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Year 5 😊✌🏼 > Path 2 > Flashcards

Path 2 Flashcards

1
Q

When do Looser’s zones occur and what are they?

A

They look like fractures but are not fractures.

caused by severe vitamin D deficiiency

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2
Q

What are brown tumours?

A
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3
Q

When do you see multinucleatted giant cells in bone histology?

A
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4
Q

Causes of hilarious lymphadenopathy

A

lymphoma
TB
sarcoidosis

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5
Q

How does sarcoidosis cause hypercalcaemia?

A

macrophages in lymph nodes express 1-alpha-hydroxylase

make increased levels of activated vitamin D

this is not controlled by PTH

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6
Q

seasonal hypercalcaemia

A

Seasonal hypercalcaemia is a feature of sarcoidosis

due to increased levels of sunlight

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7
Q

Management of saarcoidosis

A

Steroids

-> will normalise calcium and treat the lung problem.

life long condition; have to be careful, higher doses (40/day for a week, taper down) if unwell, if not unwell reassure and observe.

These patients have to be under the resp team.

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8
Q

Sarcoidosis defintion

A

systemic disease where macrophages express 1-alpha-hydroxylase

affects the lungs (but may also affect other organs, e.g. neurosarcoidosis)

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9
Q

PTHrP - why do we express it?

A

foetuses express it to make mum release calcium from bone so that they can absorb it

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10
Q

How do you manage hyperCa in 1-HPT and Cancer?

A
  1. FLUIDS

in cancer give bisphosphonates.

In primary hyperparathyroidism fo not give bisphosphonates.

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11
Q

What does nutmeg liver indicate?

A

RHF
(caused by passive venous congestion; blood stays in the liver longer than it would; congested blood vessels)

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12
Q

Causes of splenic enlargement:

A

Infection: Malaria, EBV
Malignancy: lymphoma, leukemia
Haem:
etc.

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13
Q

When is a fallopian tube most likely to rupture due to ectopic pregnancy?

A

8-11 weeks

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14
Q

Berry aneurysm

A
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15
Q

Most aggressive bran tumour?

A

glioblastoma multiforme

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16
Q

What happens to a brain when it degenerates?

A

liquefactive necrosis - turns more liquid

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17
Q

What cancers does asbestos predispose you to?

A

mesothelioma
carcinoma of the lung as well!

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18
Q

Can you put “T1 resp failure’ as cause of death?

A

not by itself.

Have to add a cause e.g. as a result of asthma

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19
Q

old age on death certificate?

A

yes, old age is a cause of death that can be on a certificate.

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20
Q

pulmonary oedema on death cert?

A

not by itself

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21
Q

common causes of sudden death

A
  • stroke
  • MI
  • ruptured AAA
  • oesophageal varices (if people do not know that they had them)
  • epilepsy
  • illicit drug use
  • trauma related to alcohol
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22
Q

What picks up haematoxilin and eosin?

A

H: nuclei (purple, dark blue)

E: cytoplasm and collagen (pink)

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23
Q

Epidermis - type of epithelium

A

stratified squamous epithelium

new cells born in the stratum basale, as they go up they lose their nucleus

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24
Q

thickest layer of skin

A

stratum spinosum

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25
Q

Tissue reaction patterns in dermatology (1-6)

A
  1. spongioitic
  2. lichenoid
  3. psoriasiform
  4. vesiculobullous
  5. granulomatous
  6. vasculopathic

There is overlap between these patterns

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26
Q

Spongiatic reaction (derm)

A
  • intrtaepidermal oedema (spongiosis)
  • can cause vesicles
  • superficial perivascular lymphocytic infiltration

example: eczema/dermatitis

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27
Q

Lichenoid inflammation (derm)

A
  • lymphocytes at junction of dermis and epidermis
  • attack keratinocytes in the ?epidermis -> kill them -> apoptotic keratinocytes

e.g. lichen planus or erythema multiform or Toxic Epidermal Necrosis (TEN) or SJS

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28
Q

Psoriasiform reaction pattern (derm)

A
  • thickened epidermis
  • reddish plaques with silvery scale
  • rapid turnover of keratinocytes (e.g. 8 days rather then 30/40ish)
  • no time for cells to fully lose nucleus -> stratum corner shows nuclei
  • neutrophils in the skin

e.g. psoriasis

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29
Q

psoriasis

A

silvery, white scale

extensor surfaces (elbows, knees)

psoriasiform reaction pattern

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30
Q

Vesiculobullous reaction pattern (derm)

