Past Years Comparison

7/28/2019 Past Years Comparison

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PAST YEARS COMPARISON

ACUTE & CHRONIC INFLAMMATION (2001,2006,2012)

COMPARISON ACUTE INFLAMMATION CHRONIC INFLAMMATION

ONSET Acute Gradual

DURATION Short LongEFFECT ON BLOOD VESSELS Vasodilatation & hyperaemia No effect

INFLAMMATORY

EXUDATES

Marked Minimal

INFLAMMATORY CELLS mainly polymorphs Lymphocytes, plasma cells & macrophages

FIBROSIS No -present

-arterioles : thickening of walls & narrowing

of lumen

(end arteritis obliterans)

LOCAL REDNESS,

HOTNESS,SWELLING

Present Absent

FEVER AND LUECOCYTOSIS Present Low grade fever

DYSTROPHIC & METASTATIC CALCIFICATION (2003,2012)

DYSTROPHIC CALCIFICATION METASTATIC CALCIFICATION

Sites In dead and degenerating tissue In previously undamaged tissue especially :

-lung alveoli

-gastric mucosa

-media of blood vessels

-kidney (from renal stones)

Deposition of calcium

salt

Dead and degenerating tissue Blood

Dependant on increase

of calcium serum level

. Does not depend Depend

Pathogenesis Examples:

1)Areas of tuberculous necrosis & caseation2) in fat necrosis with acute haemorrhagic

pancreatitis

3) Dead bilharzial ova &hydatid cysts

4) Dead foetus

5) Wall of blood vessels in arteriosclerosis &

atheroma

6) Wall of chronic abscess or old scar

7) Certain tumours with degeneration (leiomyoma)

8) In nodular goiter (thyroid degeneration)

Causes:

1)Hyperthyroidism-Primary :increased mobilization of calcium

from bone

-Secondary : Chronic renal disease with

phosphate retention > secondary

hyperparathyroidism >hypercalcaemia

2)Hypervitaminosis D :

- lead to increased absorption of calcium

from GIT

3)Destructive bone diseases (tumour)


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DRY GANGRENE & MOIST GANGRENE (2011)

DRY GANGRENE MOIST GANGRENE

Mode of onset Gradual Sudden

Site of gangrene Limbs Limbs & internal organs

Site of occlusion Artery Artery & vein

Cause of necrosis Tissue anoxia Tissue anoxia or toxins

Tissue fluids Decreased Increased

Size of affected part Shrunken & mummified Swollen

Line of demarcation Well formed Poorly formed

Toxaemia Mild Severe

Course Slow, may end in self- separation Rapid & fatal. No self-separation

DRY GANGRENE & GAS GANGRENE (2004)

DRY GANGRENE GAS GANGRENE

Def Massive tissue necrosis followed by

putrifection,dry types

-Rapidly spreading infection due to contamination of

wounds

-by anaerobic spore bearing organisms especially in fecal

matters & animal excreta-may also occur in civil life

Causes Arterial occlusion:

-minor trauma as from tight shoes

-removal or corn

From organisms (saccharolytic bacteria):

-cl.welchii

-cl oedematiens

-vibrio septique

Types 1)Senile gangrene

2)Diabetic gangrene

-

Pathological

features

I)Senile Gangrene

1)Distal to vascular occlusion :

-massive necrosis,no pulsation,no sensation

-affected part cold and pale

2)necrotic tissue:

-dry,shrunken,mummified

3)Bad odour

4)Blackening of affected part

5)Progression slowly and gradually

6)Line of demarcation & line of separation

7)Conical stump (natural amputation)

II)Diabetic gangrene

1)begin in feet

2)more rapid

3)low resistance (diabetic patient)

4)Better medium for organism to growth due to

presence of sugar.

