Histopathology EMQs Flashcards
A Monckeberg arteriosclerosis B Infective endocarditis C Dressler’s syndrome D Dilated cardiomyopathy E Rheumatic heart disease F Left heart failure G Hypertrophic obstructive cardiomyopathy H Aortic stenosis I Carcinoid syndrome
A 36-year-old man presents to accident and emergency with a 1-day history of
a fever of 39.2°C and night sweats. A new heart murmur is detected by the oncall
cardiologist. The patient admits to being an intravenous drug user.
B Infective endocarditis
Infective endocarditis (IE; B) results from bacterial-vegetation of heart
valves. Acute IE has a time course of days and is usually caused by
Staphylococcus aureus in intravenous drug users; both sides of the
heart can be affected, but the right heart is most commonly affected,
because the lungs filter out many organisms, so that the left side of
the heart gets less exposure to organisms. Subacute IE has a time
course of weeks/months and is generally secondary to Streptococcus
viridans infection after dental procedures; only abnormal valves are
affected and hence these are more likely to be on the left side of
the heart because those valves are more commonly damaged as they
are on the high pressure side of the heart. Perforation of the valve
leaflets and rupture of papillary muscles may lead to aortic or mitral
regurgitation.
A Monckeberg arteriosclerosis B Infective endocarditis C Dressler’s syndrome D Dilated cardiomyopathy E Rheumatic heart disease F Left heart failure G Hypertrophic obstructive cardiomyopathy H Aortic stenosis I Carcinoid syndrome
A 64-year-old man presents to accident and emergency due to a collapse at
home. An ejection systolic murmur is heard at the upper-left sternal edge.
H Aortic stenosis
Aortic stenosis (H) occurs when there is an opening defect in the aortic
valve. Causes include age-related degenerative calcification, rheumatic
heart disease and congenital malformations (bicuspid valve).
Calcification is confined to the cusps. Clinical presentation includes
syncope, angina and dyspnoea. On examination an ejection systolic
murmur, narrow pulse pressure and/or slow rising pulse may be detected.
If due to a bicuspid valve an ejection systolic click may be heard.
Left ventricular hypertrophy may develop as a consequence of chronic
pressure overload.
A Monckeberg arteriosclerosis B Infective endocarditis C Dressler’s syndrome D Dilated cardiomyopathy E Rheumatic heart disease F Left heart failure G Hypertrophic obstructive cardiomyopathy H Aortic stenosis I Carcinoid syndrome
A widowed 72-year-old woman who has passed away at home is sent for
autopsy due to unknown cause of death. Post-mortem examination reveals a
nutmeg liver and haemosiderin-laden macrophages in the lungs.
F Left heart failure
Left heart failure (F) results in the inability of the heart to meet the
demands of the body. It is either due to increased demand (high output
failure) or reduced supply (low output failure) of blood. Causes of
high output failure include severe anaemia and hyperthyroidism, while
low output failure occurs due to ischaemic heart disease, hypertension
and aortic/mitral valve defects. Clinical features include dyspnoea,
orthopnoea and paroxysmal nocturnal dyspnoea. Histological findings
include dilated ventricles, thin walls, nutmeg liver and haemosiderin
macrophages in the lungs.
A Monckeberg arteriosclerosis B Infective endocarditis C Dressler’s syndrome D Dilated cardiomyopathy E Rheumatic heart disease F Left heart failure G Hypertrophic obstructive cardiomyopathy H Aortic stenosis I Carcinoid syndrome
A 54-year-old man presents to accident and emergency with fever and pleuritic
chest pain. It is noted that the patient suffered a myocardial infarction 4 weeks
previously.
C Dressler’s syndrome
Dressler’s syndrome (C) is an autoimmune complication of myocardial
infarction (MI) that occurs approximately 4 weeks after the episode. It is
characterized by chest pain, fever and a pericardial rub. The complications
of MI can be classified according to how they present temporally.
Complications of MI that may occur within 1 week include arrhythmias
(most commonly ventricular fibrillation and ventricular tachycardia), myocardial rupture, valve incompetence (causing regurgitation) and
cardiogenic shock. Later developments include ventricular aneurysm,
pericarditis and the aforementioned Dressler’s syndrome.
