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109 Cards in this Set
- Front
- Back
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Ischemic heart disease |
Imbalance between supply and demand |
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Myocardial infarction |
Death of cardiac muscle resulting from ischemia s Transmural |
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Subendocardial infarction |
Inner 1/3 1/2 of ventricular wall Least perfused Circumferential |
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Other cause of transmural acute MI |
Vasospasm- cocaine users Emboli- atrial fibrillation Left side mural thrombosis Vegetative endocarditis Paradoxical thrombosis- right side Unexplained- vasculitis hematology Amyloidosis |
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Mechanism of cell death in MI |
Coagulating necrosis |
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Gross morphology and histology of MI |
4-12- dark mottling, coagulation necrosis edema hemorrhage 12-24- dark mottling, CN pyknosis nucleus nutrophilic infiltrate 1-3 day- yellow tan , loss of nucleus interstitial infiltration of neutrophil 3-7 days- hypermic borders, phagocytosis of dead cells by macrophages 7-10 day- red tan, fubrovascular granulation tissue 10-14day- red-grey new vessel formation 2-8wk- grey white, increase collagen decrease cellularity 2 months- scaring complete dense collagen |
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Consequences and complication of MI |
Contractile dysfunctions- cardiogenic shock Arrhythmia- sinus bradycardia heart block tachycardia V.fibrillation Myocardial rupture- Rupture of ventricular free wall- 3-7 days CN infiltration of neutrophils lysis of myocardium >60 female HTN lack of left ventricular hypertrophy Rupture of ventricular septum- L-R shunt Rupture of papillary muscle- mitral regurgitation Pericarditis- 2-3 days after Right ventricle infarction Infarction extension and expansion Mural thrombosis Ventricular aneurysm |
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Systolic dysfunction cause |
Ischemic injury Volume/pressure overload Dilated cardiomyopathy |
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Diastolic dysfunction |
Massive LVH Myocardial fibrosis Amyloidosis Constructive pericarditis |
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Concentric hypertrophy |
Pressure overload HTN and aortic stenosis Thickening of muscle wall |
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Extra cardiac effect of left side heart failure |
Lungs Pressure increase in pulmonary vein Pulmonary congestion and edema Perivascular and interstitial transudate Progressive edema widen alveolar septa Accumulation of edema fluid in alveolar space Kidney- decrease CO decrease renal perfusion Activate RASS Retention of salt and water expansion of blood volume Pulmonary edema Brain- brain hypoxia Pulmonary edema |
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Extra cardiac effects of right side heart failure |
Liver Hepatomegaly Fibrosis liver cirrhosis Increase pressure in portal vein Congestive splenomegaly Ascitis due to the accumulation of transudate Kidney Congested kidney Same Brain Venous congestion Brian hypoxia Pleural effusion Dependent edema |
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Rheumatic fever |
Group A streptococcus pharyngitis Fibrotic valve Mitral stenosis- fishmouth or buttonhole stenosis |
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Morphology of rheumatic fever |
Aschoft bodies Pancarditis Fibrinoid necrosis Vegetation of cusp Sunendocardial lesion MacCollum plaque |
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Changes of mitral and tricuspid valve |
Leaflet thickness Commissural fusion Shortening thickening and fusion of tendinitous cord |
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Major criteria for rheumatic fever |
Migratory polyarteritis of large joints Carditis Subcutaneous nodules Erythema marginatum Sydenham chorea |
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Minor criteria for rheumatic fever |
Fever>38 Arthralgia Increase ESR CRP Prolong PR interval Previous RF |
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Diagnosis of RF |
Evidence of Group A strep 2 majors or 1 major and 2 minor |
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Complication of rheumatic fever |
Mural thrombosis Infective endocarditis |
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Infective endocarditis |
Vegetation Consist of thrombotic debris and organism Destroy cardiac muscle Bacterial |
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Acute endocarditis |
High virulent organism damage normal heat valve 50% patients die despite antibiotics or surgery g |
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Subacute endocarditis |
Low virulent organism damage abnormal heart valve Recovery with antibiotics |
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Cardiac and vascular cause of IE |
