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Year 5 Pathology > Histopath > Flashcards

Histopath Flashcards

1
Q

Layers of the skin

A

Epidermis

  • Stratum corneum
  • Stratum lucidum
  • Stratum granulosum
  • Stratum spinosum (langerhans cells)
  • Startum basale (melanocytes)
  • Keratinocytes move up as they age

Dermis

  • made of collagen and elastic fibres
  • contains sweat glands, sebaceous glands, hair follicles, neurovascular bundles, blood vessels

Subcutaneous fat
- yum insulation

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2
Q

What are the inflammatory reaction changes and examples of vesiculobullous conditions?

A

Forms bullae

  • Bullous pemphigoid
  • Pemphigus vulgaris
  • Pemphigus foliaceus
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3
Q

What are the inflammatory reaction changes and examples of spongiotic conditions?

A

Becomes oedematous due to intracellular oedema

  • Eczema
  • Contact dermatitis
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4
Q

What are the inflammatory reaction changes and examples of psoriasiform conditions?

A

Becomes thickened

  • Psoriasis
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5
Q

What are the inflammatory reaction changes and examples of lichenoid conditions?

A

Forms a sheeny plaque

  • Lichen planus
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6
Q

What are the inflammatory reaction changes and examples of vasculitic conditions?

A

Associated with vasculitides

  • Pyoderma gangrenosum
  • Small vessel vasculitis
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7
Q

What are the inflammatory reaction changes for granulomatous conditions?

A

Associated with granulomas

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8
Q

What do the following words mean?

a) hyperkeratosis
b) parakeratosis
c) acanthosis
d) acantholysis
e) lentiginous

A

a) increase in S. corenum/ keratin
b) nuclei in S corneum
c) increase in S. spinosum
d) decreased cohesions between keratinocytes
e) linear pattern of melanocyte proliferation within epidermal basal cell layer

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9
Q

Compare acute and chronic histology of dermatitis/eczema

A

Acute

  • spongiosis
  • inflammatory infiltrate in dermis
  • dilated dermal capillaries

Chronic

  • acanthosis
  • crusting, scaling
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10
Q

Differences between atopic, contact, and seborrhoeic dermatitis

A

Clinical presentation

Atopic

  • infants (face + scalp) and older (flexural areas) affected
  • lichenification if chronic
  • FHx of atopy

Contact

  • type IV hypersensitivity
  • erythema, swelling, pruritus
  • affect ear lobes, neck, wrists, feet (jewellery, watches, shoes)

Seborrhoeic

  • inflammatory reaction to yeast
  • infants (cradle cap) and adults (face, eyebrow, eyelid, chest)
  • mild erythema, fine scaling, mildy pruritic
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11
Q

What would you see in histology of psoriasis?

A

Parakeratosis
Loss of granular layer
Clubbing of rete ridges giving ‘test tubes in a rack’ appearance
Munro’s microabscesses

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12
Q

What other conditions/signs are associated with psoriasis?

A

Nail changes (POSH)

  • Pitting
  • Onycholysis
  • Subungual Hyperkeratosis

Arthritis (5-10%)

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13
Q

Describe lesions seen in lichen planus?

A

Pruritic, Purple, Polyglonal, Papules and Plaques with mother-of-pearl sheen

Wickam’s striae also seen - fine white network on surface

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14
Q

What would you see in histology of lichen planus?

A

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

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15
Q

Name causes of erythema multiforme

A

Infections
- HSV, mycoplasma

Drugs (SNAPP)

  • Sulphonamides
  • NSAIDs
  • Allopurinol
  • Penicillin
  • Phenytoin
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16
Q

Pt has annular target lesions on the extensor surfaces of their hands and feet

Combination of macules, papules, urticarial weals, vesicles, bullae and petechiae noted

What is this?

A

Erythema multiforme

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17
Q

Based on where IgA Abs bind to, which bullous disease is it?

a) Basement membrane -> subepidermal bulla
b) Desmoglein 1 + 3 -> intraepidermal bulla
c) Hemidesmosomes of basement membrane -> subepidermal bulla

A

a) Dermatitis herpetiformis
- associated w coeliac
b) Pemphigus vulgaris
- pemphiguS - bullae are SUPERFICIAL
c) Bullous pemphigoid
- pemphigoiD - bullae are DEEP

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18
Q

Histology shows microabscesses w coalesce to form supepidermal bullae, and neutrphil + IgA deposits as tips of dermal papillae

What is it?

A

Dermatitis herpetiformis

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19
Q

Histology shows supepidermal bullae with eosinophils, and linear depositiong og IgG along basement membrane

What is it?

A

Bullous pemphigoid

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20
Q

Histology shows intraepidermal bulla with netlike pattern of intercellular IgG deposits, and acantholysis

What is it?

A

Pemphigus vulgaris

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21
Q

Compare clinical presentation of bullous diseases

A

Dermatitis herpetiformis

  • itchy vesicles on extenson surfaces of elbows, buttocks
  • associated w coeliac

Bullous pemphigoid

  • large tense bullae on erythematous base, do not rupture easily
  • forearms, groin, axillae
  • occur in elderly

Pemphigus vulgaris

  • easily ruptured bullae
  • raw red surface found on skin and mucosal membranes
  • +ve Nikolsky’s sign (top layer of skin slips away from lower layer when rubbed)
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22
Q

Salmon pink rash appears followed by oval macules in Christmas tree distribution. Pt had a cold last week.

What is it?

A

Pityriasis rosea

  • first patch is known as Herald patch
  • remits spontaenously
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23
Q

Name two derm emergencies and what you would see

A

Stevens Johnson Syndrome

Toxic Epidermal Necrolysis

  • sheets of skin detachment (<10% in SJS and >30% in TEN)
  • Nikolsky sign positive
  • commonly caused by reaction to drugs, i.e. sulfonamide abx, anticonvulsants
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24
Q

Rough plaque, waxy, ‘stuck on’ appearing in middle age/elderly

Histo shows entrapped keratin with orderly proliferation of epidermis

A

Seborrhoeic keratosis

  • entrapped keratin = horn cysts
  • benign
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25
Q

Scaly lesion biopsied on nose of elderly pt

Histo shows solar elastosis, parakeratosis, atypia/dysplasia, inflammation, not full thickness

A

Actinic (solar/senile) keratosis

  • premalignant
  • sandpaper like texture
  • sun-exposed area
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26
Q

Rapidly growing dome shaped nodule develops necrotic, crusted centre on pt back of hand

Grew over 2-3 weeks then went away, pt shows pictures and wants to know what it was

A

Keratocanthoma

  • similar histology to SCC
  • premalignant
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27
Q

Pt comes in with flat, red, scaly patches on lower leg

Wants to know what it is and should they be worried?

