Know diff morphologic features

Cell injury = what type of adaptation? Downsizing to conserve cell = atrophy

Correlated with case

We may give clinical data about pictures

Testis

Normal is left and the right is the abnormal/atrophic bec undescended testis

What is the lesion seen here what is the type of adaptation atrophy

What would be the reason behind = cryptochorchidism undescended testis of the right side
Which side do you think shows cerebral atrophy the right side

What lobe frontal lobe shows atrophy what conditions or dx alzheimers

Increase in cellular size of myocardial fibers systemic HTN

Compensatory hypertrophy of cardiac muscles

Hyperplasia

So much prominence of the folds of endometrial linings that they forms folds

Inc lining of epithelial cells

Stroma inc in number

Both glands and stroma increase size

Back to back folds

Hyperplasia

Elderly indiv males inc epithelial cells lining the glands forming papillae formation show prominence
corpora amylasaea inc number of cells

Endometrium and prostate undergo hyperplasia

Metaplasia lining epithelium of larynx

Pseudstaritifed columnar (normal encircld)

Strat squamous (left encircled) seen among smokers – squamous metaplasia of respi epithelium

Strat squamous epi undergoing this change (down)

Into gastric type epithelium (normal right up

Hypoxia; in myocardial fibers dying due to ischemic injury

You lose normal nuclei material

Small pink debris within cell bec cytoplasm is losing organells and structues within them – ghost outlines
Coag necrosis:

Cells with segmented appearance neutrophilic infiltrates that act on dead myofibers

Inflammatory process happens not just in infectious processes but also dead cells within body that
needs to be taken out

Wedged shaped appearance when it undergoes necrosis

In the kidney

Pale infarcted area: coag necrosis I nkidney with infarct

Related to hemodynamic changes: loss of blood supply affects cell and causes cell death IRREVERSIBLY

Abscess formation in liver

Liver tissue
Hepatocytes are around

Inflame infiltrates overriding the liver cells

Nectroic debris and neutrophilic is predominant infiltrates where you hav lique necrosis

You don’t see dead tissue any more just debris that occupies tissue in lique necrois
Liver abscess due to pus formation caused by what organism bacteria particularly pyogenic bacteria like
staph and strep

Correlate changes with microbiology

Clear space at center left becomes area of lique necrosis brought about by loss of blood supply or
hypoxia to brain
It will have this area aor space (cystic space) when lysed off tissue resolves?

Lique necrosis not only by loss of blood supply to brain but also pus forming infections or purulent
infections

Granuloma at casues necrosis

Central to the granulomatous lesion

Multinucleate giant cell

Lymphocytes seen at periphery of granuloma

Fibrous changes

Area of casueous necrosis as yellowish cheesy like material extensive TB infection

Neutrphilic purple???

Leakage of enzymes of pancreas to fatty tissue

Fat necrosis
Nectorit c with vague cellular …..

Fat cells adjacent t pancreatic tissue

Hemorrhage lysis of pancreas ust adjacent to adipocytes

How to diff bile pigment from hemosiderin

They would appear as reddish brown in color bile pigment in the liver, globular or definite blobs of
pigment, not assoc with hemorrhage in background
Anthra are carbon pigments in lungs – carbon inhaled by normal indiv in urban setting constantly
exposed to pollution, emission of carbon – intracellularly in bronchi and bronchioles, not symptomatic,
can still be seen normally within lung tissue and not cause any sx

Melanin – skin, basal portion of strat squam epi when there is inc melanin pigmentrelated to formation
of benign tumor (mole) (intradermal navus) (compound navus) grows inwardly into dermis

Calcification dysplasic or metaplastic NOTE DIFF

Fatty change in liver – reversible like cell swelling

Hemosiderin are related to (brown also) they are just powdery small, assoc hemorrhage at background

