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pathologies are treated in this summary, no tumors are wri5en: they will be summarized in a single table

Insane graphic review for the 2 semester exam Alessandro Mo5a, UVVG, 3rd year 1

Cardiac Pathology

Cardiac Pathologies

Rheuma;c Pericardium Myocardium Endocardium Valves

Ischemic Heart Disease

Ischemic heart disease is caused by the interrup;on, par;al or complete, of arterial blood ow to the myocardium. Disease begins to manifest when coronary blood supply no longer sa;sfy the oxygen demand myocardium. The main cause that generates cardiac ischemia is coronary atherosclerosis (narrowing of the of arterial lumen by plaque), some;mes aggravated by arterial spasm or a process of superimposed thrombosis. Cardiac ischemia may be silent or may manifest clinically in several forms: angina pectoris, myocardial infarc;on, chronic ischemic heart disease.

Angina pectoris: transient painful crises localized predominantly precordial, three types of angina: Stable angina is usually under 15 minutes, triggered by factors that overload heart (emo;ons, exercise) and resolves at rest and administra;on of coronary vasodilators (nitroglycerin); Instable angina (premyocardial infarc;on, aggravated angina) is caused by the forma;on of a non-obstruc;vely thrombus superimposed to a plaque. Prinzmetal angina is an unusual form of angina that occurs at rest, oRen during sleep, caused by arterial spasm superimposed to a atherosclerosis lesions.

Myocardial infarc6on is the most important cause of morbidity and mortality in modern society. Is an expression of brutal, complete and persistent interrup;on of blood ow through a coronary artery branch, which translates morphologically by necrosis of myocardial territory served by that artery. Comes with Atherosclerosis + superimposed thrombosis, hemorrhage into plaque, persistent arterial spasm, arteri;s, congenital coronary anomalies etc. Lab ndings: raised LDH, CPK. Types: transmural subendocardial. Chronological morphology changes: 1. First 12 hours: no macroscopical changes 2. In 1-2 days: swollen, pale yellow central area, raised neutrophils ac;on 3. In 3-7 days: necrosis area become yellowish, macrophages replace neutrophils, granula;on ;ssue forma;on 4. In 2-3 weeks: depressed area with soR texture 5. In 4-5 weeks: hard scare area, retracted, pale gray

Chronic ischemic heart disease denes slow installa;on of conges;ve heart failure due to myocardial altera;ons by chronic ischemia. Most of these pa;ents have a history of episodes of angina pectoris or myocardial infarc;on. The heart has variable dimensions, myocardium has a brown color and can some;mes be iden;ed area of infarc;on with dierent 2 seniority. There is always advanced lesions of atherosclerosis of the coronary arteries.

Cardiac Pathology

Rheuma;c Heart Disease

Is a systemic inammatory disease of connec;ve ;ssue, aects children from 5 to 15 years old, symptoms starts aRer 1-4 weeks from a tonsilli;s contrac;on, usually comes with streptococcal infec;ons. The Acute form (rheuma6c fever) has some extra-cardiac manifesta;ons such as: large joints impairments, tegumentary impairments and neurological damage. Cardiac manifesta;ons (rheuma;c pancardi;s) has rheuma;c involvements such as pericardi;s, myocardi;s (with Ascho granulomas) and endocardi;s. The Chronic phase is a sequel of the acute one and triggers valvular deforma;ons, CHF, endocardi;s and thromboembolism. Called eusions, triggers hydropericardium, haemopericardium and chill eusion (lymph). The accumula;on can be from 50 to 2000 ml with or without clinical manifesta;ons Acute: by biological factors, can be in form of: serous, brinous, suppura;ve or hemorragic. in Chronic one we nd a thick peritoneum, constric;ve, brous; triggered by TBC, staphylococcal sep;cemia and radioteraphy Conges6ve/dilata6ve: is the most common, triggered by alcohol/ drugs, dilata;on occurs in both ventricles, HF in 5 years Hypertrophy: in young pa;ents, for long ;me asymptoma;c, gene;c causes are studied, decreases the intraventricular volume Restric;ve: limi;ng diastolic lling, generate atrial dilata;on and retrograde venous stasis, bring to a global HF


Non- inammatory Inammatory

dis;nct group of primi;ve disease of the heart muscle that did not cause inamma;on and are not associated with hypertension, congenital heart disease, valvular or coronary artery disease. It is characterized by heart failure, ventricular volume and increased ventricular arrhythmias.


Dened as generalized inamma;on of the myocardium. Are classied into two broad categories, rheuma;c (discussed before) and non-rheuma;c such as: 1. Viral (toxic): by HIV, inuenza virus, generally reversible, worse in children and pregnancy status 2. Non-Viral: divided in bacterial, driven by hypersensivity to medicaments and a rare giant cells myocardi;s

Cardiac Pathology

Non-infec6ous may also be of several types: Non-bacterial, associated with metasta;c cancer Libman-Sacks, associated with SLE and valvular vegeta;on progress From Carcinoid Syndrome, genera;ng endocardial plaques at RH Valves

Infec6ous caused by bacterial coloniza;on, rarely fungal, of endocardium, with a severe impairment of valvular apparatus. Acute Bacterial, or ulcera;ve is driven by Staphylococcus Aureus and detroys the valves un;l the HF Sub-Acute Bacterial, or polypous is caused by streptococcus Viridians and triggers a polypoid vegeta;on that generate embolism

Mitral Stenosis is caused usually by rheuma;c diseases, the blood ow from LA to LV diminishes, ini;ally triggers an atrial dila;on, in ;me hypertrophy and pulmunary stasis with risk of pulmunary edema. Mitral Insuciency a very common valve disease, generated by a mitral prolapse or papillar muscle rupture, blood regurgita;on in systole triggers LV hypertrophy and LA hyp.

Tricuspid or pulmonary ones are very rare, associated with mitral problems. Pulmonary can be aected in congenital or in Fallots tetralogy Aor6c Stenosis is caused usually by calcica;ons or congenital condi;ons such as bicuspid valve. Blood ow diminishes from LV to Aorta, triggers a markes LV hypertrophy and bovine heart in radiology ndings

Aor6c Insuciency may be congenital or aRer a syphili;c aor;;s, blood regurgitates from Aorta to LV

Congenital Heart Diseases

Abnormali;es of embryonic development by gene;c causes or viral infec;ons or teratogen substances. With Blood Shunts from L to R side we nd ventricular septal defects, interatrial septal defects, fetal ductus arteriosus that trigger a late cyanosis. From L to R but with early cyanosis = Fallots tetralogy: pulmonary stenosis, v.septal defect, Dx posi;on of the Aorta, right ventricular hypertrophy. Without blood shunts there are transposi;ons of great vessels, coarcta;on of the Aorta and Situs Inversus (dextrocardia) Dened as the inability of the heart to deal with the body's demands, on the LEFT side is triggered by: ischemic heart disease, MI, arterial hypertension, valvulopathies, myocardiopathies. Generates dispnea, pulmonary edema, hydrothorax, low renal perfusion, cerebral anoxia. On the RIGHT side can be triggered by a previous leR heart failure, a pulmunary vascular hypertension, valvulopathies, cardiomyopathies. Triggers 4 peripheral edema, ascites and hepatomegaly

Heart Failure

Vascular System

Arteriolo-sclerosis can be divided in: Hyaline, in chronic ischemia, benign nephroangiosclerosis Hyperplas;c, a concentric thickening of arterioles walls, reduced lumen and malignant nephroangiosclerosis

