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:

ORGAN: UTERUS DIAGNOSIS: ENDOMETRIAL HYPERPLASIA

Endometrial hyperplasia is an important cause of abnormal bleeding Frequent precursor to the most common type of endometrial

carcinoma. ETIOLOGY:

Hormonal Imbalance Prolonged stimulation of estrogen

**HALLMARK: Cylindrical shaped endometrial glands

PATHOGENESIS:

Inactivation of the PTEN tumor suppressor gene is a common genetic alteration in both endometrial hyperplasias and endometrial carcinomas.

ADAPTIVE CHANGE: Hyperplasia

GROSS EFFECT: Thickening of the endometrium

MICROSCOPIC EFFECT:

Increased gland to stroma ratio

Increased in number of glandular cells

Normal nuclei

Cells – columnar and multilayered

CLINICAL MANIFESTATION:

Abnormal bleeding

Increased secretion

MANAGEMENT: Atypical hyperplasia is managed by hysterectomy In young women who desire fertility, a trial of progestin therapy and

close follow-up.

ORGAN: HEART DIAGNOSIS: BROWN ATROPHY OF THE HEART ETIOLOGY:

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.

ADAPTIVE CHANGE: Atrophy GROSS EFFECT:

Decreased size of the heart and cardiac contractility. MICROSCOPIC EFFECT:

Intact nucleus

Increased stromal space. Presence of LIPOFUSCIN PIGMENT – product of autophagy,

wear and tear pigment, due to oxidative phosphorylation of the membrane. Sign of free radical injury and lipid peroxidation.

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

**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

ALCOHOL CONCENTRATION EFFECT

20 mgdl a slight feeling of intoxication

80mg/dl

Constitutes the legal definition of drunk driving, Decrease in complex

cognitive functions and motor performance

200 mg/dl Drowsines, slurred speach

300 mg/dl Stupor and coma

400 mg/dl Death

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

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.

**HALLMARK: Anucleated cardiac muscle cells with intense eosinophilia of the cytoplasm due to leakage of basic nuclear contents. TYPE OF INJURY: Irreversible Injury TYPE OF NECROSIS: COAGULATION NECROSIS LOCATION OF LESION: Cardiac muscle cell HEMODYNAMIC CHANGE: INFARCTION DIAGNOSTIC MARKERS: CK-MB, AST, LDH, Troponin I, Troponin T FAVORITE QUESTION: INFLAMMATORY CELLS INVOLVED IN THE LESION:

Neutrophils

Macrophage

Fibroblast

Lymphocytes and plasma cells ARE NOT INVOLVED GROSS EFFECT: MICROSCOPIC EFFECT:

Eosinophilic in the area of necrosis.

Striations are lost with stromal neutrophilic infiltrates.

Shrunken nuclei (Pyknosis), Nuclear fragmentation (Karyorrhexis) and Karyolysis (Disappearance of the nucleus)

CLINICAL MANIFESTATION:

ANGINA

CHEST PAIN

COMPLICATIONS:

Arrythmia- most common cause of death in the first several hours following infarction.

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

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, enclosing inflammatory cells like lymphocytes.) 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, macrophages and some PMN’s enclosed in a fibrous tissue made of collagen.

ORGAN: SKIN DIAGNOSIS: MALIGNANT MELANOMA ETIOLOGY:

Excessive growth of melanoblast. UV Rays

**HALLMARK: Brownish accumulation in the cells in the dermis. 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: 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.

**HALLMARK: Infiltration of neutrophils in the muscularis layer. TYPE OF INFLAMMATION: Acute suppurative inflammation PREDOMINANT INFLAMMATORY CELL: Neutrophil LOCATION OF LESION: MUSCULARIS HEMODYNAMIC CHANGE: HYPEREMIA

PATHOLOGIC CHANGES:

Dilated arterioles and capillaries (more prominent in the lamina propria and serosa, where the wall is looser)

Loosening of adjacent interstitium indicates edema. GROSS CHANGES:

Inflamed appendix with present characteristics of inflammation (rubor, tumor, dolor, etc

Congested appendix with a swollen distal half covered by purulent exudates

Lumen contains purulent exudates and often a fecalith. MICROSCOPIC CHANGES:

In inflammation, PMN’s are present even in the muscularis layer of the appendix. In terms of hemostasis, hyperemic vessels are evident in the serosal layer.

CLINICAL MANIFESTATION:

Mcburney’s sign (rebound tenderness upon deep palpation)

Anorexia

Nausea

Abdominal pain

Fever FORMS OF APPENDICITIS:

a. ACUTE SUPPURATIVE - Neutrophil infiltrates in all layer.

b. ACUTE NECROTIZING/GANGRENOUS

- Muscularis layer is replaced with neutrophilic infiltrates - Has tendency to rupture Perotinitis Sepsis

CHEMICAL MEDIATORS

FEVER- Chemical mediators (IL-1, Prostaglandins, TNF) PAIN – Prostaglandin

COMPLICATION OF RUPTURED APPENDICITIS:

Peritonitis

LABORATORY DIAGNOSIS

Neutrophilia

Elevated WBC count

MANAGEMENT:

APPENDECTOMY

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- Oncomelania quadrasi SITE OF MALNUTRITION: Liver – They male in the portal vein

where ova are laid.

TYPE OF INFLAMMATION: CHRONIC INFLAMMATION MECHANISM OF ACTION: A parasite (S. japonium) whose larvae enter the Skin. It goes to the liver to mature and eggs go to the circulation.

PARASITE INVOLVED: Schistosoma japonicum

**INFECTIVE STAGE OF PARASITE: Four tailed cercariae

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. ACUTE SCHISTOSOMIASIS Dominant TH1 produce IFN-gamma activate macrophage to

release TNF, IL-6, IL-1 FEVER COMMON SITES: Liver, Intestines and Lungs

B. 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.

HISTOLOGICAL CHANGES:

a. MILD FORM White,pinhead-size scattered granulomas Schistosome eggs with miracidium at the center of granuloma Macrophage, lymphocyte, neutrophils and eosiniphils

b. SEVERE FORM

Pipestem fibrosis-triad (granulomas, widespread fibrosis, portal enlargement)

**S. japonicum lodge in the superior mesenteric plexus **S. mansoni lodge in the inferior mesenteric plexus

**Fork tailed cercaria are the one infective to man. They become schistosomulia & go to the

lungs & reach the liver once they mature. They mate in the tribuatries of the portal vein.

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, producing severe congestion of alveolar capillaries leading to edema of the walls and alveolar spaces.

LOCATION OF LESION: STROMA HEMODYNAMIC CHANGE: HEMORRHAGE AND CONGESTION ACCUMULATED SUBSTANCE: HEMOSIDERIN (Non-hemoglobin,

***endogenous pigment due to hemolysis of rbc which is phagocytosed by macrophages.

CHIEF COMPLAINT: DIFFICUTY O BREATHING

MICROSCOPIC EFFECT: (+) Granular, 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

ORGAN: ANUS DIAGNOSIS: HEMORRHOIDS, THROMBOSIS

Hemorrhoids can also result from primary varicose dilation of the venous plexus at the anorectal junction (e.g.,through prolonged pelvic vascular congestion due to pregnancy or straining to defecate). Hemorrhoids are uncomfortable and may be a source of bleeding; 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.

Dilated veins filled with thrombus

LINES OF ZAHN - these represent pale platelet and fibrin deposits alternating with darker red cell rich layers. Such laminations signify that a thrombus has formed in flowing blood.

3 TYPES OF HEMORRHOIDS:

EXTERNAL HEMORRHOIDS- collateral vessels within the inferior hemorrhoidal plexus which are located below the anorectal line.

INTERNAL HEMORRHOIDS- result from dilation of the superior hemorrhoidal plexus within the distal rectum

COMBINED- both plexuses are affected

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ORGAN: THYROID DIAGNOSIS: HASHIMOTOS DISEASE / THYROIDITIS ETIOLOGY: Breakdown of self-tolerance to thyroid auto-antigens MECHANISM OF ACTION: Autoantibodies against thyroglobulin and thyroid peroxidise. GENE POLYMORPHISM:

CTLA4 (Cytotoxic T lymphocyte- associated antigen-4) – most significant

PTPN22 (protein tyrosine phosphatase- 22) TYPE OF HYPERSENSITIVITY: TYPE 4 HYPERSENSITIVITY GROSS EFFECT:

Thyroid diffusely enlarged

Capsule intact, gland well demarcated

Pale, yellow-tan, 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

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. **HALLMARK: TOPHI CRYSTALS ACCUMULATED SUBSTANCE: Monosodium urate crystals ACUTE INFLAMMATORY TYPE OF LESION: TOPHUS CHRONIC INFLAMMATORY TYPE OF LESION: Fibrosis, many macrophages and giant cells around the deposits. CLINICAL MANIFESTATION:

Joint pain MICROSCOPIC EFFECT:

Well circumscribed masses of pale-staining anuclear masses.

Urate crystals and deposits appearing as slender crystals or pinkish yellow masses surrounded by macrophages

Fibrosis DIAGNOSIS: INCREASED SERUM URIC ACID LEVEL

ORGAN: UTERUS DIAGNOSIS: HYDATIDIFORM MOLE MOST IMPRESSIVE ABNORMALITY: Extensive/ Diffuse trophoblast hyperplasia or proliferation GROSS EFFECT:

Delicate, friable mass of thin-walled, transluscent, cystic, **grapelike structures w/ swollen edematous (hydropic) villi

MORPHOLOGIC FEATURES:

COMPLETE MOLES PARTIAL MOLES

All villi underwent hydrophobic regeneration (Edematous)

Only some villi are edematous

Diffused trophoblastic prolifferation Localized trophoblastic proliferation

Without fetal parts With of fetal parts

GENOTYPE

XX karyotype 46 chromosomes

2n (Diploid)

XXY or XXXY karyotype 69 chromosomes

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

cell. fertilized by 1-2 sperms

Good prognosis Poor Prognosis

Complication: malignant choriocarcinoma

Increased risk of persistent molar disease BUT NOT choriocarcinoma

CLINICAL FEATURES:

Vaginal bleeding (4TH

TO 5TH

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

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.

RISK FACTORS: 1. HEREDITARY / GENETIC Inheritance of susceptible gene. **Positive family history – greatly increased in first degree female

relatives. Inherited mutations in p53 BRCA-1 / BRCA-2 tumor suppressor genes are

associated with increased risk BRCA 1 – dominant gene

2. History of breast Ca in one breast 3. Early menarche and late menopause 4. Obesity – due to production of estrogen by adipose tissue 5. First pregnancy after 30 years of age 6. Diet high in animal fat

**SITE OF METASTASIS: Axillary lymph nodes, lung, liver and bone

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, pleiomorphic cells

Hyperchromatic nucleus

Fibrosis of stroma

Malignant glands insinuating in fibrous stroma

Glands infiltrate in adipose tissue

Comedocarcinoma (ducts healed w/ malignant cells; 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

HISTOLOGICALLY: Multifocal lesions Some tumors may be well circumscribed and even encapsulated. 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. 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

ORGAN: SKIN DIAGNOSIS: Verruca vulgaris (WART) ETIOLOGY: HUMAN PAPILLOMA VIRUS (HPV 6 & HPV 11) MODE OF TRANSMISSION:

Direct Contact

Auto inoculation OUTCOME: Self-limiting, 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, 0.1 to 1 cm papules with rough, pebble-like surface

MORPHOLOGIC FEATURES:

Acanthosis (Thickened epithelium and Spiky appearance)

Papillomathosis

Dermis - 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)

ORGAN: CEREBELLUM DIAGNOSIS: MENINGITIS MENINGITIS

Inflammation of the meninges and CSF within the subarachnoid space. Usually caused by infection, 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- S. Pneumonia and Listeria monocytogenes are more common. ** S. Pneumonia is the most prevalent microorganism.

PARTS:

Pia mater Granular layer Meningeal vessel- congested

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.

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, with as many as 90,000 neutrophils under cubic millimiter

Increased protein concentration Markedly reduced glucose content

ORGAN: COLON DIAGNOSIS: AMEOBIC COLITIS PARASITE: Entamoeba histolytica

E. 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.

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. AMEBIASIS SEEN MORE FREQUENLTY IN: Cecum and ascending colon

** although the sigmoid colon, rectum and appendix can be involved.

MODE OF TRANSMISSION: Fecal-oral route MICROSCOPIC CHANGES:

Narrow ulceration of the involved mucosa ulceration in the tunica propria where the ulceration becomes wider.

Walls of the ulcers how necrotic tissue & some inflammatory cells.

Trophozoites show a halo/empty space & they present nuclei, vacuoles & red blood cells in the cytoplasm.

On the mucosal section, with ulceration (denuded mucosal portions), with surrounding inflamm atory cells

Does not go beyond muscularis mucosa

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.typhi are able to survive in gastric acid and once in the small

intestine, are taken up by and invade M cells. Organisms are then engulfed lymphoid tissue. Unlike S.enteritidis, S.typhi can then disseminate via lymphatics and blood vessels. Causing reactive hyperplasia of phagocytes and lymphoid tissues throughout the body.

MORPHOLOGY:

Infection causes Peyer’s patches in the terminal ileum to enlarge into sharply delineated, plateau like elevations up to 8 cm diameter.

Draining mesenteric lymph nodes are also enlarged.

Neutrophils accumulate within superficial lamina propia

Macrophages containing bacteria, red blood cells and nuclear debris mix with lymphocytes and plasma cells in the lamina propia.

Mucosal sheddings creates oval ulcers, oriented along the axis of ileum, that may perforate.

The draining lymph nodes also harbour organisms and are enlarged due to phagocyte accumulation.

Spleen is enlarged and soft with uniformly pale red pulp

Obliterated follicular markings

Prominent phagocyte hyperplasia

Liver – shows small, 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.

Patient with sickle cell disease are suscetible to salmonella osteomyelitis.

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

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.pneumonia is part of the endogenous flora in 20% of adults

and therefore false positive may be obtained

Isolation of pneumococci from blood cultures is more

specific but less sensitive.

Pneumococcal vaccines containing capsular

polysaccharides from the common serotypes are used in

patient in high risk.

Staphylococcus aureus

Most important cause of secondary bacterial pneumonia in children and healthy adults following viral respiratory illness.

Important cause of hospital acquired pneumonia.

Moraxella catarrhalis

Cause of bacterial pneumonia in elderly. Second most common bacterial cause of acute

exacerbation o COPD. Constitutes one of the three most common causes of otitis

media in children.

Klebsiella pneumonia Most frequent caue of gram negative bacterial pneumonia Commonly afflicts debilitated and malnourished people,

particularly chronic alcoholics. Thick gelatinous sputum is characteristic. Patient may have difficulty expectorating.

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: (99.9% GUT FEELING HAHAHA)

1. CONGESTION Lung is heavy, boggy and red. It is characterized by vascular engorgement, intra-

alveolar fluid with few neutrophils, and oftern the presence of numerous bacteria.

2. RED HEPATIZATION Massive confluent exudation with neutrophils, red

cells and fibrin filling the alveolar spaces.

Gross appearance:

Lobe appears distinctly red, firm and airless

Liver like consistency

3. GRAY HEPATIZATION Follows with progressive disintegration of red cells

and persistence of a fibrinosuppurative exudates.

Gross appearance:

Grayish brown

Dry surface

4. RESOLUTION Consolidated exudates within the alveolar spaces

undergoes progressive enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by macrophages, expectorated, or organized fibroblast growing into it.

CLINICAL MANIFESTATIONS:

Onset of high fever

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.

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, causing the intrapleural fibrinosuppurative reaction known as Empyema

Bacteremic dissemination to the heart valves, pericardium, brain, kidneys, spleen, or joints, causing metastatic abscesses, endocarditis, meningitis suppurative meningitis.

ORGAN: LUNGS DIAGNOSIS/LESION: INTERSTITIAL PNEUMONIA ETIOLOGY: UNKNOWN GROSS EFFECT:

Early in the course, the lungs become stiff due to loss of functional surfactant.

MICROSCOPIC EFFECT:

In the acute stage, the lungs are heavy, firm, red, and boggy.

**Diffused patchy inflammation localized to interstitial areas of the alveolar walls.

They exhibit congestion, interstitial and intra-alveolar edema.

Inflammation, fibrin deposition, and diffuse alveolar damage.

Alveolar walls become lined with waxy hyaline membranes.

In most cases the granulation tissue resolves, leaving minimal functional impairment.

CLINICAL COURSE:

Profound dyspnea and tachypnea herald acute lung injury

Increasing cyanosis and hypoxemia

Respiratory failure

Appearance of diffuse bilateral infiltrates on radiographic examination.

Hypoxemia may be refractory oxygen therapy due to ventilation perfusion mismatching

Respiratory acidosis candevelop

DIAGNOSIS: Chest xray

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.

In countries where milk is pasteurized, intestinal tuberculosis is more often caused by the swallowing of coughed up infective material in patients with advanced pulmonary disease.

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

MICROSCOPIC EFFECT: Organisms are seeded to mucosal lymphoid aggregates

of the small and large bowel, which then undergo granulomatous inflammation that can lead to ulceration of the overlying mucosa, particularly in the ileum.

Healing creates strictures. LABORATORY DIAGNOSTICS:

Acid Fast Staining

Culture and Sensitivity

ORGAN: UTERUS DIAGNOSIS: LEIOMYOMA ETIOLOGY: Hormonal LEIOMYOMA

Most common tumor in women.

Benign smooth muscle neoplasms that may occur singly, but most often are multiples.

CELLS OF ORIGIN: SMOOTH MUSCLES TYPE OF DEGENERATION: HYALINE DEGENERATION

MALIGNANT TRANSFORMATION: LEIOMYOSARCOMA** PREDISPOSING FACTOR:

Women that are in the reproductive life. – due to Estrogen

In menopausal stage, they may regress and calcify GROSS EFFECT:

Sharply circumscribed, discrete, round, firm, gray white tumors varying in sizes from small. 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)

***INTRAMURAL AND SUBMUCOUS OBLITERATING CAVITY

MORPHOLOGY:

Whorled bundle of smooth muscle cells** Well-differentiated, regular, spindle shaped smooth muscles associate with

hyalinization.

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

ORGAN: OVARY DIAGNOSIS: DERMOID CYST (TERATOMA)

TERATOMA

Derived from 3 germ layers

Presence of skin, hair, sebum and cartilages

Cyst usually made up of teeth and skin (epidermis). 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, hair shaft and sebaceous glands****

NEUROECTODERM- Glial tissue and ganglion cells TYPES:

MATURE/ BENIGN

Cystic / dermoid cyst

Usually in young women during active reproductive years.

MORPHOLOGY

Cyst wall is Stratified squamous with underlying sebaceous glands, hair shafts,

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

- Madrid 2017