Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Histopathology Part 4- (p183-207- Breast, Cerebral, Neurodegenerative, Bone, Skin + Miscellaneous) > Flashcards

Histopathology Part 4- (p183-207- Breast, Cerebral, Neurodegenerative, Bone, Skin + Miscellaneous) Flashcards

1
Q

How does acute mastitis present?

A

Painful
Red breast
Fever
Either lactational or non-lactational

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes lactational and non-lactational acute mastitis?

A

Lactational- staphylococcal infection (often polymicrobial)

Non-lactational- secondary to duct ectasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Treatment of lactational acute mastitis?

A

Continued expression of milk + antibiotics +/- surgical drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatment of non-lactational acute mastitis?

A

Abx + treatment of duct ectasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Who does mammary duct ectasia usually occur in?

A

Multiparous 40-60yo women

Smokers- biggest RF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does duct ectasia present?

A

Poorly defined palpable periareolar mass with thick white nipple secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pathophysiology of duct ectasia?

A

Dilatation in one or more of the larger lactiferous ducts, which fill with a stagnant brown or green secretion, which may discharge.
These fluids irritate surrounding tissue leading to periductal mastitis or even abscess and fistula formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which condition mimics the mammographic appearance of cancer?

A

Duct ectasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What would you see on cytology for duct ectasia?

A

Proteinaceous material

Inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is fat necrosis of the breast?

A

Inflammatory reaction to damaged adipose tissue (can be delayed 10y from trauma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does fat necrosis of the breast present?

A

Painless breast mass which can mimic carcinoma by displaying skin tethering or nipple retraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is fibrocystic disease/fibroadenosis?

A

Breast lumpiness
Common group of changes caused by exaggerated hormone response:
Cystic- small cysts form by dilation of lobules and contain fluid
Fibrosis- secondary to cyst rupture
Adenosis- increased number of acini per lobule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What would you see on histology for gynaecomastia?

A

Epithelial hyperplasia

Finger-like projections into ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a fibroadenoma commonly referred to as?

A

A breast mouse- spherical and freely mobile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the most common benign breast tumour?

A

Fibroadenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When do fibroadenomas usually occur?

A

Reproductive period- usually 20-30y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What has a strong influence over fibroadenomas?

A

Hormones- increase in size during pregnancy and calcify after menopause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a duct papilloma?

A

Benign papillary tumour within the duct system of the breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does duct papilloma present?

A

Bloody discharge

No lump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where does breast cancer rank in the most common cancers in women?

A

Numero uno

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Women’s lifetime risk of breast cancer?

A

1 in 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In which age range is breast cancer more common?

A

75-80y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the risk factors for breast cancer?

A 
Susceptibility genes- BRCA1/2
Hormone exposure- early menarche, late menopause, OCP, HRT etc
Advancing age
FH
Race (Caucasian most likely)
Obesity
Smoking
Alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does breast cancer present?

A

Hard fixed lump
Paget’s disease (eczema of nipple then areola- normal eczema never affects the nips)
Peau d’orange
Nipple retraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the breast cancer screening programme in the UK?

A

47-73yo women are invited every 3y for mammography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is breast carcinoma in situ?

A

Neoplastic epithelial proliferation limited to ducts (DCIS) or lobules (LCIS) by basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is breast carcinoma histologically subcategorised?

A

Ductal- can’t be classified into one of the others, most common
Lobular- cells in single file chains/strands
Tubular- well formed tubules with low grade nuclei
Mucinous- abundant extracellular mucin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the triple assessment for breast cancer?

A

Examination
Radiological exam- mammography/USS/MRI)
FNA + cytology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are all neoplastic breast lesions assessed for?

A

Oestrogen receptor, progesterone receptor and HER2 receptor status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does ER/PR/HER2 receptor status influence prognosis?

A

ER/PR positive- good as responds to tamoxifen

HER2 positive- bad prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is tamoxifen’s MOA?

A

Mixed agonist/antagonist of oestrogen at its receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is herceptin/trastuzumab?

A

Monoclonal Ig to Her2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is it important to monitor in herceptin treatment?

A

LVEF as it is toxic to myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where do phyllodes tumours arise from?

A

Interlobular stroma with increased cellularity and mitoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the main differences between male and female breast cancer?

A

Lesions easier to find due to smaller breasts but lack of awareness may postpone treatment
Presence of gynaecomastia may mask condition
Diagnosis made later in males
Lesions less contained as don’t have to travel far to infiltrate
Almost 1/2 of male b cancer patients are stage III or IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is an infarction?

