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 Endometrial hyperplasia is an important cause of abnormal bleeding
 Frequent precursor to the most common type of endometrial
 Hormonal Imbalance
 Prolonged stimulation of estrogen
**HALLMARK: Cylindrical shaped endometrial glands
 Inactivation of the PTEN tumor suppressor gene is a common genetic
alteration in both endometrial hyperplasias and endometrial carcinomas.

 Thickening of the endometrium
 Increased gland to stroma ratio
 Increased in number of glandular cells
 Normal nuclei
 Cells – columnar and multilayered
 Abnormal bleeding
 Increased secretion
 Atypical hyperplasia is managed by hysterectomy
 In young women who desire fertility, a trial of progestin therapy and
close follow-up.

 Aging
 Ischemia
 Hypoxia
 Nutritional deficit
MECHANISM OF LESION: Decrease in cell size due to decrease protein
synthesis and increase protein degradation in cell. The cell adapts by
protein degradation through the Ubiquitin Proteosome Pathway, causing
proteolysis and cell shrinkage.
**HALLMARK: Nucleated cardiac muscle cells.
 Decreased size of the heart and cardiac contractility.
 Intact nucleus

Presence of LIPOFUSCIN PIGMENT – product of autophagy.  Increased stromal space. wear and tear pigment. . due to oxidative phosphorylation of the membrane. Sign of free radical injury and lipid peroxidation.

Decrease in complex cognitive functions and motor performance Drowsines.ORGAN: LIVER DIAGNOSIS: FATTY LIVER ETIOLOGY:  Injury secondary to Chronic alcoholism  Excess fat in the body  Kwashiorkor (Protein Malnutrition) **NAD DEFICIENCY – Main cause of accumulation of fat in alcoholics ALCOHOL CONCENTRATION 20 mgdl 80mg/dl 200 mg/dl 300 mg/dl 400 mg/dl EFFECT a slight feeling of intoxication Constitutes the legal definition of drunk driving. slurred speach Stupor and coma Death **HALLMARK: Fat vacuoles within the parenchyma TYPE OF INJURY: Reversible LOCATION OF LESION: Hepatocytes ACCUMULATED SUBSTANCE: Lipids/Triglycerol ADAPTIVE CHANGE: Fatty Change CLINICAL MANIFESTATION: Jaundice ASSOCIATED DISEASE: Hyperlipidemia .

GROSS EFFECT:  Enlarged liver with glistening capsule  Greasy  Yellowish  Soft MICROSCOPIC EFFECT:  Formation of fat vacuoles in the liver cells  Nucleus is pushed in the periphery  Small vacuoles fused to form – Fatty cyst DIAGNOSIS: LIPID PROFILE .

LDH. Troponin T FAVORITE QUESTION: INFLAMMATORY CELLS INVOLVED IN THE LESION:  Neutrophils  Macrophage . TYPE OF INJURY: Irreversible Injury TYPE OF NECROSIS: COAGULATION NECROSIS LOCATION OF LESION: Cardiac muscle cell HEMODYNAMIC CHANGE: INFARCTION DIAGNOSTIC MARKERS: CK-MB. **HALLMARK: Anucleated cardiac muscle cells with intense eosinophilia of the cytoplasm due to leakage of basic nuclear contents. AST. Troponin I.ORGAN: HEART DIAGNOSIS: MYOCARDIAL INFARCTION PREIPITATING FACTOR:  Atherosclerosis – most common cause MOST COMMON AFFECTED ARTERY: Circumflex & Left Anterior Desending Artery MECHANISM OF ACTION: Occluded blood vessel leading to ischemia causing irreversible injury.

 Striations are lost with stromal neutrophilic infiltrates. Fibroblast  Lymphocytes and plasma cells ARE NOT INVOLVED GROSS EFFECT: MICROSCOPIC EFFECT:  Eosinophilic in the area of necrosis.  Myocardial pump failure  Myocardial rupture  Ventricular aneurysm  Mural thrombosis – may lead to left sided heart failure LABORATORY DIAGNOSIS:  Elevated serum levels of cardiac muscle creatine kinase MB  EleavatedTroponin are early signs of myocardial infarction . Nuclear fragmentation (Karyorrhexis) and Karyolysis (Disappearance of the nucleus) CLINICAL MANIFESTATION:  ANGINA  CHEST PAIN COMPLICATIONS:  Arrythmia.  Shrunken nuclei (Pyknosis).most common cause of death in the first several hours following infarction.

