Systemic Pathology

Renal pathology

Glomerular syndromes

1. Acute nephritic syndrome

2. Nephrotic syndrome

3. RPGN

ACUTE NEPHRITIC SYNDROME

Hematuria

Oedema

Hypertension

Oliguria

Azotemia

Mild proteinurea

Eg. PSGN, MPGN

Nephrotic syndrome

Proteinurea >3.5(albumin)

Hypoalbuminemia

Edema

Hyperlipidemia

Lipidemia

Eg. Minimal change disease, membranous glomerulonephritis, FSGS,

MPGN

RPGN( all are nephritic syndrome)

Has features of acute nephritic syndrome+ acute renal failure

Increased proteinurea (not massive)

Eg. WG, microscopic PAN, GPS, SLE

PSGN

Post streptococcal glomerulonephritis

Group A beta hemolytic streptococcus

Type 3 HS

Type 2 is rheumatic carditis

NK cell can detect IgG

Complement is used in both type 2 and 3, it can be anywhere where there

is antibody

Antigens are from strep

Endostreptin

Nephritis strain asso. Protein NSAP

C/F

Pyoderma/ sore throat

Then ANS(acute nephritic syndrome), after 1-4 weeks

Podocytes are negatively charged and albumin gets repelled

complement comes and kills

Endothelial cells damaged much more than podocytes

Therefore RBCs are poured but not albumin

Thus leading to Hematuria and mild proteinurea

Light microscopic finding of PSGN

Since necrosis is happening

Brisk neutrophilic infiltrate in the glomeruli due to acute inflammation

This is followed by proliferation: endo capillary proliferation

Fluorescent microscopic findings

Granular deposits of IgM and C3

Electron microscopy

Electrondense( black) and electronluscent( white)

Here sub epithelial humps( characteristic) seen

And sub endothelial deposits

Prognosis of PSGN

90-95% remission and no complication

<5% land up into RPGN

Tt.

Plasmapheresis not useful as the immune complex are already deposited

in the kidney so no use filtering the plasma

Steroids also don't work

Penicillin prophylaxis not given as the no. of immune complexes formed

in reinfection are nill or very low( limited antigens)

Recurrence can occur if there is overwhelming infection by strep and

abundant antigens present

Principles of fluorescent microscopy

Antibodies against antibody or other things

We can identify

Which Ab is deposited

The pattern of deposit

All type 3 HS will show granular deposits as the immune complexes are
not specific

RPGN

C/F

ANS

ARF

Aka Crescentric GN

Coz on light microscopy we see crescent shaped structures in glomeruli

composed of fibrosis, mesangial cell, epithelial cells, inflammatory cells
and endo capillary cells

3 types of RPGN

Nephrotic syndrome
In children: MCD

Adults: FSGS

Elderly: MGN

Minimal change disease

Idiopathic is the most common cause

Secondary causes:

NSAIDs

Hodgkin's lymphoma

Other lymphomas and leukemias

SLE

C/F

Nephrotic syndrome

LM findings

No change in glomeruli

Lipid laden vacuoles in tubular cells due to reabsorption of lipids that was
being filtered

Not specific

Seen in all nephrotic syndromes

EM findings

Eacement of foot processes aka fusion or loss of foot processes

Not specific

Can be seen in any proteinuric states

Therefore the only sp change is the no change in glomeruli on LM

followed by Eacement on EM

Congenital nephrotic syndromes

Two important mutations

Nephrin: Finnish type of congenital nephrotic synd

Also asso congenital FSGS, AD form

Podocin: steroid resistant nephrotic syndrome

Other mutations

Alpha 3 integrin mutation

Dystroglycan

Proliferative means

Proliferation of

Mesangial , epithelial, endothelial, inflammatory cell

Non proliferative GN are only four

Minimal change disease

Membranous GN

Amyloid nephropathy

Diabetic glomerulosclerosis

FSGS
Focal and segmental glomerulosclerosis

C/F

Nephrotic syndromes

It is a group of conditions caused by multiple causes

Many of them are immune complex mediated

Deposited in the mesangium

Complent cells come and kill epithelial cells and mesangial cells

This happens chronically

Leading to sclerosis of the mesangium on LM which is focal and

segmental

Focal means less than half of glomeruli

Segmental means a part of the glomerulus( less than half)