A

An area of tissue death due to lack of oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the most common cause of a cerebral infarction?

A

Cerebral atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

RFs for strokes and TIAs?

A

Smoking, DM, HTN, FH, past TIAs, OCP, PVD, ETOH, hyperviscosity e.g. sickle cell or polycythaemia vera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Symptoms and signs of stroke?

A 
Sudden onset
FAST
Numbness
Loss of vision
Dysphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Symptoms and signs of TIA?

A

<24h
Amaurosis fugax- painless temporary loss of vision
Carotid bruit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Commonest area affected in a stroke?

A

MCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Investigations for stroke/TIA?

A

CT/MRI (infarct vs haemorrhage) for stroke
Carotid US for TIA
Vascular risk- BP, FBC, ESR, U+E, glu, lipids, CXR, ECG, carotid doppler

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Stroke/TIA management?

A

Aspirin +/- dipyridamole
Thrombolytics (if <3h) for stroke
+/- carotid endarterectomy
Long term- HTN, lipid reducing, anticoag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How would a stroke affecting the anterior cerebral artery (ACA) present?

A

Contralateral leg paresis
Sensory loss
Cognitive deficits (apathy, confusion, poor judgement)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How would a stroke affecting the MCA present?

A

Contralateral weakness and sensory loss of face and arm
Cortical sensory loss
Contralateral homonymous hemianopia or quadrantopia
If dominant hemisphere- aphasia
If non-dominant- neglect
Eye deviation towards side of lesion and away from weak side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How would a stroke affecting the PCA present?

A

Contralateral hemianopia or quadrantopia
Midbrain findings- CNIII and IV palsy/pupillary changes, hemiparesis
Thalamic findings- sensory loss, amnesia, decreased level of consciousness
Bilateral- cortical blindness or prosopagnosia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How would a stroke affecting the basilar artery present?

A

Proximal- impaired extraocular movement, vertical nystagmus, reactive miosis, hemi or quadriplegia, dysarthria, locked-in syndrome, coma
Distal- somnolence (sleepy), memory and behaviour abnormalities, oculomotor impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What type of haemorrhages are commonly non-traumatic?

A

Intraparenchymal

Subarachnoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the common site for intraparenchymal haemorrhage?

A

Basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are responsible for 85% of subarachnoid haemorrhages?

A

Ruptured berry aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How does a SAH present?

A

Thunderclap headache
Vomiting
LoC
Usually in F <50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Patients with which conditions are at increased risk of SAH?

A

Polycystic kidney disease
Ehler’s Danlos
Aortic coarctation pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which cerebral haemorrhages are usually due to trauma?

A

Extradural
Subdural
Traumatic parenchymal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which artery is involved in an extradural haemorrhage?

A

Middle meningeal artery ruptures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How does a subdural typically present?

A

Prev history of minor trauma -> damaged bridging veins with slow venous bleed, often elderly/alcoholic, associated with brain atrophy and fluctuating consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Six types of brain herniation?

A 
Uncal
Central- transtentorial
Cingulate- subfalcine
Transcalvarial
Upward tonsilar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which organism most commonly causes meningitis in newborns-3m olds?

A

Group B strep (90% in first 5 days)

E. Coli and Listeria monocytogenes as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which organisms most commonly causes meningitis in 1m-6y olds?

A

Neisseria meningitidis, streptococcus pneumoniae, haemophillus influenza type B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which organisms most commonly causes meningitis in >6yo olds?

A

N. meningitidis, strep pneumoniae, mumps (pre-MMR vaccine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which viruses cause meningitis?

A

Enteroviruses (80%), CMV, Arbovirus, HSV (most common in adults)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What RFs are there for meningitis?

A

Young
HIV
Immunocompromised
Environmental- crowding, poverty + close contact with affected individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What would you see in the CSF for bacterial/pyogenic meningitis (appearance, predominant cell, cell count, glucose, protein and presence of bacteria in smear or culture)?

A 
Appearance- turbid
Predominant cell- polymorphs e.g. neutrophils
Cell count- 90-1000+
Glucose- low <40
Protein- high >250
Bacteria in smear and culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What would you see in the CSF for TB meningitis (appearance, predominant cell, cell count, glucose, protein and presence of bacteria in smear or culture)?

