Part one of the full clinical anatomy micro and macroscopic slides. this part covers the first 32 microscopic slide topics. For medical students Plovdiv medical university.

1. Microscopic slides:
1. Atherosclerosis of aorta
2. Arteriolosclerotic nephrosclerosis
3. Myocardial infarction
4. Rheumatic myocarditis.
5. Fibrous endocarditis
6. Subcutaneous rheumatoid/ rheumatic nodule
7. Acute bronchitis
8. Chronic bronchitis
9. Lung emphysema
10. Abscessing bronchopneumonia (lobular pneumonia)
11. Lobar pneumonia (croup)
12. Interstitial pneumonia
13. Silicosis
14. Squamous cell carcinoma (SCC) lung
15. Undifferentiated small cell lung cancer
16. Chronic lymphogenic Leukemia (in liver)
17. Chronic myelogenous Leukemia (in liver)
18. NHL – 4 of the more common types
19. Hodgkin's lymphoma – all four types
20. Plasmacytoma
21. Leucoplakia
22. Giant cell epulis
23. Amelloblastoma (adamantinoma)
Micro continued..
24. Chronic tonsillitis
25. Atrophic gastritis
26. Acute duodenal ulcer
27. Chronic peptic ulcer
28. Massive acute necrosis liver
29. Micronodular cirrhosis of liver
30. Chronic cholecystitis
31. Crescentic GN (semilunar or subacute)
32. Mesangiocapillary GN
33. Nephrosclerotic glomerulonephritis
34. Acute pyelonephritis
35. Chronic pyelonephritis
36. Renal cell carcinoma
37. Carcinoma urinary bladder
38. Adenocarcinoma of prostate
39. Seminoma testis
40. Abortion
41. Molar pregnancy
42. Choriocarcinoma
43. In situ SSC uterine cervix
44. Adenocarcinoma of endometrium
45. Papillary cystadenoma of ovary
46. Papillary cystadenocarcinoma ovary

2. Micro continued…
47. Fibrocystic disease of breast
48. Fibroadenoma
49. Breast cancer
50. Nodular goitre
51. Graves disease (hyperthyroidism)
52. Diabetic Glomerulosclerosis
53. Acute polio encephalitis
54. Acute poliomyelitis
55. Tuberculous leptomeningitis
56. Astrocytoma
57. Glioblastoma multiforme
58. Neurinoma (schwannoma)
59. Meningioma
60. Miliary TB lungs

3. 1. Atherosclerosis of Aorta
(Microscopic)
 Numerous thin elongated “needle-like”
empty spaces – cholesterol clefts or crystals.
 Multiple lipophages (foam cells)
 Media can be atrophic – dark blue stripes or
intact.
 Ulceration of fibrous cap
 Mural thrombi
 Focal hemorrhage – red blood cells
 Calcifications
Complications of an atheromatous plaque include:
erosion, ulceration, plaque rupture, hemorrhage,
arterial aneurysmal dilation, calcification and
thrombosis.

4. 2. Nephrosclerosis Arteriolosclerotica
(Microscopic):
 Lumen of arteriole is narrowed
 Thickening of wall
 Hyalinization
 At first only arteriolar changes but later – loss of nephrons,
fibrosis, thickening and hyalinization of glomeruli.
 Hyperplastic changes: concentric laminations of arteriolar
smooth muscle – “onionskin appearance”
 Interstitium – patchy fibrosis, chronic inflame, occasional
infarction/ hemorrhage – RBC infiltrates

6. 3. Myocardial Infarction (Micro):
Earliest stage:
First 6hrs
 Contraction band necrosis (Irregular, dark,
eosinophilic, wavy bands extending
transversely across myofiber.)
 Myofibers lose their cross-striations
After 12 hours to 2/3 days – Coagulative
necrosis
 Central nuclei disappear
 Wavy fibres
 Outlines of myofibers remain
 Neutrophil infiltration at margin of infarct
 Macrophages filled with hemosiderin
 Haemorrhages
1 week – months
 Onset of capillary and fibroblastic
proliferation at margins
 Fibrosis and granulation tissue/scar
formation
 Fewer inflammatory cell infiltrates
1 Early stage
– contraction
band necrosis
(acute MI)

7. Stage 2 – Coagulative
necrosis evident after 6 –
12 hours and clearly
visible by 24 hours;
karyolysis, eosinophilia,
wavy fibers, and onset of
leucocyte infiltration.

