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200 Cards in this Set
- Front
- Back
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What is the virulence of subacute bacterial endocarditis? tempo? effects? responsiveness?
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Virulence: less aggressive organisms (Strep)
Tempo: insidious, indolent course over weeks to months Effects: slower injurious alterations in abnormal valves Responsiveness: greater potential for recovery with therapy |
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What is the virulence of acute bacterial endocarditis? tempo? effects? responsiveness?
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Virulence: aggressive organisms (Staph)
Tempo: rapid progression; death in <6 weeks if untreated Effects: rapidly destructive changes in normal valves Responsiveness: frequently unresponsive to therapy |
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True or false: a patient with bacterial endocarditis may present with systemic complications rather than heart problem
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True: the two scenarios (acute and subacute) have much overlap and can present with systemic complications rather than heart problem
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What is the main cause of potential for infection?
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any damaged valve (congenital heart disease, chronic rheumatic heart disease, mitral valve prolapse, calcific aortic stenosis, mitral valve annulus calcification, IVDA, prosthetic valves)
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What are examples of pathogenesis of bacterial endocarditis?
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transient bacteremia, catheterization, obstetrical procedures, congenital heart disease, hemodynamic factors
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What are examples of pathology of bacterial endocarditis?
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Endocardial injury, formation (point of valvular closure), result (destruction of valve leaflet), spread, infected emboli
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What are the signs and symptoms of bacterial endocarditis?
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general (fever, chills, sweat, etc), splenomegaly, neurological (headache, stroke), congestive heart failure, murmurs, skin (petechiae), emboli
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How do you treat patients at risk of bacterial endocarditis?
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antibiotic prophylaxis and appropriate antibiotics based on culture and sensitivity
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What can you do with lab testing for bacterial endocarditis patients?
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Serial blood cultures
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What surgery should be considered for patients with bacterial endocarditis?
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valve replacement as needed
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What are some of the issues observed with mechanical valves?
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site of infection for endocarditis, myocarditis, ring abscess and infection embolization
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Is a bioprosthetic valve better than a mechanical valve?
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They can both be good or bad and the selection should be tailored to the patient for the best results
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Why is hypertension called the silent killer?
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Most patients are initially asymptomatic (or ignore the symptoms)
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What is the diastolic cutoff for hypertension?
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90 (Reisner says this is arbitrary...not sure why???)
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Does diastolic or systolic pressure become more relevant as one ages?
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Systolic
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Do more men or women tend to be undertreated?
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Women
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Describe benign HTN
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chronic, progressive, cumulative injury
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Describe malignant HTN
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accelerated, acute rapid-onset life-threatening event
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Describe Primary HTN
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(essential), no single cause recognized, complex and multifactorial, 95% of most cases
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Describe Secondary HTN
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Definabe etiology in 5% of cases, treatable with potential for cure
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What is reflex BP mediated by?
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pressure sensors in the aorta and carotid (baroreceptors) and smooth muscle in the vessel (via the medulla in the CNS)
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What do the baroreceptors and/or smooth muscle of the vessels do when activated by the BP?
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activate the parasympathetic (reduce pressure) or sympathetic (increase pressure)
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What organ is critical for non-reflex related control of BP?
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the kidney
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What is secreted by the kidney that is essential in BP control?
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renin
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What product is formed from renin?
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angiotensin II
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What is a likely major cause of hypertension?
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metabolic syndrome
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What is metabolic syndrome?
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Insulin resistance/pre-diabetes, obesity
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Describe the effects of insulin resistance/pre-diabetes
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increased insulin levels, increased sympathetic activation, vascular smooth muscle cell hypertrophy
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Describe the effects of obesity.
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increased angiotensinogen (from adipocytes), augmented blood volume, increased blood viscosity (complex)
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What does LVH stand for?
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Left Ventricular Hypertrophy
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What is the warning weight for LVH?
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>400g
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What are the 3 characteristics that LVH is related to?