Artificial (prosthetic) valve Bicuspid aortic valve Degenerative calcification valvular stenosis Myxomatous mitral valve RHD |
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Predisposing factors for IE |
Alcohol IV drug users Diabetes mellitus dental procedure Therapeutic immunosuppressive Immunodeficiency Malignancy Neutropenia |
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Organism causing infective endocarditis |
Streptococcus viridans Staph aureus high virulent Gram negative bacilli HÁČEK- subacute endocarditis |
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Treatment of infective endocarditis carditis |
Ceftriaxone Augmenting (fluoroquinolone if Beta lactam allergy) |
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Organism of prostatic valve |
Coagulase negative staphylococcus Staph. Epidermis |
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Morphology of IE |
Vegetation can erode myocardium and form a abscess ring abscess Fungi- larger vegetation |
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Non bacterial thrombotic endocarditis |
Fibrin platelets and other blood components on the leaflets of valves Sterile Occurs with venous thrombosis and PE |
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Sepsis |
A clinical syndrome characterized by the present of SIRS plus a foci of infection |
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Gross pathology of the brain in shock |
Hypoperfusion cause cerebral ischemic Neurons and gliol susceptible |
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3 categories of brain shock |
Early changes- 12-24 hr Microvaculoization Eosinophilia of the cytoplasm Nuclear pyknosis and karyorrhexis Neutrophilic infiltration Subacute changes- 24hr- 2wk Tissue necrosis Influx of macrophages Vascular proliferation Reactive gliosis Repair- >2 weeks Removal of necrotic tissue Loss of CNS structure and gliosis
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Causes of pulmonary edema |
Hemodynamics disturbance Increase hydrostatic pressure Left side heart failure Pulmonary vein occlusion Decrease oncotic pressure |
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Causes of increase capillary permeability |
Infection Inhaled gas Liquid aspiration- gastric content Transfusion related Drugs and chemicals Shock and trauma |
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Gross morphology of lung shock |
Bulky firm red boggy Congestion interstitial intra-alveolar edema, inflammation Alveolar wall line with waxy hyaline membrane Hyaline membrane made of fibrin rich edema fluid |
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Stages of sepsis |
Sepsis + SIRS Sever sepsis- target organ damage Septic shock- sever sepsis + hypo-perfusion |
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Pathophysiology of sepsis |
Respond to infection burn trauma pancreatitis hemorrhage ischemia anaphylaxis Activation of the inflammatory cascade Release of Cytokines from tissue macrophages monocytes mast cells platelet and endothelial cell TNFa and IL-1 first release Works alone or active coagulation cascade or compliment cascade to realer nitric oxide platelets activator prostaglandin and leukotriene Vasodilation and increase vascular permeability Prostaglandin and leukotriene cause endotheilal damage |
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IL-1 and TNF |
Causes endothelial damage Activate tissues factor Tissue factor produces thrombin which promote coagulation fibrinolysis inhibited via IL-1 and TNFa activate plasminogen activator inhibitor Microvascular thrombosis Imbalance between inflammation and coagulation |
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Ischemic acute tubular necrosis |
Foci tubular epithelial necrosis Skip areas Tubularhexis- rupture of basement membrane Affect the proximal tubule and ascending thick limb Loss Proximal tubule brush borders Simplification of cell structure Cellular sweeping and vacuolization Sloughing of non necrotic tubular cell Interstitial edema Accumulation of leukocytes writhing dilates vasa recta Epithelial regeneration Eosinophilic hyaline |
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Septic shock |
Spread and expansion o localized infection into the bloodstream abscess peritonitis pneumonia Endotoxins producing gram -ve bacilli LPS lipopolysaccharides |
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Results of septic shock |
Systemic vasodilation- hypo perfusion Decrease myocardial contractility Widespread endothelial injury and activation- systemic leukocytes adhesion and pulmonary capillary damage- ARDS Activation of the coagulation system - DIC |
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Stages of shock |
Non progressive- reflex compensation and perfusion of vital organs Progressives- tissue hypo perfusion and acidosis Irreversible- cellular and tissue injury |
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Gross pathology of shock of the kidney |
Acute tubular necrosis - destruction of the tubular epithelium cells Causes- Ischemia Direct toxic injury of the tubules- drugs contrast myoglobin radiation Acute tubulointerstitial nephritis- hypersensitive DIC Urinary obstruction- tumor BPH clot |