A 
Appearance- fibrin web
Predominant cell- mononuclear e.g. lymphocytes
Cell count- 10-1000
Glucose- low <40
Protein- high 50-500
Bacteria often not in smear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What would you see in the CSF for viral meningitis (appearance, predominant cell, cell count, glucose, protein and presence of bacteria in smear or culture)?

A 
Appearance- clear
Predominant cell- mononuclear e.g. lymphocytes
Cell count- 50-1000
Glucose- normal
Protein- normal or high <100
Bacteria often not in smear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Symptoms of viral encephalitis?

A 
Drowsiness
Seizures
Behavioural changes
Headache
Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Viruses that cause viral encephalitis?

A 
Enteroviruses
HSV
VZV
Arboviruses
Adenoviruses
HIV
Mumps
Rubella
Rabies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Are most brain tumours primary or secondary tumours?

A

Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Which cancers are the most common primaries for secondary brain tumours?

A

Lung
Breast
Malignant melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Commonest type of primary brain tumour?

A

Astrocytomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Which familial syndromes are associated with CNS tumours?

A

Von Hippel Lindau- hemangioblastoma of cerebellum, brainstem and spinal cord
Tuberous sclerosis- giant cell astrocytoma
NF type 1- neurofibroma astrocytoma
NF type 2- Meningioma, ependydoma, astrocytoma
Li-Fraumeni- astrocytoma, primitive neuroectodermal tumour
Turcot syndrome- glioblastoma multiforme, medulloblastoma, pineoblastoma
MEN 1- pituitary adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the common pathogenic mechanism behind neurodegenerative diseases e.g. dementia?

A

Accumulation of misfolded proteins (intra or extra-cellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the four As of dementia?

A

Amnesia
Aphasia- language disorder
Apraxia- unable to do skills
Agnosia- unable to recognise people, objects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the pathological misfolded protein in Alzheimer’s disease?

A

Tau

Beta-amyloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the pathological misfolded protein in Lewy body dementia?

A

Alpha-synuclein

Ubiquitin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the pathological misfolded protein in corticobasal degeneration?

A

Tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the pathological misfolded protein in frontotemporal dementia linked to Chr 17?

A

Tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the pathological misfolded protein in Pick’s disease?

A

Tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What changes occur to the brain during Alzheimer’s

A

Generalised atrophy of the brain
Widened sulci
Narrowed gyri
Enlarged ventricles (temporal and frontal especially)
Senile plaques of beta-amyloid protein and neurofibrillary tangles of tau protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How is Alzheimer’s diagnosed?

A

Clinical diagnosis

PET and MRI may help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How is Alzheimer’s treated?

A

Symptomatic:
Anti-cholinesterases
nAChR agonists
Glutamate antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

How can Lewy Body Dementia be differentiated from Alzheimer’s?

A

Psychological disturbances- visual hallucinations- small people or animals
Day to day fluctuations
Signs of Parkinsonism (very similar)
Recurrent falls and syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the pathology of Parkinson’s disease?

A

Death of dopaminergic neurones in substantia nigra -> reduced stimulation of the motor cortex by the basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

How does Parkinsons present?

A 
TRAP
Tremor
Rigidity
Akinesia
Postural instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the pathology of multiple sclerosis?

A

Autoimmune demyelinating disease with plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How does multiple sclerosis commonly present?

A

20-40yo, focal sx e.g. optic neuritis, poor coordination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Aetiology of osteoporosis?

A

Age-related or secondary to systemic disease/drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Disease features of osteoporosis?

A

Decreased bone mass- >2.5 SD below normal (1-2.5=osteopenia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Symptoms of osteoporosis?

A

Low impact fractures- NOF or Colles’

Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

RF for osteoporosis?

A 
Age
Smoking
F
Poor diet
Low BMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Changes of x ray for osteoporosis?

A

Usually none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Histology of osteoporosis?

A

Loss of cancellous bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Biochemical changes of osteoporosis (Ca, PO4, ALP)?

A

All normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Aetiology of osteomalacia/rickets?

A

Low dietary vit D
low sunlight
Malabsorption of vit D
Genetic causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is osteomalacia/rickets?

A

Decreased bone mineralisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Symptoms of osteomalacia?

A

Bone pain/tenderness

Proximal muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Symptoms of Rickets?

A 
Bone pain
Bowing tibia
Rachitic rosary
Frontal bossing
Pigeon chest
Delayed walking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Changes of x ray for osteomalacia?

A

Looser’s zones (pseudofractures)

Splaying of metaphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Histology of osteomalacia?