.ORGAN: LYMPH NODE DIAGNOSIS: TUBERCULOSIS ETIOLOGY:  Mycobacterium tuberculosis **HALLMARK: Pinkish collected areas f necrosis TYPE OF INJURY: Irreversible TYPE OF NECROSIS: Caseous necrosis TYPE OF LESION: TUBERCLE (Composed of fibrocytes nd collagen Fibers. macrophages and some PMN’s enclosed in a fibrous tissue made of collagen.) TYPE OF INFLAMMATION: Chronic granulomatus inflammation PREDOMINANT INFLAMMATORY CELL: Lymphocyte CHARACTERISTIC CELL: EPITHELOID CELL (Modified macrophages) GROSS EFFECT:  Cheese like area of necrosis MICROSCOPIC EFFECT:  Aggregation of lymphocytes. enclosing inflammatory cells like lymphocytes.

ACCUMULATED SUBSTANCE: MELANIN TYPE OF LESION: PLAQUE CLINICAL MANIFESTATION:  Hyper pigmentation GROSS EFFECT:  Presence of an elevated mass with black/brown discoloration MICROSCOPIC EFFECT:  Melanin deposits in the dermis which can be seen as brownish/blackened accumulation.ORGAN: SKIN DIAGNOSIS: MALIGNANT MELANOMA ETIOLOGY:  Excessive growth of melanoblast.  UV Rays **HALLMARK: Brownish accumulation in the cells in the dermis. .

TYPE OF INFLAMMATION: Acute suppurative inflammation PREDOMINANT INFLAMMATORY CELL: Neutrophil LOCATION OF LESION: MUSCULARIS HEMODYNAMIC CHANGE: HYPEREMIA . **HALLMARK: Infiltration of neutrophils in the muscularis layer.ORGAN: APPENDIX DIAGNOSIS: ACUTE APPENDICITIS ETIOLOGY:  Occlusion  Secondary to bacterial infection  Pus formation  Obstruction of the lumen producing increased luminal pressure  CHILDREN: Lymphoid hyperplasia following viral infection  ADULT: Obstruction due to fecalith MECHANISM OF ACTION: Occluded blood vessel leading to ischemia causing irreversible injury.

CLINICAL MANIFESTATION:  Mcburney’s sign (rebound tenderness upon deep palpation)  Anorexia  Nausea  Abdominal pain  Fever FORMS OF APPENDICITIS: a. dolor. PMN’s are present even in the muscularis layer of the appendix. b. etc  Congested appendix with a swollen distal half covered by purulent exudates  Lumen contains purulent exudates and often a fecalith.Muscularis layer is replaced with neutrophilic infiltrates . ACUTE NECROTIZING/GANGRENOUS . MICROSCOPIC CHANGES:  In inflammation. Prostaglandins. In terms of hemostasis. tumor.Has tendency to rupture Perotinitis Sepsis CHEMICAL MEDIATORS   FEVER. where the wall is looser)  Loosening of adjacent interstitium indicates edema. TNF) PAIN – Prostaglandin COMPLICATION OF RUPTURED APPENDICITIS:  Peritonitis LABORATORY DIAGNOSIS  Neutrophilia  Elevated WBC count MANAGEMENT:  APPENDECTOMY .Chemical mediators (IL-1. hyperemic vessels are evident in the serosal layer. GROSS CHANGES:  Inflamed appendix with present characteristics of inflammation (rubor.PATHOLOGIC CHANGES:  Dilated arterioles and capillaries (more prominent in the lamina propria and serosa.Neutrophil infiltrates in all layer. ACUTE SUPPURATIVE .

Oncomelania quadrasi SITE OF MALNUTRITION: Liver – They male in the portal vein where ova are laid. It goes to the liver to mature and eggs go to the circulation. japonium) whose larvae enter the Skin. PARASITE INVOLVED: Schistosoma japonicum **INFECTIVE STAGE OF PARASITE: Four tailed cercariae . TYPE OF INFLAMMATION: CHRONIC INFLAMMATION MECHANISM OF ACTION: A parasite (S.ORGAN: APPENDIX DIAGNOSIS: SCHISTOSOMIASIS ETIOLOGIC AGENT:  Schistosoma japonicum MODE OF TRANSMISSION: Skin penetration of the cerceria (infective stage) DIAGNOSTIC STAGE: Ova excreted in feces and urine    Sexual stage and definitive host – Human Asexual stage and intermediate host.

