common in

q
id ~more
Hyperthyroidism
Neop Geis
clinical
features
Tremor

⑳I
*

simple.aboidal ee *
Tachycardia
thyroglobin en *
Walm moist skin

on activation
(seen in
Graves and
hyper] It-loss, muscle
* aleakness

agetation
*

Cuboidal pithelum -> Columnal Epithelium # Heat

*
Intolerance
*
Goiter
G medullary Carcinoma
Palafollicular Cells
- *
Exopthalmus
Atrial
↳ Secret c-cells
* ofthyroid *

fibrillations
Calcitonin Annovvenia
*

diarrhoca
*

Thyroid disorders

-
Hyper Hypo EGeiscaseadpois
Hyperthyroidism
I- ->

most
common cause
ofEndogenious
primary Secondary Hyper thyroidism

Graves disease TSH

* *
Secreting pitutar pathogensis
Type
IIHS
Tonic
* multinodulerGoiler tumor -> Rann

Tonic
* Adenoma
[Tyroid Stimulating
Fatrogenic
* antibodies ->

↳
TSI
Immuno
Globuliy
LATS
↳
Long acting thyroid
/Hyperthyremulators
Gross Hypothyroidom
->
Diffuse Enlargementofthyroid ->
m.c
=> Rodine in
Sufficiency
->

Symmetric ifthere is Rodine

Sufficiency
->

Beefy Red
thyroid. - HASHIMOTOS
HIE Tyroiditis
Hyperplastic follicles Clinical
->

conc
follicles look like papillar ->

memory
and
- >

poor
Scalloping of colloid. Poor
hearing
- >
->

- >
Cold Intolerance
Slow pulse (pericardial effusion]
egte
- >

- >
Pavasthesia
=> colloid
filledfollichs ->

Myeudema
degenerative changes delayedReflex
->

calcification
->

-> Hemocidrine Leiden

>Gross
macrophages. Engris-Inflamation ofthyroid.
↳ multinodular Guitar. /HASHIMOLO'S Thyraditis
L Goite.
↳ Common in
q
2
Diffuse ↳Auto Immune = 3-antibodies

*
anti-TSH-Receptor Ab

*
Anti
thyroglobulin Ab

*
Anti microsomal Ab

Es ->
diffuse homogenous enlargementof
thyroid
Gland.
 Ee Thyroid
my
umor's
*
Lymphoid follicles / Aggregates ->
Begnin malignant
Stroma
*
Lymphomatosom
addenoma
I
Risk of follicular pappillary ca
* *

Non-hodgekin's lymphoma *
follicular
ca

are
(a
medullary
*

monocytic /Onyphill cell/Askenji cell *

Anaplastic
* ca

Le
FNAC
ofthyroid
cell
change -x cells with abundant Criteria

Eminen
characterstic Eosinophilia granular "A
specimen should display
cytoplasm due to at least
6-groups offollicular Cell
mytochondria with each
group composed ofat least
3
10

Glide.
Cells
preferably on a
Single
Complications 3 exceptions
->
pappilary Ca
ofthyroid *
ifabundantinflamatory cells
- > NHL
[marginal zone Lymphoma] if
*
3
thick colloid is
present
-> 44 Disk
of Autoimmune ifatypical/malignant
* cell
present.
Hashi tonicosis -
-
Hypothyroidism
follicular denoma daillae
the form ofCa
-Solitary wellCircumscribe *most common

Bestprognosis
*

metastises
#

through Lymphatic Route

HE *
Usually Celical lymph node Enlargement
=>
proliferation ofSmall follicles mutation
*

ofBRAF
Gene
with scanty colloid. thyroglossal cyst
*

=> No
Capsular, vascular Invasion has hi mottos
*
thyroidits
Radiation
*
Exposure
Variants
-
&Hurthle call adenoma HE
50%
* cells ① papillar e
Jingulike projection with fibrovascular
2 denoma
Hyalinizing trabecular cove

optically
clear
⑧ Orphan dunie ↑nuclei
3
nuclei
eye clear
cell's with nuclei

3
psamomma bodies
(dense basophillic
Body
Gritty]
a
coffee bean nuclei -y nuclear Groove

pseudo
5 Anclusions in nuclei
Varients follicular Ca
->
Encapsulated
and
follicular
->
calls
allanged in
-> are

follicles butnuclear
Hematogenous
->

features all those of ->

KRAS mutation

pappillary ca - >

Goiter (Long)
Tall Valient
3 poorprognosis
->
Cell
->
Diffuse Sclerosing Valiant r/t
follicular

I
Follicular Aceno ca
->
papillary microcarcinoma.