Thus mesangial and epithelial cell proliferation can be seen on LM

IF finding

Granular deposits of IgM C3

EM finding

Electron dense deposits in mesangium

Histological variants of FSGS

1. Collapsing: asso with HIV/ aids, worst prognosis

2. Glomerular tip lesion: best prognosis

3. Cellular

4. Peri hilar

Causes of FSGS

HT nephropathy

Diabetic nephropathy

Reflux nephropathy

Sickle cell disease

Obesity

HIV nephropathy

MGN
Membranous glomerulonephritis

Immune complex mediated

Epithelial cells damaged

Therefore presents as nephrotic syndrome

LM

Thickened BM coz the deposits also get stained

But if we do special stains

Like PAS

PAS stains the BM but since there were immune complexes pushing the
BM, the BM looks irregular and spikes are seen on the BM

EM

Electron dense sub epithelial deposits

Rule of two in kidney

Two conditions where sub epithelial deposits seen

PSGN

MGN

Sub endothelial deposits:

Type 4 lupus

MGN

+/- PSGN

Two conditions that happen after sore throat

PSGN

IgA / HSP

Mesangial deposits

IgA

FSGS

Two diseases after diarrheal diseases

HUS- TTP

ATN: most common cause of acute renal failure in children

Tubular cells die as medulla has scant blood supply(10-20%)

ATN has severe dehydration compared to HUS- TTP

MPGN
Membranoproliferative glomerulonephritis

Immune complex mediated type 3( all are 3 except GPS)

deposits are everywhere, hence dense deposits

Although characteristic is sub endothelial

Therefore nephritic syndrome

Nephrotic syndrome can also happen

LM

Basement membrane thickened

Proliferation of endo capillary cells

Special stains will show tram track appearance as the complexes in the
BM don't get stained

Also ka splitting of BM

Aka duplication of BM

Aka replication of BM

EM

Sub endothelial or diuse dense deposits( even in sub epithelial)

Lupus nephritis
6 WHO types

Type 1 : least severe

Type 6: most severe, advanced sclerosing GN

Type 4 shows wire loop lesions. These are due to sub endothelial deposits

Although characteristic for type 4, can also be seen in 3 and 5

PSGN has Hematuria, not recurrent Hematuria, low complement levels

Deposits of IgM, IgG, IgA, C3: full house eect

Compliment is not decreased in pauci immune

Complement is increased in infection

IgA Nephropathy/ HSP

Both have same Pathogenesis

Immune complexes formed, IgA

Both present after resp tract inf.

Kidneys aected either concurrent or in 1-2 days

C/F of IgA nephropathy

Isolated recurrent gross Hematuria is the most common finding

Pt can also have

ANS

Nephrotic syndrome

RPGN

LM

Mesangial proliferation

Leading to mesangial sclerosis as it is recurrent

IF

Granular deposits of IgA and C3 most commonly seen

IgG and IgM can also be seen

EM

Electron dense deposits in mesangium

HUS- TTP
Micro thrombi of platelets

Aects small vessels of glomeruli

Thrombi come into capillaries and block the vessels

Leads to ischemia

Ultimately infarct of cortex as glomeruli are present in cortex

Which causes uremia( neuropsychiatric manifestations)

LM

Micro thrombi in glomerular capillaries

Small cortical infarcts

Hemolysis happens as the RBCs crossing the clogged capillaries get

damaged: microangiopathic hemolytic anemia

Happens after E. Coli and shigella

Alport syndrome
Inherited disease

Mutation of alpha 5 chain of type 4 collagen

Alpha 3 and 4 seen in 15% of the cases

X linked recessive

Females aected more due to lyonization

Disease mild in females and severe in males

C/F

Triad

Sensorineural deafness

Posterior cataracts, ???