A
  • antibodes attacking different levels of the epidermis

e.g. pemphigoid, pemphigus

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31
Q

bullous pemphigoid

A
  • IgG autoantibodies attacking the basement membrane
  • eosinophils
  • bullae are subepidermal
  • direct immunofluorescence binding to IgG can show deposit of IgG at the dermal/epidermal junction
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32
Q

pemphigus

A
  • intercellular junctions are attacked
  • this leads to epidermolysis
  • lethal, can be a very severe disease
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33
Q

pemphigus vs pemphigoif

A

pemphigus is epidermal

pemphigoid is subepidermal

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34
Q

What exactly is attacked in pemphigus vulgaris?

A

desmoglycin 3

intraepidermal blistering

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35
Q

Where do bulbar form in pemphigus valgaris?

A

intraepidermal

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36
Q

Granulomatous skin reaction

A

x

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37
Q

vasculitis reaction (derm)

A
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38
Q

How does sun damage show on pathology?

A

solar elastosis

39
Q

What is the commonest skin cancer?

A

basal cell CA

40
Q

Does basal cell Ca metastasise?

A

Virtually never metastasises

41
Q

common mutation in basal cell ca

A

PTCH (often somatic mutation due to sun exposure, but also you can inherit a mutation that causes BCC)

42
Q

How to BCCs look under the microscope?

A
  • they are blue tumours
  • some artefact
  • peripheral nests (cells at periphery of the nests align)
43
Q

SCC or BCC worse?

A

SCC is worse

they CAN metastasise and tend to be more aggressive locally

44
Q

What is Bowen’s disease?

A

SCC in situ

45
Q

SCCs colour on histopath

A

pink

there are keratin pearls

you can have increased mitotic activity and perineurial activity
because of the keratin

46
Q

Benign naevi on histopath

A
  • maturation with depth
  • nests
  • well spaced
  • …..
47
Q

ABCDE and FG of melanoma

A

AA
B
C
D
E

Firm
Growing

48
Q

melanoma on histopath

A
  • ## pagetoid spread (melanocytes high up in the epidermis)
49
Q

stains for melanoma

A

melan A
…..

50
Q

main factors in melanoma staging

A

breslow thickness
ulceration

51
Q

prognosiit cfactors in melanoma

A
  • breslow thickness
  • ulceration
  • lymphovascular invasion
  • etc.
52
Q

What mutation do you investigate in melanoma?

A

BRAF

can use a specific treatment

53
Q

How is Breslow thickness meaasured?

A

from granular layer to the deepest melanoma cell

54
Q

Breslow stage is used to stage which cancer?

A

melanoma

55
Q

What is multiple myeloma?

A

malignancy of bone marrow plasma cells, the terminally differentiated and Ig secreting B cells

56
Q

Structure of an antiibody

A

light chain:
heavy chain:

56
Q

Structure of an antiibody

A

light chain:
heavy chain:

57
Q

Somatic hypermutatoin

A
  • ## increases affinity of Ab to Ag
58
Q

Where does somatic hypermutation occur?

A

In the germinal centre of lymph nodes

59
Q

myeloma statistics

A
  • 2nd mostt common heamatological malignancy (f you count lymphoma as 1 )
  • 19th n all cancers
  • m>f
  • less common in asian and Caucasian population
  • more common in afrocarribean
  • age of onset ~67
  • 1% below age 40
  • more common in
60
Q

aetiology of multiple melanoma

A

Risk factors: obesity, increasing age

Genetics (increased incidence n black population, sporadic cases of familiar myeloma)

61
Q

Wheat is myeloma preceded by?

A

MGUS

62
Q

MGUS

A
  • premalignant condition (before multiple myeloma or lymphoma)
  • clonal plasma cells in bone marrow
  • no symptoms
63
Q

Diagnostic criteria for MGUS

A
64
Q

MGUS average risk to progression too malignancy

A

1% per year

IgG and IgA MGUS -> MM

IgM MGUS -> lymphoma

65
Q

how do you stratify MGUS?

