Pathology Tutorial (with some answers)

** double check the answers, some of them may not contain

full answers or have been written with slight
errors/incomplete explanations**

Key points of describing pathology:

What sample? (pot, slide)
What is it? (lung, liver, epithelium of skin)
Describe what it looks like? (eg. round nodular lesion, not a specific
dx)
What is the most likely dx given features?

Case 1

(a) 75 yo male presents with ulcerated lesion on leg. The

ulcer has been there for several months, but has recently
increased in size and started bleeding. A surgical excision
was performed.

Specimen No: X2985

Describe the lesion: The pot contains an excised lesion with a well
circumscribed border, which is raised, nodular, uniformly
pigmented, and measuring approximately 2 cm in diameter.

What is your differential diagnosis? Key points: SCC or BCC.

May also be seborrhoiec keratoses, wart or amelanocytic melanoma.

<Histology slide> (describe) Slide of what looks to be epithelial

cells of the skin. There looks to be infiltration through the basement
membrane by squamous cells. There are invasive nests sitting on
the BM, with signs of ulceration and the formation of keratin pearls.
<SCCs also stain pink>

What is your diagnosis now? SCC with dermal invasion.

<cf. BCC would be nests with palisading squamous cells around

edge. And would stain blue>

(b) 35yo female presents with a mole on her shoulder. There

has been a recent increase in size and bleeding. On
examination the lesion appears to be a pigmented, inflamed
nodular lesion. It has a diameter of approx 1.2cm, irregular
borders with 2 satellite nodules. An excisional biopsy is
performed under local anaesthetic for histology.

Do you agree with the management thus far? No. Whole

excision should be performed with appropriate margins. By taking
only a sample, you are distorting the architecture of the remaining
skin lesion (due to scarring), making prognostic factors such as
Breslow’s thickness less reliable. Also there is a small risk of seeding
of the melanoma.

Describe the histology slide: Epithelium of the skin, signs of cell

hyperplasia and parakeratosis. Abnormal nests of cells at the
dermo-epidermal junction. Spindle epithelioid cells (indicative of
melanoma), with no signs of maturation. Lymphocyte infiltration in
dermis.
Diagnosis? Melanoma

Prognostic factors considered in melanoma staging. What

are important histological features?
Breslow’s thickness
Clark’s staging
Also: ulceration, lymphoblastic infiltration, lymph node metastises,
margins, mitotic features.

The patient returns in 3 months with black urine, jaundice

and convulsions. Admitted to hospital, has cardiac
arrhythmia and dies. Autopsy. How do the findings in the
brain explain the signs/symptoms described?

<pot with brain> Brain, coronal view, multiple dark nodules, well
demarcated, present mainly in grey matter. c/w cannonball
description of metastises.

Black urine and jaundice: could be explained by metasises to liver,

with accompanying intrahepatic jaundice and unconjug bilirubin in
urine, causing dark coloured urine. Black urine may also be
indicative of tumour load, and excretion of melanin (dark pigment).

Seizures: Mets in brain.

Case 2

What are the 2 types of bone marrow? Yellow and red

Specimen no: X2997B <describe> thyroid w/ PTH gland. Right

PTH gland hyperplasia, nodular in appearance.

Condition caused by lesion? Primary hyperparathyroidism, due to

parathyroid adenoma.

Would serum calcium be increased or decreased? Increased

Explain mechanism. ↑PTH→ increased vit D (via kidneys), ↑

osteoclastic action (in Bone), direct action on kidneys → Vit D: ↑
absorption Ca from intestine, Kidneys: ↑ Ca reabsorption, Bone: ↑
mobilisation of Calcium stores → ↑ Calcium

Other clinical manifestations? Bones (pathological fractures,

pepper pot lesions of the skull), Moans (confusion, depression,
seizures, lethargy), Groans (stomach pain, constipation, PUD),
Stones (gallstones, kidney stones), Cardiac abnormalities (shortened
QT, arrhythmias, calcification of valves).