8. Left = Later stage
MI; A – Necrotic
myocyte (pink)
B – Fibroblast
C – Collagen
deposition
Stage three; 10 – 12
days old: extensive
granulation tissue,
few necrotic
myocytes are left as
they have mostly
been replaced.
Abundant
capillarisation,
macrophages

10. Myocardial cicatrix – HE vs. Van Gieson
staining
 3 – several weeks post-MI
 Patches of fibrosis replace the myocardial
cell dropout with intervening healthy
myocardium.
 Size of scar is directly proportionate to the
degree of preserved ejection fraction.
Larger scars lead to complication: heart
failure and arrhythmia
 Scar is rich in eosinophilic staining
collagen, healthy myocardium appears as
yellow - brown
 Scar tissue has low cellularity,
scanty chronic inflammatory
infiltrate, only a scattering of
fibroblasts
 Some semi-damaged myocytes
experience decreased size
(atrophy).
 Other undamaged myocytes
undergo reactive hypertrophy
Cicatrix
HE Cicatrix

11. 5. Fibrous endocarditis (micro);
 Fibrose endocarditis is one of four subtypes
of rheumatic endocarditis; the other three
being 1). Diffuse valvulitis/ recens/
incipiens, 2). Verrucous endocarditis and 3).
Recurrent endocarditis. These are classified
morphologically based on the prevailing
type of damage.
In fibrose type:
 Valve leaflets become thickened and
deformed
 Neovascularization and calcifications
 Commissures are frequently fused
 Chordae tendineae are thickened,
shortened and fused together.
 Metachromasia due to redistribution of
glycosaminoglycans
Other pathological processes of rheumatic heart disease can
simultaneously be occurring in the myocardium:
 Modest dilation of ventricles
 Mural softening, myocyte necrosis
 Chronic interstitial inflammation and myocardial necrosis
 Don’t forget the pathognomonic feature: Aschoff bodies (granular
fibrinoid lesions) – perivascular and subendocardial location
Right:
Normal valve
has three
clearly
defined
layers
Fibrose endocarditis
Fibrose endocarditis

12. 6. Subcutaneous rheumatoid/ rheumatic
nodule (micro);
 Associated with BOTH juvenile rheumatic
fever and adult rheumatoid arthritis
 Occur mainly over bony prominences in
the extremities.
 Mostly non-tender, pea sixed, last 6-10
weeks and coincide with concurrent
heart involvement.
 The lesion is typified by fibrinoid necrosis
and granulomatous reaction.
 Usually subcutaneous location, large,
firm, dome shaped mass that may or may
not be painless
 Typically the nodule may be surrounded
by adipocytes, may extend deep into
reticular dermis.
 Fibrin deposition and necrosis in centre
of nodule (acellular area)
 Surrounded by well-developed palisading
histiocytes, vascular granulation tissue,
Ly, plasma cells, eosinophiles, giant
multinucleated cells.
 Older lesions are more severely fibrotic.

13. 4. Rheumatic myocarditis
(Microscopic):
 Cause post-infection of pharynx
with GABHS.
 Aschoff bodies = granulomatous
inflammation/ nodular
perivascular collection of mainly
mononuclear inflammatory cells
found near blood vessels
characterised by “aschoff giant
cells” (orange arrow) – cells with
two or more nuclei and prominent
nucleoli, mononuclear cells –
activated macrophages called
“aschoff caterpillar cells” and
some neutrophils. Eosinophilic
collagen representing site of
antigen – antibody reaction.
 Aschoff bodies = areas of fibrinoid
necrosis.
 Leads to “spindle- form” scars

14. Fibrinous pericarditis (Microscopic):
 Strands of pink/ eosinophilic, amorphic fibrin
extending out from surface.
 Neutrophils (PMNs) can often be seen in this
exudate.
 Unlike other forms of pericarditis, leucocytes
do not invade the myocardium!

15. Left: Normal. Right: Acute bronchitis –
debris and mucus in lumen, thickened
oedematous mucosa
7. Acute bronchitis
(microscopic);
 Purulent exudate
 Increased number of
leucocytes mostly neutrophils
and macrophages.
 Very little pathological change
from normal anatomy
 Mucus glands normal
 Goblet cells – slightly
increased in number
 Smooth muscle is normal

16. Chronic bronchitis: A=
epithelial thickening
B=Mucous gland
hypertrophy and
metaplasia
C=Prominent smooth
muscle
Chronic bronchitis (left)
A=Bronchiole wall with
accumulation of mucus, wall
thickening, mucous gland
hypertrophy and metaplasia
and scattered mononuclear
inflammatory cells.
B=Squamous cell metaplasia
and hyperplasia of
seromucous gland.
8. Chronic
Bronchitis -
Microscopic
 Increased number of inflammatory cells in
submucosa.
 Infiltrate is mostly lymphocytes and plasma cells.
 Hyperplasia of glands (increased number),
muscular layer and hyperplastic “cupped” cells.
 Metaplastic mucosa – from ciliated cylindrical to
squamous.
 Mucous and catarrhal-purulent exudate in
lumen, mucus plugging and fibrosis.

