cardio first aid Flashcards
umbilical vein
ligamentum teres hepatis
umbilic arteries
medial umbilical ligaments
ductus arteriosus
ligamentum arteriosum
ductus venosus
ligamentum venosum
foramen ovale
fossa ovalis
allantois
urachus-median umbilical ligamnt
notochord
nucleus pulposus of intervertebral disc
where do you see increased pulse pressure?
hyperthyroidism, AR, arteriosclerosis, obstructive sleep apnea, increased sympathetic tone, exercise (transient)
where do you see decreased pulse pressure?
AS, cardiogenic shock, cardiac tamponade, advanced heart failure
contractility increases with
catecholamines
increased intracellular Ca2+
decreased extracellular Na+
digitalis
contractility decreases with
beta1 blockade heart failure with systolic dysfunction acidosis hypoxia and hypercapnea non-dihydropyridine ca2+ channel blockers
SV inreases with
anxiety
exercise
pregnancy
myocardial oxygen demand increases with
afterload
contractility
HR
ventricular diameter
venodilators effect what cardiac output variable?
decrease preload (nitroglycerin is an example)
vasodilators effect what cardiac output variable?
decrease afterload (eg. Hydralazine)
ACE inhibiors and ARBs effect what cardiac output variable?
decrease preload and afterload
how is ejection fraction effected by heart failure
decreased in systolic heart failure but normal in diastolic heart failure
what increases venous return
fluid infusion
sympathetic activity
what decreases venous return
acute hemorrhage
spinal anesthesia
what increases TPR?
vasopressors
what decreases TPR?
exercise, AV shunt
S1
MV and TV closure
loudest at mitral area
S2
AV and PV closure
loudest at left sternal border
S3
early diastole during rapid ventricular illing
patho: MR, CHF, dilated ventricles
normal: children, pregnant women
S4
late diastole
high atrial pressure
patho: ventricular hypertrophy
a wave
atrial contraction
c wave
RV contraction, closed TV bulging into atrium
x descent
atrial relaxation and downward displacement ofclosed tricuspid valve during ventricular contraction
absent in tricuspid regurgitation
v wave
increased right atrial pressure dur to filling against closed tricuspid valve
y descent
blood flow from RA to RV
aortic area sounds
systolic murmur
aortic stenosis
flow murmur
aortic valve sclerosis
pulmonic area sounds
systolic ejection murmur
pulmonic stenosis
flow murmur
what causes normal splitting?
inspiration causes a drop in intrathoracic pressure causing increased venous return to the RV which increases the RV stroke volume. Ejection time of the RV increases leading to delayed closure of the pulmonic valve. There is decreased pulmonary impedence meaning that there is increased capacity of the pulmonary circulations allowing for the delayed closure of the pulmonic valve
when do you see wide splitting
pulmonic stenosis and RBBB
when do you see fixed splitting
ASD
when do you see paradoxical splitting
delayed LV emptying like in AS and LBBB
left sternal border sounds
diastolic murmurs: aortic regurgitation and pulmonic regurgitation
systolic murmurs: hypertrophic cardiomyopathy
tricuspid area sounds
pansystolic murmur: tricuspid regurgitation, VSD
diastolic murmur: tricuspid stenosis, ASD
mitral area sounds
systolic: mitral regurgitation
diastolic: mitral stenosis
how does inspiration effect heart sounds/
increase intensity of right heart sounds
how does hand grip effect heart sounds
increasing systemic vascular resistance causes increased intensity of MR, AR, VSD
decreased intensity of AS, hypertrophic cardiomyopathy murmurs
MVP: has increased intensity and later onset of click/murmur
how does valsalva and standing affect heart sounds?
valsalva then standing decreases venous return
it decreases intensity of most murmurs including AS
it increases intensity of hypertrophic cardiomyopathy murmur
MVP: decreased murmur intensity and earlier onset of click/murmur
how does rapid squatting effect heart sounds?
it causes increased venous return and increased preload. The afterload also increases with prolonged squatting
this causes a decreased intensity of hypertrophic cardiomyopathy murmurs
increased intensity of AS murmurs
MVP: increased murmur intensity and later onset of click/murmur
what are the systolic heart sounds?
AS, PS, MR, TR, VSD
what are the diastolic heart sounds?
