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