Atherosclerosis or atheromatosis, has a mixed and not fully elucidated pathogenesis, has various risk factors (hypercholesterolemia, high LDL concentra;ons, hypertension, diabetes, aging, sex=male, smoking). Lesions are founded in the in;mal layer of arteries (atheromas) and are brino-lipidic plaques (with a lipidic center and a ibrous capsule). Evolu;ons: calcica;on, ulcera;on, superimposed thrombosis (occlusion of the arteria), hemorrage, aneurysm. Clinical manifesta;on: MI, chronic ischemia, aneurysm, emboliza;on

Inamma;on may begin in in;ma, media or adven;;a (at the level of vasa vasorum) of the arteries. In terms of these loca;ons can dis;nguish: endarteri;s, mesarteri;s or periarteri;s. Arteri6s types: Thromboangi;s obliterans, named Buergers Disease Polyarteri;s Nodosa Syphili;c Arteri;s Raynauds disease

Abnormal dilata;ons, localized, permanent of the blood vessels Atherosclero;c Celebral Dissec;ng (aorta) Arteromatous Fistula (post- trauma;c) Syphili;c

Venous Thrombosis
Forma;on of thrombi, oRen in the deep veins of the lower limbs. The process is favored by the stasis at this level caused by impeding of venous return as a result of heart failure, pregnancy, prolonged bed repose or varicose veins. Thrombophlebi6s, comes with inamma;on and can be divided into: bacterial, intravenous chemical irrita;on and post-trauma;c. Phlebothrombosis, in turn, comes without inamma;on, it can be post-opera;ve, obstetrical, medical- associated and migratory

Varicose Veins

Are abnormally dilated veins, with a tortuous course, mainly are founded in lower limbs, but we can also nd them in form of esophageal varices (portal hypertension), hemorrhoids and varicocele

Respiratory System

Respiratory System Pathologies

Bronchi Pulmonary Parenchyma Pleural

Upper Resp. Tract

Rhini6s are inamma;on of the nasal mucosa. Can be acute and chronic. Acute rhini;s, in turn, can be: Acute viral rhini6s (common cold) is caused mainly by adenoviruses. It manifests clinically with increased nasal secre;on, nasal conges;on, sneezing. Morphological substrate is represented by an acute catarrhal inamma;on of the nasal mucosa; Allergic rhini;s is caused by a type I hypersensi;vity reac;ons (IgE), following exposure to various an;gens: pollen, dust, our etc. Is manifested by abundant watery nasal secre;on, sneezing crisis. Specically, is the appearance of inammatory inltrate rich in eosinophils in the nasal mucosa; Bacterial rhini;s usually occurs as a complica;on of forms described above, characteris;c is the transforma;on of inammatory exudate from a watery into a purulent one. Chronic rhini6s, can also be of two types: Hyperplasic chronic rhini;s occurs due to repeated nasal inamma;on. It is characterized by hyperplasia of mucous glands some;mes realizing real adenomatous polyps that can extend up to the throat. They appear as mul;ple, soR, pedicled forma;ons, with bunch of grapes-looking. Chronic atrophic rhini;s (ozena) is also a possible consequence of repeated acute inamma;on. Is manifested by diminishing sense of smell due to pavimentosase metaplasia, brosis and reducing of the mucous glands. Laryngi6s are inamma;on of the larynx. May be acute or chronic. Of acute laryngi;s, the most important forms are: Catarrhal laryngi;s is in most cases caused by a viral infec;on (inuenza virus). Manifested clinically by dry throat and hoarseness. Morphologically is characterized by edema and hyperemia of the laryngeal mucosa, mucous exudate which, due to microbial superinfec;ons, becomes mucosal-purulent; Laryngeal diphtheria is now rare. It is an acute pseudomembranous inamma;on of the larynx, has a par;cular severity due to possible mechanical asphyxia;on through membranes of the pa;ent. Chronic laryngi;s may con;nue acute forms, or may have chronicity characters from the beginning, because local ac;on of chronic irrita;ve factors (smoking, pollu;on). Is manifested by hoarseness and irrita;on spas;c cough. Morphological can be described two forms: Hyperplasic laryngi;s with thickening of the pharyngeal mucosa. Some;mes may occur localized hypertrophy, pseudotumoral (singers nodules); Atrophic, dry laryngi;s. 6

Respiratory System

Bronchial Diseases

Bronchi6s are inamma;on of the large and medium bronchi. May be aected concomitant and trachea, in which case we speak of a tracheobronchi;s. Can be acute and chronic. Acute bronchi;s are ini;ated by microbes (pneumococcus, streptococcus, etc.), viruses (inuenza), or may have cause by irrita;on (pollu;on). Depending on the quality of inammatory exudate, are described several types of acute bronchi;s: catarrhal bronchi;s, ini;ally manifested by conges;on, edema and hypersecre;on of mucus, while in advanced stages occur and serous exudate. Soon there will be a microbial superinfec;on, exudate becoming purulent due to the inux of granulocytes; ulcera;ve bronchi;s is a more severe form, characterized by the occurrence of ulcers of variable depth in bronchial mucosa, at which are some;mes associated processes of necrosis and hemorrhage; pseudomembranous bronchi;s (diphtheria); gangrenous bronchi;s is rare, occurs consecu;vely to malignant tumors, infec;ons with anaerobic streptococci etc. Bronchial mucosa shows extensive necrosis with deposit of brin, necro;c material, microbial colonies. Chronic bronchi6s is characterized clinically by the appearance of more than 2 years consecu;vely of episodes of produc;ve cough for at least 3 months. It is par;cularly common in smokers and those who live in polluted urban environments. The disease is manifested with hypersecre;on of mucus, and as a result of microbial superinfec;on, there is a mucosal-purulent exudate. The main complica;ons of chronic bronchi;s include: pulmonary hypertension with cor pulmonale occurrence; squamous metaplasia of ciliated bronchial epithelium, with possibility of developing malignancies. Asthma is clinically manifested by dyspnea crisis and expiratory wheezing. From e;opathogenic point of view can be described two types: extrinsic asthma, is based on a type I hypersensi;vity reac;on, begins in childhood and usually there is an allergic family history; intrinsic asthma occurs in adults, can not be iden;ed an allergic factor and usually complicates a chronic bronchi;s. Morphologically, is characterized by hypersecre;on of mucus, by bronchial gland hyperplasia, inammatory inltrate rich in eosinophils, basement membrane thickening and bronchial muscle hypertrophy. Sputum of the pa;ents contains Charcot-Leyden crystal, produced by the disintegra;on of eosinophils. Bronchiectasis implies the existence of abnormal, persistent dilata;on of bronchi. Can be caused by several factors: sequelae of some suppura;ve pneumonia, inuenza, whooping cough; mechanical bronchial obstruc;on caused by tumors, foreign bodies etc.; congenital diseases: muciviscidosis, Kartagener syndrome (sinusi;s, situs inversus and congenital bronchiectasis by immobility cilia of bronchial epithelium). Bronchial dila;on is called bronchiectasis cavity. They can have diuse or localized character, can be single or mul;ple and may have dierent shapes: cylindrical, saccular or moniliforme (dilated por;ons alterna;ng with unaected por;ons). Bronchiectasis cavity is ini;ally dry, smooth, and aRerwards to ll with stagna;ng mucus. This mucus causes obstruc;on of the terminal bronchi and promote microbial superinfec;on, with the appearance of purulent secre;ons. Epithelium bordering the cavity is converted to metaplasia, and nally to atrophy. Bronchial wall is the seat of chronic inamma;on, with atrophy of the elas;c bers, muscle and mucous glands. In advanced stages occurs granula;on ;ssue prolifera;on with replacement brosis. 7