ANS, NS, RPGN----> always progresses to CRF in males and mild

proteinurea in females

Lab Dx

LM

Foam cells in interstitium

EM

Alternate thinning of BM

Ka splitting g of lamina densa

Aka basket weave appearance

Aka, alternate thickening

Tt. No treatment

Renal transplant

Pyelonephritis

Inflammation of pelvis usually due to infection spreading to the renal

parenchyma of the kidney

Acute

Chronic

Acute pyelonephritis is a dd of chronic GN

Irregular contraction of kidney in CPN

Regular in CGN, always bilateral and symmetrical

While CPN can be UL/ BL, and asymmetrical

Cast in Urine

Tam horsfall protein

Formed either in loop of henle and in distal tubule

Cast takes the shape of the tubule

Hyaline casts are seen normally( tam horsfall)

If RBCs in cast: RBC cast( pathology in glomeruli)

Dysmorphic RBCs in GN, isomorphic in urinary tract

WBC cast

Shows inflammation

They either come from tubules

Seen in acute pyelonephritis ( also in tubulointerstitial inflammatory dis)

WBC cast dierentiates???

If bacteria in cast

Diagnostic of acute pyelonephritis

It dierentiates it from UTI

Broad cast

Dilated tubules

Characteristically seen in CRF

Aka cast of renal failure

Others

Epithelial casts

Fatty casts

Tumors of kidney

Benign

Malignant

Most common tumor if asked, go for benign if don't know

Most common tumor of kidney is papillary adenoma

Sub centimeter in size

Incidental finding

Most common malignancy is RCC

Other benign tumors of kidney are

Angiomyolipoma

Oncocytoma: have oncocytes, cells having numerous mitochondria

Sites are

Kidney

Thyroid aka hurthle cell neoplasm

Parathyroid

Salivary gland

Adrenal

Pancreas

Malignant tumors

RCC aka hypernephroma aka adenocarcinoma of kidney:

Divided into 3 types

Clear cell: proximal tubule, CD10

Papillary: proximal tubule, CD10

Chromophobe: best prognosis , distal tubule, CD117

Genetics of RCC

Clear cell

VHL mutation 3p25

3p deletion

Papillary

Trisomy 7 ( familial papillary RCC) and 17

Chromophobe

Monosomies

Furrman's gradefor clear cell

Hematogenous route for spread for rcc(CHORIOCARCINOMA, HCC ???)

Pediatric renal tumors

Most common: wilms

Malignant tumor

Genetics

Mutation of WT-1(11p15) and WT-2(11p13)

Beckwith wiedmann

WAGR: wilms, aniridia, gonadal hypoplasia, ????

Dennis drash

Nephrogenic rests

Precursors of wilms tumor

Nephroblastomatosis

Diuse presence of nephrogenic crest

Bilateral commonly

Gross appearance of wilms: fish flesh

Histopathology

Triphasic tumor

Epithelial phase: tubular cells

Mesenchymal: spindle cells

Blastemal: blast like cells

pediatric tumors
Most common of infancy and Childhood: hemangioma

Malignancy of infancy and childhood: ALL> CNS tumors> neuroblastoma

Most common malignancy of infancy: neuroblastoma

Most common solid organ malignancy: neuroblastoma

Most common malignancy of childhood: ALL

Most common abdominal malignancy of childhood: neuroblastoma

If above 2 years, wilms will be the answer

Most common soft tissue tumor of infancy and childhood: hemangioma

Most common soft tissue sarcoma of childhood: rhabdomyosarcoma

Oral cavity

Amiloblastoma

Aka adamantinoma

Most common site: mandible, maxilla, tibia

Cell of origin: odontogenic epithelium( teeth forming cell)