A

Excess of unmineralised bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Biochemical changes of osteomalacia/Rickets (Ca, PO4, ALP)?

A

Ca- Normal or low
Decreased PO4
Increased ALP

100
Q

Aetiology of primary hyperparathyroidism?

A

Parathyroid adenoma
Hyperplasia
Carcinoma
MEN

101
Q

Disease features of primary hyperparathyroidism?

A

Excess PTH production -> Ca reabsorption and PO4 excretion

Bone changes of osteitis and fibrosa cystica

102
Q

Symptoms of primary hyperparathyroidisim?

A 
Hypercalcaemia- Moans, stones. bones and groans
Depression
Renal stones
Bone pain and fractures
Constipation
Pancreatitis
Polydipsia
Polyuria
103
Q

X Ray changes in primary hyperparathyroidism?

A

Brown’s tumours
Salt and pepper skull
Subperiosteal resorption in phalanges

104
Q

Histology of primary hyperparathyroidism?

A

Osteitis fibrosa cystica (aka brown tumour)

105
Q

Biochemical changes of primary hyperparathyroidism (Ca, PO4, ALP)?

A

Increased Ca
Decreased or normal PO4
Increased or normal ALP
Increased PTH

106
Q

Aetiology of Paget’s?

A

Disorder of bone turnover

107
Q

Disease features of Paget’s?

A

Lytic and sclerotic lesions

108
Q

Symptoms of Paget’s?

A 
Bone pain
Microfractures
Nerve compression
Skull changes increase head size
Deafness
High output cardiac failure
109
Q

RF for Paget’s?

A

> 50 + Caucasian

110
Q

X ray changes in Paget’s?

A

Mixed lytic and sclerotic
Skull- osteoporosis circuscripta, cotton wool
Vertebrae- picture frame, ivory vertebra
Pelvis- sclerosis and lucency

111
Q

Histology of Paget’s?

A

Huge osteoclasts with >100 nuclei

Mosaic pattern of lamellar bone

112
Q

Biochemical changes of Paget’s (Ca, PO4, ALP)?

A

Normal Ca
Normal PO4
Massively raised ALP

113
Q

Aetiology of renal osteodystrophy?

A

All skeletal changes associated with CKD- osteitis fibrosa cystica, osteomalacia, osteosclerosis, adynamic bone disease, osteoporosis

114
Q

Biochemical changes of renal osteodystrophy (Ca, PO4, ALP)?

A

Low Ca
High PO4
Secondary hyperparathyroidism

115
Q

What is the main way to differentiate between gout and pseudogout?

A

Gout has negatively birefringent crystals

Pseudogout has positively birefringent crystals

116
Q

What are RFs of gout?

A

Increased dietary purine intake
ETOH
Diuretics
Inherited metabolic abnormalities

117
Q

What is the aetiology of pseudogout?

A

Idiopathic
HyperPTH
Hypothyroid
Wilsons

118
Q

Which joints are affected in gout?

A

Great toe- MTP, lower extremities

119
Q

What are the clinical features of gout?

A

Hot swollen red and exquisitely painful joint

Tophus (s/c urate deposits) is pathognomic lesion

120
Q

What is the crystal type in gout?

A

Urate crystals

Needle shaped

121
Q

What is the crystal type in pseudogout?

A

Calcium pyrophosphate crystals

Rhomboid shaped

122
Q

How do you manage gout?

A

Acute- Colchicine
Long term- Allopurinol
Conservative- reduce alcohol and purine intake e.g. sardines or liver

123
Q

Management of pseudogout?

A

NSAIDs or intra-articular steroids

124
Q

What causes osteomyelitis ?

A

Haematogenous spread or local infection e.g. post-trauma

Mainly bacterial and occasionally fungal

125
Q

Which organism most commonly causes osteomyelitis in adults and which most commonly cause it in children?

A

Adults- S.Aureus

Children- haemophillus influenza, GBS

126
Q

How does osteomyelitis present?

A

Pain, swelling and tenderness

General features of malaise, fever, chills + leukocytosis

127
Q

In what condition would you see Heberden’s and Bouchard’s nodes?

A

Osteoarthritis
Heberden’s- DIPJ
Bouchard’s- PIPJ

128
Q

X ray features of osteoarthritis?

A 
LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
129
Q

How does rheumatoid arthritis present?

A

Slowly progressive

Symmetrical in small joints of hands and feet- spares DIPJ

130
Q

Characteristic deformities of rheumatoid arthritis?