Respiratory System

Pulmonary Parenchyma


Represents inammatory diseases of pulmonary parenchyma. Are caused by microbial or viral germs. Morphopathological subtypes: Lobar pneumonia represents the classic form of bacterial pneumonia, and is mainly caused by pneumococcus (Streptococcus pneumoniae). Currently complete evolu;on of the disease is rare, due to an;bio;c therapy. Clinically manifests with fever, chest pain and cough with sanguinolent sputum. The disease is limi;ng to a single pulmonary lobe (lobar pneumonia), oRen inferior, rarely more lobes. The star;ng point of the disease is pulmonary alveoli. Untreated, in terms of morphology, evolving into four phases: acute conges;on, red hepariza;on, grey hepariza;on, resolu;on. Lobular pneumonia (bronchopneumonia) usually occurs in debilitated persons, children and old, as a result of infec;on with pyogenic streptococci, Staphylococcus aureus, Klebsiella pneumoniae, etc. Unlike lobar pneumonia, the star;ng point of infec;on is bronchioles, with secondary extending in alveoli. Are aected more pulmonary lobules, which appear as outbreaks of condensa;on. Microscopically, bronchopneumonia outbreak appear centered by a bronchiolus with purulent bronchioli;s lesions. It is surrounded by alveoli with various types of pulmonary alveoli;s, which severity diminishes from the center to the periphery. Inters66al pneumonia is commonly caused by viral infec;on (inuenza virus, adenoviruses, etc.) or Mycoplasma pneumoniae. Pulmonary morphological changes occurring can be systema;zed as follows: inters;;al lesions, thickened alveolar septa, with dilated vessels and monocyte inammatory inltrate, without granulocytes; necro;zing bronchioli;s lesions, some;mes with the appearance of mul;nucleated giant cells; alveoli contain edema uid, red blood cells, brin. Pulmonary emphysema is permanent dila;on of terminal respiratory bronchioles and alveoli of the lungs. Disease pathogenesis is not fully elucidated. It is assumed that altera;on of alveolar walls may be caused by the ac;on of proteoly;c enzymes such as elastase, which destroys the elas;c bers at this level.

Pulmonary TBC
Primary tuberculosis in terms of morphology is characterized by the appearance of primary tuberculosis complex (Ranke), consis;ng of three elements: primary aect (Ghon) consists of an area of caseous necrosis with peripheral tuberculous follicles, most commonly localised subpleural the middle por;on of the right lung; connec;ng lymphangi;s: tuberculous follicles along the eerent lympha;cs of primary aec;on; hilar adenopathy, with the presence of prolifera;v-altera;ve lesions in the lymph nodes, tributary to the damaged lympha;cs. Secondary tuberculosis (postprimary) develops most oRen in debilitated persons, immunized by prior infec;on. Source of bacilli may be endogenous (reac;va;on of latent lesions from primary disease) or can talking about exogenous contamina;on by inhala;on of bacilli. The lesions begins in the best aerated pulmonary areas (apical posterior part), in the form of aggregates of tuberculous follicles (Simon outbreak). Follicles conuence and soon occurs their caseous necrosis. 8

Respiratory System

Pneumoconiosis are professional pulmonary disease caused by inhala;on of various anorganic powders. Severity of lesions is variable, depending on the type of dust, their concentra;on, dura;on of exposure and the coexistence of other pulmonary lesions. Types: Silicosis, Anthracosis, Asbestosis

Inammatory Types: Sero-brinous pleurisy can occur in rheuma;sm, uremia, tuberculosis, or may be a complica;on of pneumonia. It is characterized by the appearance of an intracavitary serous exudate, with brinous inamma;on of pleural serous. Hemorrhagic pleurisy, with exudate rich in erythrocytes, can occur in tuberculosis, mesothelioma, pulmonary infarc;on; Purulent pleurisy (pleural empyema or piotorax) appears in pleuro-pulmonary infec;on with pyogenic germs. Non-inammatory pleural eusion: Hydrothorax is characterized by the accumula;on of transudate in pleural cavity. Hemothorax represent accumula;on of blood in pleura, usually as a result of thoracic trauma or rupture of a aor;c aneurysm; Chylothorax consists in accumula;on of of lymph in pleura due to an obstruc;on of the thoracic duct; Pneumothorax is represented by the presence of air in the pleural cavity. Depending on the mechanism can be described several types: spontaneous, trauma;c or therapeu;c.

Gastric Pathology


gastric mucosal erosions small focal defects of substance in the gastric mucosa Usually supercial, may extend to the serous

Idiopathic: Supercial gastriHs is a mild form, characterized by a chronic inammatory inltrate in the

Pep;c Ulcer

lamina propriae. Glands are not aected. Atrophic gastriHs, advanced stage. It is characterized by extensive inammatory changes in the deeper gastric mucosa. Autoimmune: (Type A) occurs due to the presence of an;bodies against parietal cells, and will be complicated with achlorhydria and pernicious anemia. Lesions are located on the gastric fundic level, being similar to those seen in idiopathic gastri;s. Infec6ous: (type B) is produced by Helicobacter pylori, present lesions of chronic supercial gastri;s located in the antrum and gastric body. Germs can be iden;ed in gastric mucus and, in ac;ve forms, appear granulocytes in the neck of glands. Hyperplas6c: (Menetrier) is characterized by a highly expressed thickening of the gastric mucosa, the presence of giant folds that give the gastric area a cerebroid aspect. It is considered a precancerous condi;on. Is usually localized on the low curvature, in antral and pre-pyloric region. Appears as a solu;on of con;nuity (crater), usually single, rounded, with a diameter of 2-3 cm, with net, prominent margins. Gastric mucosa folds converge towards ulcer. Gastric wall penetra;on is variable, ulcers can have dierent depths. Some;mes there are overcoming all the structures of stomach, the basis of ulcer being composed of a rough brous ;ssue block (callos ulcer). Microscopically, the basis of gastric ulcer consists of four layers. They are, from surface to depth: Supercial, an area with brino- Gastric leukocyte exudate, area of brinoid necrosis, area of granula;on ;ssue, area of brous ;ssue with inammatory inltrate. Caused by increased acidifying of duodenal environment. Frequently, it is localized on the anterior or posterior wall of the duodenum, in the post-pyloric area. Usually unique, but there are also double duodenal ulcers, situated opposite on the anterior and posterior wall (ulcers in the mirror). Complica;ons: Haemorrhages: from occult bleedings to massive blood loss (haematemesis or melaena) Perfora6on: more common in duodenal ulcers (peritoni;s) Penetra6on -> (liver, pancreas). Pyloric stenosis, due to ulcer healing, with occurrence of a retrac;le brous scars. 10


Intes6nal Pathology

Crohn's disease

Chronic inammatory disease of unknown e;ology that can aect the en;re gastrointes;nal tract, but especially the terminal ileum and colon. The disease has two specic features: the inammatory process aec;ng all layers of the intes;ne and segmental nature of the lesions (impaired segments of intes;nes alterna;ng with unaected areas). Macroscopic interested segments: appear thickened, swollen with narrowed lumen, on mucosal surface occurs linear ulcera;on that gradually became deeper, and can be transformed into stulas. Can occur mesenteric lymphadenopathy. Microscopically, it is found: the presence of a polymorphous inammatory inltrate, a brosis process that interests all intes;nal structures, oRen can be observed non-caseous granulomas; Crohn's disease can rarely develop into a cancer of the small intes;ne or colon.

