Summary Pathology PA 1 PDF

Pathology PA slides for PA ! only mag 1 Acute pulmonary edema MICROSCOPIC ONLY 1. Lung parenchyma 2....

Pathology PA slides for PA ! only mag 1 Acute pulmonary edema MICROSCOPIC ONLY 1. Lung parenchyma 2. Congested vessels 3. Anthracotic pigment ORGAN: Lungs STAIN: Hematoxylin Eosin DIAGNOSIS: Acute pulmonary edema DEFINITION: Edema (from the greek oidaein = swelling) is an abnormal collection of fluid in: tissues —> in the intercellular compartment serosal cavities —> serous effusion PATHOGENESIS of EDEMA in general: 1. Increased hydrostatic pressure —> in the capillaries, due to venous thrombosis, congestion or heart failure (e.g. venous congestion, right heart failure) 2. Decreased blood osmotic pressure —> due to hypoproteinemia (e.g. nephrotic syndrome, liver function failure, hypoalbuminemia) 3. Increased vascular permeability —> inflammation, insect bites, allergies 4. Lymphatic obstruction —> removal of lymph nodes, parasites (Filaria bancrofti), tumoral surgery ETIOLOGY of ACUTE PULMONARY EDEMA: - acute left heart failure - shock - severe forms of pneumonia - inhalation of toxic gases - substitution acute pulmonary edema or ex vacuo - acute respiratory distress syndrome (particular form of pulmonary edema caused by (ARDS) rapid therapeutic evacuation of pleural effusion) - body over hydration (iatrogenic edema) CLASSIFICATION of EDEMA: 1. Venous edema —> heart failure, venous congestion; increasing hydrostatic pressure 2. Cardiogenic edema (heart failure) —> pitting edema (finger-shaped depression), depends on the gravitation; venous congestion + decreasing of kidneys filtration 3. Hypoalbuminemic edema —> areas with loose connective tissue (eyelid, periorbital, external genital organs); liver failure, kidney lesions, enteropathy, malnutrition, starvation, cachexia 4. Edema due to increased capillary permeability —> hypoxia, toxic and allergic factors, inflammatory edema 5. Angioneurotic edema (Quincke)—> severe, generalized, sudden onset, allergy-related, larynx, lungs 6. Lymphatic edema —> Filaria parasites, Surgical removal of the lymph nodes, Congenital, Milroy disease; It can lead to elephantiasis MORPHOLOGY of EDEMA: The macroscopic changes appear when the quantity of intercellular fluid increases with 10%: swollen and pasty tissues finger-shaped depression gelatinous aspect on section The tissues can be: - blue —> venous and cardiogenic edema - pale —> hypoalbuminemic edema - red —> inflammatory edema MACROSCOPIC DESCRIPTION: Lungs: distended, hyperemic, increased volume and weight, not collapsing on the autopsy table, pink-gray color, darker in dorsal and basal areas, pasty in consistency (similar to a wet sponge) Pleura: distended, thin, transparent, smooth, and shiny, with rib imprints on the pleural surface In case of Compression of the cut section surface → elimination of a pink-red foamy, frothy fluid, containing edema fluid, a few erythrocytes, and air bubbles MICROSCOPIC DESCRIPTION: 1. LUNG PARENCHYMA —>alveolar spaces filled with a homogenous or slightly granular, eosinophilic material = edema fluid Cair would stain pinkish , but would be white —> 2 types of edema septal edema = edema fluid inside alveolar septa alveolar edema (edema fluid - transudate, quickly extravasated and therefore mixed with optically empty spaces - air bubbles, together with rare cellular elements - desquamated alveolocytes, alveolar macrophages and leukocytes) 2. CONGESTED VESSELS > - excessive accumulation of blood —> Dilated capillaries S 3. ANTHRACOTIC PIGMENT —> black color pigment resulted from inhalation of carbon particles, ingested by alveolar/interstitial macrophages and then accumulated in the connective tissue and/or regional lymph nodes  MACROSCOPIC and MICROSCOPIC 2 Lung infarction + Chronic pulmonary congestion Respiratory epithelium lining a bronchial branch 3 1. Infarcted area 2. Chronic pulmonary congestion 3. Hyperemic narrow rim 3. Trachea (macro) ORGAN: Lungs STAIN: Hematoxylin Eosin DIAGNOSIS: Lung infarction + Chronic pulmonary congestion DEFINITIONS: INFARCTION —> (from the latin in-farcire = stuffed) tissue death/ necrosis due to insufficient arterial/oxygenated blood supply, as result of sudden vascular occlusion, more frequent of an artery, within the living body CONGESTION —> Congestion is a passive process resulting from reduced venous outflow of blood from a tissue. It can be systemic, as in cardiac failure, or localized, as in isolated venous obstruction. PATHOGENESIS of CONGESTION in general: - heart failure - restriction of respiratory movement - compression of the cava vein ETIOLOGY of CHRONIC PULMONARY CONGESTION: - chronic left ventricular failure - mitral stenosis / incompetence CLINICAL FEATURES: CONGESTION —> dyspnea, cough, clubbing fingers (chronic hypoxia); —> on auscultation → crakles (air bubbling and fluid) INFARCTION —> pyramidal shape, wedge-shaped, triangular (occluded vessel located