5)Atherosclerosis affect vessel of extremities

1)Affected muscle :

-necrosis

-gas bubbles form

2)No line of demarcation

3)Fatal condition due to:

-severe toxaemia which cause deneration and necrosis in

parenchymal organs (liver,kidney,heart,adrenal organ)

4)Causative organism secretes :

-hyaluronidase enzyme - dissolve round cement substance

-poweful toxins - cause putrefaction and gangrene


3/15

EXUDATE & TRANSUDATE (2001,2002,2004)

EXUDATE TRANSUDATE

Specific gravity >1015 3gm% sterility

Other lesion - 1)Gynaecomastia in male

2)Bone : rarefraction

Mucous membrane - 1)Site : nose,pharynx,palate, shows :

-scabs and nodularity

-abundant nasal discharge

-destruction and perforation of nasal septum

-healing causes laryngeal obstruction


4/15

LAENNECS CIRRHOSIS & BILHARZIAL PERIPORTAL FIBROSIS (2006)

LAENNECS CIRRHOSIS BILHARZIAL PERIPORTAL FIBROSIS

FINE PERIPORTAL FIBROSIS COARSE PERIPORTAL FIBROSIS

Causes 1)Prolonged severe malnutrition &

chronic alcoholism lead to :

- fatty change in liver or steatosis

1) Ova :

-Small number

-desposited in fine portal tracts

1) ova & dead worms

-large number

-deposited in coarse portal tractsG/P 1)Colour : yellow

2)Early stage: enlarged, soft

3)Late stage :

-shrinkage + micronodular outer

surface.

4) Cut surface:

-small yellowish micronodules


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PATHOLOGIC HYPERPLASIA & NEOPLASIA (01,03,05,08,10,11)

PATHOLOGIC HYPERPLASIA NEOPLASIA

INDUCTION Induced by stimulus & corrected by its removal Usually does not need stimulus

LIMITATION Self limited No limitation or control for its growth

RELATION TO STIMULUS Degree of hyperplasia related to degree of stimulation Not depend on stimulus in its growth

FUNCTION Produces function Functionless purposeless new growth

DEGREE OF

DIFFERENTIATION

-Hyperplastic cells resemble tissue of origin

-normal in shape & pattern

-Malignant neoplastic lesion differ from original

tissue

- abnormal in shape & pattern

MITOSIS Normal mitosis Abnormal mitosis if malignant

BENIGN & MALIGNANT TUMORS (2012)

FEATURE BENIGN MALIGNANT

Origin De novo -De novo-on top of premalignant or benign lesion

Size Small Reach large size in short time

Rate of growth Slow Rapid

Mode of growth -Expansion

-compression

-Infiltration

-invasion

G/P -Margin : Well-defined

-Cut surface : uniform

- no hemorrhage or necrosis

-Margin : ill-defined or irregular margin

-cut surface : areas of hemorrhage & necrosis

Capsule Present Absent

M/P Tumor cells resemble normal tissue of origin

(differentiated) with minimal or no mitosis

Cellular anaplasia in the form of :

-cellular & nuclear pleomorphism,

-nuclear enlargement

-hyperchromasia

- prominent nucleoli

-increased nucleocytoplasmic ratio

- abnormal differentiation

- abnormal mitosis

-Hemorrhage, necrosis, & degeneration are present

Metastasis (spread) Absent Present

Recurrence Rare frequent

Effects on host -Not dangerous unless those of vital or hollow organs

- may turn malignant or produce hormones

-Destruction of nearby tissue or organ

-anemia due to hemorrhage or bone marrow destruction

-econdary infection

-cachexia

- organ failure


6/15

BASAL CELL CARCINOMA & SQUAMOUS CELL CARCINOMA (2003,2004)

BASAL CELL CARCINOMA SQUAMOUS CELL CARCINOMA

Definition Locally malignant tumour from basal cell layer of

epidermis of skin and its appendages (ex: hair follicles)

Malignant tumour of stratified squamous epithelium

Sites of

origin

1) Sun exposed skin :

-middle 1/3 of face

-butterfly area

1)Skin, mucous membrane of :

-Lip, pharynx, larynx, oesophagus, anal canal, vagina &

cervix uteri.

