PATHOLOGY

SLIDES 2
Protocols 6-8

Qudsia
Liver
 Cirrhosis
hepatis
Pathophysiology:
• Causes: alcoholism, hepatotropic viruses, toxins, non-
alcoholic steatohepatitis. Primary biliary cirrhosis, genetic
predisposition
• Pathogenesis: Chronic liver damage -> necrosis of
hepatocytes -> inflammation -> activation and
proliferation of fibroblasts -> deposition of collagen fibres
in sinusoids and in place of dead hepatocytes -> portal
hypertension, chronic liver failure.
• Hepatocytes can regenerate if they have framework
from reticulum.
Regenerative lobules: if lobules are surrounded by scar
tissue, portal duct flow difficulty occurs.
• Complications: hepatic failure, jaundice, portal
hypertension, hepatocellular carcinoma

Gross Pathology:
• Liver is smaller, firm nodular surface, could
be yellowish if there is fatty change

Histology:
• (H.E and V.G staining) – in V.G staining, collagen
fibres in red, liver tissues in yellow
• Total loss of normal liver architecture
• Fibrous bands and bridges – they cut through the
liver parenchyma, connecting portal spaces with
central veins or with other portal spaces, forming
pseudo-lobules
• Pseudo-lobules – parts of liver parenchyma
surrounded by fibrosis that don’t have a central vein
• Chronic inflammatory infiltrate – lymph
• Biliary duct hyperplasia
• Regenerative nodules
Kidney
 Nephritis
purulenta
Pathophysiology:
• Causes: usually microbial
• Acute localised purulent inflammation
of the kidney cortex
• Two main ways for the microorganisms
to reach the kidney:
(1) hematogenous: through blood stream.
Multiple small abscesses all over the kidney
cortex
(2) ascending (via urine retention, infection
and reflux from the bladder. Large abscess
at one of the kidney poles: this is due to the
concave anatomical structure of the renal
pyramids at the two poles which prevents
them from closing up under conditions of
high urine pressure in the renal pelvis

Gross Pathology:
• Multiple small round soft yellow
abscesses

Histology:
• Collection of neutrophils: large purple areas
(looks like continents)

• Tissue looks cracked: neutrophils destroy

underlying structure = necrosis

• Numerous acute abscesses – roundish

structureless collections of dead renal tissue (cell
and tissue debris) surrounded by a neutrophil
infiltrate

• Rounder dark blue areas where tissue

appears cracked
Aorta
 Mesoaortitis
luetica
Pathophysiology:
• Cause: Treponema pallidum
• The ascending aorta and arch of
aorta become involved around 20
years after the initial primary
infection. The damage is mostly to
the tunica media.
• Stages:
(1) Ulcer in genitalia.
(2) Couple months/years: rash over
mucous membranes and skin.
Papillary rash
(3) 15 years later. Neurosyphilis.
Changes affect neural tissue and
cardiovascular system

Gross Pathology:
• Tree bark intimal surface

Histology:
• Inflammation around vasovasorum
• Vascularisation of tunica media
• Perivascular inflammatory infiltrates of
lymphocytes and plasma cells
• Destruction of elastic fibres and proliferation
of connective tissue
• Rare calcification
• Overlying atherosclerosis
Lungs
 Pneumonia lobularis
Pathophysiology:
• Types of inflammation:
(1) Exudative (acute): serous, fibrinous, purulent, haemorrhagic and
gangrenous
(2) Chronic
• Serous exudate: contains fluids, usually caused by viruses.
Fibrinous exudate: contains fibrin and other blood proteins.
Surface fibrinous inflammation seen in tubular organs covered by
single – layered epithelium. Deep fibrinous inflammation seen in
organs with stratified squamous epithelium.
Purulent inflammation: contains neutrophils.

• Acute localized purulent inflammation

• Cause: bacterial infection (Streptococcus/ Staphylococcus etc)

• Complications: abscess formation, pleural empyema, fibrinous
pleuritis, compensatory emphysema , sepsis

Gross Pathology:
• White/ yellowish centre of consolidation surrounded by
normal parenchyma.

Histology:
• Acute leukocytic alveolitis – some alveoli are filled
with purulent exudate, some have oedema and some
appear unaffected (filled with air)
• In beginning, centres of inflammation are scattered
but during progression, they merge and form larger
areas.
 Pneumonia lobaris
(crouposa)

Pathophysiology:
• Acute diffuse surface fibrinous inflammation of whole
lobe of lung
• Cause: pneumococcal infection.
• Stages:
(1) Active hyperaemia: vasodilation
(2) Red hepatization: exudate turns fibrinous and rich
in erythrocytes
(3) Grey hepatization: increase in leukocytes in alveoli
and interstitium
(4) Resolution/ resorption: if incomplete leads to
fibrosis.
• Complications: fibrinous pleuritis, fibrinous pericarditis,
cornification

Gross Pathology:
• Red to grey consolidation of one or more lobes

Histology:
• All alveoli are affected
• The exudate filling the alveoli may look
detached from the alveolar walls; this is due to
retraction of fibrin
 Tuberculosis
miliaris pulmonis
Pathophysiology:
• Cause: mycobacterium tuberculosis, M. Bovis
• Most commonly affected are the lungs