A Monckeberg arteriosclerosis B Infective endocarditis C Dressler’s syndrome D Dilated cardiomyopathy E Rheumatic heart disease F Left heart failure G Hypertrophic obstructive cardiomyopathy H Aortic stenosis I Carcinoid syndrome
A 46-year-old man is referred to the cardiology outpatient clinic. On investigation
he is found to have mitral regurgitation and has a past history of St Vitus
Dance when he was in school and a mild pericarditis.
E Rheumatic heart disease
Rheumatic heart disease (E) is an inflammatory condition most commonly
affecting the connective tissue of the heart (but also joints and central
nervous system). It occurs several weeks after throat infection with group
A β-haemolytic streptococci usually under the age of 10 years. Cardiac
complications include endocarditis (causing verroucous lesions of the
heart valves); myocarditis (containing Aschkoff-bodies and Anitschow
cells causing dilatation of the mitral ring, hence mitral regurgitation);
pericarditis (fibrous exudate causing friction rub). Any layer of the heart
can be affected, potentially leading to pancarditis. Many years after
recovery from acute rheumatic fever, chronic rheumatic heart disease
occurs, with fibrosis of the mitral and aortic valves that can occur. The
history of St Vitus Dance Suggests Sydenham’s chorea, a well known
feature of acute rheumatic fever
A Hyaline membrane disease B Small cell carcinoma C Extrinsic allergic alveolitis D Bronchiectasis E Non-small cell carcinoma F Chronic bronchitis G Pulmonary oedema H Cystic fibrosis I Sarcoidosis
A 40-year-old male presents to his GP with chronic cough with copious
amounts of purulent mucus production. High resolution CT scans demonstrate
dilated bronchi.
D Bronchiectasis
Bronchiectasis (D) is defined as the permanent dilatation of bronchi and
bronchioles secondary to chronic inflammation. Causes are numerous,
and include chronic pneumonia, for example due to Staphylococcus
aureus or Haemophilus influenzae infection, obstructing tumours
and cystic fibrosis. Histopathological findings include bronchial wall
destruction and transmural inflammation. High-resolution computed
tomography (CT) is the diagnostic modality of choice. Abscess formation,
haemoptysis and pulmonary hypertension are complications that
may arise as a result of bronchiectasis.
A Hyaline membrane disease B Small cell carcinoma C Extrinsic allergic alveolitis D Bronchiectasis E Non-small cell carcinoma F Chronic bronchitis G Pulmonary oedema H Cystic fibrosis I Sarcoidosis
A 14-year-old girl is admitted to hospital after suffering her third bout of
pneumonia caused by Pseudomonas aeruginosa infection. She also has a previous
admission for pancreatitis.
H Cystic fibrosis
Cystic fibrosis (CF; H) is an autosomal recessive condition caused by a
mutation in the cystic fibrosis transmembrane conductance regulator
(CFTR) protein that primarily affects the exocrine glands. There are several
mutations responsible for CF, the most common being ΔF508 mutation.
Defective CFTR causes reduced secretion of chloride ions across epithelial
cell membranes, resulting in increased sodium and hence water reabsorption
into these cells. The result is viscous secretions from exocrine glands
affecting multiple organs including the lungs (recurrent infections and
bronchiectasis), gastrointestinal tract (distal intestinal obstruction syndrome)
and pancreas (pancreatitis).
A Hyaline membrane disease B Small cell carcinoma C Extrinsic allergic alveolitis D Bronchiectasis E Non-small cell carcinoma F Chronic bronchitis G Pulmonary oedema H Cystic fibrosis I Sarcoidosis
A 58-year-old man presents to his GP with haemoptysis and weight loss. He has
a 30 pack–year history of smoking. He is referred to the oncologist for a biopsy,
who determines ‘oat-shaped’ cells on microscopy.