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Ischemic acute tubular necrosis |
Foci tubular epithelial necrosis Skip areas Tubularhexis- rupture of basement membrane Affect the proximal tubule and ascending thick limb Proximal ruble have brush borders Simplification of cell structure Cellular sweeping and vacuolization Sloughing of non necrotic tubular cell Interstitial edema Accumulation of leukocytes writhing dilates vasa recta Epithelial regeneration Eosinophilic hyaline |
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Incidence of breast cancer |
40/100000 |
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HER 2 |
Epidermal growth factor receptor Bind to tyrosine kinase increase signal transduction pathway causing cell growth and differentiation Over expression cause more aggressive worst prognosis Treat with monoclonal antibody trastuzimob |
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Site of carcinoma |
In situ- limited to the basement membrane Paget’s disease No metastatic lymph nodes or vascular involvement Invasive- invade basement membrane Metastatic invade lymph node and vascular |
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Location of breast carcinoma |
Terminal duct lobular unit |
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Ductal carcinoma in situ |
Malignancy of duct and lobules limited to the basement membrane Involve single ductal system Mastectomy cure in 90% Do no recur If recur due to residual DCIS Tamoxifen if estrogen positive |
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5 subtype of DCIS |
Comedo- central necrosis Microinvasion- foci of tumor cells less than 0.1 cm invading stroma Cribriform Solid Papillary Micropaillary |
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Lobular carcinoma in situ |
Incidental finding No calcification Affect pre menopausal women Multi centric bilateral Equal frequency in both breast Estrogen and progesterone receptors |
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Invasive breast carcinoma |
Firm hard irregular borders Irregular dense white mass with yellow adipose tissue |
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Invasive lobular carcinoma |
Meta- peritoneum retroperitoniun Leptomeningies GIT Ovary and uterus |
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Medullary breast carcinoma |
Well circumscribe Mistaken for fibroadenoma Fleshy and soft No lymph nodes Mets Good prognosis No HER2 |
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Mucinous breast cancer |
Well circumscribe Slow growing Soft Express hormones receptors Increase BRCA1 mutation |
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Specimens collection of breast cancer |
Formalin Embedded in paraffin Stain with H&E |
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Tubular breast carcinoma |
Well formed tubules No myeoepithilieal cell layer Tumor in contact with stroma Express hormone rector |
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Papillary breast carcinoma |
Fibrovascular core with features of invasion |
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Major prognosis factors for breast cancer |
Invasion and insitu Distant Mets Lymph nodes Tumor size Local advance disease Inflammation carcinoma |
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Minor prognosis factor for breast cancer |
Histological subtype- good Tumor grade Estrogen and progesterone receptor- good HER2- bad Lymphovacular invasions- bad Proliferative rate- notification count bad DNA count- flow cytometry bad |
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Differentiation |
Extent to which neoplastic cells resemble normal cell |
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Anaplastic |
Lack of differentiation |
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Lack of differentiation morphology |
Pleomorphism Abnormal nuclear morphology Mitosis Loss of polarity- grow in disorganized fashion |
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Scarf blood Richardson system for grading breast cancer |
Degrees of tumor tubular formation 1->75% 2- >10%-<75% 3-<10% Tumor mitosis activity 1- <10 mitosis in 10high power field 2- >10<20 mitosis 3- > 20 mitosis in 10 high power field Nuclear pleomorphism of tumor cell 1- cell nuclei uniform in size and shape relatively small disperse chromatin no nucleoli 2- cell nuclei pleomorphic nucleoli intermediate size 3- cell nuclei large prominent nucleoli corse chromatin vary size and shape |
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Benign breast disease |
Inflammation- acute mastitis Fat necrosis Periductal mastitis Mammary duct ectasia Non- proliferative- fibrocystic change Proliferative- proliferative change without atypia Atypical hyperplasia Benign tumors |
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Risk factors for breast cancer |