2) on top of sq. metaplasia: UB,GB bronchi & endocervix

G/P -Flattened nodule slowly enlarge

-then ulcerates.

Ulcer edges: raised, beaded & rolled in.

Floor: necrotic

Base: hard & fixed to underlying structures.

1)Small hard nodule infiltrate surrounding structures

2)in form of :

-polypoidal fungating mass

-ulcerative mass

-diffuse infiltrating carcinoma.

M/P 1)Basophilic masses of malignant cells infiltrate the

dermis. variable size + shape

2)Cell masses form of :

Outer layer :

-columnar

-show palisading of nuclei

Central cells:

-polyhedral and rounded

-no evidence of keratinization

3)Cytoplasm : scanty + bluish

Nuclei : large, oval, hyperchromatic

1)Sheets and cords of malignant keratinocytes infiltrate the

dermis,forming cell nest.variable size + shape

2)Cell nests:

Peripheral layer : darkly stained,small basal like

Intermediate layer : multiple layer of polyhedral cells

Central : complete cornificating from dark red stain mass of

keratin

2)The cells show malignant characters:

-hyperchromatism

-pleomorphism

-Increase N/C ratio

-prominent nucleoli

-increase mitotic activity

-abnormal mitosis

-loss of polarity

3)Stroma is infiltrated by chronic inflammatory cells.

Characters

of ulcer

1)Edge : Raised,beaded (rolled in)

2)Floor : necrotic3)Base : fixed to underlying structures,hard

4)Regonal LN : -

1)Edge: raised,everted (rolled out)

2)Floor : necrotic3)Base : fixed indurated

4)Regional LN : enlarged,stony,hard

Spread 1)Malignant cells invade & destroy underlying tissue

locally.

2)No distant metastasis

3)May change to SCC or baso-SCC

4)Wide safety margin

1)Slower than sarcomas.

2)Occur by :

- lymphatics to regional lymph nodes.

- blood spread (late)


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DIFFERENCES BETWEEN CARCINOMA & SARCOMA (2011)

CARCINOMA SARCOMA

Definition Malignant tumor of epithelial origin Malignant tumor of mesenchymal origin

Age Middle & old All ages especially young

Incidence More common Less common

Rate of growth Less rapid than sarcoma More rapid than carcinoma

Size Smaller than sarcoma Large,variegated

M/P -Sheets, cords, groups of cell or acini

-separate by fibrous stroma

-Cellular & individual cells

-separate by intercellular stroma

Stroma Well-formed stroma Poorly formed stroma

Hemorrhage &

necrosis

Less than sarcoma More than sarcoma

Differentiation Less anaplastic More anaplastic

Metastasis -Early : lymphatic

-late : blood

- Early : blood

-rarely : lymphatic

Radiosensitivity Radiosensitive Radioresistant

Prognosis Better than sarcoma Bad

DIFFERENCES BETWEEN HAMARTOMA AND TERATOMA (2004)

HAMARTOMA TERATOMA

Def -Tumour like developmental malformation

-composed of non-capsulated irregular mature tissue

of affected organ in abnormal arrangement.

-Tumour containing structures arising from totipotent germ

cells

-composed of tissue which are foreign to the site of origin

Site Lung hamartoma 1)Gonadal : from testis & ovary

2)Extragonadal :

-ant mediastinum -retroperitoneum

-base of skull -sacrococcygeal region

Age -Present at birth

-Stop at puberty

-Young females

-Prepubertal adolescentsTypes 1)Mature teratoma (benign teratoma)

-solid teratoma

-cystic teratoma(dermoid cyst)

2)immature teratoma (Malignant teratoma)

3)Monodermal teratoma

1)Lung teratoma

2)Some tumour like lesion

-hemangioma

-nevi

-enchondromas

-neurofibromatosis

-lymphangioma

G/P 1)Non capsulated

2)composed of mixture of cartilage,blood

vessels,smooth muscle,CT,bronchial tissue

3)Some tumour like lesions :