20yo male presents with fatigue, weight loss and vague

abdominal pains. On examination he is pale.
Bloods
Hb 7.0 g/dL (14-18)
RBC 2.2 (4.6-6)
Hct 21 (42-50)
MCV (fL) 130 (80-95)
MCHC (%) 34 (32-38)
Reticulocytes 41 (20-70)

Comment. This picture is consistent with a macrocytic anaemia.

Slide showing biopsy of ileum. What is abnormal about it?

Small intestine slide with H&E stain. It shows villous atrophy, with
sloughed epithelium, chronic inflammatory infiltrates (full thickness,
extending past lamina propria). Evidence of fissuring. There is also
evidence of ulceration and granulomas.

What do the blood results indicate given the biopsy results?

Poor absorption of B12. (ie. Megaloblastic anaemia due to poor
absorption of b12)

Would a peripheral blood film be helpful? Yes. They would

confirm megaloblastic change to RBCs. You may see Howard-Jolly
bodies (basophilic nuclear remnants in circulating erythrocytes),
anisocytosis (↑ red cell distribution width or RDW), and
hypersegmented neutrophils.

Case 3

The following questions are T/F.

A germinal centre in a lymph node:

Contains mainly T-lymphocytes → F
Contains dendritic reticulum cells → T
Contains cords and sinuses → F (medulla does)
Generates immunoglobulins via plasma cells → T
Is enlarged in a reactive lymph node → T

In Hodgkin’s lymphoma:
There are Reed-Steinberg cells on microscopy → T
Is classified via the Ann-Arbor system → T
Presents with painful lymph nodes → F (non-tender, usually 1 node)
Has associated eosinophilia → T
Is associated with Askanazy cells → F (large eosinophilic cells found
in the thyroid gland in autoimmune thyroiditis and Hürthle cell
tumors. Called also Hürthle cells).

In Burkitt’s Lymphoma:
There is a prolonged course if it is untreated → F
Is associated with EBV → T
Has a distribution pattern similar to Falciparum Malaria → T
Rarely affects the jaw → F
Is a tumour of T-lymphocytes → F

25yo patient, HIV +ve.

Specimen 3024A (pot, small bowel with mesentery attached,

nodular growth in mesentery).

What is the likely diagnosis? B-cell, non-Hodgkins lymphoma.

Likely to be Diffuse large B-cell lymphoma.

T or B cell in origin? B-cell

How aggressive is this disease? Very aggressive (and the

patient is immunocompromised as well)

What would be the B-symptoms, and would this patient be

suffering from them? Night sweats, Fever, Weight loss (rapid,
significant). Yes the patient would have these.

Case 4

70yo male, presents at ER with SOB and feeling faint. Has a

history of chest pain over the past few days which he has
attributed to indigestion. Also has hypertension and smokes
10-15 cigarettes per day. On examination he has a rapid
weak pulse and muted heart sounds.

Specimen X221A <describe>. Heart, with blood in the pericardial

space (possibly due to infarct and subsequent rupture)
Describe the pathological events that led to the outcome
above? Blockage of coronary artery → MI → ventricular rupture →
haemopericardium → cardiac tamponade → cardiogenic shock.

Slide #310 <describe> Slide of myocytes. Myocytes have no

nuclei, are widely spaced with inflammatory infiltrate (neutrophils).

How old is the infarct? 3-5 days

Tip from tutor: Know sequence of pathological changes (on histology

and gross examination) and approx time frame for changes

There are 2 patterns of infarction. What are they and which

one is more common? Subendocardial and transmural.
Transmural is more common.

What determines the extent of the infarct? Collateral blood

vessel formation, duration of ischaemia, type of tissue (ie. Oxygen
demand of tissue), size of vessel occluded, length of occlusion,
location of vessel, and associated coronary artery spasm, HR and BP
(how much blood can get into the rest of the coronary vasculature).