IL-1 FEVER  COMMON SITES: Liver. CHRONIC SCHITOSOMIASIS  Dominant TH2 mast cells to release IL-4 TH2 differentiation  TH1 is also present  TH1 and TH2 Granuloma formation  IL-13 produced by the TH2 cells Increase fibrosis by stimulating  synthesis of collagen. neutrophils and eosiniphils b. . portal enlargement) **S. They mate in the tribuatries of the portal vein. MILD FORM  White. IL-6. Intestines and Lungs activate macrophage to B. They become schistosomulia & go to the lungs & reach the liver once they mature. mansoni lodge in the inferior mesenteric plexus **Fork tailed cercaria are the one infective to man. widespread fibrosis.VECTOR: ** Snail (Oncomelania quadrasi) ` LOCATION OF DEPOSITION: Submucosal layer of the appendix /muscularis/serosa **TYPE OF HYPERSENSETIVITY: Type IV (+) Granuloma formation **COMPLICATION: Portal hypertension secondary to portal fibrosis IMMUNE RESPONSE A. SEVERE FORM  Pipestem fibrosis-triad (granulomas.pinhead-size scattered granulomas  Schistosome eggs with miracidium at the center of granuloma  Macrophage. lymphocyte. ACUTE SCHISTOSOMIASIS  Dominant TH1 produce IFN-gamma release TNF. HISTOLOGICAL CHANGES: a. japonicum lodge in the superior mesenteric plexus **S.

***endogenous pigment due to hemolysis of rbc which is phagocytosed by macrophages. producing severe congestion of alveolar capillaries leading to edema of the walls and alveolar spaces. CHIEF COMPLAINT: DIFFICUTY O BREATHING . LOCATION OF LESION: STROMA HEMODYNAMIC CHANGE: HEMORRHAGE AND CONGESTION ACCUMULATED SUBSTANCE: HEMOSIDERIN (Non-hemoglobin.ORGAN: LUNGS DIAGNOSIS: EARLY PULMONARY CONGESTION ETIOLOGY:  Left sided heart failure MECHANISM OF ACTION: Left sided heart failure blood is dammed back from the left ventricle to the lungs.

yellowish-brown pigment. either scattered in the interstitium or space or within the alveolar macrophage  Distended alveolar capillaries  Fibrotic septa LABORATORY TEST: Positive Prussian Blue reaction .MICROSCOPIC EFFECT:  (+) Granular.

through prolonged pelvic vascular congestion due to pregnancy or straining to defecate). Hemorrhoids are uncomfortable and may be a source of bleeding.g..ORGAN: ANUS DIAGNOSIS: HEMORRHOIDS.  Dilated veins filled with thrombus . THROMBOSIS  Hemorrhoids can also result from primary varicose dilation of the venous plexus at the anorectal junction (e. they can also thrombose and are prone to painful ulceration. PREDISPOSING FACTORS:  Pregnancy  Straining  Increased venous pressure HEMODYNAMIC CHANGE: THROMBOSIS CLINICAL MANIFESTATION:  Rectal bleeding  Pain MICROSCOPIC EFFECT:  Submucosal vessels become thin walled and dilated.

3 TYPES OF HEMORRHOIDS:  EXTERNAL HEMORRHOIDS.collateral vessels within the inferior hemorrhoidal plexus which are located below the anorectal line.these represent pale platelet and fibrin deposits alternating with darker red cell rich layers.  INTERNAL HEMORRHOIDS.result from dilation of the superior hemorrhoidal plexus within the distal rectum  COMBINED. LINES OF ZAHN . Such laminations signify that a thrombus has formed in flowing blood.both plexuses are affected .

yellow-tan. GENE POLYMORPHISM:  CTLA4 (Cytotoxic T lymphocyte.associated antigen-4) – most significant  PTPN22 (protein tyrosine phosphatase. gland well demarcated  Pale.’ ORGAN: THYROID DIAGNOSIS: HASHIMOTOS DISEASE / THYROIDITIS ETIOLOGY: Breakdown of self-tolerance to thyroid auto-antigens MECHANISM OF ACTION: Autoantibodies against thyroglobulin and thyroid peroxidise.22) TYPE OF HYPERSENSITIVITY: TYPE 4 HYPERSENSITIVITY GROSS EFFECT:  Thyroid diffusely enlarged  Capsule intact. firm. nodular MICROSCOPIC EFFECT: .

