltrate
associated with restrictive cardiomyopathy |
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Which cardiomyopathy has systolic dysfunction and eccentric hypertrophy?
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dilated cardiomyopathy
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Which cardiomyopathy has diastolic dysfunction and concentric hypertrophy (sarcomeres added in parallel)?
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Hypertrophic cardiomyopathy
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Restrictive cardiomyopathy has systolic or diastolic dysfunction?
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diastolic
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In CHF, what causes dyspnea on exertion?
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failure of LV output to increase during exercise
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In CHF, what causes cardiac dilation?
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greater ventricular end-diastolic volume
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In CHF, what causes pulmonary edema and PND?
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LV failure --> increased pulm venous pressure --> pulm venous distention, transudation of fluid
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In CHF, what are "heart failure" cells...and what is one abnormal place they can be found? Why?
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see hemosiderin-laden macrophages in lungs due to microhemorrhages from increased pulmonary capillary pressure
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In CHF, what causes orthopnea?
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increased venous return while supine, exacerbating pulmonary venous congestion
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In CHF, what causes hepatomegaly (nutmeg liver)?
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increased central venous pressure leads to increased resistance to portal flow
(rarely leads to "cardiac cirrhosis") |
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In CHF, what causes ankle, sacral edema?
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RV failure --> increased venous pressure --> fluid transudation
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In CHF, what causes jugular venous distention?
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RV failure, leading to increased venous pressure
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What is the most common cause of right heart failure?
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left heart failure
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Isolated right heart failure is usually due to...?
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cor pulmonale
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What is the most common symptom of bacterial endocarditis?
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fever
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What is the common presentation of bacterial endocarditis?
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Bacteria FROM JANE:
Fever Roth's spots (round white spots on retina, surrounded by hemorrhage) Osler's nodes (tender raised lesions on finger or toe pads) Murmur (new) Janeway lesions (small erythematous lesions on palm or sole) Anemia Nail-bed hemorrhage (splinter hemorrhages) Emboli |
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How is bacterial endocarditis diagnosed?
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Multiple blood cultures are necessary!
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What is the difference between acute vs. subacute bacterial endocarditis?
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Acute = S. aureus (high virulence), large vegetations of previously normal valves
Subacute = viridans streptococci (low virulence), smaller vegetations on congenitally abnormal or diseased valves (maybe from dental procedures?) --> more insidious onset |
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Non-bacterial endocarditis can be secondary to...?
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Malignancy or hypercoagulable states (marantic/thrombotic endocarditis)
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What organisms cause bacterial endocarditis?
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Acute = S. aureus
Subacute = viridans streptococci -------------------------- S. bovis = colon cancer S. epidermidis = prosthetic valves HACEK organisms cause culture-negative endocarditis |
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What valve is most frequently involved in bacterial endocarditis?
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mitral
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Tricuspid valve endocarditis is associated with...?
What organisms is it associated with? |
IV drug abuse (don't tri drugs)
S. aureus, Pseudomonas, Candida |
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What are the major complications of bacterial endocarditis?
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chordae rupture, glomerulonephritis, supperative pericarditis, emboli
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What is Libman-Sacks endocarditis?
Clinical implications? |
SLE causes LSE (lupus!)
verrocous (wartlike), sterile vegetations on both sides of valve most often benign, sometimes mitral regurg (less commonly mitral stenosis) |
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What are the histologic features and laboratory features of rheumatic fever?
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Associated with...
--Aschoff bodies (granuloma with giant cells) --Anitschokow's cells (activated histiocytes) --elevated ASO titers |
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What is the presentation of rheumatic fever? (answer is a mnemonic)
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FEVERSS
Fever Erythema marginatum Valvular damage (vegetation and fibrosis) ESR increased Red-hot joints (migratory polyarthritis) Subcutaneous nodules St. Vitus' dance (chorea) |
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Infection with what group of organisms can lead to rheumatic fever? How does this happen? What bacterial protein is important?
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pharyngeal infection with group A beta-hemolytic streptococci
immune-mediated (type II hypersensitivity); not direct effect of bacteria antibodies to M protein |
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What are the early and late sequelae of rheumatic fever?