⑦
Capsullar Invasion
⑦ ⑦
Vascular

FNAC is not
useful in
folliculdar ca

Altarya
Tumor markl=>Calcitonin

proliferation of parafollicular cell

HE
Spindle
*
cell
cal
Amyloid
* => I

under Red =>

Apple
Congo
Green
Bifelenges
 Al mea
Gross: -

PHAGOChromocytoma
- >
Turner
ofAdvenella medulla
4 Catecholamines
->

produce
drapa
Least
Rules
of10's bilateral
*
common ·
10% all

Worst
*
prognosis ·
10% in children
Rapidly Anlarging
* neck mass · 10%. Extra advenella
10%
malignant
·

H/t ·
10% No
hypertension

3
Spinale shape
calledorphism
=

Bilateral
Gaint 25%
flamial usually
=>
=>
cells is
Sarcomatoid
->
and occur
in children

& Genes

. 5-
4
↑ Growth factor activity.
Receptor Signalling hyponia
Inducable

factors
Syndromes associated with Immuno
pheochronost Histochemical markus.

-> neuron Specific Enolase (NSE]

- >

multiple Indocrine neoplasia - >

Chromogramin
->

Jambal paraganglioma
->
Synaptophysin
->
polycythemia palanganglioma Syndrome Austenticular calls - S-100
posite

Gross Electron microscopy

Brownish in colour =Dense core
secretory
->
neuro
->
Hemmoragic aleas
Granules.
Rx
Chromaffin
fresh Catecholorines.
-> tissue
Urinary
↓
Pottasium Dichromate
Solution
Neuroblastoma
due to

Catecholamines Ercolour
s

- >
mostcommon Extra Cranial
solid tumor in children
H/E ->Age < 4
years
=>
Spindle shape calle -> mostcommon site -> Adrenal
medulla
polygonal"
=>
call

Abdominal distension

mall
allanged best
clinically
patente
->
->
->

pathogensis
--
fire-
I amplification
↳ Fe
Salt and
*

pepper chromatin plea

chromatin mutation

Cells
*
Seprated by fibrous network

cells
* inside fibrous network

are called Sustentacular

Cells
 EGs-. Hammorage ic MEN =>
multiple Endocrine Neoplasia
·
necrosis

Tumors Characterstics

Its small Round blue cells with

->

->
Bilateral

younger age
Scanty Cytoplasm ->
more
aggressive
multifocal.
->

HOMER
=>

InrightRosett
·
- MENI a
=>
ifLumen is
empty it
MeNE MENIU Nb/
we call

true ROS ETTE

.Tumorin :: this is
pseudo vossets

NI

E
Intratumoral
*
Calcification WERMER
*

Syndrome
3
imp Ganglionic Differentiation
*
mutation
*

in MEN 1G
Shavanian Stroma

Clinically
*

Good prognosis
factors for Panchatic
Pititualy whyroid -

Age
* <18 months

Shwanian
* Stroma => Prolactinoma 90%.
=>
Cases 30-70%
=>

Ganglionic differentiation Adenoma

&
30-40% cases
=>
->
Insulinoma
=>

Hyper ploidDNA
*
=Y
Hyperplasia
=>
ima
&most Common

most
* common
of
site metastasis
Lymph node Site duodenum

Spontaneous Regression
*
 MENIta
Pitutary ->
Pitutary Carcinoma

↓
SippleSyndrome inthe pitutary
adenoma

L
microadenoma
functional tumor
Clinically
PPM macroadenoma

·
gross
=> Idell Circusclibed Encapsulated
Phaechromocytoma Palathyroid medullar
HE cells
ca
0
=
monomorphic pappillary patter
->