A

Mayo criteria

66
Q

Mayo criteria

A

of RFs

  • risk stratification for MGUS

Non-IgG M-spike
M-spke >15g/L
abnormal serum free light chain (FLC) ratio

0 RF -> 2% risk of progression in 20 years
1 RF -> X% risk of progression in 20 years
2 RF -> X% risk of progression in 20 years
3 RF -> X% risk of progression in 20 years

67
Q

Smouldering myeloma

A

Definition criteria:

  • serum monoclonal protein (IgG or IgA) > 30g/L or urnary monoclonal protein >500mg/24h and/or clonal bone marrow plasma cels 10-60%
  • absence of myeloma defining events or amyloidosis
68
Q

IMWG stratfication

A
69
Q

What aree MGRS and MGCS

A

monoclonal gammopathy of renal/clinical significance

70
Q

When does myeloma incidence peak?

A

84-85?

71
Q

Primary events leading to myeakima

A
  • hyperdploiidy (60%, additional odd number Cir)
  • IGH rearrangements (Chr 14q32)
72
Q

Common secondary events in myeloma pahtogenesis

A

KRAS, NRRASA
t(8:14) IGH/MYC
etc.

73
Q

CRAB criteria

A
  • Hyeprcalcaemia (>2.75, no other cause for the high Ca such as HPT)
  • Renal impairment
  • anaemia
  • bone lesions
74
Q

2014 myeloma defining events (MDE)

A
  • bone marrow plasma cells >60%
  • involved:uninvolved FLC ratio >100
  • > 1 focal lesion in MRI (>5mm)
75
Q

What areas of the skeleton are affected by multiple myeloma?

A
  • skull
  • spine
  • ribs
  • pelvis

(proximal skeleton)

76
Q

Imaging for multiple myeloma

A
  • whole body low-dose CT scan
  • CT / FDG-PET scan
  • MRI (bone marrow cellularity, active vs treated disease)
77
Q

Complications of bone disease in multiple myeloma

A
  • cord compression (emergency!) Imaging with MRI
  • Hypercalcaemia
78
Q

Cord compression in MM

A
  • emergency
  • Dx and Mx within 24 h
  • Ig and FLC studies +/- biopsy
  • dexamethasone/radiotherapy
  • neurosurgery rarely required
  • stabilise unstable spine
  • MDT meeting

magin

79
Q

Hypercalcaemia in MM

A
  • Sx: drowsiness, constipation, etc.
  • Mx with fluids, steroids and bisphosphonates
79
Q

Hypercalcaemia in MM

A
  • Sx: drowsiness, constipation, etc.
  • Mx with fluids, steroids and bisphosphonates
80
Q

Causes of myeloma kidney disease

A
80
Q

Causes of myeloma kidney disease

A
81
Q

Ix for multiple myelomaa

A
  • Ig studies
  • BM biopsy and aspirate
  • FISH studies
  • other
82
Q

Staging systems for MM

A

ISS (international staging system, looks at serum b2-microglobulin level)

R-ISS (revised international staging system, includes genetics)

R2-ISS (revised international staging system, includes genetics and 1q+)

R2-ISS now used!!!

83
Q

Amyloidosis

A
  • misfolded free light chains aggregate into amyloid fibrils in target organs
  • MGUS or myeloma in the background

-

84
Q

Clinical presentation of amyloidosis

A

insert

85
Q

Key histopathological myeloma marker?

A

CD138

(they often lose markers like CD20)

86
Q

Stain for Amyloidosis

A

Congo Red

under polarised light, it has a yellow/green colour

87
Q

Treatment of myeloma

A
  • monoclonal antibodies
  • CAR-T cell therapy
  • melphalan
  • cyclophhosphamide
  • dexamethasone and prednisolone (was first treatment used for myeloma)
  • IMiD (lenalidomine, pomalidomide)
  • CELMoDs)

Myeloma is not a curable disease.

88
Q

2 groups of myeloma patients (re treatment)

A

Transplant-eligible (ft and typically <65/70)

Transplant-ineligible (frail and usually >65/70)

89
Q

Side effects of CAR-T cells in MM

A

cytokine release syndrome (CRS)
neurotoxicity
other

90
Q

Bi-specific antibodies in MM

A

BiTE

have 2 domains
one recognises CD3 and the other target in the tumour cell)

90
Q

Bi-specific antibodies in MM

A

BiTE

have 2 domains
one recognises CD3 and the other target in the tumour cell)

e.g. Teclistamab

Year 5 😊✌🏼 (53 decks)

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