Gross Pathology:
• Multiple yellowish crumbly nodules in
lung parenchyma as big as millet seeds

Histology:
• Lung parenchyma = white spaces
• Tuberculosis granuloma = tuberculoma
• Specific structures from the centre out:
caseating necrosis (pink part)
epithelioid cells – giant Langhans cell type
T-Lymphocytes (dots)
• Central caseous necrosis surrounded by
inflammation (neutrophils, macrophages)
Heart
 Pericarditis
fibrinosa
Pathophysiology:
• Also known as cor villosum
• Acute fibrinous inflammation of the epicardium
and subepicardial fat tissue.
• Both parietal and visceral pericardial sheets are
covered in a fibrinous exudate
• Cause: kidney failure, infarct in myocardium,
autoimmune disease

Gross Pathology:
• Dull white coating of the heart surface forming
crests and strings

Histology:
• Fibrinous exudate on the surface of the epicardium
that is rich in fibrin; look for saturated pink stringy
or amorphous substance at periphery of slide
• Underlying adipose tissue contains dilated blood
vessels and perivascular Neu infiltrates
• Layers:
Subepicardial fat tissues (outer)
Epicardium – fibrinous inflammation
• Pink structure: fibrin
 Cicatrices
myocardii
Pathophysiology:
• Cause: ischemic heart disease
• Cicatrices: scar tissue
• Scar tissue is the end result of tissue repair –
the necrotic myocardial cells are replaced by
collagen fibres and fibrocytes.
• Granulation tissue turns into scar tissue
• After 24 hours, ischemia grossly visible via
granulation
• Coagulative necrosis

Gross Pathology:
• Pale white, sharply demarcated area,
glossy and tough

Histology:
• (H.E staining and V.G staining)
• Pale pink eosinophilic material= connective
tissue/ scar tissue
• Periphery of necrosis = proliferation of blood
cells
• Thick cardiomyocytes = hypertrophy in order to
compensate
Cerebrum
 Leptomeningitis
purulenta
Pathophysiology:
• Cause: microbial infection –
Neisseria meningitis,
pneumococcus, streptococcus,
staphylococcus, E.coli
• Most susceptible are newborns,
babies and young children
suffering from acute otitis media or
a tooth abscess.

Gross Pathology:
• Purulent yellow exudate, covering the
brain convexity – purulent ‘cap’.
Underlying the brain tissue is
oedematous
Histology:
• Leptomeninges covered by a purulent
exudate – abundant neutrophils,
fibrin, cell and tissue debris
• Underlying brain tissue – perivascular
and pericellular oedema (dilated empty
– appearing spaces around cells and
vessels)
• Blood vessels dilated, congested with
neutrophils
 Leptomeningitis
tuberculosa
Pathophysiology:
• Inflammatory exudate covers brain –
subarachnoid space over base
• Exudate undergoes organisation,
fibrosis, granulosis
• Yellowish exudate over brain
• Possible complication: hydrocephaly

Histology:
• Tuberculosis has lymphocytes. Purulent
has neutrophils
 Abscessus
cerebri
Pathophysiology:
• Chronic abscess: pilogenic membrane
• Acute abscess: no pilogenic membrane,
no granulation

Histology:
• Foamy cytoplasm = macrophages
Oral Cavity
 Actinomycosis
Pathophysiology:
• Cause: anaerobic, gram positive,
filamentous bacteria, part of the
normal flora in the oral cavity, GI
tract, female genital tract.

Gross Pathology:
• Sulphur granules, small yellow
granules in the centre of abscesses,
they contain bacterial colonies,
could be found in sputum

Histology:
• Solid structures =float with
inflammatory exudate
• Bacterial colonies = sulfur granules in
the centre
• Granulomas consisting of lymph, giant
cells
• In the periphery, granulation tissue
with lipophages – these give the
granuloma the yellow colour
Appendix
Appendicitis
phlegmonosa
Pathophysiology:
• Young don’t have developed
lymphoid tissue – therefore
don’t have appendicitis

Histology:
• Purple = muscularis mucosa.
Invaded by neutrophils
Others
 Granulatio
Pathophysiology:
• Two types:
(1) Amyloid deposition in white
pulp (localized type)
(2) Amyloid deposition in red pulp
(diffuse type)

Histology:
• Localised type: deposition of
amyloid in walls of arterioles in the
white pulp
• Diffuse type: deposition in the
sinuses, sparing the follicles.
• (MV staining: amyloid is red-violet)
 Granuloma
corpus alieni
Pathophysiology:
• Foreign body reaction forms
around surgical sutures, splinters,
glass fragments, injected materials
like mineral oils or paraffin,
talcosis, pilonidal disease etc.

Histology:
• All characteristics of granulation
tissue (chronic inflammatory cells,
blood vessels)
• Foreign body giant cells –
multinucleated, surrounding the
foreign material, the nuclei are
situated at the pole opposite the
foreign body
• Fibroblasts -> collagen ->
encapsulation