--
Round-polycanal cells - Simusodal pattern
#>
MEN2A
*
familial medullary Ca
ofthyroid =>
Si
sare Reticulin network =>
Diffuse patter
#>
#MEN2A Cutaneous Lychen amylodosis conventional
staining classification
E, disease Acidophil
MENGA
*
Hirschsprungs
->

->
Basoplil

EniMENI chromophobe
->

(110 3 Groups
↳Combination
acc

of -> Acidophilic Laniage.

medullary ca & pheochromocytoma +

mucosal I
marfanoid feature Corticotroph Leniage.
->

neuromas

MENE, MEN 1 +

Gereitoulinary Tumors
->
Gonadotroph Leniage.
Lactotroph
* Adenoma a dollenal Cushings
somatotropeto toph-Lachotrope
20-25%
*
*

adam a t * Low Serum ACTH

Thyrotroph adenoma
* due
* to disease in one or both

Corticotroph adenoma advenal

glands.
*

#
Gonadotroph adenoma
Null cell adenoma 3 Ectopic Cushings

nowalmewovos?
Ectopic
* I4 ACTH
Seen
* in SCC
oflung
air
aatogenic ene
-> due to Excess use
ofGlucocorticoid
of or ACTH

Cortisol ->
In
autoimmune patients.

4-types
* Clinical
features
Central/truncal
*

obesely
I
pitutary Cushings Syndrome Buffalo hump
*

# face
moon

Lesion
pilutary gland Wasting due to protien
* in breakdown
A4 ACTH Secretion
*

* Systemic hypertension
pitutary
* microadenoma Impaired Glucose tollerance.
Bilateral advenal Cortical
#
Ausomia, depression, confusion
#

hyperplasia.
 atical Enssificancy Gastrinoma (G-Cell tumor] (Zollinger - Ellison
Syndrome]
Addison's disease. triad
Diagnostic
->

90% destruction of
caus ->
progressive -> Fulminant
peptic ulcer disease
advenal cortex
ofboth sides. ->
Gastric acid hyper Secretion
tumor
TB, Histoplasmosis, Amylodosis non-B panchatic Isktcell
- > ->

Sarcoidosis, hemochromatosis etc

Gross There increased

billatually small is production ofGastrin
=x *

irregulary shrunken
=-

Gross=> Seen in wall

of deodenum
HE Histologic changes depend associated
peptic ulcers.
=> on =x with

Cause
=>
non-specific Lymphocylic Infiltrate
mical
Enteria
↳progressive weakness, Lathengy
lat LOSS

Hyperpigmentation
#

*deterial hypotension
Reduced
*
GFR
*
vague upper GI Symptoms.
 ↳ Space
of
dissae

Type 1, 3 collagen deposited

↓
88 space ofdisse =
Hatocell Lossoffenestrations
Stellate
cell Capilclasiation ofLinusoids.
↓

Hepatocytu joined by
* Cannals
of fibrosis miclonocular Cirrhosis macro

HERIN1G
Early alcoholic Late alcholic
Cirrhosis Heamechromatosis calilsons
Line disease
*
End
Stage a, AT
def
Drug Reduced
Characterstics Hepatitis
Entire Lobular
->

disruption of
the viral hepatits
architecture
nodulu addie Liner
DeGenerating paranchymal se
->

->

fibrosis
Common
* Cause ofCirrhosis
micronodular Cirrhosis
nodules (3mm
*

Gross ->
Soft, yellow and
greasy
pathogensis
in 1
Type 1 and
Type 3
collagen Stage
peliportal Centrilobular.
and HIE => Steatosis
->
fatty change
-> Reversible
change
->
chage
Earliest
 Eme
Steatosis Non-alcholic Steato Heptitis
-
microvesicular macrovesicular
Obesity
*