 Chronic vs acute pulmo edema

Acute congestion

Filled with rbc

Edema fluid (ointed) with prominent congested capillaries

Acute pulmo ingestion

Hemosiderin laden macrophage in chronic brownish and granular in pattern within macrophages
inclusion : hemosiderin
Hemorrhage (POINTED) lung tissue shows thick walled alveolar sacs markedly expanded bec
congestion of capillaries --- form microhemorrhages enricrcled macrophages activated,
macrophages engulf RBC within alveolar sacs , transudate inside alveolar spaces representing
exudation or going out of fluid bec congesiton
Active vs passive affects – compartment of vascular system arteriolar dilation and capillaries

Could be dilated and filled with blood

Active congestion another ex: when you blushface will be red because of dilatation of arteriolar
vessels

This one (left) appendix so much congestion of capillaries and arterioles of appendix microscopically
– (right) periappendicital fat – congested vessels
Thrombus inside bv (coronary artery)

Which has typical red and pink area as thrombus (more typical) the picture on the left shows
organizing thrombus

Picture on the right = alternating pink and red areas

Within lumen of coronary artery, CA also

Has thickedned wall not bec of thrombus but atheroscletotic change secondary to atherosclerotic
lesion to the wall

Wall itself shows injury to the endothelium

Predisposing factors: VIRCHOWS TRIAD or mechanism

Hyepercoag abnormal blood flow

Predisposes thrombus formation

Atherosclerotic lesion

Primary predisposing factor: bec of endothelial injury

Some slowing of flow of blood

Injury to the endothelium leads to formation of a thrombus

Atherosclerotic lesion: wall of vascular channel is affected – deposition of lipid material within the
wall (muscular and endothelial area of the vessel)

Aside from the triad to thrombus formation, what are the fates of the thrombus?

Embolization

Desolution/dissolve esp a small thrombus if it has a good hemodynamic status

It could organize like the left picture start of organization of thrombus within vessel wall but its
almost completely obliterated – occlusive problem to tissue around it

When you have an occlusion within a thrombus of a vessel what could happen?

It could have ischemic injury or necrosis ischesmic necoris it depends on thr organ involved

If brain: lique factvie necrosis

Heart: coag necrosis

Kidney: coag necrosis

FATES OF A THOMRBUS cause infarction also of surrounding tissue

When you have embolixation of a thrombus it will affect THAT ORGAN where embolization took
place and could obliterate lumen of emolized area

Embolization is DISTAL TO FIRST SITE OF THROMBUS thromboeblosu

Eventually organized and recanalized (RIGHT)

Attempt of vascular space or vessel to have recanalization to have flow of blood int thrombus

Left pic—typical thromboembolus – lines of zahn bec of diff red and alternating pink areas

Embolus bec no attachment ot wall of vessel

Thomrbus (LUNG TISSUE) this came from deep vein thrombus and it went up to the heart aor lung
tissue right chamber of heart

Smoldering effect became a large one to cause large thromboembolus

Gross infarcted small intestinal segment

If you have hemorrhagic infacrction which is true.. (ques)

A – NO the cause could not be seen in one histo exam, it’s a large one that you have to dissect
before seeing

B – NO bec it will appear as very red, hemorrhagic infarct

C- only mucosa NO BEC FULL THICKNESS OF WALL affected when colon is affected

You have to resect colon for colon to happen again for its functionality otherwise dead hemorrhagic
segment that causes poisioning

Inflammatoryc ond – dilated bv wall congestion of bv wall also

What is the cause of edema when you have inflamm?