-hemangioma

-nevi

-enchondromas-neurofibromatosis

-lymphangioma

I)Cystic teratoma (dermoid cyst)

1)Thick wall oval or rounded cyst

2)Cyst contain:

-thick yellow sebaceous gland

-hair,teeth,bone,cartilage respiratory or nerve elements

3)Tumour tissue projects in cyst cavity as nipple like

protrusion(dermoid ridge)

Precancerous -some of them are precancerous -1% of cases undergo malignant transformation


8/15

VEGETATION RHEUMATIC ENDOCARDITIS & SUBACUTE BACTERIAL ENDOCARDITIS (2003,2011)

RHEUMATIC VEGETATIONS ACUTE INFECTIVE BACTERIAL

ENDOCARDITIS VEGETATIONS

SUBACUTE BACTERIAL ENDOCARDITIS

VEGETATIONS

Characteristics -Multiple- small (1-3mm)

-firm

-adherent

-Multiple-bulky

-friable

-detachable

-yellowish

-septic

-Multiple-bulky

- friable

-detachable

-grayish

-aseptic

Type &

composition of

thrombus

Pale thrombus

-fibrin,platlets

Pale thrombus

-Fibrin,platelet,bacterial

colonies,PMNLs,pus cells

Pale thrombus

- Fibrin,platelet,bacterial

colonies,mononuclear cells

Site of

vegetation

1)On rough surface valve

2)At line of closure of cusps

-on atrial surface of mitral valve.

-on ventricular surface of aortic valve

3)May formed over:-chordae tendinae

-post wall of left atrium

1)Anywhere on cusps

2)Commonly :

- mitral & aortic valve

3)Less common :

-tricuspid & pulmonary

4) May formed over:

-chordae tendinae

-mural endocardium

1)Anywhere on cusps

2)Commonly :

- mitral & aortic valve

3) May formed over:-chordae tendinae

- post wall of left atrium (on Maccallums

patch)

Complications - 1)Detachment leads to:

-systemic pyaemia

-systemic pyaemic abscess in

kidney,spleen,lung,barin

-

DIFFERENCES BETWEEN LOBAR PNEUMONIA & BRONCHOPNEUMONIA(01,02,11,12)

LOBAR PNEUMONIA BRONCHOPNEUMONIA

Type of inflammation Diffuse fibrinous inflammation Patchy suppurative inflammation

Start of lesion in alveoli in bronchioles

Most frequent site of

affection

upper lobes lower lobes

Most common age middle age children & elderly people

Course Onset & recovery of disease are sudden Insidious onset & gradual recovery

Aetiology Primary (usually) Complication of other disease

DIFFERENCES BETWEEN ULCERATIVE COLITIS & CROHNS DISEASE (2010,2012)

ULCERATIVE COLITIS CROHNS DISEASE

Sites Large intestine Small & large intestineCause intestinal hemorrhage intestinal obstruction

Fistula and anal fissures Absent Present (50%)

Extra intestinal manifestations more common Less common

Type of inflammation Mucosal inflammation (crypt abscess) Transmural inflammation with cobblestone

appearance

Granulomatous reaction Absent Present

Fibrous thickening of wall rare Common

Incidence of carcinoma Higher incidence of dysplasia & carcinoma of

colon (10% of cases)

Carcinoma occurs in less than 1%


9/15

BENIGN ESSENTIAL HYPERTENSION AND MALIGNANT HYPERTENSION (2009)

BENIGN ESSENTIAL HYPERTENSION MALIGNANT HYPERTENSION

C/P -Hypertension

-Microscopic haematuria

-Proteinuria

-Hypertension (marked elevation)

-Haematuria

-Proteinuria

G/P In longs standing cases:

1)Size:reduces,contracted

2)consistency : firm

3)surface : finely granular showing retention cyst

4)Capsule : adherent

5)Cut surface :

-atrophy of cortex

-loss of demarcation btw cortex and medulla

-increase perinephric fat

1)Size : normal

2)Outer surface : smooth

3)Capsule : strips easily

4)Cut surface : area of haemorrhage

5)Vessels :

-thick and prominent

-narrow

M/P 1)Interlobular arteries :

-fibroelastic thickening of intima

2)Afferent arterioles :

-hyaline subendothelial material

3)Bowmans capsule :

-fibrosis & thickening of glomerular capillary walls

4)Tubules connected to fibrotic glomeruli:

-atrophy

5)Tubules connected to functioning glomeruli:

-compensatory dilatation,retention cyst

6)Increased interstitial tissue,lymphocytic infiltration

1)Interlobular arterioles :

-concentric subintimal fibrosis

2)Afferent arterioles :

-fibrinoid necrosis

3)Bowmans capsule:

-haemorrhage

-crescent formation

NEPHROTIC SYNDROME AND NEHPRITIC SYNDROME (2011)

NEPHRITIC SYNDROME NEPHROTIC SYNDROME

Disease 1)commonly in :

-acute post streptococcal glomerulonephritis

-rapidly progressive glomerulonephritis

1)In :

-minimal change disease

Manifestations -oligouria

-haematuria

-mild oedema

-mild proteinuria

-massive proteinuria

-hypoalbuminaemia

-hypercholesterolaemia

Renal Failure -Acute renal failure -Gradual renal failure

Blood pressure -High blood pressure -not affected

Age -common in adult -common in children (80%)


10/15

HYPERNEPHROMA & WILMS TUMOUR (2011)

HYPERNEPHROMA WILMS TUMOUR

Incidence -Common in males

-after 40 years of age

-Common in childhood

-first 5 years of life

G/P 1)Tumour :

-large rounded - well circumscribed

- sharply demarcated mass at one pole of kidney.

-Cut surface: yellowish.

-Areas of haemorrhage& necrosis > variegated appearance

1)Tumour

-large -well circumscribed swelling.

-Consistency: fleshy or firm.

-Cut surface: grayish white.

-Areas of cystic changes, haemorrhage& necrosis.

M/P 1)Clear cell type:

- most common form

-Large rounded cells

-clear cytoplasm & central nuclei.

- Arranged : solid sheets, cords, or tubules.

-Separate by thin fibrous trabeculae.

2)Other types:

- chromophobe cell type - papillary type

-granular cell type -sarcomatoid type.

1)Very primitive immature spindle cells that form

abortive tubules and glomeruli.

2)Cells have:

Nuclei : deeply basophilic

Cytoplasm : very scant amount

3)Background may contain smooth and striated

muscle,bone or cartilage.

Spread 1) Direct spread: renal pelvis & cause haematuria.

2) Lymphatic spread: para-aortic lymph nodes

3) Blood spread: lung, liver, bones

1) Direct spread: nearby kidney tissue to form mass.

2) Blood spread: lung.

3) Lymphatic spread: regional lymph nodes

OVARIAN SEROUS AND MUSINOUS TUMOUR (2012)

SEROUS TUMOURS MUCINOUS TUMOURS

Aetiology -common cystic neoplasm,filled with serous fluid

-30% of all ovarian tumour

-closely resemble their serous counterparts

-25% of all ovarian tumoursSites -20% of beign tumours = bilateral

-2/3 of malignant tumours = bilateral

-5% of bening tumour = bilateral

-20% of malignant tomour = bilateral

G/P 1)Benign,borderline,malignant variants are

-large spherical or ovoid cysts

-smaller masses have single cavity,

Larger masses have multilocular cavity

2)Benign has smooth glistening serosal and inner aspects

3)Cystadenocarcinoma

-small,solid nodularity or irregular thickening

1)Large cystic masses with weight of 25kg

2)Multilocular

3)Filled with sticky gelatinous fluid rich in glycoprotein

M/P 1)Benign tumour

-lined by cubical or low columnar epithelium

-Cells : ciliated,dome-shaped,serous secreting

2)Borderline tumour

-moderate mitotic activity

-nuclear atypia

3)Malignant tumours

-invasion of underlying stroma or capsule of cyst

-epithelium more than one layer

1)Lining epithelium tall columnar with:

-vacoulated cytoplasm,basal nuclei,absence cilia

2)Rupture of mucinous cyst > 2-5% of mucinous tumours

associate with pseudomyxoma peritonei lead to:

-implantation of its epithelium on peritoneal cavity

-accumulation of large gelatinous material in abdomen


11/15

HYDATIDIFORM & CHORIOCARCINOMA (2002,2011)

CHORIOCARCINOMA HYDATIDIFORM MOLE

COMPLETE PARTIAL

Features Epithelial malignancy of trophoblastic cells from any

form of previous normal or abnormal pregnancies

Common complication of gestational trophoblastic disease

(GTD),characterized by cystic swelling of chorionic villi

Causes 1)Previous normal or abnormal malignancy

2)From partial hydatiform mole (malignancy)

Abnormal fertilization of

- empty egg (dead ovum ) by 2

sperms giving

-diploid karyotype(46xx)

Abnormal fertilization of

-normal egg by 2 sperms giving

-triploid karyotype(69xxy)

G/P -Soft, fleshy

- yellow white tumour

-extensive haemorrhage& necrosis.

1) Vesicles :

-variable size & shape.

-Thin walled with

semi-translucent fluid.

2)No foetal parts seen.

1) Vesicles :

-variable size & shape.

-Thin walled with

semi-translucent fluid.

2)Foetal parts seen.

M/P 1)Does not produce chorionic villi.

2) Sheets of malignant cytotrophoblasts &

syncytiotrophoblasts infiltrate myometrium.

3) Tumour penetrate blood vessels & lymphatics to

adjacent structures.

4) Areas of haemorrhage& necrosis.

1)Chorionic villi show

-hydrophic degeneration

- avascular

(devoid of blood vessel)

2)Cyst like/translucent villi

invested by layer of :

-cytotrophoblasts

-syncytiotrophoblasts

3)Trophoblastic cells=

hyperplastic

1)Some villi :

-Oedema & dilatation.

2)Trophoblastic proliferation:-Focal & mild

3)Present of fetal part

C/P 1)Doesnt produce large bulky mass

2)Irregular spotting of bloody brown foul smelling

1)Uterus:

-bleeding

-larger than expected for the

duration of gestation

-

Metastasis Metastasizes by blood to lung,liver,bone -Liable for malignant

transformation

-Most common precursos of

choriocarcinomaSecretion of

human

chorionic

gonadotropins

High level Low level


12/15

FOLLICULAR HYPERPLASIA & FOLLICULAR LYMPHOMA (01,02,03,06,10,12)

FOLLICULAR HYPERPLASIA FOLLICULAR LYMPHOMA

Nature Inflammatory lesion Malignant neoplastic lesion

Architecturally 1) Preserved architecture2) Follicles :

-in cortex only

-variable in size & shape

3) germinal centres : well formed

4) No or slight infiltration of capsule &pericapsular fat

1) Lost architecture2) Follicles

-replace cortex & medulla

-same size & shape

3) germinal centres :fading

4) Infiltration of capsule &pericapsular fat by neoplastic

cells

Cytologically 1) Composed of many types of cells

2) Prominent phagocytic activity

3) Different types of cells inside & outside follicels,

prominent mantle

4)Frequent mitotic figures

1) Composed of one or two types of cells

2) No phagocytosis

3) Same type of cells inside, at periphery & outside

follicels, no mantle

4) Rare mitoses low grade

HODGKIN & NON-HODGKINS LYMPHOMA (2008,2011)