Small Lipia Big Lipid DM

·
· *

droplets droplets Hypercholestremia

*

pushed Insulin Resistant

*
·
nuclei in center ·
nuclei

to
periphery.
Cause:
Early AD Late AD ASH NASH

fatty River
of obese ty Alcholic Non Alcholic
*
pregney
*

chronic viral
hepitilis Heamechromososi
Obesity, DM, Hypert
*
H/0 ->
obesity
⑦ ⑰

pelisinusodal
*

inflam periportal infla

Hepatits -> Stage -
2
->
Inflamation ofLone parenchie. Neutrophilic
*
Rufiltrate monocyte
more

->
Neutrophilic Enfiltrati AST:ALT L1
mallory Hyline/
* Denk bodies = dense cosinophilia AST:ALT
* >2
bodies

composedofIntumdite
bodies
=> *
mallory hyline mallory
*
hyline bodie

fillaments. more Less prominant.

Chicken
* live
fibrosis -
perisinusoidal fibrosis
Cirrhosis
-
Stage 3

2ENNAC lahen Liver

Cirrhosis --
gets
completly fibrosed
 Metabolic Liner diseases Heart
*
-> Dilated Cardiomyopathy
Joint
*
-> Pseudo gout

is
a abandan
Testis
Atrophy.

Bean
* ->

Diagnosis
ene Fe Studies -> S. Fe4
S. Feritin
↓ S. Transferrin Saturation

Hlevidetary acquired
Live Biopsy
mutation in
Repeted blood golden yellow/Brown pigmentin hepatocyts
· · ·

transfusion pussian Blue Stain for Hemocidrin.

3 genes.
HF
* E ·

*
HAMD ·BANTW

HIV
* Sideros is
Wilson's Disease
Autosomal
Pathogenis ->
ressessive.
mutation -> Excessive Copper deposition
↓ ·
due to MTPIB mutation
gene
↓Hepcidin Cemplasmin A
my
·
↓

-
↓ :Cal
↑
Fe Load Inlitsons disease
↓ ·
Impaired(u-> Bile
Hemachromatosis Clinically
alilisons triach

Clinically
*
Kayeser
* Feber
Ring
Triad ->
Bronze skin cirrhosis
*
*
-
*
DM *
putamen and basal
Ganglia
- >
micronocular cirrhosis
neuropsychatry manifestal
Diagnosis e
HE =>
Eosinophilic Inclusions
=Y adcute and chronic Inflamation PAS
=>
the DiastantResistant.

mallory hyaline
= Steatosis =x bodies.
bodies
=Y
mallory Hyaline
Stain -> Rhodamine
Rerbearic acid

=>
Copper associated protien- orcien.

Serum Calleloplasm ↓↓
Serum 4
Copper
4
Minary Exclation
ofCa

#&1 -

Antitrypsin deficiency.
·
Autosomal Recessive
· . -Antitrypsin I
↓
↑
Neutrophil Elastase activity
↓
Damage.
DiMM-> normal
*

*PiMz=> Carrier
Piz2
* =>
Affected.
 Hepatitis
-
-
altoimmune Chronic Heptitis
Hepdena virus.

⑰viralge
HE
3 D ⑳ ->
Lymphoplasmacytic Rafituche
Jeco oral Sexual
vertical
feco oral ->
Brichgin fibrosis
->
Interface
hepatitis
palentra
m.c cause of ->
portal Inflamation
Extinine

pregnatly
mortality
-ene
Glass appearance ->
Glassy cytoplan
↳ In Hep B

HBS antigen
Hepatitis
Acute -> Shikata cell

HE = 3
balloing degeneration
=>
apporotic bodies
(Councilmen) Chronic
Hep C

belie
Gosinophilia
->

Lymphoid aggregates
fatly change
->

=>

Lymphoplasmacytic Infiltrate -> Bile duct

and
proliferation.
=>

Spolty necrosis

ttepatoryand
->
Drop

it
Kuffer cells
=> Absent
portal Inflamation
mini
Adenoma Fibralaminar Valiant
ofHCC
female->> people
->
younger
oral contraceptives ->
M F
=

male-> anabolic sterials ->

NOK AFP
Gross
laell Circumscribed He deprated by
3 Hepatocitic
Rt
Lobe => nodules
Intel Encapsulated fibrous Septae.
HE
-> Inell diffrentiated Hepatocyte marker -> Neurotensin.
->
Not much
pleomorphism
-> No vascular Ruvasion