There would be inc vasc permeability bec endothelial – extravasation of fluid – edema fluid will go
out – tumor appearance ***** enlarged organ which hhas inflam appearance

Cardinal sign: rubor or redness in the area how about when you see the diff chemokines and
cytokines in the inflame condition, what cardinal sign? Release of cytokines and chemokines : pain
sensation or dolor

Dolor, rubor, calor

Calor – heat change in temp umiinit at the area and you have the loss of function or function laesae

In inflame condition
Prominence of vascular markings at the serosal side of the appendix

Delineation of vascular markings

No more on this side because (left) because here is a material covering the surface of the appendix

Corresponds to purulent material

As it goes left : reddish

Area of hemorrhage

Vascular markings (right) vascular phase of acute inflame

Leukocytes at the periphery margination and rolling of tehcells and adhesion of neutrophils onthe
wall

Endothelial cells and surrounding tissue (emigration ebc of chemotaxis)

Prominence is chemootaxis or inflame cells have gone out of vascular channels and go to site of
injury or injurious agent should be acted upon
Serouns inflame

Linear pattern on hand – unaware of holiding boiling hot water (diba straight ayun)

Serous inflame lesion *THE SPACE) in bet the dermis and epidermis \
Meninges of the brain – prominence of vascular markings – acute inflame wherein fibrinous material
is seen all over meninges

Appendix shows suppurltive hange liquefactive necrosis

Pus on the right

Pus pointed on gross

Acute inflam in the gastric wall of the mucosa (ulecer formation)

Clean edge (pointed) vs neoplastic some neoplastic or maligntant will have ulceration that would in
turn show raised up borders and nectroci debris inside ulcer

But here, clean edg- benign ulcer

Liver shows prominently in the area of portal truad

How do you know if its portal triad =

Encircled – bile ductile

Thinning or numerous mononuclear infiltrates (lymphictyic and plasma cells

Small round mononuclear infiltrates = chronic hepatits

Jaundice

Assoc with history of injury to a previous iv drug user, previous viral heap with hepa b

Hepatocytes

Pink hepatocytes wchih have this change

Incept inflame cell is lymphocyte
Chronic inflame goes hand in hand with healing and when we see granulation tissue formation, we
see macro…(slide)

Large macrophages
Lots of macrophages

Small bv with rbc in them (the light purple) angiogenesis

Fibroblasts are spindle or

Elongated = granulation tissue formation

The tissue is healing or first phase of healing = hallmark of healing (granulation tissue = attempt to
heal)

Granulomatous lesion = it is always assoc with granulomatous inflammation

(the 3) you will also see fiboris

Epithelioid histiocytes
Granuloma has has ndular formation

Multinucleate giant cells

Lymphotcyitc
Infiltrates in background

Related ot immune dx – what type of hypersensitivity reaction type 4 or delayed type

Surrounding this yellow cheesy like = granuloma

Yellow = caseous necrosis

Healing together with chronic inflame = having healing process subsequent to chornic inflame is
healing so you have liver tissue with
Small nodules , normal should be uniform and red all thoughout but you see small nodules

Area where you see marked fibrosis in between nodules of hepatic plates
Smaller

Occupied again by hepatocytes all thogurought normallybut *******8

Portal tracts = fibrosis, lymphocytic infilterates = FIBORSIS as repair mech in liver tissue

Small nodules or hepatic plates attempting to regenerate

Liver could heal by fibrosis or regeneration bec liver is what type of cell? Stable cell
Wc means it could regrenarate otherwise stable cells are just stable, do not proliferate s

The labile stable permanent cells nomenclature may not be significant

That even permanent cells given proper condition could be stimaulated to even regenerate

Healing process when you have a clean incision on a wound ther is usually a rapid healing

Granulation ntissue formation 3-7 days just a small area to heal very well in first intetion

Surgically intervented procedures like incision of a tumor, benign tumor

Healing of area of ksin is fast bec wound healing rpop

2ndary intention – lesion of the skin wc affects great number of cells

Granulation tissue

Heals in longer period bec of large area

Large granulation tissue filling the wound

Crusting on upper portion

(microscope) small bv, lots of macrophages and infiltrates – in a healing wound

Type 1 from nasal mucosa respi mucosa

(pointed)

Submucosa in edema bec allergen it allowed a lot of inflame rxn and eosinophils

Pointed
Eosinophils with orange cytoplasm with segmented nuclei

Mast cells (encircled)

Plasma cells with peripherally located or polar nuclei

This nasal mucosa could produce nasal polyp in the long runedema inflame infiltrates