Ulcera6ve Coli6s
Chronic inammatory disease of the colon of unknown e;ology that aects young adults. 3 specic morphological features that allow dieren;al diagnosis compared to Crohn's disease: impairment limited to the colon, from ileo-cecal valve up to anus, the rectum is the most severely aected, and the small intes;ne is not interested; lesions have diuse character and not segmental character; lesions interest colon mucosa and submucosa, extending in depth is excep;onal. Macroscopically, aected the mucosa is rst red, granular and bleeds easily at touch. Then appear supercial ulcers that extend into the surface, surrounded by thickened, hyperplasic intes;nal mucosa, which protrudes into the intes;nal lumen (inammatory pseudo- polyps). Microscopically there is a congested mucosa, swollen with par;ally destroyed epithelium; are iden;ed hemorrhagic suusions and lympho-plasma cells inammatory inltrate. Specic is glandular crypts impairment, with appearance of granulocyts inammatory inltrate with large areas of necrosis (cryp;c abscesses). In advanced stages colon becomes atrophied, with the persistence of a chronic inammatory inltrate in the mucosa and submucosa.

Acute Appendici6s
Exuda;ve inamma;on of the ileo-cecal appendix. Frequently occurs consecu;vely to the appendicular orice obstruc;on through fecal (solidied faecal material), hyperplasia of lymphoid structures from appendicular wall, etc. This process promotes stagna;on of secre;ons, intense prolifera;on of local microbial ora and nally, bacterial invasion of the wall, with the massive inux of polymorphonuclears. Morphology types: conges;ve appendici;s characterized by distended appendix, congested; phlegmonous appendici;s, the whole appendicular wall is purulent inltrated; gangrenous appendici;s, characterized by the appearance of hemorrhagic ulcera;on of the mucosa and areas of gangrenous necrosis of the wall. Complica;ons of acute appendici;s are oRen serious: perfora;on, usually followed by the appearance of a purulent peritoni;s; sep;c thrombophlebi;s of meso appendicular vein with 11 pylephlebi;s and secondary liver abscess.

Urinary Tract

Types of Nephropathies

Glomerulonephri6s With nephro;c syndrome With nephri;c syndrome Chronic

Acute tubular necrosis Ischemic necrosis Nephrotoxic necrosis

Nephroangiosclerosis Benign Malign

Pyelonephri6s Acute Chronic

Most glomerulonephri;s are the result of immunological mechanisms, the most commonly involved of which are:deposit of circula;ng immune complexes in the glomeruli; local forma;on of immune complexes by reac;on between a circula;ng an;body and an an;gen from glomerular basement membrane; ac;va;on of alterna;ve pathway of complement; cell-mediated immunological mechanisms. Glomerulonephri6s characterized by nephro6c syndrome: Nephro;c syndrome is a group of pathological condi;ons arising as a result of increased basement membrane permeability by the glomerular capillary level. It is characterized by: proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia and hypercholesterolemia. In this category can be classied: Glomerulonephri6s with minimal change (lipoid nephrosis) aects young children and is the prototype disease characterized by nephro;c syndrome. Glomerulonephri6s with focal and segmental lesions may appear as a primi;ve disease (idiopathic) or as a consequence of systemic disease with glomerular involvement (polyarteri;s nodosa, subacute bacterial endocardi;s and so on). Membranous glomerulonephri6s is the main cause of developing nephro;c syndrome. E;ology is unknown and aects young adults. Some;mes there is an associa;on with hepa;;s B, syphilis, malignancy, systemic lupus. Is characterized by marked thickening (5-10 ;mes), regular and diuse of glomerular capillary basement membranes due to deposits at this level of electrondense immune complexes.
Glomerulonephri6s secondary to systemic diseases: diabe6c nephropathy is characterized by glomerulosclerosis, which may be diuse (diuse mesangial hyaline deposits) or nodular (nodular mesangial hyaline deposits - Kimmels;el-Wilson nodules). Are associated with diabe;c microangiopathy, tubular atrophy, brosis and lympho-plasma cell inters;;al inammatory inltrate. amyloid nephropathy occurs in a systemic amyloidosis. Is characterized by amyloid deposit predominantly sub-endothelial and mesangial, with gradual replacement of the en;re glomerular structures. Lesions aec;ng almost all glomeruli in varying degrees.


Glomerulonephri6s characterized by nephri6c syndrome These glomerulonephri;s are caused by inamma;on, leading to glomerular capillary rupture with subsequent hemorrhage in the urinary tract. Nephri;c syndrome is characterized by the following elements: haematuria, oliguria, azotemia, hypertension. Proteinuria and edema may occur, but low intensity. The main types of glomerulonephri;s in this category are: Poststreptococcal acute glomerulonephri6s is most oRen a sequel of an infec;on (common tonsillar) with -hemoly;c streptococcal group A. Renal impairment occurs aRer a period of 1-2 weeks, pathogenesis being by circula;ng immune complex deposit. In children evolu;on is usually favorable, but in adult renal failure may occur. Aected kidney is hypertrophied, turgid, edematous, the surface is smooth with numerous haemorrhagic points which correspond to aected glomeruli. Glomeruli are aected diusely, being hypertrophy and hypercellularity. Subacute glomerulonephri6s (rapidly progressive) is characterized by severe evolu;on with the advent of early renal failure. Can occur poststreptococcal associated with some system diseases, or may be idiopathic. Aected glomeruli are hypertrophy, hypercellularity and may develop thrombosis and capillaries necrosis. Typically, there is a prolifera;on of parietal cells of Bowman capsule with forma;on a mul;layer structure that lls the ltering space, called epithelial crescent. Goodpasture's syndrome is most commonly seen in men around the age of 20 years. Pathogenically is characterized by development of an;bodies with anity for glomerular and pulmonar alveoli basement membranes. Clinical is manifested by glomerulonephri;s and pneumonic syndrome. Chronic glomerulonephri6s Chronic glomerulonephri;s is the nal stage of evolu;on of various glomerulopathies, clinically characterized by the occurrence of renal failure. Aected kidney is hypotrophy, increased consistency and nely granular surface on sec;on (small kidney, white, granular). The capsule is adherent and on sec;on surface there is a thin cor;cal, poorly demarcated from medullary.