A

Swan neck and Boutonniere deformity of fingers
Radial deviation of wrist and ulnar deviation of fingers
Z shaped thumb

131
Q

How can you differentiate benign and malignant bone disease on xray?

A

Benign- No periosteal reaction, thick endosteal reaction, well developed bone formation, intraosseous and even calcification

Malignant- Acute periosteal triangle- Codman’s triangle, onion skin, sunburst, broad border between lesion and normal bone, varied bone formation, extraosseous and irregular calcification

132
Q

Name some malignant bone tumours?

A

Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma
Giant cell

133
Q

Who does osteosarcoma and Ewing’s sarcoma affect?

A

Adolescents

134
Q

Where is most commonly affected by osteosarcoma?

135
Q

What is seen on histology of osteosarcoma?

A

Malignant mesenchymal cells

ALP +ve

136
Q

What is the X-ray appearance of osteosarcoma?

A

Codman’s triangle- elevated periosteum

Sunburst appearance

137
Q

Which bones does chondrosarcoma affect?

A

Axial skeleton

Femur/tibia/pelvis

138
Q

X-ray appearance of chondrosarcoma?

A

Lytic lesion with fluffy calcification

139
Q

Which bones does Ewing’s sarcoma affect?

A

Long bones

Pelvis

140
Q

What is seen on histology of Ewing’s sarcoma?

A

Sheets of small round cells
CD99 +ve
T 11:22 translocation

141
Q

X-ray appearance of Ewing’s sarcoma?

A

Onion skinning of periosteum

142
Q

Who does giant cell malignancy tend to affect?

A

20-40y

F>M

143
Q

Where in the body does giant cell malignancy commonly occur?

A

Knee- epiphysis

144
Q

What is seen on histology of giant cell malignancy?

A

Osteoclast-type multinucleate giant cells on background of splindle/ovoid cells

145
Q

X-ray appearance of giant cell malignancy?

A

Lytic/lucent lesions right up to articular surface

146
Q

What benign bone tumours are there?

A 
Osteoid osteoma
Osteoma- 
Enchondroma
Osteochondroma
Fibrous dysplasia
Simple bone cyst
Osteoblastoma
147
Q

Any knowledge about osteoid osteoma?

A

Adolescents
M>F
Affects tibia diaphysis/proximal femur
Small benign bone forming lesion, night pain
X-ray- Radiolucident NIDUS with sclerotic rim ‘BULLS EYE’

148
Q

Any knowledge about osteoma?

A

Middle age
Head and neck
Bony outgrowths attached to normal bone
Gardner syndrome- GI polyps, multiple osteomas + epidermoid cysts

149
Q

Any knowledge about enchondroma?

A

Often in HANDS
Benign tumours of cartilage
Ollier’s syndrome- multiple enchondromas
Maffuci’s syndrome- multiple enchondromas and haemangiomas
X-ray- Lytic lesion, cotton wool calcification

150
Q

Which benign bone tumour is most common?

A

Osteochondroma- cartilage capped bony outgrowth

151
Q

Where do osteochondromas commonly occur?

A

Metaphysis of long bones near tendon attachment sites

152
Q

Any knowledge on fibrous dysplasia?

A

Femur
Bit of bone replaced by fibrous tissue
Chinese letters on histology- misshapen bone trabeculae
X-ray- soap bubble osteolysis, Shepherd’s crook deformity

153
Q

Any knowledge on simple bone cyst?

A

Humerus or femur
Fluid filled unilocular
X-ray- Lytic and well defined

154
Q

What is the stratum corneum?

A

Outermost layer of epidermis, consisting of keratinised cells

155
Q

What is hyperkeratosis?

A

Increase in stratum corneum/keratin

156
Q

What is parakeratosis?

A

Nuclei in stratum corneum

157
Q

What is acanthosis?

A

Increase in stratum spinosum

158
Q

What is acantholysis?

A

Decrease in cohesion between keratinocytes

159
Q

What is spongiosis?

A

Intracellular edema

160
Q

What is lentiginous?

A

Linear pattern of melanocyte proliferation within epidermal basal cell layer

161
Q

5 layers of epidermis?

A 
S corneum
S lucidum- only in hands + feet
S granulosum
S spinosum
S basale
162
Q

What is dermatitis/eczema?

A

Terms used to describe a group of disorders with same histology and presenting with inflamed dry itchy rashes

163
Q

What is the histology of all types of dermatitis/eczema?