Histopathology

Palisading tumor cells

Tumors with Palisading

A. Aminoblastoma

B. Basal cell Ca.

C. Craniopharyngioma

One causes pseudopalisading

Glioblastoma multiforme

Salivary glands
GIT

Esophagus
Most common is squamous

Middle one third

Barrett's esophagus
Intestinal Metaplasia of lower esophagus

Gold standard for diagnosis: endoscopic biopsy

On biopsy: goblet cells

Special stain: Alcian blue for these

Stomach
H. Pylori

Urease producing bacilli

MALToma : causal association

Asso. with ch. gastritis, peptic ulcer, gastric carcinoma

H. Pylori diagnosed by urea breath test

Gold standard: biopsy from Antrum as maximum colonization is there

Then the organism is demonstrated by Warthin Starry stain

Warthin finkeldi cells in measles

GIST

Gastrointestinal stromal tumor

Cell of origin: interstitial cells of Cajal

Pacemakers of GIT

Most common site is stomach(70%)

Also in large intestine

Small intestine

Esophagus

Extra intestinal rare

Genetics

Mutation of C kit

It's a proto oncogene , receptor for tyrosine kinase

Markers of gist

CD117: second best marker

CD34

DOG-1: best marker

Most common mesenchymal tumor of GIT ( or abdomen)

It can be both benign and malignant

Size and mitotic count

Benign

<2 cm

<5/10 HPF

Celiac disease
Gluten sensitive enteropathy

Wheat, barley, rye, oat

Gliadin is the main molecule

Ch. diarrhea and malabsorption syndrome

Lab diagnosis

Anti endomysial

anti gliadin Ab

Anti tissue transglutamase

None are specific

Biopsy

Taken from second part of duodenum

Villi are thrice taller than crypts

Therefore, normal C/V ratio is 1/3

Infiltration of epithelial cells by lymphocytes

Increase in intra epithelial lymphocytes

Villous atrophy seen

Hyperplasia of crypts

Reversal of C/V ratio

None of the 3 are diagnostic

Gold standard: reversal of changes after a gluten free diet

Whipples disease

Trophyryma whippelii

Chr diarrhea

Malabsorption

Biopsy

PAS positive material in macrophages of lamina propria

Polyps of intestine
Juvenile, least malignant
Hamartomatous, 2nd least malignant
PJ polyp: 10% chance of malignancy

Adenomatous: FAP due to mutation of APC gene(proto oncogene), AD

disease;

Mutation YH, seen in 10% of cases

C/F of FAP

>100 polyps
Occur only in large intestine

Risk of malignancy:100%

Prophylactic total colectomy done

Prophylactic surgeries to avoid malignancy apart of above

Mastectomy

Oopherectomy

Orchidectomy in Undescended testes

Thyroidectomy in MEN-2 to avoid medullary Ca

Diseases of liver

Mallory body/ alcoholic hyaline/ Mallory hyaline

Intra cytoplasmic hyaline inclusion

Composed of keratin intermediate filaments

Causes

Alcoholic liver disease

Indian childhood cirrhosis

PBC

HCC

WD

Not seen in secondary biliary cirrhosis

List of named bodies

Gamna Gandy body: CVC spleen, hemolytic anemia, composed of

hemosiderin, dystrophic calcification, fibrosis

LD body: leishmaniasis

Heinz bodies: G6PD def

Howell Jolly bodies: hypo splenic states like sickle cell

LE cells: SLE , are neutrophils, then monocytes, then eosinophils

Hematoxylin body: SLE

Asco's nodule: RF

Asteroid bodies: sarcoidosis

Ferruginous bodies: asbestosis

Councilman bodies: acute viral hepatitis

Psammoma bodies: papillary thyroid Ca, serous cystadenoma of ovary,

meningiomas

Schiller Duvall bodies: endodermal sinus tumor, yolk cell tumor

Call Exner: granulosa cell tumor

Malakoplakia: michalis guttman

Inflammatory condition caused by proteus( E. Coli) infection of urinary

tract , commonest site is urinary bladder

Basophilic inclusion in macrophages

Negri bodies: rabies

Hirano bodies: Alzheimer's

Lews: PD and Lewy body dementia

Pick bodies: lobar atrophy of brain

Verrucae bodies: schwannomas ( Antony A and Antony B areas seen)