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early deaths due to myocarditis
late sequelae = rheumatic heart disease, which affects the valves |
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Which valves are most affected in rheumatic heart disease?
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High pressure valves affected most
mitral > aortic >> tricuspid |
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What are the early and late problems with the mitral valve in rheumatic heart disease?
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Early lesion = mitral prolapse
Late lesion = mitral stenosis |
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What is the pathophysiology of cardiac tamponade?
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compression of heart by fluid (blood, effusions) in pericardium, leading to decreased CO
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What happens to the diastolic pressures in the heart in cardiac tamponade?
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equilibration of diastolic pressures in all 4 chambers
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What are the clinical findings of cardiac tamponade?
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hypotension, increased venous pressure (JVD), distant heart sounds, increased HR, pulsus paradoxus
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What is pulsus paradoxus? (Kussmaul's pulse)
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exaggerated decrease in amplitude of pulse during inspiration
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Name 5 diseases in which pulsus paradoxus is seen?
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severe cardiac tamponade
asthma obstructive sleep apnea pericarditis croup |
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What is syphilitic heart disease? What are the clinical manifestations?
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tertiary syphilis disrupts vasa vasorum of the aorta --> leads to dilation of aorta and valve ring
(may see calcifications of aortic root/arch...leading to "tree bark" appearance of aorta) Clinical manifestations: aneurysm of ascending aorta/arch, aortic valve incompetence |
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What is the most common primary cardiac tumor in adults?
Where does it occur and what does it cause? |
Myxomas
90% occur in atria (mostly LA) usually described as "ball-valve" obstruction in LA, associated with multiple syncopal episodes |
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What is the most common primary cardiac tumor in children?
What is it associated with? |
Rhabdomyomas, associated with tuberous sclerosis
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What is the most common heart tumor overall?
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Metastases, commonly from melanoma/lymphoma
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Chronically elevated venous pressure can lead to what problem?
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Vericose veins are dilated, tortuous superficial veins
cause poor wound healing, vericose ulcers, rare thromboembolism |
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Wegener's granulomatosis?
1. Triad 2. symptoms 3. findings 4. CXR findings 5. treatment |
1. Triad of focal necrotizing vasculitis, necrotizing granulomas in lung/upper airway, necrotizing glomerulonephritis
2. Symptoms = hemoptysis, hematuria, perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea 3. Findings = c-ANCA, red cell casts 4. CXR = large nodular densities 5. Treatment = cyclophosphamide, corticosteroids |
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1. Triad of focal necrotizing vasculitis, necrotizing granulomas in lung/upper airway, necrotizing glomerulonephritis
2. Symptoms = hemoptysis, hematuria, perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea 3. Findings = c-ANCA, red cell casts 4. CXR = large nodular densities 5. Treatment = cyclophosphamide, corticosteroids |
Wegener's granulomatosis?
1. Triad 2. symptoms 3. findings 4. CXR findings 5. treatment |
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What is microscopic polyangitis?
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like Wegener's but without granulomas
p-ANCA |
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like Wegener's but without granulomas
p-ANCA |
What is microscopic polyangitis?
