Chronic inflammation

1. Chronic cholecystitis
1. Gall bladder - organ (no submucosa is not present in gall bladder)
2. Infiltration of lymphocytes in lamina propria & muscularis
3. Inflammation -> infoldings -> Rokitansky Aschoff sinus
4. Serosa -> thickening & fibrosis
5. Complication -> Porcelain gall bladder
2. Sarcoidosis
1. Systemic disorder
2. Etiology - unknown/idiopathic
3. Formation of granuloma -> non caseating necrosis
3. TB:
1. Horse shoe shaped Giant cells -> Langhans cell
2. Caseating granuloma (cheese like appearance)
3. Acellular debris
4. Silicosis:
1. Inhalation of silica
2. Black pigment - carbon pigment -> anthracosis
3. Carbon pigment is deposited in activated macrophages
4. Diagnosis = silicosis; black pigment deposition = anthracosis
5. Collagen and scar tissue formation
6. Absence of asbestos bodies
5. Asbestosis:
1. Brown beaded structures in macrophages -> asbestos bodies (fusiform ends/dumbbell
shaped)
2. Golden brown - asbestos bodies
3. Presence of macrophages in alveoli
4. Complication -> malignant mesothelioma
6. Chronic sialadenitis
1. Tissue - salivary gland (inflammation)
2. Duct obstruction is due to sialoliths
3. Ducts -> infiltrated with lymphocytes -> form a germinal center
4. Complication -> tissue fibrosis, dry mouth & lymphomas
Tissue repair
Two forms:
1. Regeneration
2. Connective tissue deposition
1. Organizing myocardial infarct:
1. Connective tissue deposition -> scar tissue
2. Blood vessel formation - angiogenesis
3. Granulation tissue - foundation for collagen deposition
2. Old infarct necrosis:
1. Healed heart after MI
2. Less capillaries
3. CT deposition by fibroblast
3. Healing wound:
1. Lesser fibrosis is seen
2. Keloid - thick fibrosis & does not regress
4. Scar:
1. Dermis - adnexal structures like sebaceous glands, hair follicles & sweat glands
2. Loss of adnexal structures
3. Hypertrophic scar - regresses
 chronic inflammation & Repair

&

organizing myocardial
I
Blood vessels
onfarct

keloid
↑
Thick
↑

I
Fibroblasts/
alagen tibocytes
Healing wound scas

/
a

silicosis carbon pigment silicosis

Anthracosis
 ↑

Asbestosis
1Macrophages
in alveoli
IAsbestos body

/
a

Chronic Sialadent's salivary duct

 --

chronic
cholecystitis sarcoidos is

oldinfarein

By Kshithij & Anisha

 Hemodynamic: General pathology

1. Pulmonary edema
 All pink-fluid
 Pink homogenous material between alveoli
 Brown- hemosiderin laded macrophages
 RBC – microvascular leakage
 Cause- heart failure, pulmonary hypertension
 Transudate

2. Passive congestion of spleen

 2 regions – white pulp, red pulp.
 White pulp – lots of lymphocytes, central artery
 Red pulp – RBS, edema fluid, fibrin (congestion)
 Most common cause – cirrhosis, heart failure

3. Chronic passive congestion, lung

 Alveolar spaces
 Fibrin – less evident
 More number of hemosiderin laded macrophages – AKA Heart
failure cells
 Cause – left sided heart failure

4. Thrombosis
 Old thrombus –
calcific medial sclerosis
canalization, collaterals, recanalization
lipid deposition

 New thrombus –
RBC
fibrin
alternating colours of dark, light – lines of Zahn
 lipid deposition
foamy macrophages
 Calcification of tunica media – calcific medial sclerosis –
Monckeberg sclerosis – sign of aging, hardworking artery

5. Pulmonary embolism
 No hemosiderin
 No fibrin
 Blood vessel in lung parenchyma
 Thrombus, embolus – same character
 Most common origin – deep vein thrombosis of leg
 No histologic manifestation on other structures – so patients can
breathe normally
 Anthracotic pigments

6. Acute infarct of lung

 Alveolar spaces – RBC
 Alveolar walls – not clear – congestion
 Big embolus – fills entire lumen
 Alveoli – hemorrhage, necrosis
 Type – red infarct
 Necrosis – coagulative necrosis

7. Acute kidney infarct

 Necrosis – coagulative necrosis
 Type – white infarct
 Ghost outlines of tissues
 Nuclear features – absent
 Etiology – embolus, hypoperfusion
8. Acute myocardial infraction
 Eosinophilic – non viable cells
 Light pink – normal cells, nucleus
 Dark red, pink – dead cells, no nucleus
 Obstruction of coronaries
 Necrosis – coagulative necrosis
 Type – white infarct
 Karyorrhexis, pyknosis, karyolysis

9. Acute infarct of small bowel – small intestine

 Paneth cells – red cells at the bottom
 2 blood supplies – superior and inferior mesenteric artery
 Type – red infarct
 Necrosis – coagulative necrosis
 Transmural infarction – depends on location, near villus
 Hemodynamics

Chronic passive
congestion of lungs
pulmonary embolism

Acutemyocardial
Acute infarct, small infarct
bowel
 embolism
infarct, lung
Acute
pulmonary

old thrombosis
Acute
kidney infarct

old thrombosis
 Antracesis
e

Passive congestion of
spleen

pulmonary embolism

edema New thombus

pulmonary
Genpath Lab - Hypersensitivity reactions (TB not included)
Type 1 Hypersensitivty:
1. Acute allergic interstitial nephritis
2. Asthma

Acute allergic interstitial nephritis:

1. Kidney/renal tissue is involved
2. Vasodilation
3. Edematous spaces
4. Infiltration by eosinophils
5. Expanded or thickened interstitium