18. 9. Emphysema bullosa (Micro):
 Loss of distal airspaces
 Diminished number of capillaries and loss of
elastic tissue
 Remaining spaces become dilated with less
SA for gas exchange.
 Thinning and destruction of acinar walls.
 Alveolar ducts are dilated.
 Acanthotic pigment deposits (smoking)

19. 10. Bronchopneumonia (lobular pneumonia)
with abscesses – micro:
 Most common pattern of lung infection.
 Bilateral, involving lower zones of lungs,
common in terminally ill patients/classically
hospital acquired pneumonia (HAP).
 Different stages of development are seen in
different areas.
 Neutrophil predominant infiltration, patchy
intra-alveolar fibrino-purulent exudates.
 Acute bronchiolitis (hyperaemic with
suppurative exudate).
 Desquamated alveolocytes, macrophages
 Hemorrhages
may occur
occasionally.
 Complications:
- Bronchiolar
fibrosis
- Bronchiectasis
- Pulmonary
fibrosis
- Abscess
formation

20. 11. Pneumonia crouposa (Lobar) – Micro HE:
 90% = Streptococcus pneumoniae.
 Congestion phase: Predominantly eosinophilic edema fluid with bacteria
visible and congested capillaries.
 Red hepatisation: RBCs (hemorrhage) and fibrin exudate. Congested
capillaries in alveolar wall.
 Grey Hepatisation/ organizing pneumonia: (As seen in images) Alveolar
spaces filled with neutrophils, and fibrin fibers.
 Due to fibrin the exudate detaches from the alveolar wall leaving a clear
peripheral space.
 Later “Resolution;” More macrophages (predominant cell) and
fibroblasts and collagen deposition.

21. 12. Interstitial pneumonia – micro:
 Commonly caused by Viruses; RSV, CMV, influenza, parainfluenza,
adenoviruses, coronaviridae, rhinoviruses (cold virus), coxsackie viruses as
well as the bacteria mycoplasma pneumoniae.
 This pneumonia is quite distinctively without alveolar exudates.
 Thickening of alveolar walls – congestion, edema and mononuclear infiltrate
(lymphocytes, plasma cells and macrophages)
 Bronchiolar and alveolar epithelial proliferation – may form giant
multinucleated cells and syncytia
 Squamous metaplasia may occur on occasion.
 Sometimes interstitial viral pneumonias precipitate a secondary bacterial
pneumonia.
 Diffuse alveolar damage may be almost identical to that seen in ARDS
 If the disease becomes chronic, a fibrotic stage occurs.

22. 13. Silicosis - Microscopic
 Large silicotic nodules that can become confluent
 Consist of concentric lamellated bundles of pink collagen fibers with
central “hyalinization”.
 Usually occur near a bronchus or bronchiole
 Surrounded by an encasing wall of chronic inflammatory infiltrate –
mostly macrophages.
 Anthracotic (Coal/carbon) pigments are often seen in tandem in
surrounding interstitium and some laden macrophages
 Polarizing light may reveal the silica crystals within the nodule

23. 14. Squamous cell cancer lung
(microscopic)
 Sheets or islands of large polygonal
malignant cells with abundant pink
cytoplasm containing keratin.
 Grows as anastomosing nests and
chords.
 Mitotic figures and intercellular
bridges.
 Stromal reaction
 Tumour often infiltrates lymph
vessels.
 Adjacent bronchial dysplasia
 Classified as well, moderate or poorly
differentiated based on the presence
of “Keratin pearls”
 Tumour obliterating alveolar spaces or
filling alveoli
 Adjacent bronchial dysplasia
 Palisading granulomas can sometimes
be seen.

24. 15. Parvocellular carcinoma or undifferentiated small cell lung cancer
(microscopic):
 Small dark blue cells resembling “Oat grains” – minimal cytoplasm, very
high nuclear: cytoplasmic ratio.
 Cells are packed together in sheets and irregular nests
 A highly malignant form of neuroendocrine tumour with
paraneoplastic syndromes due to hormonal secretion: ACTH producing
Cushing syndrome and ADH producing SIADH leading to hyponatremia.
Others may produce calcitonin or parathyroid hormones,
gonadotropins as well as serotonin (carcinoid syndrome).
 Nuclei are hyperchromatic, tumour stroma is scant.
 Immunohistochemistry reveals presence of markers: chromogranin,
synaptophysin, pancytokeratin and neuron specific enolase.
 Clinical symptoms include: cough, dyspnea, anorexia, weightloss,
fatigue and haemoptysis as well as clubbing, acanthosis nigricans, new
onset diabetes, polymyositis, migratory thrombophlebitis and
thrombotic endocarditis.