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size, gender and condition
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There is an increased incidence of CAD, MI, and CHF in hypertensive patients. What is the percentage of patients that die of these?
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50% of hypertensive patients die of CAD, MI or CHF
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What are the characteristics of benign arteriosclerosis (setting, typical lesion, pathology)?
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Setting: chronic hypertension
Typical lesion: hyaline arteriosclerosis (hyalinosis) Pathology: thick arteriolar wall; hard, glassy, hyaline, eosinophilic |
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What are the characteristics of malignant arteriosclerosis (setting, typical lesion, pathology, microangiopathic effects)?
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Setting: accelerated hypertension
Typical lesion: acute destructive arteriopathy Pathology: multiple features of acute vascular injury microangiopathic effects: damaged erythrocytes--shearing injury |
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What do patients with hypertensive diseases of the aorta have an increased predisposition for?
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Development and acceleration of the atherosclerotic process
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Describe benign nephrosclerosis (setting, clinical, pathology)
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Setting: mild to moderate chronic hypertension
Clinical: frequently totally asymptomatic Pathology: progressive damage to kidney |
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True or false: benign nephrosclerosis cannot lead to advanced disease
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False: the so-called benign process can lead to advanced disease
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Describe malignant nephrosclerosis (setting, clinical, pathology)
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Setting: markedly elevated diastolic BP--rapid clinical onset
Clinical: acute impairment of renal function Pathology: rapid irreversible ischemic injury |
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What is the percentage of hypertensive patients die of renal failure?
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10-15%
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What is a hemorrhagic stroke?
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20% of clinical CVAs, spontaneous, non-traumatic bleed
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What is an intracerebral hemorrhage?
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Rupture, small deep penetrating artery (consequence of cerebral arteriosclerosis)
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What percentage of hypertensive patients die of stroke?
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33%
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Where is the only site that arterial vasculature can be directly visualized on a routine basis?
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The eye (hypertensive retinopathy)
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What is the main cause of secondary hypertension?
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Renal disease
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What is the structure of the pericardium?
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Double layer sac containing the heart (visceral inner layer, parietal outer layer)
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What is the function of the pericardium?
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paradox--generally asymptomatic if absent
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What is the disease potential of pericardium?
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altered stiffness and compliance; altered lubrication and friction, altered pressures and fluid volume: slow and rapid changes
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What is the special testing for pericardium?
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pericardiocentesis
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What are the infectious causes of acute pericarditis?
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virus-tuberculosis-pyogenic bacteria, fungus
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What are the immunologic causes of acute pericarditis?
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acute rheumatic fever, systemic lupus erythematosus (collagen vascular disease, post-myocardial infarction and post-pericardiotomy syndromes, drug hypersensitivities
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What are the miscellaneous causes of acute periodontitis?
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uremia: renal failure
Neoplasm: metastases radiation: treatment injury trauma: direct physical injury |
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What is post-pericardiotomy syndrome?
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manipulation of pericardial sac
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What is collagen vascular disease?
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lupus erythematosus and others
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What do drug hypersensitivites cause?
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Lupus-like syndromes
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Describe uremic pericarditis
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chronic renal failure with an nknown pathogenesis
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Describe malignant pericarditis
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Secondary to tumor metastases
Large, hemorrhagic, life threatening Breast, lung, lymphoma |
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What is radiation pericarditis induced by?
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radiation therapy
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Describe sarcoidosis
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non-infectious granulomatous inflammation
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What is constrictive pericarditis?
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Chronic fibrosing process of pericardium
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What is the etiology of constrictive pericarditis?
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Historical: tuberculosis
Current: idiopathic, radiation injury, cardiac surgery |
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Describe the pathology of constrictive pericarditis
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mmarked fibrous thickening (>2mm), rigid fibrous envelope, encasement in "concrete"
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What is the pathogenesis of cardiac tamponade?