Acute tubular necrosis is the major cause of acute renal failure. Acute tubular necrosis may be the result of prolonged renal ischemia or the ac;on of nephrotoxic substances. Ischemic necrosis is a result of shock of dierent e;ology, characterized by severe renal hypoperfusion: hemorrhagic shock, post trauma;c shock, hemoly;c shock (incompa;ble perfusions), the shock caused by extensive burns or crush syndrome, endotoxic shock (Sepsi with gram nega;ve germs) and so on Aected kidney is hypertrophied, swollen, and on the surface of sec;on there is a clear demarca;on between cor;cal and pale congested medullar. Inters;;um is swollen with discreet granulocytaire inltrate. Nephrotoxic necrosis is caused by direct ac;on of a toxic substances on tubular epithelium (an;bio;cs, cytosta;cs, anesthe;cs, mushroom toxins, venom and so on). Microscopically, is shows extensive necrosis of tubal epithelium, more expressed in proximal tubules. Tubulorexis lesions are much less common than in acute tubular necrosis due to ischemia. 13

Caused by arterial hypertension. Benign nephroangiosclerosis is caused by ischemia consecu;vely to atherosclerosis and arteriolosclerosis that aects renal vessels. Small arteries and arterioles undergoes a process of hyaline arteriolosclerosis. Interlobular and arcuate large arteries shows a characteris;c lesion that consists in duplica;on of elas;c lamina, brous ;ssue hypertrophy of the media, with narrowing of vasucular lumen (broelas;c hyperplasia). These lesions expand over ;me and at glomerular capillaries, leading to complete atrophy of the aected glomeruli. Renal tubules are atrophied or hypertrophied properly and inters;;um presents brosis with lympho- plasma cell inltrate. Malign nefroangiosclerosis is characterized by the appearance of hyperplas;c arteriolosclerosis. This consists in concentric thickening, in overlapping sheets (in onion bulb) of walls of arterioles, with consecu;vely reduc;on of the vascular lumen. Some;mes it can appear brinoid necrosis (necro;zing arterioli;s) and thromboses of aerent glomerular arterioles. These lesions extend to the glomerular capillaries, causing hyalinisa;on of glomeruli. Tubules have varying degrees of atrophy and inters;;um presents lympho-plasma cell and 14 granulocyte inammatory inltrate.

Acute pyelonephri6s is caused by bacterial infec;on propagated either by hematogenous path in the course of sepsis, either by ascending path from the urethra, usually involving Escherichia coli. Are most commonly aected women, especially during pregnancy. Clinically, the disease is manifested by pollakiuria, dysuria, pyuria, hematuria and bacteriuria. In ascending infec;ons appears a purulent exudate in the calix and pelvis renalis. In renal parenchyma is observed radial purulent stria;ons from pelvis renalis into cor;cal, that can join, producing a renal abscess. Infec;ons by hematogenous path are leading to microabscesses disseminated in all renal parenchyma. Microscopically, there is a granulocyte inammatory inltrate of variable intensity that ini;ally interested pyelocalyceal inters;;um 14 and mucosa. Chronic pyelonephri6s may con;nue an acute inamma;on or may have from the beginning characters of chronicity. Is an important cause of chronic renal failure. Aected kidney is small, with irregular surface due to retrac;le scars consecu;ve healing of acute phase injuries. The capsule is adherent and pyelocalyceal mucosa is thickened. Microscopically, lesions have mul;focal disposal, separated by areas of normal parenchyma. In outbreaks are iden;ed inters;;al brosis, the presence of a lympho-plasma cell inammatory inltrate and various types of glomerular lesions. Tubules contain hyaline cylinders, some;mes making pseudo;roidisa;on images. Basically, a chronic pyelonephri;s can not be dis;nguished by chronic glomerulonephri;s in both disease all renal structures being aected in varying degrees. 14

Female genital System

Female genital system pathology

Uterine Body

Vulvi;s are mainly caused by infec;ous agents: Human papilloma virus infec6on is characterized by the appearance of benign tumor lesions, called acuminate condyloma. These forma;ons appear as papillary, warty, located on vulvar teguments or mucosa, oRen mul;ple and conuent. Herpes viruses infec6on is common in the vulva. Ini;ally develop a rash with blisters lled with clear uid, then are converted into pustules that may ulcerate. Syphili6c infec6on is caused by the spirochete (Treponema Pallidum). Bartholin cysts occur due to glandular excretory ducts obstruc;on with accumula;on of secre;on product and consecu;vely ductal dilata;on. Content is clear, mucoid, translucent. Microbial overgrowth can cause the appearance of an abscess Bartholin, with forma;on of a circumscribed purulent collec;ons. Kera6n cysts interested oRen large labia, are supercial and small (2-5 mm). The content of the cys;c consists of acellular mass, eosinophilic of kera;n, bounded by atened squamous epithelium. Mucinous cysts are commonly located at the ves;bular level, is separated by a mucous-secre;ng epithelium, cuboidal or cylindrical type, frequently with squamous metaplasia.

Vagini;s are oRen caused by pathogens such as Candida albicans, Gardnerella vaginalis and Trichomonas vaginalis.


Acute endometri6s oRen occur consecu;vely to a birth, an abor;on or following uterine surgery. More rarely, can occur in their absence, as in gonococcal infec;on through ascendent path from the vagina. Uterine mucosa is swollen and congested, with desquama;on of surface epithelium. Is iden;ed a mucous hypersecre;on which can then become mucopurulent or purulent. Endometriosis are characterized by the presence and prolifera;on of endometrial ;ssue non-neoplas;c anywhere else than in the mucosa of the uterus. Histologically, ectopic endometrium can be completely made up of cytogenic chorion and glands, or can contain only one of these elements. In terms of loca;on, can be described two types of endometriosis: external and internal. Internal endometriosis (adenomyosis) is the presence of islands of endometrium in myometrium thickness.

Cervici;s can be divided, depending on the nature of the e;ologic agent, in infec;ous cervici;s and noninfec;ous. Both can manifest as an acute or chronic inamma;on. It can also be aected the por;on of the the cervix from vagina (exocervici;s), or the corresponding segment of cervical canal (endocervici;s). Noninfec6ous cervici6s can be caused by chemical irrita;on, use of vaginal tampons, diaphragms and intrauterine contracep;ve devices. In acute forms, the cervix is hypertrophied, erythematous, friable. Microscopically is highlighted stromal edema, vascular conges;on, and inammatory inltrate with polymorphonuclear neutrophils in chorion. Infec6ous cervici6s may complicate those noninfec;ous or can manifest from the beginning itself. Involve the ac;on of a biological agent. ). All rst manifests as an acute cervici;s, oRen with the appearance of purulent striae on the surface of exocervix or muco- purulent secre;ons that is removed from endocervical canal. 15

Mammary Gland

Mammary Gland Pathologies

Inamma;ons: Mas;;s
Acute mas66s are usually related to installa;on of lacta;on, usually aec;ng primiparous. It is a bacterial infec;on (staphylococcus aureus, streptococcus pyogenic), favored by the appearance of ssures, rhagades, nipple excoria;on due to a dicult lacta;ons. From this level, the infec;on spreads in depth by canalicular path. In breast appear hard areas, swollen and very painful, at whose compression is expressed in the nipple a purulent exudate. Microscopically, at the beginning is a sero- brinous acute inamma;on, which can progress to suppura;ve inamma;on of abscess or phlegmon type. Chronic mas66s (mas;;s with plasmocytes) are found in mul;parous, due to mammary ducts obstruc;on by secre;ons condensa;on. This induces a chronic inammatory reac;on with occurrence in mammary gland mass of some indurated areas, from which at pressure is expressed plugs of cheesy material. Microscopically, can be iden;ed dilated ducts with epithelium in large part atrophied and necro;c material in lumen. Peri-and intraductal appears a granulomatous inammatory reac;on, with deposits of cholesterol and inammatory inltrate rich in plasmocytes. Some;mes may occur a process of inters;;al brosis with nipple retrac;on, similar to that from breast cancer.