25. 16. Chronic lymphogenic leukaemia in liver (micro):
 More common in males 2:1 , often seen in older adults.
 Enlarged portal tracts
 Cells often have B cell markers CD19+, CD20+ and CD23+ and T cell
marker CD5+.
 Preserved lobular structure
 “Round cell” infiltration of perivascular area - by lymphocytes and
lymphoblasts.
 Tumour Lymphoid cells resemble healthy ones; small, mononuclear,
round hyperchromic nuclei, one small nucleolus and scanty cytoplasm
 Pseudofollicles are common – pale, ill-defined germinal/ proliferative
centres
 Lymphoblasts are larger with vesicular nuclei and mild polymorphism.
CLL peripheral smear
showing smudge cells
– fragile lymphocytes
easily damaged due to
abnormal cytoskeletal
structure, a
characteristic finding
for the disease

26. 17. Chronic Myelogenic leukaemia Liver (Micro):
 Lobular structure is erased.
 Pleomorphic leucocyte Infiltrate containing numerous myelocytes,
granulocytes in several phases of maturation as well as (more rare)
early undifferentiated cells; myeloblasts, promyelocytes
 Sinusoids fill with tumour cells. “Flows” of hyperchromic cells are
observed.
 Periportal infiltration but not to the same degree as CLL.
 Hepatocytes are atrophic and separated in arcs due to the pressure-
necrosis.
In bone marrow:
• Increased basophils
and eosinophils
• Hypercellular
marrow with large
immature myeloid
cells 5-10 layers thick
• Shrunken and hypo-
segmented
megakaryocytes

28. 18. Non- Hodgkin's lymphoma:
• NHL 80% = B cell. NK-cell are rare.
• In children: most common types are Burkitt lymphoma, acute
lymphoblastic, large B cell lymphomas and anaplastic large cell
lymphomas.
• In adults: follicular lymphoma and marginal zone lymphoma
are more common.
• More likely than HL to be extranodal (Skin, CNS, disseminated,
peripheral blood, bone marrow and GIT – most common
extranodal site) but less likely than HL to have constitutional
“B” symptoms – drenching night sweats, fever and weight-loss.
 NHL often has insidious onset with dysphagia and
odynophagia (painful swallowing) being the chief complaints,
chest/abdominal pain, pruritis, splenomegaly and weightloss
also occur frequently.
1). Acute lymphoblastic lymphoma - microscopic:
 Effacement of tissue mass or bone marrow by round, blue
cells.
 Large primitive cells resembling either pre-B or Pre-T cells
 These large blast cells may contain cytoplasmic vacuoles
 Oval shape, indented nuclei, finely dispersed chromatin,
inconspicuous nucleoli.
•Non-Hodgkin lymphomas arise from monoclonal
expansion of malignant B or T cells
• B cell lymphomas
• B cell acute lymphoblastic lymphoma (ALL)
• Chronic lymphocytic lymphoma / small
lymphocytic leukemia (CLL / SLL)
• Mantle cell lymphoma
• Follicular lymphoma
• Marginal zone B cell lymphoma
• Extranodal MALT type
• Hairy cell leukemia
• Plasmacytoma / plasma cell myeloma
• Diffuse large B cell lymphoma (DLBCL)
• Burkitt lymphoma
• T / NK cell lymphomas
• T cell acute lymphoblastic lymphoma (ALL)
• T cell CLL
• Mycosis fungoides / Sézary syndrome
• Peripheral T cell lymphoma
• Angioimmunoblastic T cell lymphoma
• Enteropathy associated intestinal T cell
lymphoma
• Hepatosplenic T cell lymphoma
• Anaplastic large cell lymphoma (ALCL)
• Extranodal NK / T cell lymphoma, nasal
type

29. :
Above panel: acute lymphoblastic (NHL “precursor type”) lymphomas. Below: Follicular lymphoma with numerous crowded follicles
2). Follicular cell lymphoma – micro:
 22% of all NHLs.
 Extranodal involvement is rare, occurs in older patients as
painless (indolent) widespread peripheral
lymphadenopathy.
 Partial or complete effacement of lymphnode
 Capsule is often invaded
 Numerous crowded irregularly shaped lymph follicles.
 If sclerosis is present, nodular growth pattern is seen
 Small to large cleaved/ indented nuclei
 Mitotic figures are rare and growth is slow