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rapid accumulation of pericardial fluid
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What is the etiology of cardiac tamponade?
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multiple causes of effusion
Most significant: metastatic neoplasm and uremia |
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Describe atherosclerosis
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Disease of large and medium-sized arteries, progressive accumulation of smooth muscle cells, lipids and conntective tissue (atheroma formation within the intima)
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What is the percentage of mortality in the US from major complications (of atherosclerosis)?
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>50%
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What is the leading cause of death in the US?
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Ischemic heart disease
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What is the classic morphology of the "classic" atheroma?
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raised focal intimal plaque with necrotic lipid core covered by a fibrous cap
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What cells are constituents of an atheroma?
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smooth muscle cells, macrophages, leukocytes
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What is in the CT ECM of an atheroma?
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collagen, elastic fibers, proteoglycans
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What are the lipid components of an atheroma?
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cholesterol and cholesterol esters; intracellular and extracellular
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What is the first stage of atherosclerosis?
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fatty streak
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Describe a fatty streak
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Early lesion, possible precursor of atheroma, not significantly raised, no disturbance of blood flow, lipid-filled foam cells with T-lymphocytes and extracellular lipid within intima
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What age do we usually see aortic fatty streaks?
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Typically seen in all children by age 10
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What is the second stage of atherosclerosis?
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Fibrofatty plaque
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Describe a fibrofatty plaque
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intermediate lesion, focal raised lesions with disturbance of blood flow, fibrous cap, lipid core
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Describe the make-up of a fibrous cap
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smooth muscle, monocytes, lymphocytes, foam cells, CT
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Describe the make-up of a lipid core
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necrotic debris, cholesterol, foam cells
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What is the third stage of atherosclerosis?
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A complicated lesion
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Describe a complicated atherosclerotic lesion.
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Advanced lesion, pathcy or massive calcification, focal rupture or ulceration of luminal surface, hemorrhage, superimposed thrombosis, weakening of the tunica media
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What are the major complications of atherosclerosis?
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myocaridal infarction, sudden cardiac death, chronic ischemic heart disease, aortic aneurysms, cerebral infarction, ischemic encephalopathy, peripheral vascular disease, mesenteric occlusion
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What is the most common type of heart disease in the USA?
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Ischemic heart disease
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What is the percentage of cardiac deaths that are attributed to ischemic heart disease?
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>80%
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What occurs that constitutes ischemic heart disease?
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coronary atherosclerosis with fibrofatty and complicated plaques
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What is the common pathophysiology shared by the acute coronary syndromes?
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coronary atherosclerotic plaque disruption and intraluminal platelet-fibrin thrombus formation
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Describe what can happen with an acute plaque change.
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hemorrhage into atheroma, rupture or fissuring of plaque with exposure of thrombogenic constituents, erosion of ulceration with exposure of thrombogenic basement membrane
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What are three characteristics we see in ischemic heart disease?
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progressive luminal stenosis, inadequate blood flow for oxygen demands, acute plaque change critical in acute syndromes
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What are the primary manifestations for ischemic heart disease?
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Angina pectoris, myocardial infarction, sudden cardiac death, chronic ischemic heart disease
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What is the most common symptom of cardiac ischemia?
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angina pectoris
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Where is the pain of angina located and how long does it last?
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substernal chest pain of limited duration
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What causes the pain felt with angina?
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stenosed arteries cannot meet oxygen demands
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How can stable angina be relieved?
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rest and nitroglycerin
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True or false: atypical and unstable angina cannot occur at rest
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False: atypical and unstable angina can occur both at rest and during activity
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What is atypical angina associated with?
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Coronary artery spasm
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What is unstable angina associated with?
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acute plaque change, nonocclusive thrombosis, vasoconstriction
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What can unstable angina progress to?
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acute myocardial infarction
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What is an acute myocardial infarction?
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discrete focus of ischemic necrosis in the heart
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What is the development of an acute myocardial infarction related to?