A

Bowen’s disease

  • premalignant
  • intra-epidermal squamous cell carcinoma in situ
  • histo: basement membrane INTACT so not invading dermis
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28
Q

Compare BCC and SCC

A

BCC

  • ‘rodent’ ulcer
  • slow growing, rarely mets
  • pearly surface w telangiectasia
  • mass of basal cells push down into dermis
  • histo: palisading (nuclei align in outermost layer)

SCC

  • when Bowen’s spreads to dermis
  • flat, red, scaly, can ulcerate
  • histo: atypia/dysplasia throughout epidermis, nuclear crowding, spreads through basement membrane into dermis
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29
Q

What would histology of a melanoma show?

A

Atypical melanocytes

  • intially grow horizontal in epidermis then vertically into dermis
  • vertical growth produces ‘buckshot appearance’ = pagetoid cells
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30
Q

What is most important prognostic factor for melanomas?

A

Breslow thickness

  • depth which tumour cells have invaded skin
  • the deeper, the worse the prognosis
  • stage 1 <1mm = 80=90%
  • stage 4 >4mm = 50% 5-year survival
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31
Q

Subtypes of melanomas

A

Lentigo maligna melanoma

  • sunexposed area of old white ppl
  • slow growing black lesion

Superficial spreading malignant melanoma
- irregular borders, variations in colour

Nodular malignant melanoma
- occur all sites, common in younger ppl

Acral lentiginous melanoma
- occur on palms, soles and subungual areas

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32
Q

Name the conditions that affect the bronchus of the lungs and compare their pathology

A

Chronic bronchitis

  • dilatation of airways and excess mucus production
  • tobacco, smoke, air pollution

Bronchiectasis

  • airway dilatation and scarring
  • post-inflammation, asthma, systemic disease, congenital disease

Asthma

  • smooth muscle cell hyperplasia, excess mucus, inflammation
  • immunological; allergens, drugs, cold air, exercise
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33
Q

Pt suffering from productive cough over last two years every winter, multiple hospital admissions for chest infections

Histo show dilatation of airways, goblet cell hyperplasia and hypertrophy of mucous glands

What is this likely to be?

A

Chronic bronchitis

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34
Q

Pt suffers from recurrent chest infections, and recently started coughing blood, background of sarcoidosis

Histo shows permanent dilation of the bronchi

What is this likely to be?

A

Bronchiectasis

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35
Q

What would you see in histology of asthamatic lungs?

A

Curschm ann spirals
- whorls of shed epithelium

Eosinophils and mast cells in surface epithelium

Goblet cell hyperplasia

Mucus plugs seen within airways

Bronchial smooth muscle thick and blood vessels dilated

Charcot-Leyden crystals
- breakdown of eosinophils

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36
Q

Name a lung condition that affects the acinus and its pathology

A

Emphysema

  • airspace enlargement, wall destruction
  • tobacco smoke*, alpha-1 antitrypsin deficiency

*Neutrophils and macrophages activated by smoking, will release proteases which degrade tissues

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37
Q

Pt has pneumothorax and dies

Autopsy histo of lung shows loss of alveolar parenchyma distal to terminal bronchiole

What did they likely suffer from?

A

Emphysema

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38
Q

Name lung condition that affects bronchiole and its pathology

A

Small airway disease/bronchiolitis

  • inflammatory scarring/obliteration
  • tobacco smoke, air pollutants
  • suffer from dyspnoea, cough
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39
Q

Congenital causes of bronchiectasis

A

Cystic fibrosis
Primary ciliary dyskinesia
Hypogammaglobulinemia
Young’s syndrome (rhinosinusitis, azoospermia, bronchiectasis)

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40
Q

Chronic changes of asthma

A

Muscular hypertrophy
Airway narrowing
Mucus plugging

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41
Q

Presentation and investigation findings of interstitial lung disease

A

PC

  • chronic SOB
  • end-inspiratory crackles
  • cyanosis, pulmonary HTN, cor pulmonale

RESTRICTIVE lung disease in spirometry
- decreased CO diffusion capacity, lung volume, compliance

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42
Q

Histology of fibrosing lung disease subtype of ILD

A

Idiopathic pulmonary fibrosis, pneumoconiosis etc

  • progressive patchy interstitial fibrosis with loss of lung architecture and honeycomb change
  • begins at periphery of lobule, sub-pleural
  • hyperplasia of type II pneumocytes causing cyst formation (honeycomb fibrosis)
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43
Q

Histology of granulomatous lung disease subtype of ILD

A

Granuloma = collection of histiocytes, macrophages, multi-nucleate giant cells

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44
Q

Histology of extrinsic allergic alveolitis/hypersensitivty pneumonitis subtypes of ILD

A

Polypoid plugs of loose connective tissue within alveoli/bronchioles

Granuloma formation (think TB!!) and organising pneumonia

Immune-mediated lung disorders due to organic antigens cause widespread ALVEOLAR inflammation

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45
Q

Based on these occupations/equipment/things, what aspect of them causes ILD?

a) Coal mines
b) Farmer
c) Bird owner
d) Water tanks
e) Malt worker
f) Cheese maker

A

a) Asbestos exposure -> benign pleural lesions -> fibrosis

Rest of them cause hypersensitivity pneumonitis

b) mouldy hay/grain -> Saccharopolyspora rectivirgula
c) proteins in excreta/feathers
d) heated water reservoirs - thermactinomyces spp.
e) germinating barley - Aspergillus clavatus/fumigatus
f) mouldy cheese - Aspergillus clavatus/penicillum casei

By removing antigen, can prevent progression to fibrosis

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46
Q

Types of pneumonia

A

Bronchopneumonia

  • patchy bronchial/peri-bronchial distrubtion
  • low virulence organisms, seen in elderly/frail

Lobar pneumonia
- fibrinosuppurative consolidation

Atypical

  • interstitial penumonitis
  • no intra-alveolar inflammation
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47
Q

Name common bacterial pneumonia organisms

A

Community-acquired

  • Strep pneum
  • Haem influ
  • Mycoplasma

Hospital-acquired

  • Klebsiella
  • Pseudonomas

Aspiration
- mixed aerobic and anaerobic organisms

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48
Q

What would you see in the histo of a lobar pneumonia?

A
  1. Congestion
    - hyperaemia and intra-alveolar fluid
  2. Red hepatisation
    - hyperaemia, intra-alveolar NEUTROPHILS
  3. Grey hepatisation
    - intra-alveolar connective tissue, FIBROSIS
  4. Resolution
    - restoration of normal tissue architecture
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49
Q

Male pt, smoker since teens, coughing up blood, SOB last 3 months, tumour noted by proximal bronchi on CXR

Biopsy shows keratinisation, intercellular prickles (desmosomes)

Which Ca?

A

Squamous cell carcinoma (30-50%)

  • local spread w late mets
  • less responsive to chemo
  • cytology: squamous cells
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50
Q

Female pt, never smoked, coughing blood, tumour on CXR

Biopsy shows gland formation and mucin production, cells contain mucin vacuoles, and EGFR mutations noted on molecular testing

Which Ca?