If the blockage is due to atheroma, what are the sequence

of events leading to occlusion of the vessel? <not atheroma
formation, just events leading to blockage>. Sudden change in
plaque (due to ulceration of the surface, rupture of the plaque or
haemorrhage) → exposure of thrombogenic factors (endothelial cell
activation/spasm from aggregation) → platelet adhesion and
aggregation and activation of the clotting cascade → thrombus
formation → occlusion.

What is reperfusion injury and why does it occur? O2 free

radicals & inflammatory mediators → further damage.
(from Robbins Ch 1)
• New damage may be initiated during reoxygenation by
increased generation of reactive oxygen and nitrogen species from
parenchymal and endothelial cells and from infiltrating leukocytes.
These free radicals may be produced in reperfused tissue as a result
of mitochondrial damage, causing incomplete reduction of oxygen,
or because of the action of oxidases in leukocytes, endothelial cells,
or parenchymal cells. Cellular antioxidant defense mechanisms may
be compromised by ischemia, favoring the accumulation of free
radicals. Other mediators of cell injury, such as calcium, may also
enter reperfused cells, damaging various organelles, including
mitochondria, and increasing the production of free radicals.
• Ischemic injury is associated with inflammation as a
result of the production of cytokines and increased expression of
adhesion molecules by hypoxic parenchymal and endothelial cells,
which recruit circulating neutrophils to reperfused tissue. The
inflammation causes additional tissue injury ( Chapter 2 ). The
importance of neutrophil influx in reperfusion injury has been
demonstrated experimentally by the ability of anti-inflammatory
interventions, such as treatment with antibodies that block
cytokines or adhesion molecules, to reduce the extent of the injury.
• Activation of the complement system may contribute to
ischemia-reperfusion injury. The complement system is involved in
host defense and is an important mechanism of immune injury
( Chapter 6 ). Some IgM antibodies have a propensity to deposit in
ischemic tissues, for unknown reasons, and when blood flow is
resumed, complement proteins bind to the deposited antibodies, are
activated, and cause more cell injury and inflammation.

4 complications of MI:
HF, AF, Infarct extension, Valvular incompetence, Rupture, Papillary
muscle dysfunction (etc etc)

Case 5

27yo female presents at GP 1 week post tooth-extraction,

complaining of tiredness and a recurrent fever. On
examination is febrile, with peripheral oedema. PR is rapid
and thready. On auscultation, MS murmur heard. Patient
also has a history of rheumatic fever as a child. She dies
from complications.

Describe the following:

#161 slide – slide, valve leaflet, cellular infiltrate and vegetation on

valve, pathological debris present (containing white cells, fibrin and
bacterial colonies)
Specimen X2324 – Pot containing heart, hypertrophy of ventricle
wall, dilated ventricle. Heart valve leaflet, presence of vegetation on
valve leaflets (given the roughened appearance). Leaflets are also
partially destroyed.
CXR – enlarged heart, boot-shaped.

Outline the disease mechanism, starting with her disease as

a child. Rheumatic fever (autoimmune damage to the heart valve
leaflets, particularly mitral valves) → valvular insufficiency →
turbulence and damaged avascular valve leaflets → tooth extraction
entry of infection → infective endocarditis → valve prolapse, HF,
sepsis/septic emboli → septic shock.
Another group of valve problems is non-infective, and non-
bacterial endocarditis falls into this. What is your
understanding of this, and give an example of when this
occurs? Formation of a sterile plaque → still vegetation on valves,
but is made up of platelets, white cells, and fibrin deposition.

Case 6

78yo male presents with fever, malaise and SOB. Has a

history of chronic alcohol abuse. On examination is pyrexial,
dehydrated, and has dull right upper area on chest
percussion. On chest auscultation, has decreased breath
sounds on the right side, and a pleural rub is heard.

Describe CXR. Opacity in the upper zone of the right lung.

Consistent with right upper lobe consolidation (most likely
pneumonia).