Age>64 Age of menarche- early menarche late menopause First child birth First degree relative with breast cancer Breast biopsy- atypical hyperplasia Race- black Radiation Estrogen exposure Contralateral breast cancer or endometrial cancer Diet Obesity in post menopausal women No breast feeding |
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2 types of breast cancer |
Sporadic- hormone exposure Hereditary- family history |
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Hereditary breast cancer |
Autosomal dominant BRCA1 BRCA2 BRCA1 increase risk of ovarian cancer BRCA2 in male breast cancer BRCA1- prostate colon pancreas BRCA2 prostate colon pancreas stomach metastatic melanoma |
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BRCA1 |
Poorly differentiate Syncytial growth pattern Lymphocytic response |
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Syndrome that increase risk of breast cancer |
Li fraumeni syndrome- mutation of p53 Age 45 Brain tumors soft tissue sarcoma acute leukemia Pegets disease- autosomal dominant Interstitial hamartomatous polyps with melanocytic macular |
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Risk factor for sporadic breast cancer |
Gender Age of menarche and menopause Reproductive history Breast feeding Estrogen exposure |
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Scarf bloom Richardson system for grading breast cancer |
Degrees of tumor tubular formation 1->75% 2- >10%-<75% 3-<10% Tumor mitosis activity 1- <10 mitosis in 10high power field 2- >10<20 mitosis 3- > 20 mitosis in 10 high power field Nuclear pleomorphism of tumor cell 1- cell nuclei uniform in size and shape relatively small disperse chromatin no nucleoli 2- cell nuclei pleomorphic nucleoli intermediate size 3- cell nuclei large prominent nucleoli corse chromatin vary size and shape |
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Cardiomyopathy |
Abnormality in the myocardium |
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Dilated cardiomyopathy |
Cardiac dilation and systolic dysfunction Hypertrophy Congestive cardiomyopathy 25-35% familial Causes by autoimmune chronic alcoholism myocarditis pregnancy associated nutrient deficiency 20-50 |
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Morphology of dilated cardiomyopathy |
Dilation of all chambers Mural thrombosis Functional regurgitation |
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Hypertrophy cardiomyopathy |
Thicken wall heavy hyper contracting Diastolic dysfunction Autosomal dominant Poor complimented decrease stroke volume Exertional dyspnea due to increase pressure in pulmonary vein Harsh systolic ejection murmur Angina myocardial ischemia |
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Morphology of hypertrophy cardiomyopathy |
Cardiac hypertrophy without ventricular dilation Disproportionately thickness |
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Problems associated with hypertrophic cardiomyopathy |
Infective endocarditis of the mitral valve Intractable cardiac failure Sudden death Ventricular arrhythmia Atrial fibrillation and mural thrombosis |
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Restrictive cardiomyopathy |
Decrease ventricular compliance Impaired ventricular filling during diastole Idiopathic amyloidosis sarcoidosis metastatic tumor radiation fibrosis |
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Morphology of restrictive cardiomyopathy |
Ventricle normal size Myocardium firm |
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Embolism |
Detach intravascular solid liquid gases mass carried by the blood away from its origin |
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Types of embolism |
Fat Air Cholesterol Tumor fragment Foreign body eg bullet Amniotic fluid |
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Fat embolism |
Due to long bone fracture Long bones contain fatty marrow Due to soft tissue trauma and burns |
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Fat embolism syndrome |
Pulmonary insufficiency Neurological symptoms Anemia- erythrocytes aggregation and hemolysis Thrombocytopenia- platelets adhere to globules 1-3 days after injury tachycardia tachpnea dypnea Petechial rash |
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Air embolism |
Gas bubbles obstruct vascular flow >100cc Decompression sickness- sudden change in atmospheric pressure Air breath at am I High pressure increase amount of gas(nitrogen) dissolve in blood and tissue |
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Amniotic fluid embolism |
Complication of labor and post postpartum period Seizures cyanosis dyspnea hypovolemic shock Survival pulmonary edema DIC from thrombotic substances from the amniotic fluid Indication of DIC- pulmonary edema Diffuse alveolar damage Systemic fibrin Due to infusion of amniotic fluid or fetal tissue in maternal circulation via tear of placental membrane or rupture of uterine vein |
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Component of blood vessel |
Endothelial cell Smooth muscle cells |