A

Adenocarcinoma (20-30%)

  • malignant epithelial tumour
  • can have atypical adenomatous hyperplasia; non-mucinous BAC, mixed pattern adenocarcinoma
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51
Q

Pt with 40 yr pack hx, cushingoid, bone pain, CXR shows central tumour by proximal bronchi

Which Ca?

A

Small cell carcinoma (20-25%)

  • arises from neuroendocrine cells
  • associated w ectopic ACTH secretion, Lamber-Eaton, cerebellar degeneration
  • highly malignant, mets early to bone, adrenal, liver and brain
  • p53 and RB1 common mutations
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52
Q

Tumour noted on CXR

Biopsy shows large cells, large nuclei, prominent nucleoli, no evidence of glandular or squamous differentiation

Which Ca?

A

Large cell carcinoma (10-15%)

  • poorly differentiated malignant epithelial tumour
  • poor prognosis
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53
Q

Name potential paraneoplastic syndromes seen in lung Ca

A

Excess of the following:

ADH -> SIADH
ACTH -> Cushing’s syndrome
PTH/PTHrP -> primary hyperparathyroidism, hypercalcaemia + bone pain
Calcitonin -> hypercalcaemia
Serotonin -> carcinoid syndrome (flushing + diarrhoea + bronchoconstriction)
Bradykinin -> coughing

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54
Q

How is lung Ca staged?

A

Tumour 1-4
- based on size and invasion of pleua, pericardium

Lymph node mets N0-2
- N1/2 = lymph node involved, depends on extent of involvement

Distant mets M0-1
- tumour spread to distant sites

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55
Q

Pt worked in coal mines 40 years ago

What signs would be suggestive of mesothelioma?

A

Extensive pleural effusion

Chest pain

Dyspnoea

*asbestos exposure

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56
Q

What do the molecular findings mean for lung Ca tx?

a) ERCC1 - NSCLC
b) EGFR
c) Kras
d) EML4-ALK

A

a) poor response to cisplatin
b) usually adeno, target for anti-EGFR for tyrosine kinase inhibitor therapy
c) adeno/squamous, poor prognosis, non-response to TKI
d) usually adeno, no benefit from TKI

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57
Q

Classification of pulmonary hypertension

A

Classified according to aetiology

  1. Pulmonary arterial hypertension
    - idiopathic, hereditary, drugs/toxins, associated congenital heart disease
  2. Pulmonary hypertension associated with left heart disease
    - systolic/diastolic dysfunction, valve disease
  3. Pulmonary hypertension due to lung disease
  4. Chronic thromboembolic pulmonary hypertension
  5. Pulmonary hypertension w unclear multifactorial mechanisms
    - metabolic disorders, systemic disorders, haematological disorders
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58
Q

Pathophysiology of pulmonary HTN

A

Pre-capillary
- chronic hypoxia/embolus

Capillary
- pulmonary fibrosis

Post-capillary
- left heart disease, veno-occlusive disease

Pulmonary vasoconstriction of arterioles
- intimal firbosis, thickened walls

Complications
- RHF, venous congestion of organs (nutmeg liver), peripheral oedema

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59
Q

Risk factors for PE

A

Anything that contributes to Virchow’s triad (stasis + vessel wall injury + hypercoagulability)

  • female
  • immobile
  • cardiac disease
  • cancer
  • childbirth
  • polycythaemia
  • contraceptive pill
  • DIC
  • anti-phospholipid syndrome
  • trauma/surgery
  • obesity
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60
Q

Path of pulmonary oedema

A

Intra alveolar fluid accumulation leads to poor gas exchange

Usually result of left heart filure

Histo: intra-alveolar fluid, iron laden macrophages (heart failure cells)

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61
Q

Path of diffuse alveolar damage

A

ARDS in adults
- infection, aspiration, trauma

HMD in neonates

  • hyaline membrane
  • insufficient surfactant production in prems
  • rapid onset resp failure

Histo: lung expanded, firm, plum-coloured, airless

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62
Q

How is breast disease investigated?

A

Triple Assessment

  1. Clinical examination
  2. Imaging - sonography, mammography, MRI
  3. Pathology - cytopathology, histopathology
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63
Q

Who do we offer mammograms to?

A

35+

Pts have less glandular tissue and more fat, contrast more visible

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64
Q

How is cytopathology obtained and coded for suspected breast disease?

A

Fine needle aspiration via 16/18 gauge needle

C1 - inadequate sample
C2 - benign
C3 - atypia
C4 - sus of malignancy
C5 - malignant
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65
Q

What is the diagnostic gold standard of breast cancer?

A

Core biopsy for histopathology

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66
Q

What would you see on normal breast histology?

A

Branching ducts ending in terminal-duct lobular units (functional unit of breast)

Duct-lobular system lined by an inner glandular epithelium and an outer myoepithelium

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67
Q

Painful, red breast, hot to touch

Pt has fever and recently gave birth, finding it difficult to breastfeed

What caused this and its tx?

A

Lactational acute mastitis

Staphylococcal infection via cracks in nipple and stasis of milk

Tx: continue breastfeeding + abx +/- surgical drainage

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68
Q

What causes non-lactational acute mastitis?

A

Keratinising squamous metaplasia blocking lactiferous ducts leading to peri-ductal inflammation and rupture

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69
Q

What FNA cytology findings do you expect from the following benign breast conditions:

a) acute mastitis,
b) mammary duct ectasia,
c) fat necrosis,
d) fibroadenoma,
e) intraductal papilloma?

A

a) abundance of neutrophils
b) proteinaceous material and macrophages
c) empty fat spaces, histiocytes and giant cells
d) branching sheets of epithelium, bare bipolar nuclei and stroma
e) (of nipple discharge) - branching papillary groups of epithelium

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70
Q

45 yr old woman comes in with green nipple discharge. She is a smoker and has 4 children.

Poorly defined periareolar mass palpated.

What caused this and its possible complications?

A

Mammary duct ectasia

Inflammation and dilation of large breast ducts that fill up with stagnant brown/green secretion

Fluids can be irritant and lead to

  • periductal mastitis
  • abscess
  • fistula formation
  • fibrosis (slit-like nipple retraction)
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71
Q

54 year old obese woman comes in after noticing breast mass and skin tethering. There is no breast pain and she was involved in a recent car accident.

What is this and its causes?

A

Fat necrosis

Inflammatory reaction to damaged adipose tissue

Causes

  • trauma
  • radiotherapy
  • surgery
  • nodular panniculitis
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72
Q

What is the most common benign breast tumour and its clinical findings?

A

Fibroadenoma

  • spherical, freely mobile, variable size and rubbery tumour
  • occur in reproductive period
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73
Q

How could intraductal papilloma present and what does it affect?