Factors contributing to presentation? History of chronic alcohol

abuse (↑ likelihood aspiration pneumonia) and age.

Slide 105 – slide of lung tissue. Inflammatory response, neutrophils

present but no evidence of organization. Slide consistent with early
red hepatization as in pneumonia.

3 possible complications Disseminated sepsis, Empyema,

abscess formation, carnification (lung tissue resembles skeletal
muscle).
Describe the following pots (histological appearance) and
likely diagnosis.

Specimen X3432 – pot with lung, Gohn complex (lesion on lung,

and also in mediastinal lymph nodes) TB.

Specimen X2898C – Lung, small white lesions, over entire lung

(consistent with Miliary TB)

Both contain granulomas with central caseation.

Name the organism involved. What are the pathways from a

primary TB to the above specimens?
Mycobacterium tuberculosis. Pictures from Chapter 8 Robbins.
Case 7

Describe the lesion in X-ray A. What is the likely diagnosis

and histological appearance? Coin lesion, right lung, lateral and
lower zone. Likely to be a haematoma.

Describe the lesion in X-ray B, and specimen X2158. What is

the likely diagnosis and histological appearance?
Right apical lung tumour. Cavitating. Most likely to be a SCC or
Pancose tumour.

Describe the neurological complications of the lesion in X-

ray B.
Sympathetic: Horner’s syndrome (think MEAT) – Miosis,
Enophthalmos, Anhydrosis, pTosis.
<Also brachial plexus compression, and recurrent laryngeal nerve
compression>

Define paraneoplastic syndrome. A symptom complex that

cannot be explained by local or distant infiltration by the tumour.
They are defined as clinical syndromes involving nonmetastatic
systemic effects that accompany malignant disease. In a broad
sense, these syndromes are collections of symptoms that result
from substances produced by the tumor, and they occur remotely
from the tumor itself. The symptoms may be endocrine,
neuromuscular or musculoskeletal, cardiovascular, cutaneous,
hematologic, gastrointestinal, renal, or miscellaneous in nature.

What are the three common paraneoplastic syndromes that

occur in lung cancer? SIADH, Cushing’s (ACTH), Myasthenia
gravis. (others include 5HT, bradykinin, gonadotrophins, PTH)

Case 8

68yo male presents at GP with indigestion. On examination

he has tenderness in the epigastrium. Doctor suspects PUD
and prescribes cimetidine and advises the patient to stop
smoking. 2 weeks later, patient presents with haematemesis
to hospital. On examination his PR is 108, and BP 100/65.

What are the causes of haematemesis? Oesophageal varices,

Mallory weiss tears, gastritis, PUD, oesophagitis, cancer.

On further examination, the doctor finds ascites, spider

naevi, gynecomastia. Now what is the likely explanation of
the haematemesis? Oesophageal varices.

What are the pathological processes for ascites, varices,

spider naevi and gynecomastia?
Liver dysfunction/cirrhosis and portal system hypertension.
Varices: portosystemic shunts in oesophagus, distension of low
resistance/thin walled veins in oesophagus. With the rise in portal
system pressure, the flow is reversed from portal to systemic
circulation by dilation of collateral vessels and development of new
vessels. Venous bypasses develop wherever the systemic and portal
circulation share common capillary bed.
Ascites: low albumin in blood (low oncotic pressure) and increased
pressure through liver. Sinusoidal hypertension, altering Starling's
forces and driving fluid into the space of Disse, which is then
removed by hepatic lymphatics; this movement of fluid is also
promoted by hypoalbuminemia. Percolation of hepatic lymph into
the peritoneal cavity: Normal thoracic duct lymph flow approximates
800 to 1000 mL/day. With cirrhosis, hepatic lymphatic flow may
approach 20 L/day, exceeding thoracic duct capacity. Hepatic lymph
is rich in proteins and low in triglycerides, which explains the
presence of protein in the ascitic fluid. Splanchnic vasodilation and
hyperdynamic circulation. These conditions were described earlier,
in relationship to the pathogenesis of portal hypertension. Arterial
vasodilation in the splanchnic circulation tends to reduce arterial
blood pressure. With worsening of the vasodilation, the heart rate
and cardiac output are unable to maintain the blood pressure. This
triggers the activation of vasoconstrictors, including the renin-
angiotensin system, and also increases the secretion of antidiuretic
hormone. The combination of portal hypertension, vasodilation, and
sodium and water retention increases the perfusion pressure of
interstitial capillaries, causing extravasation of fluid into the
abdominal cavity.
Gynecomastia/Spider naevi: liver dysfunction, unable to metabolise
oestrogen. Increased oestrogen causes spider naevi and hyperplasia
of breast tissue.