HODGKINS LYMPHOMA NON-HODGKINS LYMPHOMA

Site Localized in axial group of nodes

(cervical, mediastinal&para-aortic)

Multiple & at peripheral nodes

Spread Spreads by contiguity Non-contiguous spread

Mesenteric Nodes &

Waldayers ring

Rare in mesenteric nodes &Waldayers ring Common in mesenteric nodes &Waldayers ring

Extranodal sites Uncommon in extranodal sites Commonly extranodal


13/15

COMPARE BETWEEN OSTEOCLASTOMA & OSTEOSARCOMA (2011)

OSTEOCLASTOMA OSTEOSARCOMA

Type of

tumours

Locally malignant tumour Primary malignant tumour

Aetiology -Males

- 20 & 40 years.

-Males

-Primary type: 10-20 years

-Secondary type: > 40 years

Sites Ends of long bones:

Lower end of femur

Upper end of fibula or tibia

Lower end of radius

Upper end of humerus

1)Metaphysis of long bones:

-Lower femur -Upper tibia

2)Flat bones:

-Scapula -Pelvis -Jaw

G/P -Begins : extremities of bone.

-Grows slowly.

-Firm grayish mass.

-Areas of haemorrhage & necrosis.

-Formation of multiple cystic cavities filled with blood.

-Expansion of bone with thin shell of new bone formed

by periosteum surround tumour (egg shell crackling

sensation)

-Begins : metaphysis.

-Grows rapidly.

-Grayish white bulky fleshy mass.

-Areas of haemorrhage& necrosis.

Medullary parts:

-Diffusely infiltrate towards shaft

-does not invading epiphysis or joint.

Subperiosteal part:

-Surround shaft completely-periosteum firmly attached to epiphyseal cartilage.

-New bone deposited at :

*junction of raised periosteum (Codmans triangle)

*perpendicular to the shaft (sun ray appearance).

M/P 1)Tumour cells:

-Small mononuclear stromal cells with dark nuclei

-varying degrees of atypia.

2)Giant cells:

-Numerous of osteoclastic type (10-100 nuclei)

-Areas of haemorrhage, necrosis, haemosiderin&

osteoid.

1) Pleomorphic spindle-shaped cells

- varying degrees of atypia

-increased mitotic activity.

2) Osteoid formation :

-appear as homogenous pink matrix directly laid down

by tumour cells.

3)Thin wall blood vessels

4)Intervening tissue includes

osseous,cartilaginous,myxomatous,fibrous elements

Metastasis -No metastasis to other organ -Blood spread : lung

HASHIMOTOS THYROIDITIS & GRANULOMATOUS THYROIDITIS (2005,2006)

HASHIMOTOS THYROIDITIS GRANULOMATOUS THYROIDITIS

Aetiology -Autoimmune reaction against thyroid gland

- manifested by cytotoxic cell mediated hypersensitivity

reaction.

-Autoimmune disorders

-Subacute thyroiditis

-Viral infection: Epstein-Barr virus,mumps vrs

Age & sex -Female

-Middle age (30-50 years old)

-Female

-3rd

to 5th

decades

G/P 1)Early stage:diffusely enlarged thyroid gland,firm,nodular

2)Later stage: smaller with fibrosis & atrophy.

1) Diffusely nnlarged thyroid gland

2) consistency :firm

3) colour : yellowish white

3) adherent to surround structures.

M/P 1)Small thyroid follicles lined by :

-ample amount of granular eosinophilic cytoplasm (Hurthle

Cells)

2)Infiltrated by :

-lymphocyte -plasma cell

3)Lymphoid follicle formation

4)Well develop germinal center

1) Extensive follicular destruction & fibrosis.

2) Aggregation of macrophages & giant cells

around colloid form granuloma-like lesion.

Clinical

features

1) Diffuse enlarged thyroid gland.

2) Patients either euothyroid or mildly hypothyroid.

1) Painful enlarged thyroid.