A

Bloody nipple discharge

Benign papillary tumour in duct system of breast

  • small terminal ductules => peripheral papillomas
  • larger lactiferous ducts => central papillomas
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74
Q

Pt presents with palpable lump in breast

Stellate mass seen on mammography

Histology shows central, fibrous, stellate area

What is this?

A

Radial scar

Benign sclerosing lesion - central scarring surrounded by proliferating glandular tissue in stellate pattern

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75
Q

What is a Phyllodes tumour?

A

Breast: interlobular stroma mass with increased cellularity and mitoses

Presents >50yrs as palpable mass

Most benign, can be aggressive thus excised with wide local excision/mastectomy to limit recurrence

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76
Q

32 year old woman comes in with lumpiness in breasts that comes and goes every month

What would histology show?

A

Fibrocystic disease, changes w menstrual cycle

Dilated large ducts which may become calcified

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77
Q

Name three proliferative breast conditions that risk becoming malignant

A

Usual epithelial hyperplasia
- slight increase risk Ca

Flat epithelial atypia
- x4 risk of Ca

In situ lobular neoplasia
- x7-12 risk of Ca

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78
Q

How many breast Ca present?

A

Hard fixed lump
Paget’s disease (eczema of nipple then areola)
Peau d’orange
Nipple retraction

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79
Q

Compare breast carcinoma in situ types and histology

A

Neoplastic epithelial proliferation limited to ducts/lobules by basement membrane

Lobular

  • cells lack adhesion protein E-cadherin
  • no microcalcifications or stromal reactions

Ductal

  • ducts filled with atypical epithelial cells
  • high risk progressing to invasive Ca
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80
Q

How can invasive breast carcinomas be categorised and their histology?

A

Malignant epithelial tumours

Ductal

  • most common
  • big, pleiomorphic cells, invade into stroma

Lobular
- cells aligned in single file chains/strands

Tubular

  • well-formed tubules with low grade nuclei
  • <1cm rarely palpable

Mucinous
- produce abundance of extracellular mucin, dissects into surrounding stroma

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81
Q

What medication types are used to treat breast Ca?

A

Tamoxifen
- mixed agonist/antagonist of E2 receptors

Herceptin/trastuzumab

  • monoclonal Ig to Her2
  • needs LVEF monitoring due to toxic effect on myocardium
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82
Q

Which genes and receptors impact breast Ca mx?

A

BRCA1/2

  • susceptibility gene
  • prophylactic treatment

+ve ER/PR receptor
- associated with good prognosis, predicts response to tamoxifen

+ve HER2 receptor
- associated w bad prognosis

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83
Q

What is basal-like carcinoma in breast associated with and what would histology show?

A

Associated with BRCA, vascular invasion and distant mets

Triple negative: EP/PR/Her2 negative

Histo: sheets of markedly atypical cells w lymphocytic infiltrate, +ve stain for CK5/6/14

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84
Q

How are breast biopsies coded for in the screening programme?

A

Screening programme for 47-73 year old women every 3 years

Core biopsy of abnormal area:
B1 = normal breast tissue
B2 = benign abnormality
B3 = lesion of uncertain malignant potential 
B4 = sus of malignancy
B5 = malignant

B5a -> DCIS
B5b -> invasive Ca

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85
Q

What is the role of the pancreas?

A

Produces enzymic HCO3- rich fluid stimulated by secretin and CCK

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86
Q

What does secretin do?

A

Produced by s-cells in the duodenum

Controls gastric acid secretion and buffering with HCO3-

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87
Q

What does CCK do?

A

Made by l-cells in the duodenum

Stimulates digestion of fast and protein by causing release of digestive enzymes

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88
Q

What are the exocrine functions of the pancreas?

A

Digestive function by secreting proteases, lipases, amylases into ducts

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89
Q

What are the endocrine functions of the pancreas?

A

Secretes the following into the bloodstream

  • glucagon
  • insulin
  • somatostatin
  • D1 (vasoactive peptide)
  • pancreatic polypeptide
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90
Q

What do D1 and PP do for the pancreas?

A 
D1 = stimulates secretion of H2O into pancreatic system
PP = self regulates secretion activities (pancreatic polypeptide)
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91
Q

Where are the following hormones made by the Islets of Langerhans in the pancreas?

a) glucagon
b) insulin
c) somatostatin

A

a) Alpha cells
b) Beta cells
c) Delta cells

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92
Q

Features of metabolic syndrome

A 
Fasting hyperglycaemia > 6 mmol/l
BP > 140/90 
Central obesity (> 94cm M, > 80cm F) 
Dyslipidaemia (decreased HDL < 1 mmol/l, increased TGs > 2 mmol/l) 
Microalbuminaemia
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93
Q

Complications of diabetes

A

Macrovascular

  • cardiac = MI
  • renal = glomerulonephritis, pyelonephritis
  • cerebral = CVA

Microvascular

  • ocular = diabetic retinopathy
  • PVS = claudication, change in colour/temp, poor healing ulcer
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94
Q

Diagnosis of diabetes mellitus

A

Fasting plasma glucose > 7 mmol/l

Random plasma glucose > 11.1 mmol/l

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95
Q

Compare T1DM and T2DM

A

T1DM
- autoimmune destruction of beta cells by CD4+ & CD8+ T-lymphocytes, may present with DKA, insulin dependent

T2DM
- strongly linked to obesity and insulin resistance

Both

  • polyuria due to osmotic diuresis
  • polydipsia due to raised plasma osmolality
  • hyperglycaemia, predisposing to recurrent infections
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96
Q

54 yo male presents with severe epigastric pain radiating to the back, relieved by sitting forward, and has associated prominent vomiting

Ix: increased amylase and lipase

What are the possible causes of his presentation?

A

Acute pancreatitis (most common)

Idiopathic

Gallstones*
Ethanol*
Trauma

Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia 
ERCP
Drugs (thiazides)
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97
Q

What would you see on histology of acute pancreatitis?

A

Coagulative necrosis

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98
Q

Complication of alcoholic pancreatitis

A

Formation of pseudocyst (pathological collection of fluid)

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99
Q

What would you see on histology of chronic pancreatitis?

A

Fibrosis and loss of exocrine tissue
Duct dilatation with thick secretions
Calcification

*similar to Ca pancreas

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100
Q

Complications of chronic pancreatitis

A

Pseudocysts
Diabetes
Pancreatic Ca

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101
Q

64 yo presents with epigastric pain radiating to their back, complain of white stool and weight loss, and have a hx of diabetes

What are possible causes of their presentation?

A

Chronic pancreatitis

  • wt loss & steatorrhea = malabsorption
  • 2o diabetes = lack of enzymes to digest food
Alcoholism 
CF
Hereditary 
Pancreatic duct obstruction (stones/tumours)
Autoimmune (IgG4 sclerosing)
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102
Q

What would you see on the histology of acinar cell carcinoma of the pancreas?