A liver biopsy is scheduled. What blood tests should be done

before this?
Hepatitis serology and coag studies.

Slide 112 (biopsy). Describe features seen and what these

findings suggest? Nodules of liver parenchyma with band fibrosis.
Malory’s hyaline and steatosis present. Consistent with cirrhosis?

Specimen X3495. Describe the lesion seen and suggest a

diagnosis. What is one complication of the disease? Large
irregular pale area in right liver lobe. Consistent with hepatocellular
carcinoma.

Case 9

Draw and label a diagram with features seen in slide 108. Is

it acute or chronic and why? (slide is histo of ulcer)
Defect of epithelium, extends into muscularis mucosa. Just need to
draw ulcer with the four layers of chronic inflammation. Necrosis →
Acute inflammation → granulation → fibrosis.

What is the likely organism? Helicobacter pylori.

How do you determine whether the lesion is an erosion or

ulcer? It is to do with the depth of the lesion. An ulcer will
penetrate into the muscularis mucosa, whereas an erosion will only
affect the superficial layers of the gut wall (and not extend into the
MM).

When do Cushing and Curling ulcers occur?

Cushing – associated with operations, tumours, surgery, intracranial
injury
Curling – associated with burns, trauma.

What are 2 complications of PUD?

Haemorrhage, perforation, stricture formation (from fibrosis).

Describe the lesion in specimen X3574. Give a name to this

lesion? Stomach, leather bottle stomach. Consistent with Linitis
plastica. (type of stomach cancer)

How do gastric adenocarcinomas spread, and what is a

Krukenberg tumour?
Adenocarcinoma spread – can be via direct spread, seeding in the
perotineum, lymphatic or vascular spread.
Krukenberg tumour – Gastric tumour (or any other tumour) that
spreads to the ovaries through the peritoneum.

Case 10

What condition is illustrated by slide 205? FAP (familial

adenomatous polyposis) tubular adenomas, polyps

Why is it important to diagnose this condition? Because it can

have malignant transformation, and is familial (genetic component)

What is the diagnosis illustrated by specimen X823A? Pot

contains portion of large bowel. Has multiple outpouchings along
the wall. Consistent with diverticulosis.

Give a definition of the above specimen. Diverticulosis. Blind

ended pouch, lined with epithelium and all layers of the gut wall.
Pouch communicates with the gut lumen.

2 factors that are involved in the pathogenesis of the

condition above? Focal weakness in the gut wall, ↑ intraluminal
pressure.

The following questions are T/F

Bacterial causes of intestine infection:

Giardia lamblia → F (protozoal)
Balantidium coli → F (protozoal)
Schistosoma mansoni → F (fluke)
Escherichia coli → T
Histoplasma capsulatum → F (fungus)

Hirschsprung’s disease:
Usually affects the right colon → F (usually affects left)
Failure of migration of the neural crest cells → T
Not associated with meconium ileus → F
Abnormality is in the distended portion of the bowel → F (distal to
distension)
Causes constipation → T

Which of the following polyps in the large bowel are

precancerous?
Tubular adenoma → T
Inflammatory polyps → F
Metaplastic polyps → F
Lymphoid polyposis → F
Villous adenoma → T