A 
DISCA
Acute:
Dilated dermal capillaries
Inflammatory infiltrate in dermis
Spongiosis

Chronic:
Crusting, scaling
Acanthosis

164
Q

Different types of dermatitis?

A

Atopic
Contact
Seborrhoeic

165
Q

Where does atopic dermatitis commonly affect in infants and older?

A

Infants- face and scalp

Older- flexural area

166
Q

What type of hypersensitivity reaction is contact dermatitis?

167
Q

What causes seborrhoeic dermatits?

A

Inflammatory reaction to a yeast

168
Q

What is psoriasis?

A

A common chronic inflammatory dermatosis with well-demarcated red scaly plaques- cells have increased proliferation rate

169
Q

What is the commonest form of psoriasis?

A

Chronic plaque affecting extensor surfaces and scalp

170
Q

What is Auspitz’ sign?

A

Rubbing psoriatic plaques causes pinpoint bleeding

171
Q

What is Koebner phenomenon?

A

Lesions form at sites of trauma

172
Q

What is seen on histology for psoriasis?

A

Parakeratosis, loss of granular layer, clubbing of rete ridges giving test tubes in a rack appearance, Munro’s microabscesses

173
Q

Pathophysiology of chronic plaque psoriasis?

A

Type IV T cell hypersensitivty reaction

174
Q

What are other forms of psoriasis and how do they typically present?

A

Flexural- seen in later life, groin, natal cleft and submammary areas
Guttate- rain drop plaques, children, seen 2w post STREP
Erythrodermic/pustular- severe widespread, systemic symptoms, can be limited to hands and feet (palmo-plantar)

175
Q

What nail changes are seen in psoriasis?

A

Pitting
Onycholysis
Subungal keratosis

176
Q

What are lesions like in lichen planus?

A 
6ps 
Pruritic
Purple
Polygonal
Papules
Plaques
Pearl sheen
White network on surface called Wickam's striae
177
Q

Where is lichen planus usually seen?

A

On inner surface of wrists but can affect oral mucosa

178
Q

Histology of lichen planus?

A

Hyperkeratosis with saw-toothing of rete ridges and basal cell degeneration

179
Q

What lesions are seen in erythema multiforme and where?

A

Annular target lesions
Most commonly on extensor surfaces of hands and feet
Can be a combination of macules, papules, weals, vesicles, bullae and petechiae

180
Q

Causes of erythema multiforme?

A 
Infections- e.g. HSV, mycoplasma
Drugs- SNAPP:
Sulphonamides
NSAIDs
Allopurinol
Penicillin
Phenytoin
181
Q

Which condition is dermatitis herpetiformis associated with (not herpes lol)?

182
Q

Pathophysiology of dermatitis herpetiformis?

A

IgA Abs bind to basement membrane -> subepidermal bulla

183
Q

Clinical features of dermatitis herpetiformis?

A

Itchy vesicles on extensor surfaces of elbows and buttocks

184
Q

Histology of dermatitis herpetiformis?

A

Microabscesses which coalesce to form subepidermal bullae

Neutrophil and IgA deposits at tips of dermal papillae

185
Q

Pathophysiology of pemphigoid?

A

IgG Abs bind to hemidesmosomes of basement membrane -> subepidermal bulla

186
Q

Pathophysiology of pemphigus?

A

IgG Abs bind to desmosomal proteins -> intraepidermal bulla

187
Q

How can you easily differentiate between pemphigoid and pemphigus?

A

PemphigoiD- Deep bullae

PemphiguS- Superficial bullae

188
Q

Clinical features of pemphigoid?

A

Large tense bullae on erythematous base
Often on forearms, groin and axillae
Elderly
Do not rupture as easily as pemphigus

189
Q

Histology of pemphigoid?

A

Subepidermal bulla with eosinophils

Linear deposition of IgG along basement membrane

190
Q

Clinical features of pemphigus?

A

Bullae are easily ruptured

Found on skin and mucosal membranes

191
Q

Histology of pemphigus?

A

Intraepidermal bulla
Netlike pattern of intracellular IgG deposits
Acantholysis

192
Q

What are seborrhoeic keratosis?

A

Benign rough waxy plaques with a ‘stuck on’ appearance

193
Q

What is an actinic keratosis?

A

Rough sandpaper-like scaly lesion on sun-exposed area

194
Q

Histology of actinic keratosis?