A

Neoplastic epithelial cells with eosinophilic granular cytoplasm
+ve immunoreactivity for lipase, trypsin, chymotrypsin

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103
Q

What is acinar cell carcinoma and its presentation?

A

Rare, arises from acinar cells and leads to enzyme production by neoplastic cells

Causes non-specific sx, abdo pain, wt loss, N&V

10% get multifocal fat necrosis and polyarthralgia due to lipase secretion

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104
Q

Prognosis of acinar cell carcinoma

A

Median survival from diagnosis: 18 months

5 year survival: < 10%

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105
Q

What is the most common pancreatic Ca?

A

Ductal adenocarcinoma of the pancreas (85% cases)

- usually affects the head of the pancreas

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106
Q

Risk factors for ductal adenocarcinoma of pancreas

A

Smoking
BMI, diet
Chronic pancreatitis
Genetic = FAP, HNPCC

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107
Q

Signs and sx of ductal adenocarcinoma of pancreas

A 
Wt loss, anorexia
Upper abdo and back pain (chronic, persistent, severe)
Painless jaundice, pruritus, steatorrhoea
DM
Trousseau's syndrome (25%)
Ascites
Abdominal mass
Virchow's node
Courvoisier's sign
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108
Q

What is Trousseau’s syndrome?

A

Acquired blood clotting disorder that results in migratory thrombophlebitis (inflammation of a vein due to a blood clot) in association with an often undiagnosed malignancy

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109
Q

What is Courvoisier’s sign?

A

In the presence of a palpably enlarged gallbladder and accompanied with mild/painless jaundice, the cause is unlikely to be gallstones (malignancy instead)

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110
Q

Ix seen in ductal adenocarcinoma of pancreas

A 
Low Hb
High bilirubin
High Ca2+
CT/MRI/ERCP for imaging
CA19.9 > 70 IU/mL
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111
Q

Mx of ductal adenocarcinoma of pancreas

A 
Palliative chemo (5-FU) 
Surgical resection (15% cases) = Whipple's procedure
5 year survival rate = < 5%
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112
Q

What is MEN?

A

Multiple endocrine neoplasia

  • group of genetic syndromes where functioning hormone-producing tumours appear in multiple organs
  • MEN1, MEN2A, MEN2B
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113
Q

Which organs are affected in MEN1?

A

‘PPP’
Parathyroid hyperplasia/adenoma
Pancreatic endocrine tumour (often phaeo)
Pituitary adenoma

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114
Q

Which organs are affected in MEN2A?

A

Parathyroid, thyroid, phaeo

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115
Q

Which organs are affected in MEN2B?

A

Medullary thyroid, phaeo, neuroma

Marfanoid phenotype

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116
Q

Functional neuroendocrine tumour presentations

A

Present with sx related to hormone excess:

  • insulinoma = hypoglycaemic attack
  • gastrinoma = Zollinger-Ellison syndrome, high acid so recurrent ulceration
  • glucagonoma = necrolytic migrating erythema
  • VIPoma = diarrhoea
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117
Q

Non-functional neuroendocrine tumour presentation

A

Picked up incidentally on imagine or when grow large enough to produce sx of local disease or mets

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118
Q

What do the following pancreatic malformation mean?

a) ectopic pancreas
b) pancreas divisum
c) annular pancreas

A

a) commonly in stomach, small intestine instead
b) dorsal and ventral buds fail to fuse, increased risk of pancreatitis
c) bad shape that can constrict duodenum, presents with duodenal obstruction around 1yo

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119
Q

Which mutation is present in most ductal pancreatic carcinomas?

A

K-Ras (95% cases)

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120
Q

Where does ductal pancreatic Ca spread?

A 
DIRECT: bile ducts, duodenum
LYMPHATIC: lymph nodes
BLOOD: liver
SEROSA: peritoneum
Nerves
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121
Q

Common pathology of the gallbladder

A

Gallstones
Inflammation
Cancer

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122
Q

Complications of gallstones

A

Bile duct obstruction = painful, reflux of bile and acute pancreatitis
Acute and chronic cholecystitis
Gallbladder cancer
Pancreatitis

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123
Q

What are Rokitansky-Aschoff sinuses?

A

Pressure diverticula involving muscularis that form in chronic cholecystitis as a result of the gallbladder contracting against an obstruction

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124
Q

Which cells are affected in gallbladder cancer?

A

Adenocarcinoma – mucin-secreting epithelium

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125
Q

Which pathological protein is present in the following diseases that cause dementia?

a) Alzheimer’s
b) Lewy body dementia
c) Corticobasal degeneration
d) Frontotemporal dementia
e) Pick’s disease

A

a) Tau, beta-amlyoid
b) Alpha-synuclein, ubiquitin
c) Tau
d) Tau, progranulin (linked to chr 17)
e) Tau

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126
Q

Rx of Alzheimer’s

A

Symptomatic based

  • anti-cholinesterases
  • nAChR agonists
  • glutamate antagonists
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127
Q

What is seen on imaging of Alzheimer’s?

A

MRI and PET may be done though clinical diagnosis
Generalised atrophy of brain
Widened sulci
Narrowed gyri
Enlarged ventricles
Most marked in temporal and frontal lobes with loss of cholinergic neurons

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128
Q

What presentation of dementia points towards Lewy body?

A 
Psychological disturbances early 
Day-to-day fluctuation in cognitive performance
Visual hallucinations
Spontaneous motor signs of Parkinsonism
Recurrent falls and syncope
Pathologically indistinguishable from PD
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129
Q

What causes Parkinson’s disease?

A

Decreased stimulation of motor cortex by basal ganglia

Due to death of dopaminergic neurons in substantia nigra

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130
Q

Parkinsonism symptoms

A

T remor
R igidity
A kinesia
P ostural instability

Psychiatric features late in disease (hallucinations, anxiety)

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131
Q

Fluctuating cognition, visual hallucinations, early dementia

Which dementia type is this?

A

Lewy Body Dementia

- parkinson plus syndrome

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132
Q

Downgaze, early falls, early rigidity and akinesia, dysarthria and dysphagia

Which dementia type is this?

A

Progressive supranuclear palsy

- parkinson plus syndrome

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133
Q

Unilateral parkinsonism, dystonia/myoclonus, apraxia ‘alien limbs’, progressive non-fluent aphasia

Which dementia type is this?

A

Corticobasal syndrome

- parkinson plus syndrome

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134
Q

What are the two presentations of multiple system atrophy?

A

Cerebellar predominant or parkinsonism predominant

- both associated with early autonomic dysfunction

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135
Q

Multi-infarct presentation, gait instability, lower body parkinsonism, less likely to have a tremor

Which dementia type is this?