AR, PR, MS, TS
speed of conduction of the cardiac cells
purkinge > atria > ventricles > AV node
pacemaking capability of cardiac cells
SA > AV > bundle of his > purkinge/ventricles
what causes torsades de points
drugs, decreased K+, decreased Mg2+
how do you treat torsades de pointes
magnesium sulfate
what meds prolong QT?
sotalol risperidone macrolodes chloroquine preotease inhibitors quinidine thiazide
what is romano ward syndrome
AD
congenital long QT syndrome
purely cardiac phenotype
what is jervell and lange-nielsen syndrome?
AR
congenital long QT syndrome
also sensorineural deafness
what is Wolff-Parkinson white syndrome?
ventricular pre-excitation
abnormal fast accessory conduction pathway from atria to ventricle that bypasses the rate slowing AB node
ventricles partially depolarize earier
delta wave appearance with shortened PR on ECG
leads to reentry circuit –> supraventricular tachycardia
what is ANP
released from atrial myocytes in response to increased blood volumeand atrial pressure. It causes vasodilation and decreased Na reabsorption at the renal collecting tubule. It constricts efferent renal arterioles and dilates afferent arterioles via cGMP promoting diuresis and leading to aldosterone escape mechanism
what is BNP
released from ventricular myocytes in response to increased tension. Has longer half life than ANP, used for diagnosing heart failure
recombinant form: nesirtide is used for treatment of heart failure
what do the receptors on the aortic arch respond to and how is the information transmitted?
only increased BP
via the vagus to solitary nucleus in medulla
what do the receptors on the carotid sinus respond to and how is the information transmitted?
both increased and decreased BP
via the glossopharyngeal to solitary nucleus of medulla
describe the baroreceptor response to hypotension
the decreased arterial pressure leades to decreased stretch and decreased afferent baroreceptor firing.
This leads to increased efferent sympathetic firing and decreased efferent parasympathetic stimulation leading to vasoconstriction increased HR, increased contractility, and increased BP. this response is important in severe hemorrhage
what is carotid massage?
it is the increased pressure on the carotid sinus that leads to increased stretch, increased afferent baroreceptor firing and then to increased AV node regractory period which decreases HR
what is the cushing reaction?
it is the triad of hypertension, bradycardia, and respiratory depression
the increased intracranial pressure causes constriction of the arterioles and leads to cerebral ischemia and reflex sympathetic and increase in perfusion pressure. There is increased stretch and reflex baroreceptor induced bradycardia
what stimulates the chemoreceptors in the carotid and aortic bodies?
decreased PO2
increased PCO2
decreased pH
what stimulates the central chemoreceptors
pH and PCO2 changes of the brain interstitial fluid. These are influenced by arterial CO2 and do not directly respond to PO2
what does PCWP approximate?
left atrial pressure
measured with pulmonary artery catheter (Swan-Ganz)
autoregulation of the heart
local metabolites, CO2, adenosine, NO
autoregulation of the brain
local metabolites, CO2
autoregulation of the kidneys
myogenic and tubuloglomerular feedback
autoregulation of the lungs
hypoxia induced vasoconstriction
autoregulation of the skeletal muscle
local metabolites, lactate, adenosine, K+, H+, CO2
autoregulation of the skin
sympathetic stimulation
what causes edema?
increased capillary pressure (heart failure)
decreased plasma proteins (nephrotic syndrome, liver failure)
increased capillary permeability (toxins, infections, burns),
increased interstitial fluid colloid osmotic pressure (lymphatic blockage)
what are the causes of right to left shunting
truncus arteriosus transposition of the great vessels tricuspid atresia tetralogy of fallot total anomalous pulmonary venous return
how do you treat right to left shunts
surgical or maintenance of PDA
persistent truncus arteriosus
fulture of TA division
accompanied by VSD
D-transposition of great vessels
separation of the systemic and pulmonary circulations
not compatible with life
failure of AP septum spiral
needs surgery and presence of shunting to allow blood mixing
tricuspid atresia
absence of tricuspid valve and hypoplstic RV
requires ASD and VSD for viability
tetralogy of fallot
anterosuperior displacement of the infundibular septum
- pulmonary infundibular stenosis
- RVH
- overriding aorta
- VSD
how does squatting improve cyanosis in tet.
increased SVR leads to decreased right to left shunting and improves cyanosis
what is the treatment for tet
surgery
what do you see on CXR in tet
boot shaped heart
total anomalous pulmonary venous return
pulmonary veins drain into right heart circulation
associated with ASD and sometimes PDA to allow right to left shunting to maintin CO
What are the causes of left to right shunting?
VSD, ASD, PDA, eisenmenger syndrome
VSD
asymptomatic usually , may self resolve
larger lesions may lead to LV overload and heart failure
ASD
loud S1 and wide fixed split of S2
septum secundum defect
symptoms: none to heart failure
different than patent foramen ovale because septa are missing tissue rather than unfused
PDA
fetally: right to left
with decreased lung resistance the shunt becomes left to right
can lead to RVH, LVH or heart failure
machine like murmur - continuous
maintained patency with PGE and low O2 tension
can result in cyanosis in the lower extremities
what opens and closes PDA?
indomethacin closes, PGE opens
eisenmenger syndrom
uncorrected LtoR shunting leads to increased pulmonary blood flow and pathologic remodeling of vasculature leading to pulmonary arteriolar hypertension
RVH occurs to compensate the the shunt bcomes right to left
causes late cyanosis, clubbing and polycythemia
coartation of the aorta associations
bicuspid aortic valve and other heart defects
what is the infantile type of coarctation of the aorta
aorta narrowing is proximal to insertion of the ductus arteriosus
associated with turner syndrome
closure of ductus arteriosus (can reverse with PGE2)
what is the adult type of coarctation of the aorta
aorta narrowing is distal to ligamentum arteriosum
associated with notching of the ribs (collageral circulation), HTN in the upper extremities and weak, delayed pulses in the lower extremities
22q11 syndromes
truncus arteriosus, tetralogy of Fallot
down syndrome
ASD, VSD, AV septal defect (endocardial cushion defect)
congenital rubella
septal defects, PDA, pulmonary artery stenosis
turner syndrome
bicuspid aortic vavlve, coarctation of the aorta (preductal)
marfan syndrome
MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
infant of diabetic mother
transposition of great vessels
xanthomas
plaques or nodules composed of lipid laden histiocytes in the skin - eyelids
tendinous xanthoma
lipid deposits in tendon (esp achilles)
corneal arcus
lipid deposits in cornea, early in life wit hypercholesterolemia, or in elderly
monckeberg
medial calcific sclerosis calcification in the media of the arteries, radial and ulnar, benign pipestem areteries on x ray does not obstruct blood flow intima not involved
arteriolosclerosis
common
two types: hyaline (thickening of the small arteries in essential HTN or DM) and hyperplastic (“onion skinning” in severe HTN)
what are the types of arteriosclerosis
monckeberg and arteriolosclerosis
describe the progression of atherosclerosis
endothelial dysfunction leads to macrophafe and LDL accumulation. Foam cell formation –> fatty streaks –> smooth muscle cell migration + proliferation + ECM deposition –> fibrous plaques –> complex atheromas
common locations of atherosclerosis
abdominal aorta> coronary artery > popliteal artery > carotid artery
difference in abdominal and thoracic aortic aneurysm presentations
abdominal is associated with atherosclerosis and more often in HTN males smokers > 50yrs
thoracic: cystic medial degeneration due to HTN in older patients, Marfans, tertiary syphillis
what is aortic dissection
longitudinal intraluminal tear forming a false lumen that can be limited to ascending or propogate to descending aorta
what are aortic dissections asscoatied with
HTN, bicuspid aortic valve, inherited connective tissue disorders (marfans)
how does aortic dissection present
tearing chest pain of sudden onset radiating to the back
possible unequal BP in arms
mediastinal widening on CXR
can lead to pericardial tamponade, aortic rupture, death
what is angina
chest pain from ischemic myocardium secondary to coronary artery narrowing or spasm
no myocardia necrosis
what is stable angina
exertional chest pain
often secondary to atherosclerosis
ECG: ST depression
resolves with rest
what is variant or prinzmetal angina?
occurs at rest secondary to coronary artery spasm
ECG: transient ST elevation
triggers: tobacco, cocaine, triptans
tx: Ca2+ channel blockers, nitrates, smoking cessation
what is unstable/crescendo angina?
thrombosis with incomplete coronary artery occlusion
ECG: ST depression
coronary steal syndrome
distal to coronary stenosis
maximally dilated vessels
vasodilators (dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas. This leads to decreased flow and ischemia in the post stenotic region
used in pharmacologic stress tests
MI
acute thrombosis due t coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis
SCD
within 1 hour of symptoms, lethal arrhythmias, CAD, cardiomyopathy, hereditary ion channelopathies (long QT)
chronic ischemic heart disease
progressive onset of CHF over many years due to chronic ischemic myocardial damage
commonly occluded coronary arteries
LAD > RCA > circumflex
symptoms of MI
diaphoresis, nausea, comiting, severe retrosternal pain, pain in left arm and jaw, shortness of breath, fatigue
What do you see on ECG in Mis
ST elevations if transmural
ST depression if subendocardial
pathologic Q waves if evolving or old transmural infarcts
what are the biomarkers that you use in MI evaluation
cardiac troponin I rises after 4 hours and is increased for 7 to 10 days, more specific than other protein markers
CK-MB is good for reinfarction diagnosis because it returns to normal after 48 hours. Also released from skeletal muscle
where do you see q waves if the infarct is in the anterior wall (LAD)?
V1-V4
where do you see q waves if the infarct is in the anteroseptal (LAD)?
V1-V2
where do you see q waves if the infarct is in the anterolateral (LAD or LCX)?
V4-V6
where do you see q waves if the infarct is in the lateral wall (LCX)?
I, aVL
where do you see q waves if the infarct is in the inferior wall (RCA)?
II, III, aVF
when is the greatest risk of having a ventricular free wall rupture?
6-14 days postinfarct
when is the greatest risk of having ventricular pseudoaneurysm formation?
1 week post MI
what do you see with ventricular pseudoaneurysm formation?
decreased CO, risk of arrhythmia, embolus from mural thrombus
when is the greatest risk of having postinfarction fibrinous pericarditis?
1 to 3 days post-MI
what is dressler syndrome?
autoimmune thing that results in fibrinous pericarditis several weeks post-MI
what are the types of cardiomyopathies?
dilated cardiomyopathy
hypertrophic cardiomyopathy
restrictive/infiltrative cardiomyopathy
causes of dilated cardiomyopathy
idiopathic congenital alcohol abuse, wet Beri beri Coxsackie B chronic cocaine chagas doxorubicin toxicity hemochromatosis peripartum cardiomyopathy
dilated cardiomyopathy findings
heart failure
S3
dilated heart on echo
balloon appearance of heart on CXR
treatment of dilated cardiomyopathy
Na+ restriction ACE inhibitors beta blockers diuretics digoxin ICD heart transplant
causes of hypertrophic cardiomyopathy
familial (AD), sometimes friedreich ataxia
athletes
hypertrophic cardiomyopathy findings
S4
systolic murmur
treatment of hypertrophic cardiomyopathy
cessation of high intensity athletics
beta-blockers or non-dihydropyridine calcium channel blockers (verapamil)
ICD
causes of restrictive/infiltrative cardiomyopathy
sarcoidosis amyloidosis postradiation fibrosis endocardial fibroelastosis loffler syndrome hemochromatosis
what is loffler syndrome
endomyocardial fibrosis with prominent eosinophillic infiltrate
what is CHF
cardiac pump dysfunction
symptoms: dyspnea, orthopnea, fatigue, rales, JVD, pitting edema
right heart failure often with left heart failure
systolic dysfunction CHF
low EF, poor contractility, secondary to ischemic heart disease or DCM
diastolic dysfunction
normal EF and contractility, impaired relaxation, decreased compliance
isolated right heart failure is usually due to?
cor pulmonale
what drugs are used in CHF?
ACE inhibitors, beta blockers (except acute decompensated), Ang II receptor blockers, spiranolactone
thiazide or loop diuretics for symptomatic relief
hydralazine and nitrate therapy for symptoms and increased mortality
what causes cardiac dilation
greater ventricular EDV
what causes dyspnea on exertion?
failure of CO to increase during exercise
what are symptoms of left heart failure
pulmonary edema
orthopnea
PND
pulmonary edema
increased pulmonary venous pressure leads to pulmonary venous distention and trsudation of fluid
presence of hemosiderin-laden macrophages in the lungs
orthopnea
shortness of breath when supine becaouse of increased venous return from redistribution of blood exacerbating pulmonary vascular congestion
PND
breathless awakening from sleep: increased venous return from redistribution of blood, reabsorption of edema
what are symptoms of right heart failure
hepatomegaly
peripheral edema
JVD
symptoms of bacterial endocarditis
fever new murmur roth spots (round white spots on retina surrounded by hemorrhage) osler nodes janeway lesions anemia splinter hemorrhages
cause of acute endocarditis
s. aureus (leads to large vegetations on previously normal valves)
rapid onset
cause of subacute endocarditis
ciridans streptococci
smaller vegetations on congenitally abnormal or diseased valves
gradual onset
sequela of dental procedures
cause of culture negative bacterial endocarditis
coxiella burnetti and bartonella
non bacterial causes of endocarditis
malignancy hypercoagulable state lupus s. bovis in colon cancer s.epidermidis on prosthetic valves
what valve is most commonly effectd in bacterial endocarditis?
mitral
what causes tricuspid valve endocarditis?
IV drug abuse, s. aureus, pseudomonas, candida
what are complications of bacterial endocarditis
chordae rupture
glomerulonephritis
supporative pericarditis
emboli
what causes rheumatic fever
s.pyogenes
what valves are effects in rheumatic fever?
mitral > aortic»_space; tricuspid
what are the early and late lesions associated with rheumatic fever?
early: MR, late: mitral stenosis
what histological and clinical features are present in rheumatic fever?
aschoff bodies (granulomas with giant cells) anitschkow cells (enlarged macrophages with ovoid wavy, rod like nucleus) increased ASO titers
what type of immune mediated hypersensitivity is rheumatic fever?
II, antibodies to M protein cross react with self antigens
how does acute pericarditis present?
sharp pain aggravated ith inspiration and relieved with sitting up and leaning forward
friction rub
ECG: widespread ST segment elevation and/or PR depression
fibrinous acute pericarditis
causes: dressler syndrome, uremia, radiation
presents with loud friction rub
serous acute pericarditis
viral pericarditis, noninfectious inflammatory diseases (rheumatoid arthritis, SLE)
suppurative/purulent
caused by bacterial infections (pneumococcus, streptococcus)
cardiac tamponade
compression of heart by fluid in the pericardium that leads to decreased CO
equilibration of diastolic pressures in all 4 chambers
hat are findings associated with cardiac tamponade
beck triad
increased heart rate
pulsus paradoxus
kussmaul sign
what is the beck triad
hypoTN
distended neck veins
distant heart sounds
what is seen on ECG with cardiac tamponade?
low-voltage QRS and electrical alternans (due to “swinging” movement of heart in large effusion)
pulsus paradoxus
decreased amplitude of systolic blood pressure by > 10 mmHg during inspiration
seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis and croup
syphillitic heart disease
tertiary syphillis disrupts vaso vasorum of aorta –> atrophy of the vessel wall and dilation of the aorta and valve ring
calcification of the aortic root and ascending aortic arch
tree bark aorta
what is the most common heart tumor?
metastasis (from melanoma, lymphoma)
myxsomas
most common primary cardiac tumor in adults
mostly in the atria (left)
ball valve obstruction
associated with multiple syncopal episodes
rhabdomyomas
most frequent primary cardiac tumor in children
associated ith tuborous sclerosis
kussmaul sign
increasee in jvp on inspiration instead of the normal decrease
the negative intrathoracic pressure from inspiration ins not transmitted to the heart so there is impaired filling of the right ventricle. Blood backs up into the vena cava and causes JVD
when do you see kussmaul sign
constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors
what is raynaud’s phenomenon?
decreased blood flow to the skin (fingers and toes usuually) due to arteriolar vasospasm in response to cold temperature or emotional stress
disease if primary idiopathic
syndrome if caused by disease process
what are causes of raynaud’s syndrome?
mixed connective tissue disease
SLE
CREST
strawberry hemangioma
benign capillary hemangioma of infancy
first few weeks
grows rapidly and regresses spontaneously at 5-8
cherry hemangioma
benign capillary hemangioma of the elderly
does not regress
pyogenic granuloma
polypoid capillary hemacioma that an ulcerate and bleed
associated with trauma and pregnancy
cyctic hygroma
cavernous lymphangioma of the neck
associated with turner syndrome
glomus tumor
benign painful red-blue tumor under fingernails
arises from modified smooth muscle cells of the glomus body
bacillary angiomatosis
benign capillary skin papules found in AIDS patients
caused by bartonella henselae
mistake for kaposi
angiosarcoma
rare blood vessel malignancy occurring in head neck and breast areas
usually in elderly on sun-exposed areas
associated with radiation therapy and arsenic exposure
very aggressive and difficult to resect due to delay in diagnosis
lymphangiosarcoma
lymphatic malignancy associated with persistent lymphedema (post-radical mastectomy
kaposi sarcoma
endothelial malignancy
commonly effects skin, mouth, GI tract, respiratory tract
associated with HHV8 and HIV
mistake for bacillary angiomatosis
what are the large vessel vasculitis
temporal (giant cell) arteritis
takayasu arteritis
what are the medium vessel vasculitis
polyarteritis nodosa kawasaki disease buerger disease (thromboangiitis obliterans)
what are the small vessel vasculitis?
granulomatosis with polyangiitis (wegener’s)
microscopic polyangitis
churg-strauss syndrome
henoch-schonlein purpura
epidemiology of large vessel vasculitis
temporal - elderly females
takayasu - asian females <40
temporal (giant cell) arteritis symptoms and associations
elderly females
unilateral headache, jaw claudication
irreversible blindness due to ophthalmic artery occlusion
associated with polymyalgia rheumatica
what is the pathology of temporal arteritis
focal granulomatous inflammation with increased ESR
what arteries are most commonly affected in temporal arteritis
branches of the carotid
how do you treat temporal arteritis
high dose corticosteroids prior to temporal artery biopsy to prevent vision loss
takayasu’s arteritis symptoms
pulseless disease (weak upper extremity pulses) fever night sweats arthritis myalgias skin nodules ocular disturbances
pathology of takayasu’s
granulomatous thickening and narrowing of the aortic arch and great vessels
increased ESR
treatment of takayasu’s
corticosteroids
epidemiology of medium vessel vasculitis
polyarteritis nodosa: young adults
kawasaki disease: asian children <40
polyarteritis nodosa symptoms
fever, weightloss, malaise, headache
ab pain, melena
HTN, neuro dysfxn, cutaneous eruptions, renal damage
hep B seropositivity in 30%
arteries effected in polyarteritis nodosa
renal and visceral vessels, not pulmonary arteries
pathology of polyarteritis nodosa
immune complex mediated
transmural inflammation of the arterial wall w/ fibrinoid necrosis
innumerable microaneurysms and spasm on arteriogram
treatment of polyarteritis nodosa
corticosteroids, cyclophosphamide
symptoms of kawasaki disease
fever cervical lymphadenitis conjunctival injection strawberry tongue hand-foot erythema desquamating rash possible coronary artery aneurysm thrombosis leading to MI and rupture
treatment of kawasaki’s
IVIg, aspirin
buerger disease symptoms
intermittent claudication may lead to gangrene, autoamputation of digitis, superficial nodular phlebitis
raynaud’s
(segmental thrombosing vasculitis)
treatment of buerger’s
smoking cessation
symptoms of granulomatosis with polyangiitis
upper respiratory tract: perforation of nasal septum, chronic sinusits, otitis media, mastoiditis
lower respiratory tract: hemoptysis, cough, dyspnea
renal: hematuria, red cell casts
what is the triad that is associated with granulomatosis with polyangiitis
focal necrotizing vasculitis
necrotizing granulomas in the lung and upper airway
necrotizing glomerulonephritis
what are the ANCA associated vasculitis?
PR3-ANCA/c-ANCA (anti-proteinase 3): wegner’s
MPO-ANCA/ p-ANCA (anti-myeloperoxidase): microscopic polyangiitis and churg strauss
what do you see on CXR in wegners
large nodular deposits
how do you treat wegner’s
cyclophosphamide and corticosteroids
microscopic polyangiitis symptoms
necrotizing vasculitis ommonly involving lung, kidneys and skin ith pauci-immune glomerulonephritis and palpable purpura
like wegners without nasopharyngeal involvement and no granulomas
treatment of microscopy polyangiitis?
cyclophosphamide and corticosteroids
symptoms of churg-strauss?
asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist and foot drop)
can involve heart, GI, kidneys
pathology of churg-strauss
granulomatous, necrotizing vasculitis with eosinophilia, increased IgE
henoch-schonlein purpura presentation
follows URI
classic triad: skin (palpable purpura on buttocks and leg), arthralgias, and GI (abdominal pain, melena, multiple lesions of same age)
cause of henoch-schonlein purpura?
vasculitis secondary to IgA complex deposition, associated with IgA nephropathy