Lafora bodies: neuro cutaneous lipofuschiniosis

Civette bodies: lichen planus

Liver
Tumors of liver

Most common malignancy of liver is secondaries

Organs where secondaries are most common

Liver

Lungs

Lymph node

Bone

Brain

Peritoneum

Pleura

Pericardium with heart

Most common primary malignancy: HCC

Most common in children : hepatoblastoma

Most common primary tumor : cavernous hemangioma

Most common site of primary in hepatic secondary

Colon

Breast

Most common site for a hepatic secondary

Lungs

Marker for HCC: alpha feto protein

Hep Par 1 is the most specific marker

HCC sub type

Fibro lamellar HCC

Good prognosis

Not asso with viral hepatitis

Common in young age(28 years is the median age of presentation)

Relatively females are more aected( with respect to other HCC)

Histopathology

Absence of cirrhosis

Diseases of blood vessels

Atherosclerosis

Atherosclerotic plaque

lipid core has foam cells( lipid laden macrophages or sm ms)

Fibrous cap is composed of collagen and smooth muscle cells

Shoulder is composed of sm ms cells, T lymphocytes and macrophages

Large vessels aected

Abdominal aorta

Coronary arteries

Large vessels which are Spared

Mesentric

Renal

Upper limb arteries

Complications of atherosclerosis

Ischemic heart diseases

Atherosclerotic aneurysms

Two types

Abdominal aortic: atherosclerosis, below the renal artery

Thoracic aortic: hypertension, syphilis, collagen vascular diseases

Vasculitis

Large vessel:

GCA

>50 years,

Site

Temporal

Vertebral

Ophthalmic

Takayasu

<40 years

Arch of aorta

Histopathology of both show giant cell and granulomas

Medium vessel

PAN

Site is renal artery

Middle age

Pulmonary vessels are spared

No GN in PAN

Kawasaki

Coronary

Children

Both will show transmural inflammation and fibrinous necrosis

Small

WG

Respiratory tract granulomas, Crescentric GN, granulomatous vasculitis

Microscopic PAN

Leukocytoclastic vasculitis( neutrophils seen)

>90% have GN

Pulmonary vessels are involved

P- ANCA

Churg Strauss

Neoplasm of blood vessels

Most common tumor: capillary hemangioma

Sub type

Lobular capillary hemangioma

Aka pyogenic granuloma

Granuloma gravidorum( since happens in pregnancy)

Granuloma which are neoplasms

Pyogenic granuloma

Eosinophilic granuloma( langerhans cell histiocytosis)

Stewarts granuloma

Non Hodgkin's lymphoma of the nodes

Most common malignant tumor of the blood vessel

Angiosarcoma

Kaposi sarcoma: intermediate malignant potential

Caused by HHV-8

Asso with HIV

Heart

Myocardial infarction

Time required for myocyte to go into irreversible injury: 20-40 min

Vegetations of heart

rheumatic fever
Small

Verrucous

Sterile

Located along the lines of closure of valves

Infective endocarditis
Large

Friable

Non sterile

Located along the chordae tendinae

Libman Sachs
SLE

Sterile

Small

Located at Both the surface of valve(AV valve)

More commonly under the surface

NBTE
Small

Sterile

On the surface of the valve

Tumors of heart

Most common tumor of heart is secondaries

Most common primary for cardiac secondary is bronchial Ca

Most common primary overall and adult : myxomas

Child: rhabdomyoma

Myxomas most common site is left atrial

Rhabdomyoma most common site is left ventricular 100%

80% rt ventricle

Rhabdo has spider cells

Stellate cells in myxomas

Most common primary malignancy is angiosarcomas

Thyroid

Hashimoto thyroiditis

Follicular lysis: infiltration of follicular cells by lymphocytes

Some follicular cells go into metaplasia

Forms Hurthle cells, which have abundant mitochondria

Therefore cells of origin hoe hurthle cell tumor are follicular cells

Later dense lymphocytic infiltrate

Which malignancies can arise

Hurthle cell tumor

Non Hodgkin lymphoma

Tumors of thyroid

Papillary carcinoma, most common, best prognosis

Follicular, hemat spread

Medullary, arises from para follicular or C cells( neural crest cells, reach
through ultimo branchial body, C cell secrete calcitonin, marker of the
tumor

