PATHOLOGY 1ST PRACTICAL EXAM part 1

THANK YOU FAISAL FOR MOST OF THE PICTURES.

Please do read your manuals. Don’t solely rely on this reviewer. There are other questions in the manual that I did not include in the slides.

CELLULAR INJURY, ADAPTATION, AND DEATH

CELLULAR SWELLING, kidney

Organ: Kidney – convoluted tubules

Size of lumen: decreasedCytoplasm: enlarged, increased pinkish colorReversible cell injury, but may become irreversible if stress is not removed

Pathogenesis: Swelling Is due to failure of membrane pumps because of lack of cellular ATP allowing the cell to accumulate fluid

FATTY CHANGE, liverHISTO:Organ: Liver – hepatic cordsCytoplasm: lipid vacuoles replacing the normal cords of hepatocytesNucleus: displaced peripherallyPathogenesis: impaired metabolism of fatty acids that leads to accumulation of triglyceridesConditions that give rise to fatty liver:1.Alcoholism2.Obesity3.Diabetes Mellitus

GROSS:Yellow and glossy appearancePale liver

DSCN6513

BROWN ATROPHY, heartPigment: LIPOFUSCINCell: Cytoplasm of Myocardial CellColor: brown or golden yellow granular appearance

DSCN6516

ANTHRACOSIS, hilar lymph nodePigment: CARBON/coal dustCell: Parenchymal cellsColor: black

DSCN6519

MALARIA, liverPigment: HEMOZOINCell: Kupffer cells

CHRONIC PASSIVE CONGESTION (CPC), lungPigment: HEMOSIDERINCell: alveolar/laden macrophageColor: yellow, golden brown

“heart failure cells (macrophages) in the alveoli are indicative of left sided heart failure”

DSCN6531

BILE NEPHROSIS, kidneyPigment: BILIRUBINCell: Tubular LumenColor: Reddish or golden brown

DSCN6533

SQUAMOUS METAPLASIA, lungsOrgan: Bronchi, lungs

Lining Epithelium: pseudostratified ciliated columnar epithelium was replaced by stratified squamous epithelium

Adaptive change: METAPLASIA

Seen in: chronic smokers and vitamin A deficiency

FAT NECROSIS, pancreas“acute pancreatitis” – pancreatic enzymes leak out of the acinar cells and liquefy the membranes of fat cells in the peripancreatic adipose tissue

Presence of numerous chalky white spots; necrosis of surrounding peripancreatic adipose tissue

Fat cells: pinkish-shadowy outline

DSCN6542

TUBERCULOSIS, lungsCASEOUS NECROSIS

White cheese-like appearance(granular amorphous debris)

MICROSCOPIC: formation of granulomas

NOTES:Other types of necrosis:1.Coagulative – common in kidney2.Liquefactive – brain3.Gangrenous – DM4.Fibrinous – connective tissue

GROSS:-Decrease in size of organ-White lesions on cut surface

DSCN6545

INFLAMMATION AND REPAIR

ACUTE APPENDICITISCells: PMN,

Edema present in mucosa, muscularis, and propria

(+) congestion of vessels and thrombosis

Type of necrosis: Suppurative Inflammation

Pathogenesis: initiated by progressive increase in intraluminal pressure that compromises venous outflow

APPEARANCEGROSS: dilated lumen; thickened wall; serosal surface has fibrinopurulent exudateHISTO: thickened edematous cell wall with neutrophilic infiltrates and vascular congestion with focal hemorrhages; eroded mucosa; presence of segmenters densely occupying the appendiceal wall

BRONCHOPNEUMONIA, lungsGROSS: with patches of consolidation, multiple abscess in the lungs

HISTO: bronchi, alveoli filled with NEUTROPHILS; congested septal capillaries

Tissue damage or necrosis

Acute inflammation

Marked neutrophilic response with tissue destruction

Abscess formation

OUTCOMES:1.Complete resolution2.Healing by CT replacement3.Progression to chronic inflammation

TUBERCULOSIS, lungsGRANULOMATOUS-Epitheloid cells, Langhans giant cells

Role of lymph nodes:-Filters and drains extravascular fluids that have seeded out of the capillaries

Conditions that cause chronic granulomatous inflammation:1.Leprosy2.Syphilis3.Cat-scratch disease4.Sarcoidosis5.Chron’s Disease

BENIGN ULCER, stomachExcavation of surface produced by the shedding of inflamed necrotic tissue; breach on the mucosal layer and penetrates into muscularis mucosa, submucosa, or deeper

EARLY PHASE – intense PMN infiltration and vascular dilation in margins

CHRONIC PHASE – fibroblastic proliferation, lymphocytes, macrophages, plasma cells

It is caused by an imbalance between damaging factors (gastric acid and peptic enzymes) and protective factors (gastric mucus secretion, local secretion of alkali)

GRANULATION TISSUESeen in the vagina

Presence of highly lymphocytic infiltrates with numerous angiogenesis

Plasma cells are also present and fibroblastic formation is seen

*Granuloma – no angiogenesis and focal accumulations of activated macrophages *Granulation tissue – angiogenesis, mononuclear cells (lymphocytes, plasma cells), some fibroblasts

END OF PART 1SHOUTOUTS:

hi to elmer, choy, kent, trixie, arlyn, and mark. i love you guys.Reinald, when is our next ice cream test? –ratatouille

To my thesis mates: HANS AND GIL. Good job to us! Kahit tatlo lang tayo. ICS 9, may our 15th member rest in peace.

Med Group 8. HI GUYS! I think dr. rosario will be leaving for 2 weeks. According to choy.Madame, sino na ang pipiliin mo? Si P, si M, si E, or si R? hihi. <3

Santi, my ever sipag patho lab buddy, thank you sa notes! Perfect dapat to ha!To justin, hi. I miss you. I love you. Hahaha. Adik lang!

Irene, get well soon. Good luck with the 2nd long exams. Kaya mo yan!

2013 a, good luck. 100% passing rate kahit dito lang sa patho exam. God bless everyone!

Love lots, RENEE GULA. 2013 A.

Hello to the Mann Hann Boys, CO6, ICS groupmates, and to the conyo people of sec A (Sam, Fifi, Ana, Xtian B.)Faisal, Salam-alaikum sibal! Koos arnab!

GOOD LUCK AND GOD BLESS 2013A!-Santi. 2013A