A

Vascular parkinsonism

- parkinson plus syndrome

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136
Q

What causes multiple sclerosis?

A

Autoimmune demyelinating disease

- gets rid of myelin produced by oligodendrocytes that wraps around axons for axon conduction

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137
Q

How can MS be classified?

A

Primary progressive
- 10% cases, continually getting worse

Relapsing remitting
- better between episodes but progresses over years

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138
Q

What proteins are seen in MS?

A

Myelin basic protein

Proteo-lipid protein

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139
Q

32 yo presents with blurry vision and a previous admission of loss of sensation on their R side of their body

What pathology would you expect to see?

A

MS plaques showing sharp margins of myelin loss

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140
Q

Neuropathology seen due to Alzheimer’s disease

A

Extracellular plaques
Neurofibrillary tangles
Cerebral amyloid angiopathy
Neuronal loss (cerebral atrophy)

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141
Q

When does tau protein start causing problems?

A

Tau protein becomes hyperphosphrylated -> accumlates inside the cell -> causes cell death

Found throughout the brain

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142
Q

Benign bone disease findings on X ray

A

No periosteal reaction
Thick endosteal reaction
Well developed bone formation
Intraosseous and even calcification

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143
Q

Malignant bone disease findings on X ray

A

Acute periosteal reaction (Codman’s triangle, onion skin, sunburst)
Broad border between lesion and normal bone
Varied bone formation
Extraosseous and irregular calcification

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144
Q

16 yo presents with right knee pain

X ray shows an elevated periosteum and sunburst appearance of the right knee

What would you expect to see on histology?

A

Osteosarcoma

  • malignant mesenchymal cells
  • ALP +ve

common in adolescents and affects knee in 60% cases

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145
Q

Osteosarcoma X ray findings

A 
Elevated periosteum (Codman's triangle)
Sunburst appearance
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146
Q

45 yo presents with leg pain and swelling

X ray shows lytic lesion wit fluffy calcification

What would you expect to see on histology?

A

Chondrosarcoma

  • malignant chondrocytes
  • affects axial skeleton, femur/tibia/pelvis in > 40yos
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147
Q

Chondrosarcoma X ray findings

A

Lytic lesions with fluffy calcification

Axial skeleton affected

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148
Q

14 yo presents with leg pain

X ray shows onion skinning of periosteum

What would you expect to see on histology?

A

Ewing’s sarcoma

  • sheets of small round cells
  • CD99 +ve
  • T11:22 translocation
  • affects long bones, pelvis in < 20 yos
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149
Q

Ewing’s sarcoma X ray findings

A

Onion skinning of periosteum

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150
Q

32 yo female presents with knee pain

X ray shows lytic lesions up to the articular surface

What would you expect to see on histology?

A

Giant cell borderline malignancy

  • osteoclast-type multinucleate giant cells on background of spindle/ovoid cells
  • sheets of osteoclast cells
  • knee-epiphysis affected
  • occurs in 20-40 yo, F > M
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151
Q

Giant cell X ray findings

A

Lytic/lucent lesions right up to articular surface

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152
Q

Small benign bone forming lesion of which its night pain is relieved by aspirin

A

Osteoid osteoma

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153
Q

Osteoid osteoma X ray finding

A

Radiolucent nidus with sclerotic rim ‘Bull’s-eye’

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154
Q

Osteoid osteoma features

A

Affects tibia diaphysis/proximal femur
Arises from osteoblasts
Affects adolescents, M:F = 2:1

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155
Q

Bony outgrowths attached to normal bone commonly occurs in middle aged pts

A

Osteoma

- head + neck commonly affected

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156
Q

Gardner syndrome

A

GI polyps
Multiple osteomas
Epidermoid cysts

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157
Q

Benign tumours of cartilage commonly occurs in middle aged pts

A

Enchondroma

- hands mainly affected

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158
Q

Enchondroma X ray findings

A

Lytic lesions
Cotton wool calcification
Expansile, O ring sign

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159
Q

Ollier’s syndrome

A

Multiple enchondromas

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160
Q

Maffuci’s syndrome

A

Multiple enchondromas

Haemangiomas

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161
Q

Cartilage capped bony outgrowth

A

Osteochondroma/exostosis

  • most common benign tumour
  • affects metaphysis of long bones near tendon attachment sites
  • occurs in adolescents
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162
Q

Osteochondroma X ray findings

A

Well defined bony protuberance from bone

Cartilage capped bony spur on surface of bone ‘mushroom’ on X ray

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163
Q

Hereditary multiple exostoses

A

aka diaphyseal aclasis

  • multiple exostoses (osteochondromas)
  • short stature
  • bone deformities
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164
Q

Bit of bone replaced by fibrous tissue commonly occurs in middle aged pts

A

Fibrous dysplasia

  • F > M
  • misshapen bone trabeculae on histology (chinese letters)
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165
Q

Fibrous dysplasia X ray findings

A

Soap bubble osteolysis

Shepherd’s crook deformity

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166
Q

Fluid filled unilocular with well defined lytic lesion on X ray

A

Simple bone cyst

- humerus or femur commonly

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167
Q

X ray shows speckled mineralisation of small benign bone forming lesion

A

Osteoblastoma

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168
Q

Albright syndrome

A

Polyostotic dysplasia
Cafe au lait spots
Precocious puberty

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169
Q

Pt has serositis, arthritis, red rash on their nose and cheeks, and has had a history of kidney issues

Which autoantibody do you expect to find?

A

SLE pts have anti-nuclear antibodies (ANA, 95% cases)

  • anti dsDNA
  • anti-SM
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170
Q

Which HLA is associated with SLE?

A

HLA DR3 or 2

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171
Q

Which HLA is associated with scleroderma?

A

Both limited and diffuse: HLA DR5 & DRw8

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172
Q

Pt recently struggling with swallowing, lumps in hands, and hard skin changes on face and elbows and knees as well as hands that go white when it is cold

Which autoantibody do you expect to find?

A 
Limited scleroderma (CREST)
- anti-centromere
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173
Q

Which pulmonary complications are limited and diffuse scleroderma associated with?

A 
Limited = pulmonary hypertension
Diffuse = pulmonary fibrosis
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174
Q

Which autoantibodies are present in diffuse scleroderma?

A

Anti Scl-70
Fibrillarin
RNA pol I, II, III
PM-Scl

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175
Q

Which connective tissue disorder is +ve for anti-Jo-1?

A

Polymyositis
Dermatomyositis

*anti Jo-1 = tRNA synthetase

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176
Q

What are polymyositis and dermatomyositis associated with?

A

Underlying malignancy

Pulmonary fibrosis

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177
Q

Histology shows increased collagen in skin and organs as well as onion skin thickening of arterioles

What is this?

A

Limited scleroderma

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178
Q

What would histology show for diffuse scleroderma?