30. 3). Diffuse large B-cell lymphoma:
 Many NHL’s in adults are of the large cell variety, most of which are
sporadic and B cell type (CD19+/ CD20+).
 Large cleaved cells with large eccentric nuclei and prominent nucleoli
(1-2) and moderate amount of metachromatic/ amphophilic pale
cytoplasm
 Mitotic figures are frequent
 Diffuse growth pattern
 Tend to be localised in early stages but with rapid aggressive nodal
enlargement and higher tendency to become extranodal in later stages
than other NHLs.
4). Burkitt's lymphoma – microscopic:
 Very common in children (30% of cases) but rare in adults.
 Highly aggressive but often curable.
 Three subtypes: African endemic – associated with EBV and usually
presents in the jawbone, Sporadic form – more pleomorphic/
multinucleated than the others and immunodeficiency-related form – in
children with HIV.
 Sheets of monotonous intermediate sized cells with “Starry sky pattern”
– produced by cellular debris phagocytosed by large macrophages
 Mitosis is commonly seen.
 Round nuclei, finely clumped chromatin and several nucleoli
 Neoplastic cells have squared-off borders from pressing against one-
another.

31. 19. Hodgkin's lymphoma 4 types (micro):
 Classic finding = Reed-Sternberg cells (large
multinucleated cells, bi-lobed with “mirror-like”
symmetry, 1-5% of neoplastic cell population,
nuclei appear like owl eyes due to prominent
nucleoli.)
 Normal lymphnode structure is effaced/ destroyed.
 Reactive cells include lymphocytes, macrophages,
eosinophils and fibroblasts.
 Cell-mediated immunity is usually reduced in these
patients (immunocompromised)
 There are four subclasses of Hodgkin's disease:
 Patients often have splenomegaly
1). Mixed cellularity 2). Nodular sclerosing 3).
Lymphocyte predominant and 4). Lymphocyte
depleted
1). Mixed cellularity type: Many different types of cells
are see; small Lymphocytes, Mafs and eosinophils.
 Many large pale lacunar cells: multinucleated,
nuclei frequently overlap or have surrounding
vacuolar halos – “coins on a plate appearance”).
 Reed-Sternberg cells present
Right: mixed
cellularity type HL
Below: Lacunar cells
– money on a plate

32.  More likely to occur in older age and B
symptoms are very common
 Capsule of affected LN is fibrotic, thickened
and infiltrated.
 Moderate vascularisation, necrosis and
fibrosis
2). Nodular sclerosing Type:
 Prominent bands of pink collagenous tissue
divides the cellular infiltrate into nodular
growth pattern.
 Lacunar cells may aggregate into syncytiates.
 usually cells are confined within the
thickened capsule
 Mitotic figures are uncommon.
 Most common form of HL (60% of all cases,
most common in young adults)
 Background infiltrate = lym, plasma, eos (often
numerous) and mafs (may be foamy).
 Reed-Sternberg cells and lacunar cells are
frequent
 Necrotic foci
 Most cases when diagnosed are low stage: I or
II
Top right: Mixed cellularity HL, all other images = Nodular sclerosing HL
with eosinophilic connective tissue bands clearly visible

33. 3). Lymphocyte predominant HL:
 Lacks many Reed- Sternberg cells – therefore difficult to
distinguish from small cell lymphomas.
 Characteristic cell present = “Popcorn cells” – these are
multilobulated, large nuclei histiocytic and lymphocytic
cells.
 Unlike lymphocyte depleted HL this variant is
dominated largely by presence of lymphocytes, the
lymphnodes are very frequently destroyed and usually
there is still some nodularity and rarely diffuse pattern
with lack of nodularity.
 T zone attenuation: Germinal centres (bright) are
regressed and small/ absent
4). Lymphocyte depleted HL:
 Has very numerous RS cells, look very bizarre, often in
sheets
 Few lymphocytes or other reactive cells
 Least common form, mostly in old men, assoc. with EBV
 Diffuse fibrosis is usually present
 Complete effacement of LN, not order to the
connective tissue and no clear nodules like in nodular
sclerosing HL
 Focal coagulative necrosis
Right and below:
lymphocyte predominant
Left and below:
lymphocyte depleted HL

34. 20. Plasmacytoma (Microscopic HE):
• Composed of malignant cells that resemble plasmacytes but with larger, eccentric and peripheralized nuclei and abundant
basophilic cytoplasm.
• Grossly the mass is jelly-like and induces local osteolysis.
• May contain mature (pear-shaped or oval), immature, plasmablastic (dispersed chromatin and much larger cells) and
anaplastic plasma cells
• Amyloidosis may be present in extraosseous plasmacytomas and presents as a pink amorphous material scattered with
multi-nucleated giant cells.
• Most common extraosseous location is near the nasopharynx and sinuses as focal accumulations of submucosal lymphoid
tissue.