Tyoe 2 bec of complement

Note that the antigen coats the red cell – circulating ab now detect ag and acts on them via
complement system

CS produces c59 MAC

This may be seen in transfusion binasal ang niya slide

 Bind and induce lysis –

This ADCC
Transplant rejection, neoplastic or tumor cells you see lots of neutrophilic infiltrates * around it
ADCC

ACH on motor end plate – it will block receptor and dimisnih muscular response
Ab against entire GBM

Immunofluorescence with goodpasture – linear pattern of ab deposition

Promotes tissue damage binasa niya

These are trapped (the Y) acted upon c3b on the wall of small bv inciting complement cascade –
ongoing infalmm response
Type iv delayed which induces macrophages by cd4t

Binasa niya

Epitheloid cells and accumulate and form multinucleated giant cells supposed to ingest MTB

And continues to accumulate

Granuloma formation shown : mode of axtion is due to (incited to granulomatous dx) : tuberculin
skin rxn : type 3

Diff benign from malignant

We have a tumor of the breast that was excised – delineable mass

Delinateion between tumor and surrounding tissue

Fibroadenoma proliferation of both glnular and stromal elements

Flattened bec of prominence of fobromyxoid stroma

Benign

Breast tissue excised

Irregular borders infiltrating surrounding tissue

You do not see lineation anymore tumor is invading the stroma and surrounding tissue

Periphery of tumor = invasion of surrounding tissue

Benign tumor of the colon showing denilabel area

Delineable area (circled)

Exophytic growth of tumor

(right encircled) inc intensity of staining of nuclei and inc cells within glands vs the linig

Of the unaffected one

There is inc number of glands in the area of the tumor

Benign tumor bec still localized = tubular adenoma

Tubular bec they form tubular glands (tubulovillous, villuos adenoma) risk of having malignant
degeneration

Clear delineation

Malingnent

Lesion has rugged edge

Central flattened vs surrounding elevated

Tumor cells infiltrating stroma

Glands have invaded stroma

Occupying colonic wall not confined to submucosa but also muscular

Tumor cells around – marked fibrosis

Inflamm **********

Benign tumor – left gross piture of uterus cut section leiomyoma

Multiple leiomyomas of the uterine wall

Intramural

The checked intruamoura

The subserous is outward to the surface

Submucosal (impinges in uterine wall)

Binigen whirling pattern of tumor cells

Very well delineated borders

Typical smooth muscle appearance but in varying directions

Varying in direction of tumor cells of smooth muscle bundles – benign myeolieomya

Malignant looking

Uteruscervix is down
Endomertrial lining

Big mass that is hemorrhagic partly necrotic cut section

Shows necrosis

Cells are hyper chromatic

Leiomyosarcoma

Spindle cells at right down

A benign

B malignant

Capsule is infil
Capsular invasion folluclar carcinoma B-

A – denoma ** CASE

Papilarry carcinoma of the thyroid – GOGOEL

Benign lipoma well delinated borders of the tumor

Microscope typical clusters of adipocytes or fat cells

And they form lesion (gross)

Neoplasia try to study lab demo of dra Trinidad she will be using slides given

Malignant liposarcoma fat cells microscopic – of diff sizes and shapes and very dark nuclei and this is
liposarcoma even gross picture is

Not so delineable mass

What syndrome trisomy 21 or down syndrome

Congential abnormality

KNOW THE COMMMON ONES

Differentiate autosomal dom vs recessive

And who are affected, what is the cause

Auto dom- structural failure vs recessive – substrate to product failure

Affected enzyme involved – with affectation at 50% with dominant

While in recessive, dependent on combination of the carriers

** KNOW FOR CLUSTER EXAM

Classificatiojn of this

Reminder to review the SGD concepts and study guide questions pls. Thank you po – doc yolo

Cellular adaptation
all are side
questions so all are
HOTS you have to
identify dra santos
Pedigree can be asked in genetics