A 
SPAIN
Solar elastosis
Parakeratosis
Atypia/dysplasia
Inflammation
Not full thickness
195
Q

What is a keratoacanthoma?

A

Rapidly growing dome shaped nodule which may develop necrotic crusted centre
Grows over 2-3w and clears spontaneously

196
Q

Histology of keratoacanthoma?

A

Similar to SCC- difficult to distinguish

197
Q

Characteristics of Bowen’s disease?

A

Intraepidermal squamous cell carcinoma in situ

Flat red scaly patches on sun-exposed areas

198
Q

Histology of Bowen’s disease?

A

Full thickness atypia/dysplasia

Basement membrane intact- not invading the dermis

199
Q

When does Bowen’s disease become an SCC?

A

When it invades the dermis

200
Q

What is referred to as a ‘rodent’ ulcer?

201
Q

Characteristics of a BCC?

A

Pearly surface often with teleangiectasia

202
Q

Histology of BCC?

A

Mass of basal cells pushing down into dermis

Palisading

203
Q

What is a mole?

A

A benign melanocytic naevus

204
Q

Histology of melanoma?

A

Atypical melanocytes, initially grow horizontally in epidermis (radial growth phase) then vertically into dermis (vertical growth phase) which produces Buckshot appearance

205
Q

Most important prognostic factor in melanoma?

A

Breslow thickness

206
Q

Subtypes of melanoma?

A

Lentigo maligna melanoma- sun exposed area of elderly
Superficial spreading malignant melanoma- irregular borders with colour variation
Nodular malignant melanoma
Acral lentiginous melanoma- palms, soles and subungal areas

207
Q

How can you differentiate between Stevens Johnson syndrome and Toxic Epidermal Necrolysis?

A

Sheets of skin detachment- <10% BSA= SJS, >30%= TEN

208
Q

What commonly causes SJS and TEN?

A

Drugs- Sulphonamide antibiotics, anticonvulsants

209
Q

How does pityriasis rosea typically present?

A

Salmon pink rash appears first (Herald patch) followed by ovule macules in Christmas tree distribution
Post-virus

210
Q

What type of hypersensitivity reaction is involved in SLE?

211
Q

RFs for SLE?

A

In pts with classical complement deficiencies
Drug induced
Afro-Caribbeans
F>M

212
Q

HLA association of SLE?

213
Q

Autoantibody involved in SLE?

A

ANA (95%)
Anti dsDNA
Anti-Sm
Anti-histone

214
Q

Histology of SLE?

A 
LE bodies
Kidney- 
CNS- small vessel angiopathy
Spleen- onion skin lesions
Heart- Libman-Sack endocarditis
215
Q

Diagnostic criteria for SLE?

A 
4 of 11 ACR criteria- SOAP BRAIN MD
Serositis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders (AIHA, ITP, leucopenia)
Renal involvement
ANA +ve
Immune phenomena 
Neuro symptoms
Malar rash
Discoid rash
216
Q

HLA association of scleroderma?

A

HLA DR5 + DRw8

217
Q

Autoantibody in limited and diffuse scleroderma?

A

Limited- anti-centromere
Diffuse- anti-Scl70, fibrillarin, RNA pol I, II, III
PM-Scl

218
Q

Histology of limited scleroderma?

A

Increased collagen in skin and organs

Onion skin thickening of arterioles

219
Q

Histology of diffuse scleroderma?

A

Inflammation within or around muscle fibres

220
Q

Signs and symptoms of limited scleroderma?

A

Skin changes on face and distal to elbows and knees

Calcinosis
Raynaud's
Esophogeal dysmotility
Sclerodactyly
Telangiectasia
221
Q

Signs and symptoms of diffuse scleroderma?

A

Skin changes can occur anywhere
Widespread organ involvement
Pulmonary fibrosis association

222
Q

Autoantibody in polymyositis + dermatomyositis?

A

Anti Jo-1 (tRNA synthetase)

223
Q

Signs and symptoms of polymyositis + dermatomyositis?

A

Proximal muscle weakness
Increased CK + abnormal EMG
DM has cutaneous features- heliotrope rash + Gottron papules

224
Q

Name some large vessel vasculitides?

A

Takayasu’s arteritis

Temporal arteritis

225
Q

Name some medium vessel vasculitides?

A

Polyarteritis nodosa
Kawasaki’s
Buerger’s disease

226
Q

Name some small vessel vasculitides?