Asthma:
1. Airway disease
2. Increase in thickness of the wall
3. It is a progressive disease
4. Mucus plug is seen - Curschmann’s spirals
5. Smooth muscle hypertrophy
6. Hypertrophy & hyperplasia of submucosal glands
7. Vasodilation & edema
8. Eosinophils are seen
9. Basement membrane thickens due to protein deposition (adjacent edema)

Type 2 Hypersensitivty:
1. Goodpasture syndrome - lung
2. Graves’ disease
3. Pemphigus

Goodpasture syndrome:
1. Autoimmune
2. Antibodies agains the basement membrane
3. Involvement of lungs, kidneys or any tissue with basement membrane
4. Rupture of capillaries leading to bleeding into alveolar spaces
5. Necrotising hemorrhagic interstitial pneumonitis
6. Thickened interstitium & hypercellular stroma
7. Presence of hemosiderophages (hemosiderin laden macrophages); indicates that bleeding
took place
Grave’s disease:
1. Thyroid tissue
2. Diffuse hyperplasia & hypertrophy of follicular cells
3. Chronic inflammation
4. Autoantibodies - anti TSH receptor antibodies are formed
5. Anti TSH receptor antibodies -> Activate TSH receptors instead of inhibiting them
6. Scalloping of colloid - reabsorption area is seen
7. Patients - hyperthyroidism
8. Serum TSH value is low due to negative feedback

Pemphigus:
1. Blistering skin disorder
2. Autoantibodies -> antidesmoglein
3. Autoantibodies attack antidesmogelin present at the desmosomes in the stratum spinosum
layer
4. Spaces may contain serous fluid or seropurulent fluid during infection

Type 3 Hypersensitivty:
1. Fibrinoid necrosis of vascular wall
2. Membranous glomerulonephritis
3. Amyloidosis - heart, kidney, liver

Fibrinoid necrosis of vascular wall:

1. Tunica intima - contains exudate
2. Tunica media - inflammatory cells
3. Pinkish acellular areas -> fibrinoid

Membranous Glomerulonpehritis:
1. Glomerulus - subepithelial deposition of immune complex
2. Results in thickening of the BM
3. Podocytes are affected
4. Expansion of thickening of glomerular tufts
5. Can lead to end stage renal disease
6. Oliguria progresses to Anuria
7. Patient might need to undergo hemodialysis

Amyloidosis:
1. Heart - pressure atrophy, between myocytes - amyloid bodies are seen; heart is unable to
 1.
contract - cardiac failure
2. Kidney - all parts of the renal tissue has amyloid body deposition; can lead to end stage renal
disease
3. Liver - hepatic plates are separated & thin; space of Disse disappears & there is amyloid
deposition

Type 4 Hypersensitivty:
1. Psoriasis
2. Crohn’s disease
3. Ulcerative colitis
4. TB lungs
5. Hashimoto’s thyroiditis

Psoriasis:
1. Hyperkeratosis
2. Acanthosis
3. Papillamatosis
4. Micro abscesses within epithelium
5. Thickening of scales - silver scales
6. Lymphocytic reaction

Crohn’s disease:
1. Inflammatory bowel disease - IBD
2. Skip lesions are seen
3. Non caseating granuloma is seen along w/ giant cells
4. Involves muscular & serosa layer
5. Can affect the rectum, sigmoid & transverse colon.

Ulcerative colitis:
1. Affected till submucosa
2. Vasodilation & congestion is seen
3. No skip lesions
4. Can affect transverse colon, sigmoid colon, ascending colon & splenic flexure mucosa
5. Mucosa appears red
6. Wide ulcers are seen
7. T cell mediated inflammation

Hashimoto’s thyroiditis:
1. Follicles are not seen, only remnants are seen
2. Lymphocytic infiltrates are only seen
3. Patient presents with hypothyroidism
4. TSH levels in the serum are high
5. Can be type 2 Hypersensitivty -> autoantibodies against TSH receptor -> inhibitory effect
6. Granuloma in germinal center (strong activation of T lymphocytes)
 Eosinophils Edemalous space

~
I
ALLERGIC INTERSTITIAL NEPHRITIS
ACUTE

/
urscheat
-
I

I ASTHMA
W cartilage
mucus
 Blood in alveolar spaces

-1

GOODPASTORE
SYNDROME

scalloping of
colloid
↑
Reabsorption
-
ava

GRAVE'S DISEASE
 -Blistening skin

PEMPHI aUS

TA
-
TM-
- 7. I ->

Inflamm
alls

Infiltration

FIBRINOID NECROSIS
OF VASCOLAR WALL
MEMBRANOUS GLOMERULONEPHRITIS

HE ART LIVER KIDNEY

AMYLOIDOSIS
PSORIASIS CROHN'S DISEASE

pilated Blood vessels

↑
W

ULLERATIVE
COLTIS
j HASHIMOTO'S
THYROIDITIS
Lymphocytic
infiltrate By Kshithij & Anisha
Adenomalous polyp, colon villous polyp, colon

/
Capsule & Follicule Adenoma-Thyroid
 Spindle shaped muscle
smooth

I
Liomyoma iomyoma

SCHWAN
1 Antonia

I
Palisading
I
Nuclei
 cardiac
Lipoma mysoma

Hemangioma Astrocyloma
 chonanomymoid
Appearance

Plomorphic Adenoma Fibroadenoma

I
-steomal
Triphasic
-

Epithelial pattern

Blastemal
->

Wilms tumor
 aands(sebaceous)
-

--
Adipocytes
--stealified squamous
In spithelium
cartilage

CYSTIC TERATOMA

Cartilage cap-

Osteochondroma-
-kshithij