Fibrocys;c Breast Disease

Condi;on that occurs in women with hormonal ac;vity caused by the excess of estrogen. Some;mes it can evolve to breast cancer. Histologically, the disease is characterized by a variable lesional complex, which in essence can be systema;zed into three major categories: Simple brocys6c moca6on (non-prolifera;ve) is the most common form of the disease. It is characterized by the appearance, oRen unilateral, of single or mul;ple mammary nodules, elas;c and mobile to surrounding ;ssues. They consist of a mass of stromal brosis, in which are found terminal ducts with cys;c dilated. Prolifera6ve brocys6c modica6on is characterized, in addi;on to previous form, by prolifera;on (hyperplasia) of ductal epithelium. Some;mes it can be very marked, forming papilliferous structures that can ll distended ductal lumen (ductal papilloma). Sclerosing adenosis is characterized by increasing the number of small ducts or acini. They appear microscopically as nests, cordons of ductal cells embedded in a brous stroma. Some;mes, the ducts can be in a large number, placed back to back, being deformed by bands of brosis, in which case the dieren;al diagnosis with breast cancer is very dicult. 16

Male Genital System

Male Genital System Pathologies

Inamma;on of the tes;cles is called Orchi6s. These can be acute or chronic, and may be associated with inamma;on of the epididymis (orchiepididymi;s). Acute orchi;s are oRen of gonococcal nature, but may also include syphili;c or viral, some;mes complica;ng an epidemic paro;di;s. They are rarely encountered in inamma;on of tuberculous nature. Aected tes;cle is swollen, painful and microscopically shows a polymorphous inammatory inltrate, predominantly with neutrophils. Gonococcal orchi6s evolves towards suppura;on, with the forma;on of abscess. Acute orchi;s unhealed can become chronic, and bilateral forms can be complicated by sterility

Prostate Pathology
Prostate inamma;ons are called prosta66s. They are oRen bacterial (gonorrhea, streptococci, coli, etc..) consecu;ve of an urinary infec;on. Acute prosta;;s is characterized by a glandular painful swelling, with urethral expression of a sero-purulent uid at compression. Microscopically, there is a rich granulocy;c inammatory inltrate located in the prosta;c glands and stroma. Chronic prosta66s are the result of repeated acute inamma;on. Clinically, is manifested by nocturia and dysuria, and in ;me occurs progressive atrophy of the prostate. Some;mes can occur characteris;c injuries for tuberculous prosta;;s.

Other Condi6ons: Cryptorchidism is lack of descent of the tes;s into the scrotum. It frequently accompanies by tes;cular atrophy with sterility, and an increased rate of malignant degenera;on. Torsion of sperma;c cord, compromising blood perfusion, which can lead to tes;cular gangrene. Hydrocele is caused by the accumula;on of serous uid, with distension of the tunica vaginalis, for most of the ;me is idiopathic, but may be congenital, secondary to infec;on or as a result of lympha;c blocking of tumoral origin. Hematocele is an accumula;on of blood that relax tunica vaginalis, is usually postrauma;c, but may indicate the presence of a renal tumor. Varicocele is a varicose dilata;on of the sperma;c cord vein. Spermatocele is a cyst oRen intrates;cular containing sperm. 17

Pathology of Blood

Post-Hemorrhagic: Acute as a result of sudden, severe, internal or external hemorrhage. In the early stages there is not a decrease of hematocrit and hemoglobin concentra;on due to concomitant loss of red blood cells and plasma uid. A litle later, hypervolemia is compensated by the body through an increased produc;on of plasma liquid, with the advent of hemodilu;on. Chronic posthaemorrhagic anemias occur aRer repeated small haemorrhages (gastric ulcer, tumor, meno-metrorrhagia and so on). Anemia becomes signicant only aRer deple;on of body iron deposits (iron deciency anemias) Hemoly6c: caused by an excessive destruc;on of red blood cells, with reducing their lifespan. Destruc;on can occur in macrophages from spleen, bone marrow, or within blood vessels (intravascular hemolysis). As a compensatory response, erythropoiesis is s;mulated, anemia became manifest only when damage rate exceeds the produc;on of red blood cells. Hemoly;c anemia is characterized by the following elements: increased serum levels of unconjugated bilirubin, appearance in the blood and urine of free bilirubin (hemoglobinemia and hemoglobinuria), intensica;on of erythropoiesis, Splenomegaly Iron Deciency: can be caused by inadequate dietary intake, an increase in body iron requirements (pregnancy, growth period) or may complicate malabsorp;on syndromes and chronic hemorrhages. It is characterized by the appearance in the peripheral blood of erythrocytes of small size (microcytes), pale, hypochromic. Signicant is a decrease serum level of ferri;n, which reects a decrease of iron reserves in the body. Megaloblas6c anemias are the consequence of a reduced DNA synthesis, due to deciency of folic acid or vitamin B12. Most common cause in vitamin B12 deciency is the absence of intrinsic factor necessary for intes;nal absorp;on of the vitamin. This deciency occurs in atrophic gastri;s (pernicious anemia).


Dyshematopoie6c: result of deciencies of factors required for normal erythrocyte matura;on, despite the existence of an adequate number of marrow precursors for their synthesis. Most important in this category are megaloblas;c and iron deciency anemia.

Aplas6c: result of altera;on of bone marrow stem cells with pancytopenia occurrence and bone marrow cell depopula;on. Impairment may be idiopathic or may be due to the ac;on of marrow toxic agents: chemotherapy, sulphonamides, benzene, radia;on, viruses, etc. Anemia is oRen macrocy;c, and leukocytes and thrombocytes are greatly reduced in number. The popula;on of normal bone marrow is replaced by fat ;ssue prolifera;on. 18

Pathology of Blood


Or Erythrocytosis, is characterized by increased total mass of circula;ng erythrocytes, a process most accurately reected by increasing hematocrit. The direct consequence is increased blood viscosity, with aec;ng its ow and the possible occurrence of ;ssular hypoxia. Polycythemia may be rela;ve, occcurred as a result of the decrease in plasma volume (hemoconcentra;on), and absolute (per se), characterized by increased number of erythrocytes.

Primi6ve erythrocytosis (polycythemia vera) is a neoplas;c altera;on of mul;potent stem cells, resul;ng in prolifera;on of all marrow cell lines, but more of erythrocyte series. The disease occurs mainly in men, in old age; heredity seems to play an important role. In peripheral blood is an increase in the number of erythrocytes (over 6 million / ml) with increasing hematocrit (60%) and hemoglobin concentra;on (over 2 g%). In addi;on, increases the number of leukocytes and thrombocytes. Hematogenous marrow is hypercellular, with the presence of numerous precursors of all cell lines. Secondary erythrocytosis is the consequence of hypersecre;on of erythropoie;n. This increase is typically reac;ve, consecu;vely to a arterial hypoxia(high al;tude with rareed air, lung disease, hemoglobinopathies, etc.). Some;mes, the disease may be caused by the appearance of erythropoie;n-secre;ng tumors (renal carcinoma, liver carcinoma etc.).

It is a decrease in thrombocytes number below 150.000/ml. More severe decreases, under 50.000/ml, increase the risk for postrauma;c hemorrhages or by surgery, and at values less than 20.000/ml spontaneous bleeding occurs. Thrombocytopenia may be the result of reduced medullary thrombocytopoiesis (aplas;c anemia, leukemia) or destruc;on, excessive sequestra;on of thrombocytes at spleen level. The most common manifesta;on, but not pathognomonic, of thrombocytopenia is purpura Primary thrombocytopenic purpura (essen;al) have immune e;ology, being the result of appearance in the blood of an;thrombocy;c or an;megakaryocy;c an;bodies. This may occur in adults as a consequence of serious chronic diseases (collagenosis, leukemia, AIDS), or in children during viral infec;ons.

Secondary thrombocytopenic purpura may occur due to thromboly;c ac;on of chemical agents, drugs, or secondary to myelo-or lymphoprolifera;ve neoplas;c processes.

Leukemia will be discussed in the table dedicated to tumors and cancers


Pathology of Blood

Lymphadeni;s are inamma;on of lymph nodes, secondary to the ac;on of exogenous agents, oRen biological (bacteria, viruses, parasites, etc.). Acute lymphadeni6s occur in the lymph nodes that drain lymph from ;ssular territories in which it take place an acute inammatory process. Aected lymph nodes are hypertrophied, have a low consistency and are painful at palpa;on. Microscopic lymph node histological structure is altered by the appearance of a prolifera;on of sinusal his;omacrophages (sinus his;ocytosis) and the occurrence of a subcapsular granulocy;c inltra;on (catarrhal lymphadeni;s). Some;mes inamma;on can get a suppura;ve character with extension to surrounding ;ssues.


Chronic lymphadeni6s may be:- Nonspecic chronic lymphadeni;s accompanies chronic infec;on with various sites, having appropriate regional topography. Lymph nodes are hypertrophied, with bro;c capsule; microscopic presents sinusal his;ocytosis and hypertrophy of lymphoid follicles. Specic chronic lymphadeni;s are characterized by the appearance of lesions characteris;c of underlying disease: in tuberculosis appear tuberculous follicles and and caseous necrosis, in syphilis, vasculi;s with plasmocytes rich in inammatory inltrate. Reac6ve splenomegaly accompanies some acute or chronic inamma;on such as bacterial, viral, parasi;c or immunological. In bacterial infec;on spleen is moderately increased in volume, red pulp being intensely populated with macrophages and polymorphonuclear neutrophils. In sep;cemia may appear abscesses and sep;c splenic infarcts, as well as involvement of capsule and surrounding structures (perispleni;s). In infec;ous mononucleosis splenomegaly is due to occurrence of an inltrate rich in lymphocytes and immunoblasts located in the sinuses and medullary cordons. In malaria, the spleen is much hypertrophied (10 kg), of gray-blackish colour due to increased an;malarial pigment content (hemateina).


Conges6ve splenomegaly occurs in portal hypertension (hepa;c cirrhosis, heart failure). The spleen is moderately hypertrophied, hard, with bro;c capsule. Microscopically, in the early stages, sinusoids are dilated, with a large number of macrophages. In advanced stages, red pulp tends to become hypocellular due to a process of brosis. Inltra6ve splenomegaly can occur in several circumstances: intrasplenic advent of cellular inltrates (macrophages in haemoly;c anemia, malignant cells in lymphoma or leukemia) or extracellular deposits of abnormal substances (amyloidosis). Others: Splenomegaly due to primi;ve or metasta;c splenic tumoral processes / Splenomegaly due to occurrence at this level of hyda;d cysts. 20



Pathology of Hypophysis
Injuries associated with hypofunc;on of adenohypophysis: Pituitary cachexia is caused by panhypopituitarism, can be produced by any factor that destroys the pituitary gland (various tumors, postpartum necrosis of pituitary gland). Selec6ve decits of one or more pituitary hormones: growth hormone deciency (retarda;on in growth), gonadotropin deciency (delayed sexual matura;on), TSH deciency (hypothyroidism), ACTH deciency (hypocor;cism). Injuries of neurohypophysis: ADH secre6on deciency is manifested by diabetes insipidus (polyuria, dehydra;on, permanent thirst). Can occur consecu;vely to any process that leads to the destruc;on of the posterior hypophysis (trauma, tumors, inamma;on and so on). Ectopic secre6on of ADH is the preroga;ve of some tumors such as small cell lung carcinoma. It is characterized by reten;on of water and concentrated urine.

***Nope Zappala, these are not tesHcles


Acute thyroidi6s are usually bacterial, occurring as a result of infec;ous hematogenous dissemina;on, rarely spread from a neighboring organ. The thyroid is enlarged in volume and painful. The most common encountered are suppura;ve forms, abscess or phlegmon type Subacute thyroidi6s (de Quervain) have most likely a viral e;ology (mumps virus, Coxsakie etc). It is a self-limited inamma;on, characterized by focal destruc;ons of thyroid ;ssue with granulomtoase lesions. In advanced stages may occur a process of brosis with symptoms of hypothyroidism. The thyroid is enlarged in volume, not adhering to the surrounding organs, increased consistency and irregular surface

Hashimoto's thyroidi6s (diuse lymphocy;c thyroidi;s) is an autoimmune disease with familial aggrega;on, more common in women. In advanced forms is manifested by hypothyroidism. The thyroid is diusely and moderately increased in volume, with increased consistency and intact capsule, nonadhesive Riedl thyroidi6s (ligneous thyroidi;s) has unknown e;ology and may clinically mimic the carcinoma. The thyroid is usually reduced in volume, with irregular surface, adherent capsule and very high consistency.





Dene the increase in volume and weight of the thyroid, in the absence of inammatory processes or tumors. From a func;onal perspec;ve, there may be simple goiters, without endocrine disorders, and goiters associated with hyper- or hypothyroidism.

With Euthyroidsm
(Simple, non-toxic) are caused by iodine deciency due to either an insucient exogenous or an increased need of the body (pregnancy, growth period, etc..). Iodine deciency leads to a defec;ve synthesis of thyroid hormones, with consequent decrease of serum level of these. This abnormality is felt by hypophysis, which will intensify the synthesis of TSH. Under its ac;on will produces compensatory hypertrophy and hyperplasia of thyroid follicular epithelium with the advent of goiter. Simple goiter may be diuse or nodular. Simple difuse goiter is accompanied by euthyroidism, and is characterized by a uniform damage of all thyroidian mass. May be endemic, occurring in mountain areas (Andes, Alps, Carpathians). Evolves in two stages: hyperplas;c phase, colloid involu;on phase

With Hyperthyroidism
(toxic) are manifested clinically by a complex clinical picture: irritability, tremor, heat intolerance, tachycardia with arrhythmia, diarrhea, menstrual disorders etc.. Morphologically can be dis;nguished: Diuse toxic goiter (exophtalmos goiter, Graves - Basedow Disease) is the most frequent goiter associated with hyperthyroidism. The disease has a hereditary component, and in;mate produc;on mechanism is autoimmune. .. Clinically, presents signs and symptoms of hyperthyroidism, plus exophthalmia and inltra;ve dermatopathy. The thyroid is overall enlarged in volume, but oRen with unequal lobes; is hard, britle and highly vascularized; the capsule is integral and nonadhesive. Toxic nodular goiter is rare, occurs more frequently in women with a history of simple goiter. The thyroid is uneven increased in volume, with the presence of nodules of varying sizes.