2) Fever, malaise, muscle aches.


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SIMPLE GOITER & TOXIC GOITER (2002,2003)

NODULAR GOITER SIMPLE GOITER TOXIC GOITER (GRAVES DISEASE)

Aetiology -2ry to repeated attack of

hyperplasia

-involution of thyroid glans

due to increase physiologic

demand of thyroid gland.

Ex:puberty,pregnancy

1)Metabolic disease

2)Absolute chronic deficiency of

iodine

3) Relative deficiency of iodine:

increased requirement (pregnancy

& lactation).

4)Dietary factors:

-block thyroid hormone synthesis

1)Organ-specific autoimmune disease.

2)Hyperfunction of thyroid gland

-due to Stimulation of thyroid by

autoantibodies of IgG against TSH

receptors in thyroid follicular cells.

G/P 1)Nodular enlargement of

thyroid

2)Nodules:

-irregular -variable size

3)Cut surface:

-brownish with foci of

hemorrhage and calcification

-each lobe is surrounded by

fibrous tissue

1) Diffuse Enlargement of thyroid.

2) Cut surface:

-translucent

-brownish (large amount of stored

colloid)

1) Diffuce symmetrical thyroid

enlargement.

2) Fleshy appearance &

hypervascularity.

M/P 1)Nodules formed of thyroid

follicles :

-variable size

-distended with colloid = lined

by flat follicular cells

-diminish colloid = lined by

hyperplastic columnar

follicular cells

-seperated by fibrous septa

-lymphocytic infiltration

2)Papilllary formation

(hyperplastic papillae)

-with thick CT core

1)Large colloid filled follicles.

2)Lined by low cubical epithelium.

3)Compressed follicles in between.

1)Diffuse epithelial hyperplasia of follicle

cells.

2)Hyperplastic follicles cells:

-Closely packed together

-lined by tall columnar epithelium with

papillary infoldings.

-Scanty colloid

3)Stroma:

-intervening

-lymphocytic infiltration

-Lymphoid follicles with GC


15/15

FOLLICULAR,PAPILLARY,MEDULLARY,ANAPLASTIC CARCINOMA OF THYROID GLAND (08,11,12)

PAPILLARY CARCINOMA FOLLICULAR CARCINOMA ANAPLASTIC CARCINOMA MEDULLARY CARCINOMA

Cells of origin Follicular epithelial cells Follicular epithelial cells Follicular epithelial cells Parafollicular or C-cells

Incidence 70% 20% 5% 5%

Age & sex

incidence

F>M (3:1)

15-35 years

F>M all ages

>30 years

F>M

>50 years

F=M

30-60 years

G/P Vary from microscopic

occult to large mass

1)Encapsulated large mass

2) difficult to be

differentiated from

adenoma

1)Massive infiltrating mass,

2)hard, gritty, grayish white

3) areas of hemorrhage &

necrosis

1)Infiltrative hard mass

2)grayish white

M/P 1)Papillary overgrowth

covered with malignant

epithelial cells with:

- ground glass nuclei

-nuclear grooves with

intranuclear inclusions

1) follicles :

-variable size

-devoid of colloid

- lined by pleomorphic cells

-capsular & vascular

invasion

1)Highly malignant spindle &

giant cells

2)massive pleomorphism &

mitotic figures

1) Nests, cords & sheets or

small ovoid cells & spindle

cells

2) separated by

fibrovasularstroma

containing amyloidal

substance.

3) Course is slow

Local:

Lymphatic:

Blood:

+++ (intragranular)

+++To cervical LN

-Rare,late,less than follicular

+++(to nearby tissue)

+to cervical LN

+++tolung & bones

+++ to the neck structures

+++

+++

+++

+

+

5 years survival 90% 65% -Nil. Highly malignant.

-Death after 1 year.

50%

Tumour markers Thyroglobulin Thyroglobulin none Calcitonin

Documents

Past Years Comparison