Anaplastic, worst prognostic

Marker for follicular cell origin(rest three) tumor thyroglobulin and TTF-1

Anaplastic is locally aggressive, invades trachea and adjacent organs

Papillary carcinoma
Lymphatic spread

Nuclear features are diagnostic

Orphan Annie eye nuclei

Follicular neoplasms
Adenoma and carcinoma

Carcinoma has capsular and vascular invasion not seen in adenoma

Therefore on FNAC, can't dierentiate adenoma and carcinoma

lungs

Most common malignancy of lungs: secondaries

Most common primary: Squamous cell carcinoma

Smoker and men: squamous cell is most common

Non smoker and women: adenoma

Overall : squamous

Tumor of lung can be divided into

Small cell

Poorly dierentiated carcinoid

Neuroendocrine tumors

Most aggressive Ca

Frequently metastasizes to brain

Histopathology

Nuclear moulding

Azzopardi eect: due to necrosis, released DNA deposits on the blood

vessel, vessel appear blue and thick

Markers of small cell ca: chromogranin( best and most specific),

synaptophysin, neuron sp enolase,

For all primary lung Ca: TTF-1( except for squamous cell Ca)

Genetics of small cell ca.

L-myc: proto oncogene

Non small cell Ca

Two important types

Squamous

Adenoma

Squamous cell

Genetics

Mutation of P53

Adenocarcinoma

Genetics: RAS, EGFR, P53, Rb

Subtype of adenocarcinoma ka bronchiolo alveolar Ca

Endobronchial spread, lepidic pattern

Good prognostic type

Pleura
Most common tumor or malignancy is secondaries

Most common primary for pleural secondaries is lungs

Most common primary malignancy is mesothelioma

Asso with asbestosis

Marker for mesothelioma is Calretinin

Next common site is peritoneum

Types of emphysema
Centriacinar

Panacinar

Paraseptal

in centriacinar

Smoking releases ROS

Oxidation of Alpha1 anti trypsin

Pro elastase mOre than anti elastase

Pan acinar will have alpha 1 anti trypsin def

Para septal will be asso with spontaneous pneumothorax

Reid index in chronic bronchitis

Mucosa to the wall of the bronchus upto the cartilage

Ratio is 1.4

This ratio is increased in bronchitis

Female genital tract

Ca cervix
Most common is squamous in India

Adeno in west, less HPV due to sanitation, vaccination also

HPV 16,18

E6 causes proteolysis of p53 and p21

E7 phosphorylates Rb( Rb acts mainly on G1S)

HPV requires mature squamous cells

superficial cells are mature( estrogen dependent)

Therefore no superficial and intermediate cells in post menopausal female

Only basal and para basal cells seen ( atrophic smear)

Thus Ca cervix is less common in post menopausal woman

Pap smear basically collects superficial and intermediate cells

We look for ???

Hybrid capture assay is not Pap. It tells us whether there is HPV infection
or not, therefore not a good screening test

Liquid based cytology is modified pap

Low grade squamous intra epithelial lesion( earlier CIN-1)

High grade squamous intra epithelial lesion(CIN -2 and 3)

LSIL has just 5% chance of malignancy

40-70% in HSIL

Bathesda System

Nucleus/ cytoplasmic ratio increases

Cellular atypia

Diagnosis of

Candidiasis

Bacterial vaginosis

Trichomonas

Actinomycosis

Can be done by Pap smear

.TUMORS of Ovary

Surface Epithelial tumor

Three types

Serous: resemble tubular epithelium

Benign and malignant

Serous cystadenoma and serous adenocarcinoma

Current consensus is that serous tumors arise from tube

Mucinous: resemble endo cervical epithelium

Mucinous cystadenoma and Mucinous adenocarcinoma

Brenner: has transitional epithelium

Germ cell tumor

Teratoma( dermoid cyst tumor is most common)

Mature and immature

Mature are well dierentiated, prognosis is good

Immature are malignant, most common immature element found is neuro

epithelial

Dysgerminoma

Markers are

PLAP placental alkaline phosphatase and LDH

Endodermal sinus tumor( yolk sac tumor)

Marker is AFP

Choriocarcinoma

B- HCG

Endodermal sinus tumor

Schilla duvar bodies

Mixed

Sex cord stromal tumor

Secrete sex hormones

Granulosa cell tumor

Secretes inhibin and estrogen

Any tumor secreting estrogen can cause endometrial ca.