Interfa
Alcohol
*
Aflatoxin
*

*
Hep B, C Ruf emochrotosis
#

Gross -> multiple nodules

->
multiple forci
H/G 3
=

Hepatocyte can be
allanged
in sheets, chords, trabuclae
->
mallory hylene bodies
=Y vascularisation
markers >
-
AFD

=>
Hep Par 1

Neurotesin.
=>
 Unavys Ammonium Mate Stones
fanative abuse.

fall
->

Hayline
* Cast -
Ene protien.

E all caste
Kidney Biops y

present in

① Glomeules
Tam & Tubular
Horsfall protient see a
*

* 71
③ Rutelstium
*
Broad Inlany Cast => Chronic Renal Disord ④ Blood vessel
*
fatCast ->
Nephrotic Syndrome

Urinary Crystals
*StruviteCrystals (5
->
Staghorn Calculi
coffin lid shaped
->

*
Cystine Stone
->
Hexagonal shape
Acidic
-> wine

# Ulic acid Crystals

-> Rhomboid or
pallelogra
shape

*Calcium monohydrate
oxalate
-> dumbell shape
*
Calcium oxalate dihydrate
-> Envolop shape
⑩Sidney
disease
mulliyst Real Dispen
↳ Adult PCKD Gross=> Unilatual or bilatual
↳
Refantile PCKB
dysplastic kidney
=>
is almost

always cystic
#AdultPCKD => Looks like bunch
ofGrapes.
-> Autosomal Dominant
a tie undiffrentiated mesenchyme.
genesis "
->
=>
Smooth
=> muscle

Kidney's abnormal & birth

=scarte
->

dee
kidney functions Retained
-

->

collecting
Symptoms appear in adulthood.
->

Grossvariable
signage te
a plan
enlarged

-
=

kidneys are

pele's
is
usually
=> Bilateral ->
medullary sponge kidney
involved -Y
heavy
=>

Cut
=
Lobulated
Section
Surface
we can see

nacin
ofValying

18
Cysts Size.
Acka
HE x
= tissue
b/w cysts show normal
Renal
parenchyma
=>
nephro Sclerosis
=Y
Euflamation is seen

=>
cyst alise
from all of
parts
nephron [=> fibrosis is also seen]
 #eptic yes
EN [Rapidly Progressive Glomerulonephritis]
protinuria
*

Hematuria
#

Types
Hypertension
*

*
Azotemia Y ammonia in blood. I
- -
T #

GN Antibodies In mane complex Paucimme

to Glomerular Antibody mediate No Ab

postStreptococcal
*

Defection Basmentmembrane NO IC
IIHS ↓
*
Type Ren Internet
Immune Complexe
*
Good pasture Glam
2-3
after B-hemolytic Strep. Syndrome
*
weeks

#Lightmicroscopy
Glomulli
->
Anlarged Hyper cellular morphology-
-
->

neutrophillic proliferation 2M =x Cresent shaped Gromulli

-> Endo andno
proliferation of >50%

Capillaries Cresentis
=>
formed by
parital cell, fibrin, Leucocyte
#Electron microscopy

wrinkling of
ithal
Sub GM=Y Rupture
hamPosition
-> or

13 M

Linear deposite
ofRamune IF Type 1 ->
Y
complexes. =

#
Ammunofluosence Type 2 ->
Granullar deposite
=> Grannular pattern
Stary sky pattern. Type
->
3 No
=>
deposits
 Nephrotic Syndromes
Membraneous proliferative Gromulonephets.
- >
massive protienuria
->
Edema
Type 1
Immune
dilutional
Coagubility Complexe.
- >
*