B Small cell carcinoma
Small cell carcinoma (B) is also known as ‘oat-cell’ carcinoma due
to the appearance of the malignant cells under the microscope. They
appear as nests of small round hyper-chromatic cells that are fragile
(chromatin smudging) and possess nuclear moulding. Small cell carcinomas
are very aggressive with approximately 80 per cent of cases having
metastasized at the time of diagnosis. Small cell carcinomas also express
neuroendocrine markers and can cause paraneoplastic syndromes such
as Lambert–Eaton myasthenic syndrome. On chest X-rays, the cancer
may be seen arising centrally.
A Hyaline membrane disease B Small cell carcinoma C Extrinsic allergic alveolitis D Bronchiectasis E Non-small cell carcinoma F Chronic bronchitis G Pulmonary oedema H Cystic fibrosis I Sarcoidosis
A 62-year-old man presents to his GP with shortness of breath, lethargy and
weight loss. The patient’s chest X-ray reveals a peripheral focal lesion in the left
lung field.
E Non-small cell carcinoma
Non-small cell carcinomas (E) comprise adenocarcinoma, squamous
cell carcinoma and large cell carcinoma. Adenocarcinomas are gland
forming and therefore will have mucin vacuoles within. This sub-type
of non-small cell carcinoma may lead to atypical adenohyperplasia
whereby atypical cells are seen to line the alveolar walls; hence adenocarcinoma
is usually a peripheral lung cancer. Squamous cell carcinomas
are histologically characterized by keratinization and intracellular
‘prickle’ desmosomes. Large cell carcinomas are undifferentiated forms
of adenocarcinoma or squamous cell carcinoma.
A Hyaline membrane disease B Small cell carcinoma C Extrinsic allergic alveolitis D Bronchiectasis E Non-small cell carcinoma F Chronic bronchitis G Pulmonary oedema H Cystic fibrosis I Sarcoidosis
A 53-year-old woman with a history of rheumatic fever presents to accident
and emergency with severe shortness of breath, and has been coughing up pink
frothy sputum for the past 2 days.
G Pulmonary oedema
Pulmonary oedema (G) is defined as fluid collections in the alveoli
which impairs gas exchange that can potentially lead to respiratory
failure. Increased hydrostatic pressure causes of pulmonary oedema
include heart failure, mitral stenosis, fluid overload and renal failure.
Increased capillary permeability can also cause pulmonary oedema,
for example due to pneumonia. Chest X-rays can distinguish between
cardiac and non-cardiac causes of pulmonary oedema; the former will
demonstrate alveolar oedema (bat’s wing appearance), Kerley B-lines,
cardiomegaly, upper lobe diversion of blood vessels and effusions.
A Systemic lupus erythematosus B Sjögren’s syndrome C Diffuse scleroderma D Amyloidosis E Takayasu arteritis F Dermatomyositis G CREST syndrome H Polymyositis I Microscopic polyangitis
A 35-year-old woman is referred to the rheumatology clinic due to recent onset
dysphagia. The patient also reports that her fingers have turned very pale and
cold. One examination she is found to have tightening of the skin near her finger
tips and small dilated vessels on her skin.
G CREST syndrome
CREST syndrome (G), also known as limited scleroderma, represents a
combination of conditions: calcinosis (calcium deposition in the skin),
Raynaud’s disease (vasospasm of blood vessels in response to triggers
such as cold), oesophageal dysmotility, sclerodactyly (thickening and
tightening of skin surrounding fingers/hands) and telangiectasia (dilation
of blood capillaries causing red marks on the surface of the skin). The
pathogenesis relates to excessive release of PDGF causing widespread
fibroblast activation and multi-organ fibrosis. Chronic fibrosis leads to
initimal thickening of the microvasculature known as ‘onion skinning.’
A Systemic lupus erythematosus B Sjögren’s syndrome C Diffuse scleroderma D Amyloidosis E Takayasu arteritis F Dermatomyositis G CREST syndrome H Polymyositis I Microscopic polyangitis
A 35-year-old woman with a history of recurrent miscarriages presents to her
GP with joint pains. Blood tests reveal she is anti-double stranded DNA antibody
positive.
A Systemic lupus erythematosus
Systemic lupus erythematosus (SLE; A) is a multi-system connective tissue
disease that is antinuclear antibody (ANA) positive. The underlying
pathology of SLE relates to failure in the regulatory mechanisms of selftolerance.