 Extensive mononuclear inflammatory infiltrate (Small lymphocytes and Plasma cells)  Well-developed germinal centers  Atrophic thyroid follicles lined by HURTHLE CELLS (Presence of abundant eosinophilic & granular cytoplasm)  Replacement of thyroid parenchyma by lymphocytic infiltrates CLINICAL COURSE:  Painless enlargement of the thyroid (symmetric and diffuse)  Some degree of hypothyroidsm – may be preceeded by transient thyrotoxicosis d/t disruption of thyroid follicles with secondary release of thyroid hormones (hashitoxicosis)  Free T4 and T3 are elevated  TSH diminished  Radioactive iodine uptake decreased LABORATORY DIAGNOSIS:  Decreased T3 and T4  Increased TSH  Immunoassay: Antiglobulin antibodies .

. many macrophages and giant cells around the deposits. **HALLMARK: TOPHI CRYSTALS ACCUMULATED SUBSTANCE: Monosodium urate crystals ACUTE INFLAMMATORY TYPE OF LESION: TOPHUS CHRONIC INFLAMMATORY TYPE OF LESION: Fibrosis. CLINICAL MANIFESTATION:  Joint pain MICROSCOPIC EFFECT:  Well circumscribed masses of pale-staining anuclear masses.ORGAN: JOINTS / METATARSOPHARYNGEAL JOINT TYPE OF JOINT: SYNOVIAL JOINT BASED ON MOVEMENT: DIARTHRODAL JOINT DIAGNOSIS: GOUT ETIOLOGY:  Hyperuricemia  Increased intake of purine rich foods  Alcoholism **HEAVY METAL ASSOCIATED WITH THE DEVELOPMENT OF LESION: LEAD – Decreases uric acid secretion Saturnine gout MECHANISM OF LESION: Formation of monosodium urate crystals in the soft tissues.

 Urate crystals and deposits appearing as slender crystals or pinkish yellow masses surrounded by macrophages  Fibrosis DIAGNOSIS: INCREASED SERUM URIC ACID LEVEL .

**grapelike structures w/ swollen edematous (hydropic) villi MORPHOLOGIC FEATURES: COMPLETE MOLES PARTIAL MOLES All villi underwent hydrophobic Only some villi are edematous regeneration (Edematous) Diffused trophoblastic prolifferation Localized trophoblastic proliferation Without fetal parts With of fetal parts GENOTYPE XX karyotype XXY or XXXY karyotype 46 chromosomes 69 chromosomes 2n (Diploid) 3n /4n (Triploid/Quadruploid) Both chromosomes from the father One from the mother Ovum is empty. fertilized by sperm Egg has lost its chromosomes and .ORGAN: UTERUS DIAGNOSIS: HYDATIDIFORM MOLE MOST IMPRESSIVE ABNORMALITY: Extensive/ Diffuse trophoblast hyperplasia or proliferation GROSS EFFECT:  Delicate. friable mass of thin-walled. transluscent. cystic.

cell. fertilized by 1-2 sperms Good prognosis Complication: malignant choriocarcinoma Poor Prognosis Increased risk of persistent molar disease BUT NOT choriocarcinoma CLINICAL FEATURES: TH TH  Vaginal bleeding (4 TO 5 month AOG)  Rapid increase in uterine size  HCG levels are greatly increased  Spontaneous pregnancy loss DIAGNOSIS:  Ultrasound  IMMUNOSTAINING FOR P57 (CELL CYCLE INHIBITOR)  INCREASED SERUM HCG** MANAGEMENT:  Dilatation and Curettage  Serum HCG monitoring until they fall and remain zero for 6 months to 1 year .