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Layers of the artheriosclorotic plaque |
Fibrous cap- macrophages and extracellular matrix SCM T lymphocytes Necrotic core- disorganized lipid cholesterol dead cell fibrin foam |
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Pathological changes of advance lesion of artherosclorosis |
Focal rupture ulceration or erosion Hemorrhage Superimposed thrombosis Aneurysmal dilatation |
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Non modifiable risk factor for artheriosclorosis |
Age male >45 female >55 Gender male>females = after menopause Family history Genetic abnormality |
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Modifiable risk factor for artheriosclorosis |
Hyperlipidemia Hypertension Diabetes Cigarette smoking Homocysteineuria Lipoprotein lpa |
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Function of the endothelium of the heart |
Control the transport of molecules- impermeable to large molecules(plasma protein) Maintenance of non thrombotic blood tissue interference Modification of blood flow and vascular resistance Metabolism of hormones Regulation of immune and inflammatory reaction |
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Arteriosclerosis |
Thickening and loss of elasticity of the arterial wall |
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Arteriolosclerosis |
Affect small artery and arterioles Hyaline and hyper-plastic form Thickening of the vessel wall and lumen narrow HTN and DM |
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Monckeberg medial calcific sclerosis |
>50 Calcification of the muscular arteries Radiographically visible and may be palpable Does not include vessel lumen |
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Artheriosclerosis |
Atheroma plaque Obstruct vascular lumen Weaken the media |
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6 types of artherosclorosis lesion |
Type 1- isolated macrophage foam cells Type 2- fatty streak intracellular lipid accumulation 1cm or longer Type 3- intermediate lesion- type 2 and small extracellular lipid pool Type 4- atheroma lesion- type 2 and core of extracellular lipid Type 5- fibroartheroma lesion - lipid core and fibrotic layer or mainly calcific mainly fibrotic Type 6- complicated lesion- surface defect hematoma- hemorrhage thrombosis |
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Complication of artherosclerosis |
Myocardial infarction Mesenteric ischemic Aortic aneurysms Peripheral vascular disease Stroke Sudden cardiac death Ischemic heart disease Ischemic encephalopathy |
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Gross morphology of of artherosclorosis |
Soft yellow core of lipid(cholesterol) Eccentric lesion Affect the lower abdominal aorta coronary artery |
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Components of the artheriosclorotic plaque |
Cells- SMC macrophages leukocytes Extracellular matrix- collagen elastic fibers proteoglycon Intracellular and extracellular lipid |
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Bladder obstruction |
Males BPH or cancer Due to cytocele in women from prolapse of the bladder into the vagina |
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Causes of bladder obstruction |
Congenital narrowing or stricture of the urethra Inflammatory stricture of the urethra Inflammatory necrosis or construction of the bladder Bladder cancer- benign or malignant Secondary invasion Mechanical obstruction- foreign body or calculus Injury to innervation of the bladder- neurogenic bladder |
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Gross morphology of bladder obstruction |
Thicken of the bladder wall due to smooth muscle hypertrophy Progressive hypertrophy leads to trabeculation of the wall Cryps form are converted to true diverticulum In acute obstruction no trabeculation |
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Prostate weight |
20g |
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Prostate zone |
Peripheral- cancer Central Transitional- hyperplasia Anterior |
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Benign prostate hyperplasia |
>50 Hyperplasia of the prostate stroma and epithelial cells Discrete nodules in the periurether region Nodular hyperplasia is mediated by testosterone Dihydrotestosterone mediate testosterone which cause prostate hyperplasia Synthesis by 5 alpha reductase (stromal cells) |
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Gross morphology of BPH |
Weight 60-100 In the transitional zone First stromal cells then epithelial nodules |
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Symptoms of BPH |
Compression of the urethra- difficulty urination Retention of urine in the bladder- distention and hypertrophy UTI cystitis renal infection Frequency Noctouria Dysuria Hesitant Overflow dripping Residual urine Hydronephrosis Azotemia/uremia |
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Mucinous carcinoma of the breast |
Well circumscribe Slow growing Soft with gelatin Have hormone receptor Increase BRCA 1 mutation |
