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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
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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
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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
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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
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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%
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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%)
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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
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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
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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¶-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
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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
7/28/2019 Past Years Comparison
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