A

Wegener’s granulomatosis
Churg Strauss
Microscopic polyangiitis
Henoch Schonlein Purpura

227
Q

What is Takayasu’s arteritis also referred to as?

A

Pulseless disease- absent pulse, bruits and claudication

Increased in Japanese women

228
Q

Key features of temporal arteritis?

A 
Elderly
Scalp tenderness
Temporal headache
Increased ESR
Overlap with polymyalgia rheumatica
229
Q

Histology of temporal arteritis?

A

Granulomatous transmural inflammation + giant cells + skip lesions

230
Q

Key features of polyarteritis nodosa?

A

Renal involvement main feature
Spares lungs
30% have Hep B
Microaneurysms on angiography

231
Q

Key features of Kawasaki’s?

A 
Children <5
Fever>5d
Rash- red palms and soles
Conjunctivitis
Inflammation of lips, mouth or tongue (STRAWBERRY)
Cervical LNs
Coronary arteries may be involved
232
Q

Key features of Buerger’s disease?

A 
Heavy smokers usually men >35
Inflammation of arteries of extremities
Pain
Ulceration of toes, feet and fingers
Angiogram- corkscrew appearance from segmental occlusive lesions
233
Q

Key features of Wegener’s granulomatosis?

A

Triad of
URT- sinusitis, epistaxis, saddle nose
LRT- cavitation, pulmonary haemorrhage
Kidneys- crescentic glomerulonephritis

cANCA +ve

234
Q

Key features of Churg Strauss?

A

Asthma, allergic rhinitis
Eosinophillia
Later systemic involvement

pANCA +ve

235
Q

Key features of microscopic polyangiitis?

A

Pulmonary renal syndrome- pulmonary haemorrhage and glomerulonephritis

pANCA +ve

236
Q

Key features of Henoch Schonlein purpura?

A 
IgA mediated vasculitis
In children <10
Preceding URTI
Palpable purpuric rash- lower limb extensors + buttocks
Colicky abdo pain
Glomerulonephritis
Arthritis
Orchitis
237
Q

What is amyloidosis?

A

Multisystem disorder caused by abnormal folding of proteins that are deposited as amyloid fibrils in tissues. disrupting their normal function

238
Q

What is the primary form of amyloidosis?

A

AL- deposition of amyloid L protein

239
Q

Key features of AL amyloidosis

A

Most associated with plasma cell dyscrasias and with paraproteins e.g. MM
Most have monoclonal Ig, free light chains in serum and urine (Bence Jones) and increased bone marrow plasma cells

240
Q

What is the secondary form of amyloidosis?

A

AA amyloidosis- Amyloid A (an acute phase protein) secondary to chronic infection and inflammation e.g. autoimmune disease- RA, ank spond, IBD, chronic disease- TB, IVDU+ non-immune- RCC, Hodgkin’s

241
Q

Clinical features of amyloidosis?

A

Caused by amyloid deposits in various organs-
Kidney- nephrotic syndrome (most common presentation)
Heart- conduction defects, HF, cardiomegaly
Liver/spleen- hepatosplenomegaly
Tongue- macroglossia in 10%
Neuropathies- inc carpal tunnel

242
Q

How can amyloidosis be identified by staining?

A

Apple green birefringence with Congo red stain under polarised light (otherwise pink/red)

243
Q

What is sarcoidosis?

A

A multisystem disease of unknown cause, commonly affecting young adults, characterised by non-caseating granulomas in many tissues

244
Q

What is seen on histology of sarcoidosis?

A

Non-caseating granulomas, also get Schaumman and asteroid bodies (inclusion of protein and calcium)

245
Q

How is sarcoidosis most commonly detected?

A

Routine CXR - bilateral hilar lymphadenopathy and pulmonary infiltrates leading to fine nodular shadowing in mid zones
Most seek help with SOB, cough, chest pain + night sweats

246
Q

Extrapulmonary manifestations of sarcoidosis?

A

Skin- erythema nodosum, lupus pernio, skin nodules
LNs
Joints- arthritis + bone cysts
Eyes- anterior uveitis
Liver/spleen- hepatosplenomegaly
Blood- leukopenia/anaemia
Hypercalcaemia/hypercalcuria -> renal calculi + nephrocalcinosis
Heart- dysrhythmias, cardiomyopathy, conduction defects
CNs
Constitutional symptoms- FLAWS

247
Q

How is sarcoidosis diagnosed?

A

Exclusion

Ix- Raised Ca, ESR + ACE, transbronchial biopsy

Pathology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions