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Thrombotic vein
(33) Hemorrhoids - Rectal• varicose dilation of venous plexus at anorectal junction• Common lesions affect 5% pop. & develop 2° elevated venous
pressure within hemorhoidal plexus• causes:
– constipation– venous stasis of pregnancy
• morphology – varicosities develop:1. external hemorrhoids – varicosities develop in inferior hemorhoidal
plexus & located below anorectal line2. internal hemorrhoids – develop from dilation of superior hemorhoidal
plexus• histology
– Lesions: thin-walled, dilated, submucosal varices protruding beneath anal or rectal mucosa
– becomes thrombosed & recanalized in exposed, traumatized position– may develop
• superficial ulceration• fissure formation
– infarction w/strangulation
Landmark: Cardiac tissue
Infarction w/ thrombus
(15) Myocardial Infarction - Heart
• Infarct: area of coagulation necrosis• Cause
– ischemia because of blood supply obstruction– cells die & cellular protein undergo denaturation &
coagulation in absence of blood
• nuclear changes as:1. Karyopyknosis (shrunken nuclei)2. Karyorrhexis (nuclear fragmentation)3. Karyolysis (nuclei disappear)
• more red than normal cells in area of infarct• striation are lost with neutrophilic infiltrates in stroma• Note: cardiac architecture still recognizable• Landmark features: Lines of Zahn
RBC in interstitial Space Dilated
BV w/RBC
Edema Fluid - Pink
Dilated Cap Bed
Interestial Hemorrhage
Edema
(50) Chronic Passive Congestion - Lungs• long standing congestion• stasis of poorly oxygenated blood causes chronic hypoxia
cell death• capillary rupture causes:
1. hemorrhage2. breakdown & phagocytosis of red cell debris hemosiderin – laden
macrophages• Septa becomes thickened & fibrotic• Alveolar spaced – contain hemosiderin – laden macrophages
(heart failure cells)• Hemosiderin
– yellow to brown pigment containing Fe– Fe stored in cells w/apoferritin to form ferritin micelles
• Thickened-alveolar wall– granular yellowish-brown pigment scattered in:– interstitial alveolar space– alveolar macrophages (hear-failure cells)– alveolar capillaries – distended w/blood
Tumor Emboli
(57) Tumor - Embolus• Embolism
– detached intravascular, solid, liquid, or gaseous mass which goes w/circulation to be trapped in distant BV
– 99% emboli are detached thrombi– Foreign materials: air bubbles, BM tissue, fat droplets, tumor cell
• pulmonary embolism– most common preventable cause of death in hospital– large vessels of LE are sources of 95% pulmonary emboli
• Small Blood Vessels in alveolar wall contain aggregate cells atypical with pleomorphism
• Note: congested BV & presence of interstitial & alveolar edema• Fate of emboli:
1. Propagation2. Embolize3. Dissolution4. Recanalize5. organization
Landmark: Bronchiole – filled with exudate
Leaked exudate into lung tissue
Leaked exudate into lung tissue
(47) Bronchopneumonia - Lungs
• Lesion caused by bacteria:– Staphyloccus– Streptococcus– Pseudomonas– Coliform
• Characteristic lesions: patchy lung consolidations
• Infants & elderly more affected by disease• Lung sections
– Lumen has bronchi sections with mucopurulent exudates
– Walls infiltrated by acute inflammatory cells– Adjacent alveolar walls & spaces filled with exudates
(consolidation)– Alveolar vessels are hyperemic– Intervening alveolar walls may not be all consolidated
(51) Lobar Pneumonia - Lungs
• Acute• Inflammatory cells everywhere• Lesions & infiltrates located in alveolar spaces,
accompanied by edema• Dilated alveolar capillaries w/ lots of neutrophils
and some RBC, edema fluid.• Fibrino-suppurative exudates filling the alveolar
space.• Makes the lung air-less (consolidated). This is
the “red hepatization” stage.• Stages: Congestion, Red hepatization, Gray
hepatization, Resolution
Infiltrates in the lungs:Most are macrophages and Lymphocytes
(54) Interstitial Pneumonia - Lungs
• Lesion – thickened alveolar walls due to edema & congested blood vessels
• Inflammatory infiltrate in septa consists of– Lymphocytes– Plasma cells– Macrophages (mononuclear cells)
• Early lesions show interstitial location of cells• Hyaline membranes on septal walls appear
pinkish• Alveolar spaces not consolidated or filled up• Acute edema exudate
TB - Lung
• Lung granuloma• TB caseating granuloma• Granulomatous lesions
– Epitheloid cells– Giant cells– Fibrosis– Chronic inflammatory cells
• Area of caseation at center• Epitheloid cells surrounded by fibroblasts
zone & lymphocytes that usually contain Langhan’s giant cells
(19) TB – Lymph node
• Huge granuloma that fills nearly entire node
Landmark: Brain
Thickened edematous and inflammed meninges
(108) Acute meningitis - Brain
• Meningitis – inflamed meninges & subaracnoid area• 3 types of meningitis
1. Acute pyogenic (bacterial)2. Acute lymphocytic (viral)3. Chronic (fungal or bacterial)
• Common causative organism of pyogenic meningitis:1. Neonates – Escherichia coli2. Infants & children – Hemophiluz influenzae3. Adolescents & young adults – Neisseria meningitis
(Meningococcus)4. Very young & elderly ff. trauma – Pneumococcus
• Subarachnoid space filled w/polymorphonuclear neutrophils
• Congested meningeal vessels• Inflammatory cell infiltration at Meningeal walls, Sulci,
Blood vessels• Brain stroma not affected
Schistosoma - Skin• Helminth disease• Types - S.mansoni, S.japonicum, S.mekongi, S.haematobium• Transmitted via fresh-water snails in living in slow-moving
water• Hallmark are severe portal HPN, esophageal varices, &
ascites• Morphology
– Mild Schistosomiasis1. White pinheaded granulomas in gut & liver2. Granuloma contains schistosome3. Composed of macrophages, lymphocytes, neutrophils, eosinophils4. Liver darkened by regurgitated heme-derived pigments
– Severe Schistosomiasis1. Inflammatory patches form in colon2. “pipe-steam” fibrosis, fibrous triads resemble stem of clay pipe3. Granulomas & scar as seen in arteries of lungs
– S.haematobium1. Bladder inflamed patches due to massive egg deposition2. Granulomas appear early
Leprae cells aggregates containing mycobacterium leprae
Leprosy - Skin
• Known as “Hansen’s Disease”• Caused by mycobacterium leprae• Divides every 13 days & fails to grow above 36°C• Lacks exotoxin & endotoxins & has no lytic enzyme• 2 forms of leprosy:
1. Tuberculoid leprosy (TL)a. Good cell-mediated immunityb. Characterized by formation of tuberculoid granulomas w/few bacilli in
tissue2. Leromatous leprosy (LL)
a. Lacks T-cell mediated immunityb. Lesion show nodular or diffuse aggregates of foamy macrophagesc. Many bacilli found in macrophages
• Nodules in dermis appear foamy & show lipid-ladened macrophages
• Nuclei pushed to one side or at center & called “leprae cells”• Slight fibrosis around• No giant cells seen
(129) Verruca Vulgaris - Skin
• Most common type of war• Caused by papilloma virus (DNA-Papva virus group)• Lesions appear rough fard, papillary structures w/ brown
to gray-white color• Note:
– Thickened epidermis– Papillary thickening formation of epidermal cells– Hyperkeratosis & keratinocytes vacuolization
• Inclusion bodies in keratinocytes• Reddish & smooth in cytoplasm w/dark blue nuclei• Underlying stroma shows:
– Lymphocytes– Plasma cells– macrophages
Cysticercus - Muscle
• Taenia solium – cestode parasites (tapeworms) that invade tissues & cause infections
• Morphology– Found in any organ but mostly in brain, muscle, skin,
& heart– Cerebral symptoms include; meninges, gray & white
matter, sylvian aqueduct, & ventricular formaina– Cysts are ovoid & white to opalescent, does not
exceed 1.5 cm, & contain invaginated scolex w/hooklets that bathe in clear cyst fluid
– Cyst wall >100um thick, rich in glycoproteins, & evokes little host reaction when intact
– Inflammation occurs when cysts degenerate followed by focal scarring, & calcifications
Intestine landmark
Tubercle – inflammatory lesion
(30) TB - Intestine
• Infection caused by Mycobacterium tuberculosis• Chronic granulomatous inflammation• Tissue reaction – inflammatory lesion (tubercle)• Tubercle composition
– wall of fibrocytes & collagen fibers– Enclosing inflammatory infiltrates (lymphocytes, plasma
cells, macrophages (epitheloid cells), giant cells
• Caseation necrosis area– Tissue damage at tubercle center has pink, granular material– Area of tubercle center appears “cheese-like” (caseous)
AmoebaTrophozoiteentamoeba histolytica
(29) Intestinal Amoebiasis
• Amebic colitis – colon inflammation in amoebiasis• Parasite caused by Entamoeba hitolytica• Trophozoite has glycogen vacuoles in cytoplasm & aggregate
DNA-RNA at nuclear membrane• Infective stage: Forms cysts w/4 nuclei under adverse
conditions• Mode of transmission – fecal food & water contamination• Pathogenic stage: Cysts exits & become motile trophozoites in
intestine after being ingested• Common sites involved – cecum & ascending colon• Narrow ulceration located in mucosa• Ulceration widens at tunica propria• Ulcer walls show necrotic tissue & inflammatory cells• Trophozoites found in ulcer walls which shows halo or empty
space around, nuclei, vacuoles, & RBC in cytoplasm (not to be mistaken for macrophages)
Acute Pyelonephritis
(1) Acute Pyelonephritis - Kidney
• Acute suppurative kidney inflammation caused by bacterial infection
• Morphology– Patchy interstitial suppurative inflammation– Unpredictable lesion distribution– Damage occurs in lower & upper poles in pyelonephritis
associated w/reflux– Neutrophilic infiltration reaches tubules & produces
characteristic abscess w/destruction of engulfed tubules– 3 complications
1. Papilary necrosis
2. Pyonephrosis
3. Perinephric abscess
Appendix LandmarkAppendix LandmarkLymphoid Folicle
Neutrophil in the Muscular Layer
(27) Acute Appendicitis
• inflammation: RLQ, assoc. with fecalith & gallstone, tumor or worms
• manifestations: (1) pain, (2) nausea & vomiting, (3) abdominal tenderness, (4) mild fever, (5) increase WBC
• morphology:– neutrophilic exudate found in mucosa, submucosa, & muscularis propria– subserosal vessels congested & Perivascular neutrophilic infiltrate– early acute– inflammatory reaction transform normal serosa into dull,
granular, red membrane– acute suppurative – abscess formation w/in wall, along w/ ulcerations &
foci of Suppurative necrosis in mucosa– acute gangrenous – large areas of hemorrhagic green ulceration of
mucosa
• histologic:– Diagnosis of acute appendicitis is neutrophilic infiltration of muscularis
(40) Chronic peptic ulcer - abdomen• Produced by imbalance between gastroduodenal mucosal defense
mechanism & damaging forces• Gastric acid & pepsin are requisite of peptic ulcerations• Morphology
– 98% located in 1st of duodenum or stomach (ratio 4:1)– Small lesions (<0.3cm) shallow erosions– >0.6cm are ulcers– Size does not differentiate between benign from malignant– Round to oval, sharply punched out defect w/ relatively straight walls
• Histological– Active necrosis to chronic inflammation & scarring, to healing– 4 zones:
1. Base & margins – thin necrotic layer2. Non-specific infiltrate w/neutrophils3. Deep layer – active granulation tissue4. Solid fibrous or collagenous scar
• Complications1. Bleeding2. Perforation3. Obstrcution from edema4. Intractable pain
Chronic Cholecystitis – Gall Bladder
• Inflammation caused by obstruction of neck of cystic duct in 90% cases
• Associated w/gall stones
• Prostaglandins released from dilated gall bladder wall contribute to mucosal inflammation
• Bacterial infection develops in later course of disease
Band of fibrotic tissue under repair
(102) Liver cirrhosis
• Area of liver lobules & portal areas
• Note:– Fatty change in liver cells– Fibrosis bridging from central vein to portal area,
trapping islands of regenerative liver cells– Few lymphocytic infiltrates are seen in portal area