35. 21. Leucoplakia - micro:
 Squamous epithelium is thickened – hyperplasia of basal
and keratin layers with enlarged papillae which deeply
invaginate the underlying supporting tissue (acanthosis).
 Parakeratosis is seen – abnormal preservation of nuclei
in the upper strata of the epithelium.
 Hyperkeratosis – excessive accumulation of corneous
substance
 There are several subtypes: classic, hairy, verrucous, and
erythroplakia.
 Erythroplakia (grossly red and eroded type) have higher
chance of malignant transformation
 Nuclear hyperchromasia or increased nuclear:
cytoplasmic ratio may be seen. Inflammatory infiltrate is
scanty or absent in this lesion.
 Underlying submucosa has increased collagen
deposition.
 There is no cellular atypia however leucoplakia is a pre-
cancerous lesion due to its tendency for squamous
metaplasia.
 Mechanical irritation (ill-fitting dentures), alcohol and
tobacco use are etiological factors.
Left: verrucous
subtype with
undulating
structure, no
cellular atypia
but marked
hyperkeratosis
Left: classic type
with increased
collagen
deposition in
stroma and
acanthotic
squamous cell
epithelium but
no cellular
atypia.

36. 22: Giant Cell Epulis (giant cell granuloma) –
microscopic:
o Epulis is a tumour-like process in the gingiva.
o It is a hyperplastic reaction of the connective tissue to
repeated trauma and inflammation.
o It is covered with multi-layered squamous epithelium
with parakeratosis (retention of nuclei in the upper
layers of the epithelium – stratum corneum).
o Epulis is often ulcerated with granulation tissue below
the epithelium.
o Two constituent cells are: A). Fibroblast-like cells, B).
Giant multinucleated cells resembling osteoclasts.
This cellular zone is separated from the epidermis by a
layer of connective tissue.
o The giant cells are surrounded by a vacuolar halo
separating them from the rest of the tissue. They are
round, basophilic and with dozens of oval nuclei.
o Epulis is very highly vascularised, they hemorrhage
very frequently and evidence for this is seen in the
often abundant hemosiderin deposits.
o Variable mitotic activity
o Non-encapsulated growth
o Most common type is giant cell epulis but other types
include angiomatous and fibromatous epulis.
Above circle: a giant cell with halo, right: oblong cut-out
showing dark brown hemosiderin deposits, rectangle
highlights connective tissue dividing multi-layered squamous
epithelium (orange arrow) from cellular region.

37. :
23. Ameloblastoma (adamantinoma) – microscopic:
 Rare, non-cancerous/ benign tumour that
develops in the jawbone near the molars. Though
benign, the tumour is locally aggressive and
often grows rapidly.
 It is derived from the germinal tooth epithelial
cells that produce enamel.
 Follicular type: most common, germinal
epithelium is arranged on oval follicles, with clear
linear palisade arrangement around the
periphery but haphazard organisation in the
centre.
 Follicles are multiple and of various size with
fibrous septae between.
 Centrally the cells have a starry-like appearance,
cells show reverse polarisation of nuclei away
from basement membrane.
 Cystic spaces form between tumour nests, cystic
destruction of bone shows on radiograph as
characteristic “soap bubbles” lesion.
 Other variants include plexiform ,
acanthomatous, granular, desmoplastic and basal
cell variants.
Left close-up: Reverse
polarisation of nuclei away
from basement
membranes

38. 24. Chronic tonsillitis - microscopic:
 During active infection bacteria colonies and purulent exudate may be
seen in the tonsillar crypts
 Has two forms: atrophic and hypertrophic
 Atrophic type: epithelial atrophy, fibrosis and inflammatory infiltrate.
 Hypertrophic type: hyperplasia and hypertrophy of lymph follicles with
light germinal centres.
 Sclerotic tissue is found in bands below them.
 Lacunae are dilated
 Epithelium is desquamated (flaking off).
 Some cellular debris may be concentrically compacted into cholesterol
deposits that over time calcify – amygdalites (tonsil stones).

