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73 Cards in this Set
- Front
- Back
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blowing murmru
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regurgitation
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harsch murmur
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stenotic valve
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aortic murmus
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2nd right intercostal space
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mitral murmur
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apex, and radiate to left axila
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aortic stenosis
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harsh systolic murmur
due to age, congenital bicuspid valve (before 40 yo) |
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aortic regurg
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blowing diastolic murmur
due: chronic htn, leutic aneurysm (3 syphilis), disectic aortic aneurysm, ankylosing spondylitis |
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mitral stenosis
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harsh diastolic murmus
due: rheumatic heart dis |
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mitral regurg
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blowing systolic murmus
due: rheumatic dis, advanced mitral prolapse,damage from infectiuos endocarditis, papillary musle rupture secondary to MI, CHF |
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Mitral valve prolapse
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midsystolic click
due: marfans sysndrom, ehlers danlos, fragile X syndrome (CGG trinucleodite repea) |
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right side murmus
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increase in intensity with inspiration
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left side murmur
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increase in intensity wiht expiration
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vsd
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ventricular septal defect
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ASD
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1) ostium primum: defect next to AV valve
2) ostium secundum: fenestrated ovale fosa (90 % or ASD) |
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Acyanotic congentital heart defects
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VSD, ASD, PDA
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cyanotic CHD
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tetralogy of fallot, transpositon of great vessels, persistent truncus arteriosus, eisenmengers syndrome
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tetralogy of fallot
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pulmonic stenosis + VSD + overriding aorta + right vent hypertropy
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eisenmengers syndrome
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reversal of left to right shunt (such as VSD), to a right to left shunt (secondary to the development of pulmo HTN)
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preductual obstruction: infant type
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very high afterload-->rapid develep CHF due to very aortic press
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postductal obstruction: adult type
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manny blood vessel come of aorta prior to the obstuction-->allow bllod flow to the body-->high BP in arms and low BP in legs
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stable angina
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exersice induced
decreased cardiac perfusion wiht increased demand persistent but unchanged plaque in coronary art that limits max blood flow pain when increase O2 demand (exersice, sex, arguing) pain stops when stop the stimulant |
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unstable angina
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disruption of plaque-->form thrombus-->form occlusinve platelet formation-->clot obstructs blood flow
heart tissue cant survive for more thatn 30 min w/out blood supply-->infarction |
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prinzmetal's angina
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cornonary artery spasm
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MI
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when unstable angina lasts longer thatn 30 min-->cause infarction
1)subendothelial: nonQ wave, NSTEMI, inner 1/3 wall is infarcted 2)transmural: Qwace, STEMI, whole wall is infarcted, worse blood supply to heart is from epi to endo so endo dies first |
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MONA
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treatment for anyone suspected to chest pain
Morhpine: optional after nitroglycerin, not the 1st thing to be given. potent vasodilator-->devrease venous return-->dec preload-->dec work load of heart-->decr O2 demand. also an opiate-->decre HR from anxiety-->decre work of heart-->decrease O2 demand O: oxygen: increase O2 levels in blood-->incre O2 going to heart even wiht low blood flow N: nitorglycerin: 1st thing given. vasodilator of coronary art-->increase blood flow. diagnostic and therapeutic (decrease pain in stable, and prizemetal) Aspirin: chewable-->inhits Cox-->inhbit increase in clot |
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stable angina
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pain: <30 min
EKG: st depression Troponin: marker for cell death: negative Ck-totat, Ck-Mb: (marker for cell damage) negative pain relief wiht nitro glycerin: yes because vasodilates and increase blood flow |
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unstable angina
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pain: <30 min
EKG: ST depression Troponin: neg CK MB: yes (some cell damage) Nitroglycerin: no because vasodilation is usualy counteracted wiht increase in clot formation so blood flow remains restricted. |
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Non Q wave MI/ subendothelial
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pain: >30
EKG: St depr troponin: positive: cell death usually after 30 min occlusion of vessel Ck-MB: yes Nitroglycerin: no because vasodilation is usualy counteracted wiht increase in clot formation so blood flow remains restricted. |
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Q wave MI/transmural
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pain: >30
EKG: St elevattion (marker for heart surface damage) troponin: positive: cell death usually after 30 min occlusion of vessel Ck-MB: yes Nitroglycerin: no because vasodilation is usualy counteracted wiht increase in clot formation so blood flow remains restricted |
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prinzemetal angina
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pain: <30 min
EKG: ST elevation becasue only spasm of CA on surface of heart cause prinzemetal troponin: no CK: non nitroglycerin: yes--> vasodilates CA-->stop spasm |
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acute coronary syndromes
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unstabe angina, subendothelial mi, transmural MI: once diagnoseed continue Aspirin, give IV heparin, IV nitroglycerin, Beta Blocker (block B1 receptor-->Decr HR and force of contraction-->decrease work and O2 demand)
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M. infarction
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death of tissue-->attract neutrophils-->dead tissue replaced by scar in about 8 weeks
too much damage-->develp heart failure |
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Lt heart failure
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due to chronic HTN, MI, valve pathology
result in pulmo edema and fluid overload (due to activation RAAS) signs and symps: dyspnea, othropnea, fatigue |
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rt heart failure
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#1 cause is Lt HF, pulmo HTN(usualy young women), lung pathology
results in Peripheral edema, NUtmeg liver S&S: ankle edema, JVD RT HF w/Lt HF: cor pulmonale |
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Infective endocarditis
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cause: Roth spots (retinal hemorrhages), Janeway lesions (red macule on palms and soles), oslers nodes (painful papule on finges and toes)
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acute infective endocarditis
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no prior valvulr patholo required
casued by skin microbes: s. Aureus, Strep. spp. acute onset chills, high fever high death rate most common in IV drug users, adn diabetitics, construction workrers of who cut themselfves a lot |
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subactue infective endocartditis
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only prior valve pathology
usually casued by mout or GI organisms strep spp of the viridans group (live in the mouth) E. coli and other gram - bacteria from endoscopy, colonoscopy valve patho: mandates ABX propylaxi before dental work low death rate insidiuor, slow onset, fatique, low grade fever |
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non-infective endocarditis
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Acute rheumatic fever: 3-4 wks after s. pyogenes infx
marantic endocarditis: thrombi develop on endocardium, higher risk in severe or chronic illness especially adenocarcinoma (release mucin-->hypercoaguable state)most colon cancers) Libman sacks endocarditis: only in SLE pats, huge vegetation on AG-AB complexes on valves-->valve damage, seen on echocardio |
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new onset murmur
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think endocarditis
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pericarditis
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fibrinous: #1 in world: due to transmural MI, dressler syndrome
serous: #1 in US: due to Coxsackie B, uremia, ARF, scleroderma, rheumatic heart dis, SLE suppurative: purulent, pathogens into pericadium (usually sterp pneumonia, stap. aureus) untreated pericarditis lead to pericardial effusion-->tamponade |
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Acute rheumatic fever
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immune mediated
follow 3-4 weeks after St. pyogenes infx (GABHS) more in children cause pancarditis histolologically characterized by ASCHOFF BODY: pathognomic, focal area of myocardial inflammation, contains collagen, enlarged myocytes (anitschkow myocytes) and some aschoff cells (giant cells) cause mitral valve damage-->--rheumatic heart dis Major JOnes criteria: SPECS S: subcutanious nodules P: polyarthritis migratory E: erythema marginatum C; carditis S: syndeham chorea Minor jones critera: fever, arghrlagia, High ESR, CRP, high WBC, prolonged PR interval, Hx of rheumatic fever DX: evidence of st. pyogenes infx + 2 Major criteria 1 major + 2 minor |
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obsttuctive lung dis
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increased restriction to airflow during force expiration, hyperinflated lungs, flat diaphragms
low FEV1, adn ratio high TLC treatmen: beta agonists (albuterol), +/- anticholinergics (ipratropium), +/- O2 COPD: pulmo emphysema, chronic chronchitis, bhronchiectsis Asthma |
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pulmo emphysema
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destroy alveolar walls by proteolytic enzymes
panacinar: throughout lobule assoc w/alpha1antitrypsin def centrilobular: in center of lobule due to smoking pink puffer: adequate oxygenation in early dis + pursed lips for PEEP barrell chest, dyspnea decreased/absent breath sounds |
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chronic bronchitis
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due to prolonged exposure to bronchial iritants-->hypersecrestion of mucus and bronchial structural change
symps: must be present for atleast 3 months for 2 consecutive eyars BLUE BLOATER: hypoxemic in ealry dis-->secnondary edema to Rt HF wet procuctive cough dyspnea ronchi |
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bronchiecatisi
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irrevesible bronchial dilation + infx
acquired: Kartagners syndrom: recurrent bronchial infx, bronchiextasis, situs inversus, male sterility, heraring defects cystic fibrosis: recurrent bronchial infx +bronhiextasis+malabsorption+gall stones |
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Asthma
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IgE mediated, reversible
spasm of smooth muscle FEV1 increase after albuterol expiratory wheezing, tachypnea, cough, SOB charcot-leyden crystal and curschmann spirals in mucus |
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Restrictive lung dis ((RLD)
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FEV1: normal or low
TLC: very low ration: normal very small lung volume usual due to fibrosis or scarring |
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Restrictive lung dis ((RLD)
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FEV1: normal or low
TLC: very low ration: normal very small lung volume usual due to fibrosis or scarring |
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Sacroidosis (RLD)
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form noncaseating granuloma that become surrounded by scars
dyspnea, cough night sweats bilateral hilar adenopathyon chest xrays +/- panda sign (bilat sacroidosis of parotid glands) blacks highest risk |
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Sacroidosis (RLD)
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form noncaseating granuloma that become surrounded by scars
dyspnea, cough night sweats bilateral hilar adenopathyon chest xrays +/- panda sign (bilat sacroidosis of parotid glands) blacks highest risk |
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Adult ARDs (RLD)
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from diffuse injury to endothelium of vessel of lung
characterized by : pulmo edema, resp distress, hypoxemia |
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Adult ARDs (RLD)
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from diffuse injury to endothelium of vessel of lung
characterized by : pulmo edema, resp distress, hypoxemia |
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Neonatal ARDs(RLD)
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Hylane membrande dix
due to insufficient surfactant (pramture birth (before 34 weeks) occurs when lecithin: sphingomyelin ration is <2.0, measured in amniotic fluid |
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Neonatal ARDs(RLD)
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Hylane membrande dix
due to insufficient surfactant (pramture birth (before 34 weeks) occurs when lecithin: sphingomyelin ration is <2.0, measured in amniotic fluid |
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Asbestosis Pneumoconciosis (RLD)
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chronic inhalation of asbestos
ferruginous bodies lower lobes--> casue fibrotic plaques of pleura high risk for SCC, and malignant mesoltheioma insulating agents, shipyard workers |
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Asbestosis Pneumoconciosis (RLD)
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chronic inhalation of asbestos
ferruginous bodies lower lobes--> casue fibrotic plaques of pleura high risk for SCC, and malignant mesoltheioma insulating agents, shipyard workers |
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Anthracosis pneumoconiosis (RLD)
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Coal workers's pneumoconiosis--> cause black lung dis
upper lungsa |
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Anthracosis pneumoconiosis (RLD)
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Coal workers's pneumoconiosis--> cause black lung dis
upper lungsa |
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berylliosis
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inhale berylium (elctronics, floureceent light bulb)
lower lobes |
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berylliosis
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inhale berylium (elctronics, floureceent light bulb)
lower lobes |
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silicosis
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inhale quartz dust from sand blasting, granite cutting
raises one's suseptibility to TB uppr lung lobes |
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silicosis
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inhale quartz dust from sand blasting, granite cutting
raises one's suseptibility to TB uppr lung lobes |
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farmers lung
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inhale thrmophilic actinomycetes from moldy hay
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farmers lung
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inhale thrmophilic actinomycetes from moldy hay
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bird farmers lung
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inhale bird droppings or feathers from parakeets pigeions chickens, turkeys
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bird farmers lung
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inhale bird droppings or feathers from parakeets pigeions chickens, turkeys
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tobacco work's lung (RLD)
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inhale mold on tobacco
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bagassosis (RLD)
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inhale thermophilic actinomycetes on moldy bagasse (sugar cane)
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goodpasture's syndrome
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glomerulonephritis, pulmo hemmorage, dyspnea
antiglomerular basement antibodies --> destruction casue fibrosis |
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pulmo hemisiderois
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blood accumulates in interstitial space--> inflamation --> fibrosis
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alveolar proteinosis
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alveoli fill wiht proteinaceous and other material --> inflam-->fibrosis
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eosinophilic pneumonia
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usually idiopathic but occasionally due to roundworms, drugs, fungi
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diffues idiopathic fibrosis/hamman rich syndrome
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honecomy lung
fatal within years |
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collagen vascular dis
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chronic inflmmation can start the cycle to a restrictice lung dis.
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