on the apex) - early infarct: bulging area delimitated by a hyperemic narrow rim - old infarct: retracted scar tissue EVOLUTION/COMPLICATIONS: CONGESTION —> superinfection, pulmonary fibrosis, chronic cor pulmonale INFARCTION —> organization / scaring, encapsulation, ulceration (cavity), superinfection (abscess) CLASSIFICATION: CONGESTION —> Acute pulmonary congestion: alveolar capillaries engorged with blood, serum extravasation (due to increased intracapillary hydrostatic pressure and increased capillary permeability), alveolar and septal edema —> Chronic pulmonary congestion: pulmonary fibrosis, sclerosis (septa thickening) + intraalveolar and septal hemosiderin laden macrophages, brown induration of the lungs INFARCTION —> White / anemic infarct: in solid/compact tissues, such as Myocardium (heart attack), Spleen, Kidney, Brain (liquefactive necrosis), Liver (hepatic artery), Limb (gangrene) —> Red (hemorrhagic) infarct: in spongy tissues with dual or collateral circulation, such as Lungs and Intestine —> Zahn infarction: pseudo-infarction in the Liver, caused by portal vein obstruction; the area of congestion, atrophies, but no necrosis MACROSCOPIC DESCRIPTION: 1. Infarcted area (triangular shape, with the tip pointing towards the hilum -> occluded vessel, well defined, dark red color) 2. Chronic pulmonary congestion (increased weight, brown color due to the presence of siderophages, firm consistency = brown induration) 3. Trachea MICROSCOPIC DESCRIPTION: 1. Infarcted area —> well defined, red color, due to erythrocyte flooding, with preserved alveolar architecture, but loss of nuclei - “ghost-like appearance” or „Hiroshima effect“ indicating the necrosis 2. Chronic pulmonary congestion —> thick fibrotic interalveolar septa, due to hypoxia and reaction to deposited hemosiderin and cardiac cells/ heart failure cells/siderophages 3. Hyperemic narrow rim —> hypercellular area separating the infarcted tissue from the surrounding parenchyma, composed of congested vessels, extravasated erythrocytes and acute inflammatory infiltrate —> it is the area where the granulation tissue starts forming, so there are many macrophages, fibroblasts, fibrocytes and leukocytes  MICROSCOPIC ONLY. 3 Pulmonary thromboembolism 1. Bronchial lumen 2. Anthracotic pigment, lymph node 3. Large branch of the pulmonary artery, containing a thromb-embolus M ORGAN: Lung STAIN: Hematoxylin Eosin DIAGNOSIS: Pulmonary thromoembolism (deep vein thrombosis of the leg ) DEFINITION / PATHOMECHANISM of THROMBOEMBOLISM: 1. Thrombus detachment 2. Migration – usually anterograd 3. Lodge (fixation), which can result in a - blocking embolus - “saddle” embolus (across the bifurcation) CONSEQUENCES of THOMBOEMBOLISM: - acute respiratory and cardiac disorders - ischemia, necrosis (infarction) - congestion (lung) - sudden death (pulmonary embolism) - bacterial (infective) emboli - abscesses  MACROSCOPIC and MICROSCOPIC 4 Chronic hepatic congestion 1. Hyperemic areas in the center of the hepatic lobules 2. Normal, preserved hepatocytes 3. Portal space/triad ORGAN: Liver STAIN: Hematoxylin Eosin DIAGNOSIS: Chronic hepatic congestion DEFINITION: *See slide 2 of Chronic pulmonary congestion ! * (the right ) ! ETIOLOGY: Right ventricular failure liver is on the PATHOMECHANISM of HEPATIC CONGESTION: 3 stages 1. Acute congestion The central veins (CLV) of the hepatic lobules are dilated and filled with erythrocytes —> Macroscopic view: Enlarged liver on section alternance between yellow (hepatic parenchyma) and red areas (dilated central veins and surrounding sinusoid capillaries) —> Microscopic view: distended central vein and sinusoids in hepatic lobules cockade appearance 2. Chronic congestion Sinusoid capillaries (C) are also dilated and the nutmeg liver aspect can be observed —> Macroscopic view: „Hemorragic bridges“ = alternation between yellow (hepatic parenchyma) and red color (dilated capillaries) —> Microscopic view: dilatation of the central veins and sinusoid capillaries and their fusion with neighboring lobules nutmeg liver 3. Persistent congestion or Cardiac Cirrhosis Pale areas of fibrosis (F) replace the congested areas (here the hepatocytes are destroyed) —> Macroscopic view: fibrosis (liver induration), followed by regeneration of the liver parenchyma (cardiac cirrhosis) fern (felce) appearance —> Microscopic view: Areas of fibrosis = connective tissue; Destruction of hepatocytes in those areas MICROSCOPIC DESCRIPTION: In the nutmeg liver we can observe fragments of hepatic parenchyma showing numerous hyperemic areas alternating with normal-looking areas. 1. Hyperemic areas in the center of the hepatic lobules: Dilated central veins of the hepatic lobules and sinusoid capillaries from which erythrocytes were extravasated; Hepatocytes suffer from hemorrhagic / coagulation necrosis 2. Normal, preserved hepatocytes at the periphery of the hepatic lobules, in the periportal areas 3. Portal space/triad