39. 25. Atrophic gastritis – microscopic:
• Glandular atrophy – their height is significantly diminished. Covering
epithelium looks squished/ flattened.
• Glands are compressed and later destroyed.
• Intraglandular areas widen as glands are reduced in number and in them
we find chronic inflammatory infiltrate (lympho + plasma cells).
• Thinned mucosa is interspersed with fibrous CT between the glands.
• Often duodenal or gastric ulcers are seen in association with this condition
• Intestinal metaplasia is seen in gastric epithelium – increased number of
vacuolated mucous producing goblet cells.
• Giemsa staining can visualise blue-grey stick like organisms; helicobacter
pylori.
• A subtype exists; follicular gastritis where lymphoid follicles develop.
Left: Normal gastric
mucosa
Right: atrophy and
sparsity of glands,
intestinal metaplasia,
increased connective
tissue and leucocytes

40. 26. Acute duodenal ulcer – microscopic:
• Ulcer is usually small <1cm and round.
• The margins are sharply circumscribed with abrupt change from
normal mucosa to ulceration.
• Ulcer base may contain brownish-black deposit – digested blood
(hematin).
• Mucosal defect that penetrates through muscularis mucosae
(unlike an erosion) to reach muscularis propria.
• The cavity is filled with fibropurulent exudate and lymphocytic
infiltrate in surrounding tissue.
• Glands in the ulcerated area are destroyed.
• Underlying duodenal layers are not fibrosed and there is no blood
vessel thickening unlike gastric ulcers.
• Helicobacter pylori is often present (Grey-blue on giemsa staining)
• Often surrounding proximal duodenal villi are edematous (active
duodenitis).
• Gastric foveolar metaplasia may be present when chronic.

41. 27. Chronic peptic ulcer – microscopic:
 Focal loss of gastric epithelium
 Ulcer extends down to lamina muscularis of the submucosa. The
ulcer is well-demarcated.
 Vessels at the base of the ulcer are often eroded and local
hemorrhage is often observed
 Nearby vessels are hyperaemic and often have thickened walls
(endarteritis and endophlebitis) due to stimulation by chronic
inflammatory cytokines.
 Peripheral nerves in the affected area may hypertrophy reactively
to become amputation neuromas
 Bacteria, pus (neutrophils) and necrotic debris may be seen in and
around the ulcer if active.
 Muscular wall replaced by fibrose tissue, proximal gastric glands
are hypertrophic.
 Lymphoid follicles may develop close to the ulcer or pre-existing
ones will be hyperplastic.
 Base of ulcer shows fine dark pink line (fibrinoid necrosis).
 Below the base we can see an inflammatory infiltrate consisting of
mafs, lymphocytes and plasma cells.
 Immature connective tissue is laid in proximity to the lesion
 Granulation tissue can be seen in the lesion.
 Non-active ulcers that are healing will show regeneration of fresh
epithelium over the ulcer as well hyalinisation of submucosal and
intestinal metaplasia.

42. 28. Massive acute necrosis Liver – microscopic:
 Entire liver lobules are necrotic and microscopic lobular structures
are unclear/ ill-defined.
 Panacinar necrosis with collapse of the reticular framework.
 Peripherally there may be some small concentrations of spared
healthy hepatocytes.
 Hepatocytes show balloon (hydropic) degeneration.
 Nuclei undergo karyolysis and karyorrhexis.
 Proliferated and dilated bile ductules
 Scanty inflammatory infiltrate
 Regeneration is sparse and where it does occur it is highly irregular
and disorganised
 Unlike cirrhosis, fibrosis is not a prominent feature of acute fulminant
hepatitis (no time to form).
 Clinically, the patient will be experiencing severe haptic failure;
jaundice, ascites, coagulopathy, edema, hepatic encephalopathy,
hepatorenal/ hepatopulmonary syndromes.
Left: healthy normal
hepatic lobular structure
Right: severe
widespread destruction
of hepatic architecture

43. 29. Micronodular Cirrhosis of Liver – microscopic
 Micronodules are less than 3mm this type is associated with
alcoholic disease.
 No normal lobular architecture
 Central veins difficult to see.
 Early: Delicate fibrous septae spanning from central vein to
portal triad or from portal –to portal regions. Extensive fatty
change is also typical at this stage.
 Late: fibrous septae become much thicker, denser and
confluent with one another. Fatty change is replaced/ not as
prominent as before.
 Regenerative nodules (pseudo-lobules) can be observed –
islands of isolated/ stranded hepatocytes proliferate in a
disorganised mass, mostly without development of a central
vein. These nodules are at increased risk for malignant
transformation (HCC).
 Bile ducts may proliferate in response to biliary stasis as may
additional blood vessels.
 Mallory bodies (eosinophilic hyaline globule inclusions in
hepatocytes that indicate injury/ disease especially alcohol
consumption) become rarer to spot as cirrhosis progresses.
 Fibrose septae around the micronodules usually have mild
macrophage/ lymphocyte infiltration and hemosiderin
deposits.

44. 30. Chronic Cholecystitis – microscopic:
• Almost always seen in conjunction with gallstones but
can happen with thickened sludgy bile alone
(acalculous cholecystitis)
• 2 histological forms exist; A). Hypertrophic and B).
Atrophic.
• hypertrophic type: epithelium intact, wall and
mucosal folds are abnormally thickened, blunting of
villi, infiltration by lymphocytes and plasma cells.
• Atrophic type: usually due to long standing increase in
intraluminal pressure due to gallstones. Thinned wall
with shrunken, small villi, muscle in the wall is
atrophic and almost completely replaced with fibrose
tissue. The wall is infiltrated with leucocytes.
• Deep invaginations between mucosal folds are called
Rokitansky-Aschoff sinuses.
• Difference with acute cholecystitis: In acute
cholecystitis, the inflammatory reaction is neutrophilic
not lymphocytic. Also the acute form tends to be
purulent with the presence of bacterial overgrowth
while infection is rarely implicated in the chronic form.

45. Normal Kidney histology

46. Acute proliferative Glomerulonephritis (micro):
• Associated with NEPHRITIC SYNDROME
• Lots of neutrophils infiltrate around capillary loops. Capillary
loops are poorly defined.
• Increase in number of mesangial, epithelial and endothelial cells.
• Interstitial edema varies.
• No tubular changes
• Usually occurs 1-4 weeks after strep (GABHS) infection as a result
of immune-complex deposition, but one third of cases are non-
strep; pneumococci, staph, meningococci, pseudomonas etc.
• Enlarged/ inflamed and hypercellular glomeruli.
• All glomerular capillary loops are involved
• Inflammation = “diffuse”/ “Global”

47. 31. “Rapidly progressive” or Crescentic (semi-
lunar glomerulonephritis) - microscopic:
• Obliteration of bowmans capsule
• Semi-lunar “fibrin” cap develops – proliferation
of epithelial cells/ podocytes and mafs
(basophilic) in response to leaking fibrin.
• Crescents in >50% of Glomeruli.
• Compressed capillary loops
• Narrowing and closure of bowmans space.
• RBCs in bowmans space
• Causes NEPHRITIC SYNDROME
Causes: idiopathic, post-infectious with
streptococcus, SLE immune complex deposition,
vasculitis (pauci immune – little evidence of
hypersensitivity), Goodpastures syndrome (auto-
antibodies to basement membrane).
• Tends to have fulminant course, poor prognosis.

48. Membranous GN (micro):
• Looks “Pink” / eosinophilic due
to thickened glomerular capillary
wall membranes.
• No hypercellularity
• Later in disease there is
doubling” or duplication of the
basement membrane which can
be seen as black with silver
impregnation.
• Most common cause of nephrotic
syndrome in adults.
• Loss of anticoagulant proteins
from blood pre-disposes patient
to renal venous thrombosis.
Silver impregnation (above)

49. 32. Membranoproliferative (Mesangiocapillary) GN:
• Hypercellular but unlike Acute GN there are no
neutrophils (PMNs).
• Mesangium proliferation and increased matrix pushes
on endothelium increasing the lobular appearance of
the tuft.
• Capillary wall thickens (GBM)
• 50% of patients develop renal failure within a decade.
Some cases become rapidly progressive. Corticosteroids
seem to be ineffective.
• Causes are numerous: Hep B/C, Malignancies, Jones
silver stain will show “tram-track” doubling of GBM.

50. Focal proliferative or “mesangioproliferative” GN –
micro:
• Only affects a portion of some of the glomeruli (focal).
• Hyalinosis is involved (sclerotic) – as disease
progresses the affected glomerular retract/ shrink.
• Thickened pink glomerular looks can sometimes be
seen – “wire loops” appearance.
• Not hypercellular.
• Causes: vasculitis, IgA nephropathy, SLE, goodpastures
(autoimmune).

51. Focal segmental GN- micro:
• Only some glomeruli are
affected (focal) and only small
parts of their tufts (segmental).
• Characterised by sclerosis and
hyalinosis – hardening – of one
or more lobules.
• Eosinophilic, PAS (collagen
=red) positive, homogenous
hyaline material can be seen
on inner side of peripheral
capillary loops.
• Tubular epithelium is
atrophied and degenerates.
• Interstitial fibrosis and
infiltration by leucocytes can
be seen.

52. Very important to
understand which
GN types cause
which syndrome ,
as well as the key
differences
between these
renal syndromes!