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Primary pauci-iummune crescentic glomerulonephritis
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vasculitis limited to kidney
Pauci-immune = paucity of antibodies |
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vasculitis limited to kidney
Pauci-immune = paucity of antibodies |
Primary pauci-iummune crescentic glomerulonephritis
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Churg-Strauss syndrome
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Granulomatous vesculitis with eosinophilia
Asthma, sinusitis, skin lesions, peripheral neuropathy (wrist/foot drop) Can involve heart, GI, kidneys p-ANCA |
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Granulomatous vesculitis with eosinophilia
Asthma, sinusitis, skin lesions, peripheral neuropathy (wrist/foot drop) Can involve heart, GI, kidneys p-ANCA |
Churg-Strauss syndrome
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Sturge-Weber disease
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Congenital vascular disorder affecting capillaries (small vessels)
Manifests with port-win stain on face (nevus flammeus), ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, early-onset glaucoma |
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Congenital vascular disorder affecting capillaries (small vessels)
Manifests with port-win stain on face (nevus flammeus), ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, early-onset glaucoma |
Sturge-Weber disease
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Henoch-Schonlein purpura
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Most common form of childhood systemic vasculitis
skin rash on buttocks and legs (palpable purpura) Association with IgA nephropathy Common triad: skin, joints, GI multiple lesions of the same age |
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Most common form of childhood systemic vasculitis
skin rash on buttocks and legs (palpable purpura) Association with IgA nephropathy Common triad: skin, joints, GI multiple lesions of the same age |
Henoch-Schonlein purpura
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Buerger's disease/thromboangiitis obliterans
(including symptoms and treatment) |
idiopathic, segmental, thrombosing vasculitis of small/med peripheral ateries and veins
seen in heavy smokers Symptoms = intermittent claudication, Raynaud's, gangrene/autoamputation of digits Treatment = smoking cessation |
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idiopathic, segmental, thrombosing vasculitis of small/med peripheral ateries and veins
seen in heavy smokers Symptoms = intermittent claudication, Raynaud's, gangrene/autoamputation of digits Treatment = smoking cessation |
Buerger's disease/thromboangiitis obliterans
(including symptoms and treatment) |
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Kawasaki disease
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acute, self-limiting necrotizing vasculitis in infants/children
asian ethnicity Symptoms = fever, conjunctivitis, strawberry tongue, may develop coronary aneurysms Treatment = IV immunoglobulin, aspirin |
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acute, self-limiting necrotizing vasculitis in infants/children
asian ethnicity Symptoms = fever, conjunctivitis, strawberry tongue, may develop coronary aneurysms Treatment = IV immunoglobulin, aspirin |
Kawasaki disease
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Polyarteritis nodosa
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Immune-complex mediated transmural vasculitis with fibrinoid necrosis
Symptoms = fever, weight loss, malaise, abd pain, melena, headache, HTN, neurologic dysfunction Findings = Hep B seropositivity in 30% of patients Treatment = corticosteroids, cyclophosphamide Lesions are different ages does not affect pulmonary arteries |
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Immune-complex mediated transmural vasculitis with fibrinoid necrosis
Symptoms = fever, weight loss, malaise, abd pain, melena, headache, HTN, neurologic dysfunction Findings = Hep B seropositivity in 30% of patients Treatment = corticosteroids, cyclophosphamide Lesions are different ages does not affect pulmonary arteries |
Polyarteritis nodosa
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Takayasu's arteritis
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pulseless disease = granulomatous thickening of aortic arch, proximal great vessels
associated with increased ESR Affects Asian females <40 years old Symptoms = FAN MY SKIN On Wednesday --Fever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in UE |
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pulseless disease = granulomatous thickening of aortic arch, proximal great vessels
associated with increased ESR Affects Asian females <40 years old Symptoms = FAN MY SKIN On Wednesday --Fever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in UE |
Takayasu's arteritis
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Temporal arteritis (giant cell arteritis)
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Most common vasculitis affecting med/large arteries, usually branches of carotid
Focal, granulomatous inflammation Affects elderly females Symptoms = unilateral headache, jaw claudication, impaired vision Findings = associated with increased ESR, 50% of pts have systemic involvement and polymyalgia rheumatica Treatment = high-dose steroids |
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Most common vasculitis affecting med/large arteries, usually branches of carotid
Focal, granulomatous inflammation Affects elderly females Symptoms = unilateral headache, jaw claudication, impaired vision Findings = associated with increased ESR, 50% of pts have systemic involvement and polymyalgia rheumatica Treatment = high-dose steroids |
Temporal arteritis (giant cell arteritis)
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Give the most likely vasculitis for these classic/stereotypical patients:
1. Asian females <40 2. Heavy smokers 3. Elderly females 4. Asian infants/children 5. Pts have Hep B |
1. Takayasu's arteritis
2. Buerger's disease 3. Temporal arteritis 4. Kawasaki disease 5. Polyarteritis nodosa |
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Give the most likely vasculitis for these classic/stereotypical symptoms or findings:
1. c-ANCA 2. Strawberry tongue 3. IgA nephropathy 4. p-ANCA with asthma and eosinophilia |
1. Wegener's granulomatosis
2. Kawasaki disease 3. Henoch-Schonlein purpura 4. Churg Strauss syndrome |
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Give the most likely vasculitis for these classic/stereotypical symptoms or findings:
1. unilateral headace, jaw claudication, impaired vision 2. Multiple lesions of different ages 3. Multiple lesions of the same age 4. Port-wine stain (aka nevus flammeus) on face, seizures, glaucoma |
1. Temporal arteritis
2. Polyarteritis nodosa 3. Henoch-Schonlein purpura 4. Sturge-Weber disease |
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Give the most likely vasculitis for these treatments:
1. Smoking cessation 2. High-dose steroids 3. Corticosteroids, cyclophosphamide (two!) 4. IV immunoglobulin, aspirin |
1. Buerger's disease
2. Temporal arteritis 3. Polyarteritis nodosa, Wegener's granulomatosis 4. Kawasaki disease |
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What vasculitis typically involves renal and visceral vessels, not pulmonary arteries?
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Polyarteritis nodosa
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In which vasculitis do you see the common triad of skin, joint, GI involvement?
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Henoch-Schonlein purpura
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Vascular tumors: strawberry hemangioma
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Benign capillary hemangioma of infancy, grows then regresses
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Benign capillary hemangioma of infancy, grows then regresses
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Vascular tumors: strawberry hemangioma
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Vascular Tumors - Cherry hemangioma
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Benign capillary hemangioma of elderly, does not regress
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Benign capillary hemangioma of elderly, does not regress
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Vascular Tumors - Cherry hemangioma
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Vascular Tumors - Pyogenic granuloma
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Polypoid capillary hemangioma that can ulcerate and bleed, associated w/ trauma and pregnancy
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Polypoid capillary hemangioma that can ulcerate and bleed, associated w/ trauma and pregnancy
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Vascular Tumors - Pyogenic granuloma
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Vascular Tumors - Cystic hygroma
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Cavernous lymphangioma of the neck; associated with Turner's syndrome
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Cavernous lymphangioma of the neck; associated with Turner's syndrome
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Vascular Tumors - Cystic hygroma
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Vascular Tumors - Glomus tumor
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Benign, painful, red-blue tumor under fingernails, arises from modified smooth muscle cells of glomus body
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Benign, painful, red-blue tumor under fingernails, arises from modified smooth muscle cells of glomus body
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Vascular Tumors - Glomus tumor
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Vascular Tumors - Bacillary angiomatosis
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Benign capillary skin papules found in AIDS patients caused by Bartonella henselae infections; often mistaken for Kaposi's
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Benign capillary skin papules found in AIDS patients caused by Bartonella henselae infections; often mistaken for Kaposi's
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Vascular Tumors - Bacillary angiomatosis
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Vascular Tumors - Angiosarcoma
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Highly lethal malignancy of the liver; associated with vinyl chloride, arsenic and thorotrast exposure
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Highly lethal malignancy of the liver; associated with vinyl chloride, arsenic and thorotrast exposure
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Vascular Tumors - Angiosarcoma
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Vascular Tumors - Lymphangiosarcoma
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Lymphatic malignancy associated with persistent lymphedema (e.g. in post radical mastectomy)
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Lymphatic malignancy associated with persistent lymphedema (e.g. in post radical mastectomy)
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Vascular Tumors - Lymphangiosarcoma
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Vascular Tumors - Kaposi's Sarcoma
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Endothelial malignancy of the skin associated with HHV-8 and HIV, frequently mistaken for bacillary angiomatosis
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Endothelial malignancy of the skin associated with HHV-8 and HIV, frequently mistaken for bacillary angiomatosis
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Vascular Tumors - Kaposi's Sarcoma
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When is PCWP > LV diastolic pressure?
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mitral stenosis
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