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duration of ischemia and metabolic rate of ischemic tissue
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What length of time of ischemia can cause an infarct?
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As little as 20-30 minutes
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What is a frequent result of acute myocardial infarction?
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acute plaque change with coronary artery thrombosis
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How quickly can dissolution of thrombus be seen?
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frequently within 12-24 hours
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Which ventricle is involved with an infarct more frequently
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the left ventricle is more commonly and extensively involved than the right ventricle
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In sudden cardiac death, how quickly does unexpected death occur?
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within 1 hour of onset of cardiac symptoms
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What is often the initial presentation of IHD (ischemic heart disease)?
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sudden cardiac death
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True or false: sudden cardiac death can only occur with coronary thrombosis
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False: sudden cardiac death can occur with or without a coronary thrombosis
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What does regional ischemia frequently cause?
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lethal arrhythmia
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In patients that experience sudden cardiac death, what is frequently found?
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severe coroary atherosclerosis with critical (>75%) stenosis
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How long does it take to see a mature scar (from infarction) macroscopically?
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>2 months
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In contrast to the macroscopic features, what is seen microscopically from an infarct at >2months?
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dense collagenous scar
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What type of necrosis can be seen at 12-24 hours after infarct?
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coagulative necrosis and contraction band necrosis
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What can be a complication of myocardial infarction?
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myocardial free wall rupture, aneurysm, mural thrombosis
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When does a myocardial free wall rupture occur?
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during first 3 weeks, but most commonly between days 1-4 when the wall is weakest
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When do we see a myocardial free wall rupture?
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It is a complication of a large infarct, >20% of LV
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Where does the myocardial free wall rupture occur?
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at the junction of infarct and normal muscle
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What are the results of a myocardial free wall rupture?
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Hemopericardium and death from tamponade
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What percentage of deaths from AMI in hospitalized patients is caused from myocardial free wall rupture?
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10%
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Describe the process of an aneurysm after MI.
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Wall bulges outward during systole, fibrous scar progressively stretches
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What are the results of an aneurysm after MI?
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increased risk of myocardial rupture, predisposes to mural thrombosis, increases workload
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How often is a mural thrombosis seen?
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in almost 50% of fatal AMI, especially after apical infarcts
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What does mural thrombosis predispose the patient to?
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systemic embolization
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What feature of the MI predicts morbidity and mortality?
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size
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What is the goal of therapy for MI?
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to limit the size of the MI
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What therapy is usually used for MI?
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restoration of arterial blood flow through thrombolytic enzymes (TPA, streptokinase), percutaneous transluminal coronary angioplasty (PTCA), or coronary artery bypass graft (CABG)
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What is the definition of a vascular aneurysm?
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localized abnormal dilatations of blood vessels cause by a congenital or acquired weakness in the vessel media
May also occur in the cardiac chamber |
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Where do we normal see a vascular aneurysm?
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aorta or heart
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How are vascular aneurysms usually classified?
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location, configuration, etiology
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What is the definition of abdominal aortic aneurysm?
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abnormal aortic dilatation with diameter increased by at least 50%
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What is abdominal aortic aneurysm always associated with?
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severe atherosclerosis
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What are some of the characteristics of abdominal aortic aneurysm?
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male predominence, half the patients have hypertension, familial clustering (possible genetic predisposition), 6% incidence in >80 yr population but rare before age 50
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What is the most frequent aneurysm type?
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abdominal aortic aneurysm
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What is the general morphology of the abdominal aortic aneurysm?
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severe atherosclerosis with ulcerated, calcified plaques, medial destruction and fibrosis, usually fusiform dilatation
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Where do we usually see dilatation in the abdominal aortic aneurysm?
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Distal to renal arteries, proximal to iliac bifurcation
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What complications can you usually see abdominal aortic aneurysm?
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Frequent mural thrombosis with potential for thromboembolism
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Typically, how big is a symptomatic aneurysm?