A

Inflammation within or around muscle fibres

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179
Q

What would histology show for polymyositis and dermatomyositis?

A

Endomysial inflammatory infiltrate

‘Drop out’ of capillaries and myofibre damage

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180
Q

Histology expected in SLE

A 
Lupus Erythematosus (LE) Cells 
- neutrophils that engulfed lymphocyte nuclei coated with and denatured by antibody to nucleoprotein

Affects kidneys, CNS, spleen, heart

  • kidney: nephrotic syndrome
  • CNS: small vessel angiopathy
  • spleen: onion skin lesions
  • heart: Libman-Sack endocarditis
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181
Q

Signs & sx of SLE

A

4/11 ACR criteria needed => SOAP BRAIN MD

Serositis
Oral ulcers
Arthritis
Photosensitivity

Blood disorders (AIHA, ITP, leucopenia)
Renal involvement
ANA +ve
Immune phenomena (dsDNA, anti-Sm, antiphospholipid Ab) 
Neuro sx 
Malar rash 
Discoid rash
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182
Q

Signs & sx of limited scleroderma

A

Skin changes on face and distal to elbows and knees + CREST syndrome

Calcinosis 
Raynaud's 
Esophageal dysmotility 
Sclerodactyly
Telangiectasia
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183
Q

Signs & sx of diffuse scleroderma

A

Thickening of skin occurs anywhere

Widespread organ involvement

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184
Q

Signs & sx of polymyositis and dermatomyositis

A

Proximal muscle weakness
- increased CK and abnormal EMG

DM has cutaneous features

  • heliotrope rash
  • gottron papules
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185
Q

Name large vessel vasculitides

A 
Takayasu's arteritis
Temporal arteritis (GCA)
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186
Q

Name medium vessel vasculitides

A

Polyarteritis nodosa (PAN)
Kawasaki’s disease
Buerger’s disease (thrombangitis obliterans)

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187
Q

Name small vessel vasculitides

A

Granulomatosis with polyangiitis (wegener’s = nazi)
Eosinophilic granulomatosis with polyangiitis (Church Strauss)
Microscopic polyangiitis
Henoch Schonlein Purpura

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188
Q

Woman comes in with absent pulse, low BP in arms, cold hands, bruits and claudication

Which vasculitides?

A

Takayasu’s arteritis

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189
Q

72 year old with painful shoulders and hips comes in with scalp tenderness and a temporal headache

ESR is raised

What ix would be diagnostic?

A

Temporal artery biopsy for temporal arteritis (GCA)

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190
Q

72 year old with painful shoulders and hips comes in with scalp tenderness and a temporal headache

ESR is raised

What would histology show?

A

Granulomatous transmural inflammation
Giant cells
Skip lesions

*for temporal arteritis (GCA)

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191
Q

72 year old with painful shoulders and hips comes in with scalp tenderness and a temporal headache

ESR is raised

What is the mx?

A

Oral prednisolone

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192
Q

What would you see on angiography of a patient with polyarteritis nodosa?

A

‘Strings of pearls/rosary bead’ appearance due to microaneurysms

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193
Q

What would histology show for polyarteritis nodosa?

A

Fibrinoid necrosis

Neutrophil infiltration

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194
Q

Features of polyarteritis nodosa

A

Systemic inflammation
Renal involvement
Lungs usually spared
30% have underlying hep B

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195
Q

Would would you see on angiogram of a patient with Buerger’s disease?

A

Corkscrew appearance from segmental occlusive lesions

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196
Q

32 year old man with a heavy smoking hx presents with painful inflammation of his arms and legs, as well as ulceration on his toes, feet, and fingers

Which vasculitides could this be?

A

Buerger’s disease (thrombangitis obliterans)

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197
Q

Pt presents with saddle nose due to chronic sinusitis, pulmonary haemorrhage as well as haematuria and proteinuria

Which autoantibody would they be +ve for?

A

Granulomatosis with polyangiitis -> cANCA (anti-PR3) +ve

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198
Q

What features are seen in granulomatosis with polyangiitis?

A

Triad

  1. Upper resp tract: sinusitis, epistaxis, saddle nose
  2. Lower resp tract: cavitation, pulmonary haemorrhage
  3. Kidney: cresenteric glomerulonephritis (blood & protein)
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199
Q

Features of eosinophilic granulomatosis with polyangiitis

A

Asthma, allergic rhinitis
Eosinophilia
Later systemic involvement

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200
Q

Which autoantibodies are seen in the following vasculitides?

a) Granulomatosis with polyangiitis
b) Eosinophilic granulomatosis with polyangiitis
c) Microscopic polyangiitis

A

a) cANCA (anti-PR3)
b) pANCA (anti-MPO)
c) pANCA (anti-MPO)

ANCA = antinuclear cytoplasmic antibody

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201
Q

Features of microscopic polyangiitis

A

Pulmonary renal syndrome

  • pulmonary haemorrhage
  • glomerulonephritis
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202
Q

Features of Henoch Schonlein Purpura

A 
IgA mediated 
Occurs in children < 10 years 
Preceding URTI 
Palpable purpuric rash (lower libs extensors + buttocks)
Glomerulonephritis
Colicky abdo pain, arthritis, orchitis
203
Q

Features of primary amyloidosis

A

Deposition of amyloid L protein
Associated with plasma cell dyscrasias with paraproteins, i.e. multiple myeloma
Monoclonal Ig, free light chains in serum and urine (Bence Jones)
Increased bone marrow plasma cells

204
Q

Features of secondary amyloidosis

A

Amyloid formed from serum amyloid A (acute phase protein)
Secondary to chronic infections/inflammation
- AI disease: TA, ank spond, IBD
- Infection: TB, osteomyelitis, IVDU (skin)
- Non-immune: renal cell carcinoma, Hodgkin’s

205
Q

What is haemodialysis associated amyloidosis?

A

Deposition of beta2-microglobulin resulting in amyloidosis due to longstanding chronic renal failure, especially when on peritoneal dialysis

Associated with carpal tunnel syndrome

206
Q

Most common familial amyloidosis

A

Familial Mediterranean Fever (AR)

  • +++ production of IL-1 attacks serosal surfaces (pleura, peritoneum, synovicum)
  • associated gene encodes pyrin
  • AA amyloid, predominant renal deposition
207
Q

Clinical features of amyloidosis

A

Kidney: nephrotic syndrome (main presentation)
Heart: conduction defects, heart failure, cardiomegaly
Liver/spleen: hepatosplenomegaly
Tongue: macroglossia in 10%
Neuropathies: carpal tunnel syndrome

208
Q

What staining is used for amyloidosis and what does it show?