Autoantibodies form against nuclear components such as DNA,
RNA and histones. This leads to complement activation and complex
formation, which are deposited in organs. Cytology of tissues reveals
haematoxylin bodies which are denatured nuclei that are produced when
ANA bind to exposed nuclei. LE cells are also visible on microscopy;
these are macrophages that have phagocytosed a haematoxylin body.
A Systemic lupus erythematosus B Sjögren’s syndrome C Diffuse scleroderma D Amyloidosis E Takayasu arteritis F Dermatomyositis G CREST syndrome H Polymyositis I Microscopic polyangitis
A 68-year-old man presents to accident and emergency with symptoms suggestive
of heart failure. All initial investigations do not determine an underlying
cause. However, a tongue biopsy sample gains an apple-green birefringence
under polarized light using Congo red stain.
D Amyloidosis
Amyloidosis (D) occurs due to the extracellular deposition of fibrillar
proteins that accumulate in tissues and organs. Amyloid proteins
arise due to dysfunctional folding resulting in non-branching fibrils.
Proteins aggregate into insoluble crossed beta-pleated sheet tertiary
conformation. Amyloid proteins contain P-component which causes
biopsy samples to characteristically gain an apple-green birefringence
using polarized light and Congo red stain. Four major amyloid proteins
exist: AA, derived from serum amyloid assisted protein and associated
with inflammation; AL, derived from IgG light chains and associated
with myeloma; αβ2, linked with Alzheimer’s disease; β2 microglobulin,
associated
with patients undergoing dialysis treatment.
A Systemic lupus erythematosus B Sjögren’s syndrome C Diffuse scleroderma D Amyloidosis E Takayasu arteritis F Dermatomyositis G CREST syndrome H Polymyositis I Microscopic polyangitis
A 45-year-old woman presents to accident and emergency with signs suggestive
of renal failure. She is found to be p-ANCA positive.
I Microscopic polyangitis
Microscopic polyangitis (I) is a small vessel vasculitis affecting the arterioles,
venules and capillaries. The pathology involves a trigger factor
such as microorganisms and drugs causing immune complex formation
in a previously sensitized host. These immune complexes deposit in small vessels leading to neutrophil-related inflammation. Microscopic
polyangitis affects the skin, heart, brain and kidneys. Histopathological
features of affected vessels include fibrinoid necrosis that leads to fragmented
neutrophilic nuclei within vessel walls. Microscopic polyangitis
is associated with p-ANCA.
A Systemic lupus erythematosus B Sjögren’s syndrome C Diffuse scleroderma D Amyloidosis E Takayasu arteritis F Dermatomyositis G CREST syndrome H Polymyositis I Microscopic polyangitis
A 52-year-old man presents to his GP with limb weakness and shortness of
breath. A distinctive rash is noted around both eyes as well as plaques on the
joints of his hands.
F Dermatomyositis
Dermatomyositis (F) is an inflammatory myopathy that involves skeletal
and thoracic muscles. Skeletal muscle involvement will lead to
proximal muscle fatigue, especially in the hips and shoulders. Thoracic
muscle involvement can affect the lungs (dyspnoea), heart (arrhythmia)
and oesophagus (dysmotility). There is, however, sparing of the ocular
muscles which differentiates dermatomyositis from myasthenia gravis.
Dermatomyositis is also defined by a heliotrope rash (violet erythema
around the periorbital region) and Gottron papules (violet scaly plaques
over hand joints). Muscle inflammation will also cause an increased
blood creatine kinase level.
A Subarachnoid haemorrhage B Parkinson’s disease C Extradural haemorrhage D Vascular dementia E Subdural haemorrhage F Intracerebral haemorrhage G Multiple sclerosis H Duret haemorrhage I Alzheimer’s disease
A 54-year-old man is seen in the neurology clinic due to tremor and rigidity. A
DAT scan reveals reduced uptake in the substantia nigra.
