Transcript Photo Album - Caangay.com

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 line
2. 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
Infarction w/ thrombus
Landmark: Cardiac tissue
(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
Dilated Cap Bed
Interestial Hemorrhage
Edema
Edema
Fluid Pink
RBC in
interstitial
Space
Dilated
BV
w/RBC
(50) Chronic Passive Congestion - Lungs
• long standing congestion
• stasis of poorly oxygenated blood causes chronic hypoxia 
cell death
• capillary rupture causes:
1. hemorrhage
2. 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.
2.
3.
4.
5.
Propagation
Embolize
Dissolution
Recanalize
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.
2.
3.
•
Common causative organism of pyogenic meningitis:
1.
2.
3.
4.
•
•
•
•
Acute pyogenic (bacterial)
Acute lymphocytic (viral)
Chronic (fungal or bacterial)
Neonates – Escherichia coli
Infants & children – Hemophiluz influenzae
Adolescents & young adults – Neisseria meningitis
(Meningococcus)
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 Schistosomiasis
1.
2.
3.
4.
–
Severe Schistosomiasis
1.
2.
3.
–
White pinheaded granulomas in gut & liver
Granuloma contains schistosome
Composed of macrophages, lymphocytes, neutrophils, eosinophils
Liver darkened by regurgitated heme-derived pigments
Inflammatory patches form in colon
“pipe-steam” fibrosis, fibrous triads resemble stem of clay pipe
Granulomas & scar as seen in arteries of lungs
S.haematobium
1.
2.
Bladder inflamed patches due to massive egg deposition
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.
b.
2.
Leromatous leprosy (LL)
a.
b.
c.
•
•
•
•
Good cell-mediated immunity
Characterized by formation of tuberculoid granulomas w/few bacilli in
tissue
Lacks T-cell mediated immunity
Lesion show nodular or diffuse aggregates of foamy macrophages
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)
Amoeba
Trophozoite
entamoeba
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
Neutrophil in the
Muscular Layer
Appendix Landmark
Lymphoid Folicle
Appendix Landmark
(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.
2.
3.
4.
•
Base & margins – thin necrotic layer
Non-specific infiltrate w/neutrophils
Deep layer – active granulation tissue
Solid fibrous or collagenous scar
Complications
1.
2.
3.
4.
Bleeding
Perforation
Obstrcution from edema
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