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>5-6cm diameter
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What do the clinical signs of an abdominal aortic aneurysm depend on?
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location and size
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What are the general clinical signs/symptoms?
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abdominal mass simulating a tumor (pulsatile); abdominal pain from aneurysm expansion, ureteral compression, vertebral erosion; acute ischemia of lower limb or kidneys from emboli
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Rupture is a feared and ominous complicaton. Why?
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Pain, shock and pulsatile abdominal mass--rupture and massive hemorrhage = high mortality
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What is the percentage of rupture of a large aneurysm (>5cm diameter)?
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25-40% incidence within 5 years
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What are the key features of the classic abdominal aortic aneurysm?
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severe atherosclerosis, infrarenal location, fusiform dilatation, mural thrombosis, thromboembolism risk, atheroembolism risk, rupture
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What is the definition of aortic dissection?
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dissection of blood in between and along the laminar plane sof the media, forming a blood-filled channel within the aortic wall
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True or false: aortic dissection is not usually associated with aneurysmal swelling
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true
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What are the 2 groups with a predisposition to aortic dissection?
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men, 40-60 years old, antecedent HTN
younger patients with CT disorder |
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What is a common factor of aortic dissection?
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weakening of aortic media
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What is the most frequent preexisting lesion for an aortic dissection?
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Cystic medial degeneration (CMD)
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What may trigger an event of aortic dissection?
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spontaneous intimal laceration or vasa vasorum hemorrhage
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What is the general morphology of an aortic dissection?
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intimal tear in ascending aorta, within 10cm of aortic valve; may involve great vessels, coronary, renal, mesenteric or iliac ateries
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What is the most frequent cause of death in regard to aortic dissection?
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extravascular rupture (pericardial, pleural or peritoneal)
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What are some of the clinical signs/symptoms of aortic dissection?
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acute onset of severe "tearing" pain in anterior chest, radiating to the back; loss of arterial pulse; murmur of aortic regurgitation; MI; hypotension; cardiac tamponade
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With current surgical methods and control of HTN, what is the overall mortality rate in regards to aortic dissection?
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<20%
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What is the pathogenesis of venous thrombosis?
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stasis, injury, hypercoagulability, advanced age, sickle cell disease
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Where do >90% of venous thromboses occur?
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in the deep leg veins
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What are the clinical signs/symptoms of DVT?
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frequently asymptomatic; calf tenderness (Homan sign); occlusive DVT associated with congestion, edema and cyanosis
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What can happen to a large DVT?
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It is a potential hazard to life as it can dislodge and be carried to the lungs as pulmonary emboli
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What is the clinical outcome of a pulmonary embolism?
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massive pulmonary embolism, cardiovascular collapse and sudden death; pulmonary infarction with pleuritic chest pain, hemoptysis and effusion; pulmonary embolism without infarction, transient dyspnea and tachypnea
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What are the potential sources of emboli? Which is the most frequent?
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Sources: thrombi, air, tumor, fat, amniotic fluid
Most frequent: thrombi (specifically DVT) |
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What type of heart failure is a massive thromboembolism associated with?
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acute right heart failure
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What are the T-cell phenotype (low numbers)?
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CD1, 2, 3, 4, 5, 7, 8
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What are the myelomonocytic cells?
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CD 13, 14, 15 (granulocyte, monocyte, granulocyte respectively)
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What are the B-cell phenotype?
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CD 19.20.21.22.23
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What other markers can we use in immunophenotyping?
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CD 34 stem cell, CD 33 myeloid
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What is immunophenotyping?
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identifying the phenotype using fluorescently labeled antibodies (probe)
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How is leukemia diagnosed?
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According to the prominent cell type involved
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Describe acute leukemia.
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rapid onset, aggressive, usually poorly differentiated (blasts)
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Describe chronic leukemia.
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insidious onset, usually less aggressive and more mature appearing
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What percentage of patients diagnosed with chronic myeloid leukemia (CML) are asymptomatic?