B Parkinson’s disease
Parkinson’s disease (B) is a degenerative disorder associated with basal
ganglia dysfunction. Clinical features can be remembered by the mnemonic
SMART: shuffling gait, mask-like-face, akinesia, rigidity and
tremor. Degeneration of the substantia nigra and locus coeruleus of the
basal ganglia leads to reduced production of dopamine. At the microscopic
level, inclusion bodies known as Lewy bodies are deposited in
the cytoplasm of neurons that are made up of α-synuclein. Parkinson’s
disease may be associated with Lewy body dementia.
A Subarachnoid haemorrhage B Parkinson’s disease C Extradural haemorrhage D Vascular dementia E Subdural haemorrhage F Intracerebral haemorrhage G Multiple sclerosis H Duret haemorrhage I Alzheimer’s disease
A 74-year-old man presents to accident and emergency with increasing headache
and confusion. The man’s wife suggests her husband may have tripped and
fallen 3 days previously.
E Subdural haemorrhage
Subdural haemorrhage (E) occurs between the dura and arachnoid due
to an acute tear in bridging veins. This tends to occur after a clear history
of trauma. Bleeding results in features of raised intracranial pressure.
As the bleeding is venous in nature, haematoma development is slow (usually taking 48 hours) and as a result raised intracranial
pressure takes time to become apparent. Chronic subdural haemorrhage
refers to a re-bleed of a previous bridging vein subdural haemorrhage.
Patients will usually present with an altered mental state.
A Subarachnoid haemorrhage B Parkinson’s disease C Extradural haemorrhage D Vascular dementia E Subdural haemorrhage F Intracerebral haemorrhage G Multiple sclerosis H Duret haemorrhage I Alzheimer’s disease
A 45-year-old woman presents to accident and emergency with the worst headache
she has ever experienced. She is noted to have polycystic kidney disease.
A Subarachnoid haemorrhage
Subarachnoid haemorrhage (A) occurs in the subarachnoid space. Potential
causes include a saccular ‘berry’ aneurysm (most commonly occurring
at artery bifurcations of the anterior circulation), hypertension, trauma,
arteriovenous malformations and coagulation disorders. Clinical features
include a severe ‘thunder clap’ headache radiating to the occiput; this may
be preceded by a warning bleed causing a sentinel bleed. Subarachnoid
haemorrhages are more commonly associated with polycystic kidney disease,
coarctation of the aorta and fibromuscular dysplasia.
A Subarachnoid haemorrhage B Parkinson’s disease C Extradural haemorrhage D Vascular dementia E Subdural haemorrhage F Intracerebral haemorrhage G Multiple sclerosis H Duret haemorrhage I Alzheimer’s disease
A 35-year-old woman presents to the neurology clinic with weakness of her left
side. On examination she is found to have nystagmus and an intention tremor.
The patient complains of blurred vision for the past month.
G Multiple sclerosis
Multiple sclerosis (MS; G) is a demyelinating disease of the upper
motor system which follows a relapsing and remitting course.
Histological features along the central nervous system include active
(contain lymphocytes and macrophages) and inactive plaques (reduced
nuclei and myelin). Clinical features include optic neuritis, intranuclear
opthalmoplegia (disruption of medial longitudinal fasciculus) and
cerebellar signs, as well as spasticity and weakness of limbs. Variants
of MS include Devic disease (a more aggressive form) and Marburg MS
(a fulminant form).
A Subarachnoid haemorrhage B Parkinson’s disease C Extradural haemorrhage D Vascular dementia E Subdural haemorrhage F Intracerebral haemorrhage G Multiple sclerosis H Duret haemorrhage I Alzheimer’s disease
A 42-year-old man who suffers from Down syndrome is brought to see his GP
by his carer. The carer describes how the patient has been wandering out of the
house with increased frequency as well as becoming uncharacteristically aggressive,
especially in the evening.
I Alzheimer’s disease
Alzheimer’s disease (I) is a progressive degenerative disease which
mainly occurs in patients over the age of 50 years and the condition
is most commonly sporadic. In some instances, there may be a genetic
component such as the amyloid precursor protein as well as presenelins
1 and 2 mutations associated with Down syndrome. Inheritance of the
ε4 allele of apolipoprotein E increases risk of developing Alzheimer’s
disease. Histological features include vascular wall deposition of
β-amyloid (amyloid angiopathy), neurofibrillary tangles and neuritic
plaques.