Therefore 80% asso with endometrial hyperplasia and 5% endometrial

Ca.

Inhibin is a marker

Sertoli cell tumor

Leydig cell tumor

Theca cell tumor

Fibroma

Male genital tract

Most common germ cell tumor of testes is seminoma

Prostate
Adenocarcinoma

Markers are

Prostatic acid phosphate

PSA : more specific

PSA is specific for prostate and not prostate Ca.

Therefore PSA increases in

BPH

Prostatitis

Adenocarcinoma

Prostatic intra epithelial neoplasia: PSA not raised

Gleasons grade and score

5 dierent grades

Score is sum of two most recurring grades

Therefore min score is 2 and max is 10

Breast
Most common tumor is fibro adenoma

Most common Malignancy is Ductal carcinoma

Worst prognosis is Ductal

Lobular is frequently bilateral

Most common site of distant metastasis in Ductal is spine and lungs

For lobular, it is leptomeninges and pleura

Male only have Ductal breast carcinoma as no lobules present

Current new classification of breast Ca

Gene expression profiling of breast Ca.

Divides into four sub types

Luminal: cyto keratin 8 and 18 positive

Luminal A and luminal B

Strong ER positive is A, only good prognosis, rest all bad

B is ER negative or low, bad prognosis

Basal: 5 and 17 positive, ER negative, her 2 negative, bad prognosis

Her 2 neu over expressing, her 2 neu positive

Normal breast like

Soft tissue tumors

Most common soft tissue tumor is lipoma in adults

STT In children : hemangioma

Most common soft tissue sarcoma is

Malignant fibrous histiocytoma

Or

Liposarcoma

In children: rhabdomyosarcoma

Adipocytic tumor

Three types

Lipoma: nape of neck

Liposarcoma: retro peritoneum, lipoblast, marker is S-100

Hibernoma is tumor of brown fat

Smooth ms tumors

Leiomyoma: markers are desmin( positive in both skeletal and smooth

ms) and smooth ms actin

Leiomyosarcoma : necrosis and mitosis seen

Skeletal / cardiac ms

Malignant are rhabdomyosarcoma

Common age group is children

Site is peri orbital

Next common site is genitourinary

Divided into

Pleiomorphic: worst prognosis

Embryonal: botryoid is the best prognosis

Alveolar

Marker for RMS is

Desmin

Myogenin

MyoD1

synovial sarcoma

Cell of origin: unknown

Most common site: around knee joint

Biphasic tumor: epithelial and spindle cell phase

Markers are mic-2(CD99) and cytokeratin

Bad prognosis

CNS

Most common tumor of CNS : secondaries

Most common primary for CNS secondary: lungs

Most common primary tumor of CNS: glioma>meningiomas>

astrocytomas

Most common primary tumor of brain: astrocytomas( benign) in children

and glioblastoma( malignant) in adults

Most common malignancy of CNS: secondaries

In children: medulloblastoma

Most common primary tumor of CNS in HIV: primary CNS lymphomas( B

non Hodgkin lymphoma)

Meningiomas

Most common site : cerebral convexicities followed by Falx cerebri

Arises from Dura, inner layer

Cell of origin: arachnoid cap cells aka meningiothelial cells

Histopathology

Psamomma bodies

Tumor whirling

Glioblastoma multiforme
Primary: de novo malignant

Secondary: benign progressed to malignant

Histopathology

Pseudopalisading

Micro vascular proliferation, over expression of VEGF , glomeruloid

vessels

Prognosis is bad