With Hypothyroidism
may be encountered in children from goitrous regions, as a result of chronic decit of iodine or administra;on of an;thyroid agents. It has a hereditary character resul;ng from co-blood families. Are nodular goiters, in which predominate microscopic aspects of pseudo-thyroidian hyperplasia. Hypothyroidism is manifested in adults through myxedema and in children by cre;nism. Myxedema is characterized by a localized edema predominantly on the face, tongue and hand, dry skin with tendency to peeling, litle hair and harshly. To this can be added cold intolerance, tendency to gain weight, mental retarda;on, cons;pa;on etc. Cre;nism of thyroidian cause is manifested mainly by severe mental retarda;on, delayed bone development, macroglossia and protuberant abdomen. The thyroid is much increased in volume, with marked epithelial hyperplasia. 22

Pathology of CNS


and the spaces between them


Histo Review

Dura Mater Arachnoid PiaMater

Epidural (Extradural) Subdural Subarachnoid, containing CSF

Cerebral Infarc;on

infarc;on (soRening) is the result of a total and persistent ischemia, caused by cerebral artery occlusion. The main causes of this event are: thrombosis, embolism. clinical consequences depend on the place of vascular obstruc;on and the possibility of development of collateral circula;on. Most commonly it is aected middle cerebral artery. In this case occurs controlateral paralysis, with motor and sensory decit, and aphasia. Cerebral infarc;on may be single or mul;ple, of various sizes, depending on the size of artery aected. In general, infarc;ons of thrombo;c cause are white, and those caused by emboli are red infarcts. Microscopically stands a liquefac;on necrosis due to the emergence of a large amount of lipids from the disintegra;on of the myelin sheath. Intracerebral hemorrhage (apoplexy) is dened as bleeding within the brain substance. Most frequently occurs in the basal nuclei, the internal capsule and thalamus.The most frequently involved in the produc;on of intracerebral hemorrhage is arterial hypertension. Under the ac;on of this there is a decrease in the resistance of walls of brain arterioles, with the forma;on of micro aneurysms, which can be easily broken. More rarely, are involved arteriovenous malforma;ons, hemorrhages diatheses or tumoral processes. Subarachnoid hemorrhage is a bleeding into the subarachnoid space. Most oRen it is the result of a ruptured aneurysm in the arteries of Willis polygon. Some;mes subarachnoid hemorrhage may also have trauma;c cause. Epidural hematoma usually occurs as a result of trauma;c fracture of the temporal bone, with the middle meningeal artery injury and accumula;on of blood in the extradural space. Clinically, it is characterized by a short asymptoma;c period, and then occur compressive cerebral phenomena and, in the absence of treatment, death. Subdural hematoma is the result of trauma;c rupture of the connec;on veins between cerebral substance and venous sinuses of the dura, with the accumula;on of blood between the arachnoid and dura mater. Typically locates in the fronto-parietal region. It is characterized by gradual appearance of signs of compression of the brain (some;mes over a period of several week).

Non trauma;c brain hemorrhage

Post trauma;c brain hemorrhage


Pathology of CNS



inamma;on of the conjunc;ve membranes that cover the central nervous system organs. May be aected rough meninges, process wearing in this case the name of pachymeningi;s, or soR meninges (arachnoid, pia mater and subarachnoid space), dened with the leptomeningi;s term.

Meningococcal meningi;s aects mostly children, is characterized by the appearance of a sero- purulent inammatory exudate, yellowish. Exudate contains a small amount of brin and a large number of granulocytes and macrophages. Brain substance is edematous, with punctate hemorrhages and peri vascular inammatory inltrate. Pneumococcal meningi;s is characterized by the appearance of green exudate, jelly; has increased tendency to delimita;on (forma;on of enclosed spaces lled with pus); Staphylococcal and streptococcal meningi;s are secondary to neighborly suppura;ve processes. Exudate has sero-purulent appearance for streptococcus and yellowish, creamy for staphylococcus; the process have an increased tendency for intracerebral abscess forma;on, epi-or subdural.

occurs secondary, in the context of generalized miliary tuberculosis. It is a non-purulent inammatory process, with predilect loca;on in the brain. Here may occur exuda;ve or prolifera;ve (miliary tubercles) lesions. May be complicated by meningeal brosis and consequent obstruc;on of ventricular system.

(enterovirus, mumps virus, Epstein-Barr virus, etc.) predominantly aects young ages, usually with a benign evolu;on. The disease is characterized by the appearance of an intense cephalalgia and the diagnosis is made by spinal puncture (CSF with numerous lymphocytes, increased amount of protein and normal glucose content).

(dened inamma;on of cerebral substance (encephali;s) and of spinal cord (myeli;s). Important in medical prac;ce are inamma;ons of viral e;ology, and of these, due to their seriousness, polipomyeli;s and rabies encephali;s. Poliomyeli6s (infan6le paralysis) is caused by one of three types of polioviruses. It is an acute inamma;on that par;cularly interested in the anterior corns of the spinal cord, leading to destruc;on of motor neurons with paralysis and atrophy of corresponding soma;c muscle. Macroscopically, medulla spinalis is with intense hyperemia, edematous (glassy) aspect with hemorrhagic suusions on sec;on. Rabies encephali6s is caused by the rabies virus, transmited by the bite of infected animals. From the entrance gate, virus spreads by axonal path un;l spinal cord, brain and internal organs (including salivary gland). The disease manifests itself as a severe encephali;s with increased CNS excitability, violent muscle contrac;ons and convulsions triggered by minimal s;muli. Histologically, the disease is characterized by neuronal degenera;on, perivascular lymphocy;c inammatory inltrate in the cerebral hemispheres, cerebellum and spinal cord; pathognomonic are Babes - Negri corpuscles 24

Pathology of CNS


and the spaces between them


Histo Review

Dura Mater Arachnoid PiaMater

Epidural (Extradural) Subdural Subarachnoid, containing CSF

Mul;ple Sclerosis

Mul;ple sclerosis is the most common demyelina;ng chronic disease of the CNS. Predominantly aects young women, with a progressive evolu;on, occurring in spikes. E;ology is unknown. Characteris;c lesions are represented by plates of sclerosis visible by naked eye in the cerebral white substance and spinal cord. It presents as oval patches, irregular, in sizes up to 2 cm, translucent, with color variable, depending on their age. These correspond to areas of axonal demyelina;on. Microscopically, there is complete disappearance of the myelin sheath in these areas, with local prolifera;on of glial cells and connec;ve ;ssue.

Alzheimers Disease

Is a degenera;ve disease of unknown e;ology, which is the most important cause of demen;a. En;ty refers to demen;a occurring at any age, associated with clinical manifesta;ons and specic pathological changes. Clinical manifesta;ons: slowly progressive intellectual deteriora;on: ini;ally short term memory loss, then and the long-term memory, inability to write, count, speak, etc.. motor problems:contractures and paralyzes specic to terminal phase Morphological abnormali;es: neurobrillary disorder: intraneuronal fascicles (microtubules and neurolament) disorganiza;on in cerebral cortex neuri;c plaques (senile): eosinophils neuronal processes with center consis;ng of a amyloid deposits in the cerebral cortex and hippocampus neuronal granulocyte-vacuolar degenera;on at pyramid level Hirano bodies: dendri;c eosinophilic inclusions generalized cerebral atrophy more expressed in hippocampus and frontal areas.

This work is not subsHtute of doctor Paiusans material, even if evry single word is extracted by his word les so it will matches what we need for the nal exam May The Force Be With You Your beloved colleague, Alessandro Mo5a