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20-40%--these patients are diagnosed incidentally
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If left untreated, what will the chronic phase progress to?
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it will transform to a "blast phase" with additional genetic abnormalities and increased blasts
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What is the most common form of cytogenetics see in leukemia?
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deletion of 13q14 (found in >50% of cases)
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What is acute myeloid leukemia?
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Clonal expansion of myeloid blasts
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What is the most frequent molecular abnormality in AML?
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FLT3
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What is the characterizing distinctive cell of malignant (Hodgkin) lymphoma?
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Reed-Sternberg cell
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Describe the age distribution of Hodgkin Lymphoma.
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Bimodal: peak in 20s and smaller peak at >50
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How does Hodgkin lymphoma spread?
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Along contiguous lymph node chains
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What is the diagnosis based on?
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finding Reed Sternberg cells in appropriate cellular background
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Does Hodgkin lymphoma have a good or bad prognosis?
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good
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Which is more important: stage or histologic subtype? (in regards to HD lymphoma)
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stage
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What is the current treatment of choice for HD lymphoma?
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ABVD: adriamycin, bleomycin, vinblastine, dacarbazine
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What is the most common type of NHL (non-Hodgkin lymphoma)?
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Diffuse large cell lymphoma
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Define esophagitis
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inflammation of esophageal mucosa
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What is the etiology of relux esophagitis?
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gastric contents reflux back into the esophagus
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What is the pathogenesis of reflux esophagitis?
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gastric fluid causes esophageal mucosal damage
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What morphologic changes do we see with reflux esophagitis?
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inflammatory cells in esophageal squamout epithelium; basal zone hyperplasia; elongation of lamina propria papilla; spongiosis
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What are the clinical findings of reflux esophagitis?
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dysphagia, heartburn/chest pain, hematemesis
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What are the consequences/complications of reflux esophagitis?
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bleeding, ulceration, stricture, Barrett esophagus
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What is the etiology of infectious esophagitis?
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fungal (candidiasis) or viral (herpes and CMV)
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What is the pathogenesis of infectious esophagitis?
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inflammation and resulting tissue damage in response to infectious viral or fungal agent
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What morphologic changes do we see with infectious esophagitis?
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candida, Herpes virus
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What are the clinical findings assoicated with infectious esophagitis?
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immunosuppressed patients, dysphagia, pain
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Define Barrett Esophagus.
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replacement of the distal esophageal squamous epithelium by metaplastic columnar epithelium (with intestinal type goblet cells)
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What is the etiology of Barrett esophagus?
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chronic reflux injury (GERD)
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What is the pathogenesis of Barrett esophagus?
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injury from reflux of gastric acid results in metaplasia
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What morphologic changes do we see with Barrett esophagus?
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replacement of the squamous epithelium of the distal esophagus with columnar epithelium containing goblet cells
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What are the two criteria for diagnosing Barrett esophagus?
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endoscopic findings (red, velvety mucosa), histologic findings of columnar mucosa with goblet cells in biopsy material
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What are the clinical findings associated with Barrett esophagus?
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Risk factors: Age >40, caucasian, male, any underlying cause for long standing reflux esophagitis
Same symptoms as GERD |
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What are some complications observed with Barrett esophagus?
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Dysplasia, adenocarcinoma
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Define gastritis
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inflammation of the gastric mucosa
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What is the most common type of chronic gastritis in the US?
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H. pylori
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What is a peptic ulcer?
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disruption of the mucosa that extends through the muscularis mucosa in region of GI tract exposed to acid secretions (stomach and duodenum)
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Define celiac disease.
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immune mediated disease characterized by: malabsorption, small intestine mucosal flattening, symptomatic response to removal of gluten from diet
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Define acute appendicitis
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inflammatory disease of the wall of the appendix
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What are the 2 types of inflammatory bowel disease?
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Crohn disease, ulcerative colitis
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