->

Frothy wine
->
Lipial casts. Type 2
disease
Dense
*

deposit
Minimal
ener Change Disease (MCD] Activation
*
ofComplimentpathway
in
mostcommon
* children
2-bycar Type 3
* Nil depositdisease use
*
ofdrugs

morphology
mine morphology
2 M x Lipid deposition in 2M=y TRam track
=

appearance
tubules
deposition of Immune
=> Normal feature complex and
complete

GM =Y
fusion ofpodocytes
foot =>

Enlarged
hypercellular Glowd
process
Endo
=>

capillary proliferation
= Lobulear
apparace
IF=
>
No deposits are freen.
GM =Y
Type 1 => Subendothelial depest
Good
* Response to Steroid.
Type 2 b = dense deposit

IF Type
>
= 1 4
=
Grannular deposits
Type 2 Linear, Ribbon
=>

pattern.
Persistant Hypocomplementina.
Dimic Nephropathy Lupus Nephritis
Graces

wingalmaratgaleener
1 DM
Type
*

duration
*
ofdisease 22

>I

morphologiy
"I
Diffuse Proliferative
-
I membraneous

Gross -> Renal

papillary necrosis 11

HIE =>

thickening ofCappillary wall

= Y
37

ofBM Chronic
Pyelonephitits
=>
Diffuse Glomerulo Screosis

=> Nodular Glomurnosclerosis Gross -> asymmetyly Shrula

kidney.
↓
Kimmel steel decision
HE => Tubular
atrophy
=x Fibrin Caps -> in
capillary wall Thyroidisation
=>
ofRenal table
=>
Capsular drops ->
hayline in
Lymphocytic enfiltrate
=>

Bowmans Peri
glomber fibrosis
=

Capsule.
=> clear cells in PCT

eBstien Zeision

dusto, y
 Tumors
-
Real all Comma
lalilms tumor 60-70
Age
·

years
=>

Nephro
* blastoma ⑧ m> > F

Abdominal
Smoking
* mass ⑧

Children
*
0

Obesety
mutation (T1
offunction
⑧
Petroleum
4
Loss products
I
=

gene
Y IT2 mution.
⑧
Asbestos
gene
=

H/t Triad
tumor Abdominal
=>
Triphasic -> mass

- Flank Pain
- >

- >
Hematuria
Epithelial mesenchymal Blastemal
·
Glands ·

Spindle all ·
primitive Para neoplastic Syndrome
all ->
Polycytlemia
Small Round blue cells tumor -> 44ESR

*
Histologic anaplasia
- >

Hypercalcemia.
-> P53 mutation
needed.
->
chemotlapy Types
precessor
*
Lesion=> nephrogis Cell Rust.
① Clear cell RCC
& Papillary RCC

Gross ③ Chromophobe RCC

=>
Vely Large mass
Replacing kidly ⑭ Collecting Duat RCC
aleas
=>
hemnoragic
=>
Softfish-flesh like grey-Iahit Gross=Y Ischemic necrosis

aleas
to
clean-yellow appear Hemmoragic
Cystic changes.
#Clear call RCC #
Chromophobe RCC
unilateral
solitary Bestprognosis
-> ->

->
YHL mutation ->
Arises
from Ritucallated alls
gene
from ICI
from duct.
-

collecting
->

with
-> Associated Birt
Hog Syndrom
HE => Sheaths ofcells with
clearing ->
Hypodiploidy
because
=>

of Glycogen and
fat
=>
PAS andoil Redo
positive. H/E ->
polygonal shape calls
-> Daisin nucleus

Pappillary RCC ->

perinuclear Halo ->

plantlike appeare
Bilateral and multicentric defined outlines
usually
-> -> Well
->

andmostcommon -> colloidal

Hale's Stain
PCT DCT
->
from or

dialysis. duct Carcinoma

-> seen in
collecting
->
AP2M amyloid ->
Calorst
prognosis
->
Loss ofchromosome ->
Last common

2-
Types H/E - >
Desmoplasia
Cells.
Heridetry pappillary RC2 - > HoBNail

HL-PRCC ->
Enzyme deficry. Medullary RCC
-> Sickle call trait.
HIE -> Smarc B
gene def
->
Papplica
- >

Fomay macrophages
-> Psamomma bodies

foci ofdystrophic calcification

->