liver and bone .  **Positive family history – greatly increased in first degree female relatives. 4. 6.  Inherited mutations in p53  BRCA-1 / BRCA-2 tumor suppressor genes are associated with increased risk  BRCA 1 – dominant gene 2. 5. lung. 3.ORGAN: BREAST DIAGNOSIS: INFILTRATING DUCTAL CARCINOMA ETIOLOGY:  Most common breast mass in post-menopausal patients  Occurs more frequently in the upper quadrant of the breast  Major risk factors are hormonal and genetic. HEREDITARY / GENETIC  Inheritance of susceptible gene. RISK FACTORS: 1. History of breast Ca in one breast Early menarche and late menopause Obesity – due to production of estrogen by adipose tissue First pregnancy after 30 years of age Diet high in animal fat **SITE OF METASTASIS: Axillary lymph nodes.

pleiomorphic cells  Hyperchromatic nucleus  Fibrosis of stroma  Malignant glands insinuating in fibrous stroma  Glands infiltrate in adipose tissue  Comedocarcinoma (ducts healed w/ malignant cells.GROSS EFFECT:  Firm to hard mass with irregular border due to desmoplastic reaction  Nipple inversion  Skin retraction  ORANGE PEEL LIKE APPEARANCE DUE TO EDEMA (malignant)  Punctate areas of necrotic material (comedone-like) MORPHOLOGIC FEATURES:  Cells are large invading the stroma or basement membrane  Large. tumor necrosis at the center). solid tumor cel CLINICAL MANIFESTATION  Pain  Nipple discharge  Palpable mass DIAGNOSIS:  Mammography  Biopsy MANAGEMENT:  Mastectomy  chemotherapy .

ORGAN: LYMPH NODE DIAGNOSIS: PAPILLARY CARCINOMA. THYROID METASTATIC TO THE LYMPH NODE. CELLS OF ORIGIN: THYROID FOLLICLES **PATHWAY OF SPREAD: LYMPATHIC SPREAD **PREDISPOSING FACTOR:  Ionizing radiation PATHOGENESIS: Defect in the gene for .Gain of function of  Map kinase pathway  Phosphatidyl-inositol-3-kinase (P13K/AKT Pathway) GROSS:  Grossly discernible papillary structures  Well formed papillae .

 Empty appearing nuclei or “ORPHAN ANNIE EYE”**  Intranuclear inclusions a  Presence of Psamomma bodies – dystrophic calcification structures present within the lesion ihin the cores of the papillae.HISTOLOGICALLY:  Multifocal lesions  Some tumors may be well circumscribed and even encapsulated.  Papillary tumor has the appearance of Finger-like processes CHIEF COMPLAINT:  Anterior neck lump with enlarged cervical lymph nodes CLINICAL MANIFESTATIONS:  Mass in cervical lymph node  Hoarseness  Dysphagia  Cough  Dyspnea DIAGNOSTICS:  Radionuclide scanning  Fine needle aspirations  **Papillary masses are cold masses on scintiscans .

pebble-like surface MORPHOLOGIC FEATURES:  Acanthosis (Thickened epithelium and Spiky appearance)  Papillomathosis  Dermis .1 to 1 cm papules with rough.ORGAN: SKIN DIAGNOSIS: Verruca vulgaris (WART) ETIOLOGY: HUMAN PAPILLOMA VIRUS (HPV 6 & HPV 11) MODE OF TRANSMISSION:  Direct Contact  Auto inoculation OUTCOME: Self-limiting. 0.scanty lymphocytic infiltrates  Hyperkerathosis (Abundant keratin at the surface of the skin)  Koilocytosis (Cytoplasmic vacuolization involving more superficial epidermal laters  halos of pallor surrounging infected nuclei) **PATHOMNEMONIC SIGN: KOILOCYTES (Cells with vacuolated cytoplasm and perinuclear halo) . regressing spontaneously within 6 months to 2 years GROSS EFFECT: Verruca vulgaris (VIRAL WART) – MOST COMMON  Lesions occur anywhere but most frequent on hands. particularly dorsal and periungual areas  Gray-white to tan  Flat to convex.

S. ** S.  Usually caused by infection. PARTS:  Pia mater  Granular layer  Meningeal vessel. Pneumonia and Listeria monocytogenes are more common. but AREA OF INFLAMMATION: SUBARACHNOID SPACE ETIOLOGY:  NEONATES – Escherichia coli and Group B streptococci  INFANTS & CHILDREN .S. Pneumonia (most common)  ADOLESCENT & YOUNG ADULTS – Neisseria meningitides  OTHER EXTREMES OF LIFE.congested . Pneumonia is the most prevalent microorganism.ORGAN: CEREBELLUM DIAGNOSIS: MENINGITIS MENINGITIS  Inflammation of the meninges and CSF within the subarachnoid space.

 Vascular congestion MICROSCOPIC EXAMINATION:  Exudate found in the leptomeninges  Neutrophils fill the subarachnoid space in severely affected areas and are found predominantly are found in the leptomeningeal blood vessels in less severe.  Fulminant meningitis o Inflammatory cells infiltrate the wall of leptomeningeal vein and may extend into the substance of the brain. with as many as 90.000 neutrophils under cubic millimiter  Increased protein concentration  Markedly reduced glucose content .  Leptomeningeal fibrosis o May follow pyogenic meningitis and cause hydrocephalus CLINICAL MANIFESTATIONS:  Headache  Photophobia  Irritability  Clouding of consciousness  Neck stiffness CONFIRMATORY TEST:  CSF CULTURE AND SENSITIVITY/LUMBAR TAP o A spinal tap yields cloudy or purulent CSF under increased pressure.

ORGAN: COLON DIAGNOSIS: AMEOBIC COLITIS PARASITE: Entamoeba histolytica  E.  Trophozoites o Pathogenic form o Ameboid form that reproduce under anaerobic conditions. o Leads to destruction of the epithelial lining of the mucosa forming ulcer. . MODE OF TRANSMISSION: Fecal-oral route MICROSCOPIC CHANGES:  Narrow ulceration of the involved mucosa ulceration in the tunica propria where the ulceration becomes wider. AMEBIASIS SEEN MORE FREQUENLTY IN: Cecum and ascending colon ** although the sigmoid colon. histolytica cyst o Infective stage o Have a chitin wall and four nuclei – resistant to gastric acid a characteristic that allows them to pass through the stomach without a harm. Cyst then colonize the epithelial surface of the colon release the trophozoites.  Walls of the ulcers how necrotic tissue & some inflammatory cells. rectum and appendix can be involved.

   Trophozoites show a halo/empty space & they present nuclei. vacuoles & red blood cells in the cytoplasm. with ulceration (denuded mucosal portions). On the mucosal section. with surrounding inflamm atory cells Does not go beyond muscularis mucosa .

are taken up by and invade M cells.typhi can then disseminate via lymphatics and blood vessels. plateau like elevations up to 8 cm diameter. Causing reactive hyperplasia of phagocytes and lymphoid tissues throughout the body.  Neutrophils accumulate within superficial lamina propia . MORPHOLOGY:  Infection causes Peyer’s patches in the terminal ileum to enlarge into sharply delineated.typhi are able to survive in gastric acid and once in the small intestine.  Draining mesenteric lymph nodes are also enlarged. Organisms are then engulfed lymphoid tissue. Unlike S. S.enteritidis.ORGAN: SMALL INTESTINE / ILEUM DIAGNOSIS: TYPHOID FEVER / ENTERIC FEVER CAUSATIVE AGENT:  Salmonella typhi – common in endemic countries  Salmonella paratyphi – common among travelers MODE OF TRANSMISSION: Fecal-oral route PATHOGENESIS:  S.

red blood cells and nuclear debris mix with lymphocytes and plasma cells in the lamina propia. that may perforate.    Spleen is enlarged and soft with uniformly pale red pulp Obliterated follicular markings Prominent phagocyte hyperplasia  Liver – shows small. CLINICAL MANIFESTATION:  Anorexia  Abdominal pain  Bloating  Nausea  Vomiting  Bloody diarrhea  Followed by a short asymptomatic phase bacteremia  Fever with flu-like symptoms EXTRAINTESTINAL COMPLICATIONS:  Encepalopathy  Meningitis  Seizures  Endocarditis  Myocarditis  Pneumonia  cholecystitis DIAGNOSIS:  Blood cultures . oriented along the axis of ileum.  Patient with sickle cell disease are suscetible to salmonella osteomyelitis. The draining lymph nodes also harbour organisms and are enlarged due to phagocyte accumulation.   Macrophages containing bacteria. Mucosal sheddings creates oval ulcers. randomly scattered foci of parenchymal necrosis in which hepatocytes are replaced by macrophage aggregates typhoid nodules – may also develop in bone marrow and lymph nodes.

ORGAN: LUNGS DIAGNOSIS/LESION: LOBAR PNEUMONIA TYPE OF INFLAMMATION: FIBRINOSUPPURATIVE INFLAMMATION ETIOLOGIC AGENTS:  Streptococcus pneumonia  Most common cause of community acquired pneumonia  DX: Examination of gram stained sputum  Presence of numerous neutrophils containing typical gram positive. lancet shaped diplococci.    S. Pneumococcal vaccines containing polysaccharides from the common serotypes are patient in high risk.pneumonia is part of the endogenous flora in 20% and therefore false positive may be obtained Isolation of pneumococci from blood cultures specific but less sensitive.  Important cause of hospital acquired pneumonia. . of adults is more capsular used in  Staphylococcus aureus  Most important cause of secondary bacterial pneumonia in children and healthy adults following viral respiratory illness.

 Patient may have difficulty expectorating. GRAY HEPATIZATION  Follows with progressive disintegration of red cells and persistence of a fibrinosuppurative exudates. firm and airless  Liver like consistency 3. intraalveolar fluid with few neutrophils. CONGESTION  Lung is heavy.  Constitutes one of the three most common causes of otitis media in children. Moraxella catarrhalis  Cause of bacterial pneumonia in elderly.  Klebsiella pneumonia  Most frequent caue of gram negative bacterial pneumonia  Commonly afflicts debilitated and malnourished people. boggy and red. CLINICAL MANIFESTATIONS:  Onset of high fever . ingested by macrophages.9% GUT FEELING HAHAHA) 1. particularly chronic alcoholics. and oftern the presence of numerous bacteria. red cells and fibrin filling the alveolar spaces. semifluid debris that is resorbed. RESOLUTION  Consolidated exudates within the alveolar spaces undergoes progressive enzymatic digestion to produce granular. expectorated. 2.  Gross appearance:  Lobe appears distinctly red.  Thick gelatinous sputum is characteristic. RED HEPATIZATION  Massive confluent exudation with neutrophils.  Second most common bacterial cause of acute exacerbation o COPD.  Pseudomonas aeruginosa  Most commoly caused hospital acquired infections LOBAR PNEUMONIA  Fibrinosuppurative consolidation of large portion of a lobe of an define lobe  FOUR STAGES OF INFLAMMATORY RESPONSE: (99.  Gross appearance:  Grayish brown  Dry surface 4. or organized fibroblast growing into it.  It is characterized by vascular engorgement.

   Shaking chills Cough productive mucopurulent sputum Occasionally patients may have hemoptysis  If fibrinosuppurative pleuritis is present o Pleuritic pain o Pleural friction rub  The whole lobe is radiopaque in lobar pneumonia whereas there are focal opacities in bronchopneumonia. endocarditis. causing metastatic abscesses. kidneys. or joints. . spleen. causing the intrapleural fibrinosuppurative reaction known as Empyema  Bacteremic dissemination to the heart valves. brain. DIAGNOSIS  Chest xray  Culture and sensitivity  Examination of gram stained sputum COMPLICATIONS:  Tissue destruction and necrosis abscess formation (common in Klebsiella and Type 3 pneumococci)  Spread of infection to the pleural cavity. pericardium. meningitis suppurative meningitis.

. and diffuse alveolar damage.  They exhibit congestion. firm. the lungs become stiff due to loss of functional surfactant. and boggy. MICROSCOPIC EFFECT:  In the acute stage.  **Diffused patchy inflammation localized to interstitial areas of the alveolar walls.  Alveolar walls become lined with waxy hyaline membranes.ORGAN: LUNGS DIAGNOSIS/LESION: INTERSTITIAL PNEUMONIA ETIOLOGY: UNKNOWN GROSS EFFECT:  Early in the course. fibrin deposition. red. interstitial and intra-alveolar edema. the lungs are heavy.  Inflammation.

leaving minimal functional impairment.  Hypoxemia may be refractory oxygen therapy due to ventilation perfusion mismatching  Respiratory acidosis candevelop DIAGNOSIS:  Chest xray . CLINICAL COURSE:  Profound dyspnea and tachypnea herald acute lung injury  Increasing cyanosis and hypoxemia  Respiratory failure  Appearance of diffuse bilateral infiltrates on radiographic examination. In most cases the granulation tissue resolves.

 In countries where milk is pasteurized. TYPE OF NECROSIS: Caseous necrosis TYPE OF LESION: GRANULOMA CHARACTERISTIC CELL: EPITHELOID CELL (Modified macrophages) PREDOMINANT INFLAMMATORY CELL IN THE LESION: Neutrophil** TYPE OF HYPERSENSITIVITY: TYPE IV HYPERSENSITIVITY GROSS EFFECT:  Cheese like area of necrosis .ORGAN: SMALL INTESTINE DIAGNOSIS: TUBERCULOSIS ETIOLOGY:  Mycobacterium tuberculosis  Contracted by the drinking of contaminated milk is common incountries where bovine tuberculosis is present and milk is not pasteurized. intestinal tuberculosis is more often caused by the swallowing of coughed up infective material in patients with advanced pulmonary disease.

which then undergo granulomatous inflammation that can lead to ulceration of the overlying mucosa. LABORATORY DIAGNOSTICS:  Acid Fast Staining  Culture and Sensitivity .  Healing creates strictures. particularly in the ileum.MICROSCOPIC EFFECT:  Organisms are seeded to mucosal lymphoid aggregates of the small and large bowel.

ORGAN: UTERUS DIAGNOSIS: LEIOMYOMA ETIOLOGY: Hormonal LEIOMYOMA  Most common tumor in women. – due to Estrogen  In menopausal stage. Barely visible nodules to massive tumors that fill the pelvis.  Large tumors: develop yellow-brown to red softening (red degeneration)  They occur within the: o Myometrium (intramural) o Just bemeath the endometrium (submucosal) o or beneath the serosa (subserosal) . CELLS OF ORIGIN: SMOOTH MUSCLES TYPE OF DEGENERATION: HYALINE DEGENERATION MALIGNANT TRANSFORMATION: LEIOMYOSARCOMA** PREDISPOSING FACTOR:  Women that are in the reproductive life. round. discrete. firm.  Benign smooth muscle neoplasms that may occur singly. gray white tumors varying in sizes from small. but most often are multiples. they may regress and calcify GROSS EFFECT:  Sharply circumscribed.

regular. spindle shaped smooth muscles associate with hyalinization.***INTRAMURAL AND SUBMUCOUS OBLITERATING CAVITY MORPHOLOGY:  Whorled bundle of smooth muscle cells**  Well-differentiated.  Individual muscles cells are uniform in size and shape  Oval nucleus  Bipolar cytoplasmic processes  Atypical or bizarre tumors with nuclear atypia and giant cells CLINICAL MANIFESTATIONS:  Abnormal bleeding  Compression of the bladder  Urinary frequency  Sudden pain if disruption of blood occurs  Impaired fetility  In pregnant women: o Increase frequency of spontaneous abortion o Fetal malpresentation o Uterine inertia o Postpartum hemorrhage .

hair shaft and sebaceous glands****  NEUROECTODERM. hair.Glial tissue and ganglion cells TYPES: MATURE/ BENIGN Cystic / dermoid cyst Usually in young women during active reproductive years.ORGAN: OVARY DIAGNOSIS: DERMOID CYST (TERATOMA) TERATOMA  Derived from 3 germ layers  Presence of skin.  MORPHOLOGY . CELLS OF ORIGIN: TOTIPOTENT CELLS **MALIGNANT CELL TRANSFORMATION: SQUAMOUS CELL CARCINOMA – MOST COMMON GERM LAYERS:  ENDODERM – Respiratory and GUT epithelium  MESODERM – cartilage and smooth muscle  ECTODERM – Skin. sebum and cartilages  Cyst usually made up of teeth and skin (epidermis).

and skin adnexal structures. Structures from other germ layers may be identified GROSS Unilocular cysts Contains hair shaft Presence of hair and cheesy sebaceous material Tooth structures Areas of calcification MANAGEMENT: SURGICAL REMOVAL “NOTHING WORTH HAVING COMES EASY” #OPERATION VNECK #NO TO REMEDS 2015 GOD BLESS GUYS  . hair shafts.Cyst wall is Stratified squamous with underlying sebaceous glands.Madrid 2017 .