A

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

  • this is due to beta-pleated sheet configuration
  • misfolded proteins unstable and self-associated to form fibrils
209
Q

Characteristic feature of sarcoidosis

A

Non-caseating granuloma in many tissues

- also get Schaumann and asteroid bodies (includes proteins and calcium)

210
Q

Typical presentation of sarcoidosis

A

F>M, more severe disease in black pts
Lungs commonly involved
- Bilateral hilar lymphadenopathy
- Pulmonary infiltrates (fine nodular shadowing in mid zones)
Insidious SOB, cough, chest pain and night sweats

211
Q

Ddx of bilateral hilar lymphadenopathy

A

TB
Sarcoidosis
Lymphoma
Bronchial Ca

212
Q

Extrapulmonary manifestations of sarcoidosis

A

Skin: erythema nodosum, lupus pernio, skin nodules
Eyes: anterior/posterior uveitis, keratoconjuctivitis, lacrimal gland enlargement
Blood: leucopoenia, anaemia
Heart: dysrhythmias, cardiomyopathy, conduction defects, pericarditis, valvular lesions

Lymphadenopathy, hepatosplenomegaly, arthritis, bone cysts, FLAWS, hypercalcaemia/hypercalciuria

213
Q

How is sarcoidosis diagnosed?

A

Diagnosis of exclusion

  • CXR: bilateral hilar lymphadenopathy, fine nodular shadowing mid zones (pulmonary infiltrates)
  • hypercalcaemia
  • increased ESR, ACE
  • transbronchial biospy
214
Q

Stain for melanoma

A

Fontana stain

215
Q

+ve Fontana stain

A

+ve for melanin -> melanoma

216
Q

Stain for amylodosis

A

Congo red + apple green birefringence

217
Q

Congo red stain with apple green birefringence

A

+ve for amyloid -> amyloidosis

218
Q

Stain for Wilson’s disease

A

Rhodanine stain

*golden brown against blue counterstain

219
Q

+ve Rhodanine stain

A

+ve for copper -> Wilson’s disease

*golden brown against blue counterstain

220
Q

Stain for haemachromatosis

A

Prussian blue

Perl’s stain

221
Q

+ve Prussian blue stain

A

+ve for iron -> haemochromatosis

222
Q

+ve Perl’s stain

A

+ve for iron -> haemochromatosis

223
Q

Stain for epithelial carcinoma

A

Cytokeratin

224
Q

Stain for lymphoid cells

A

CD45

225
Q

Stain for TB

A

Ziehl-Neelson
*red against a blue background

Auramine stain
*bright yellow

226
Q

+ve Ziehl-Neelson

A

+ve for acid-fast bacilli -> TB

*red against a blue background

227
Q

+ve Auramine stain

A

bright yellow -> TB

228
Q

Which stain shows flying saucer shaped cysts?

A

Gomori’s methanamine silver stain

229
Q

Which stain diagnoses Pneumocystic jirovecii?

A

Gomori’s methanamine silver stain

230
Q

+ve Gomori’s methanamine silver stain

A

Flying saucer shaped cysts -> Pneumocystic jirovecii

231
Q

+ve modified Kinyoung acid fast stain

A

Cryptosporidium parvum

232
Q

Which stain shows yeast cells surrounded by halos?

A

India ink stain

233
Q

Which stain diagnoses Cryptococcus neoformans?

A

India ink stain

234
Q

+ve India ink stain

A

Yeast cells surrounded by halos -> Cryptococcus neoformans

235
Q

Which stain shows cystoplasmic inclusions?

A

Giemsa stain

236
Q

Which stain diagnoses Chlamydisa psittaci?

A

Giemsa stain

237
Q

+ve Giemsa stain

A

Cystoplasmic inclusion -> Chlamydisa psittaci

238
Q

+ve Fite stain

A

Mycobacterium leprae

239
Q

Stain for Mycobacterium leprae

A

Fite stain

240
Q

Histology seen for osteoporosis

A

Loss of cancellous bone

241
Q

Histology seen for osteomalacia

A

Excess of unmineralise bone (osteoid)

242
Q

Histology seen for primary hyperparathyroidism

A

Osteitis fibrosa cystica

  • marrow fibroisis + cysts
  • aka Brown Tumour
243
Q

Histology seen for Paget’s disease

A

Huge osteoclasts w >100 nuclei

Mosaic pattern of lamellar bone (jigsaw due to re-modelling)

244
Q

What would you see in the x-ray of ostemolacia?

A

Looser’s zones
- pseudo fractures

Splaying of metaphysis

Bowing of legs in Ricket’s

245
Q

What would you see in the x-ray of primary hyperparathryoidism?

A

Brown’s tumours
- collection of multinucleate giant cells

Salt and pepper skull

Subperiosteal bone resorption in phalanges

246
Q

What would you see in the x-ray of Paget’s disease?

A

Mixed lytic and sclerotic

Skull

  • osteoporosis circumscripta
  • cotton wool appearance

Vertebrae

  • picture frame
  • ivory vertebra

Pelvis
- sclerosis and lucency

247
Q

Stages of Paget’s disease

A

Osteolytic
Mixed
Osteosclerotic

=> results in lytic and sclerotic lesions

248
Q

Diagnosis of osteoporosis

A

DEXA scan

  • T-score < -2.5 = osteoporosis
  • T score -1 to -2.5 = osteopenia
  • T-score compares to healthy population
  • *Z-score compares age-matched control (useful for bone loss in younger pts)
249
Q

Sx of Paget’s disease

A 
Bone pain
Microfractures
Nerve compression
- sensorineural deafness
- sciatica
Skull changes cause larger head size
Deafness
High output cardiac failure
250
Q

Sx of vit D deficiency in children

A 
Bone pain 
Bowing tibia
Rachitic rosary 
Frontal bossing 
Pigeon chest
Delayed walking
251
Q

Skeletal changes associated with CKD

A 
Increased bone resorption (osteitis firbosa cystica)
Osteomalacia
Osteosclerosis
Growth retardation
Osteoporosis
252
Q

Clinical features of RA

A 
Symmetrical joints affected
DIP joints SPARED 
Mild anaemia 
Raised ESR
Rheumatoid nodules (25%) 
Can be multisystem disease
253
Q

Serology for rheumatoid arthritis

A

Rheumatoid factor +ve 60-70% cases

anti-CCP more sensitive + specific

254
Q

Characteristic deformities in RA

A

Radial deviation of wrist

Ulnar deviation of fingers

Swan neck = hyperextension of PIP & flexion of DIP

Boutonniere = flexion of PIP & hyperextension DIP

Z shaped thumb

Synovial swelling

255
Q

Extra-articular features

A

Pulmonary fibrosis

Vasculitis

Amyloidosis

Pericarditis

Subcutaneous nodules

DVT

256
Q

Histopathology seen with RA

A

Proliferative synovitis

  • thickening of synovial membranes
  • hyperplasia of surface synoviocytes
  • intense inflammatory cell infiltrate
  • fibrin deposition and necrosis

Pannus formation
- inflamed synovium overlies articular surface

257
Q

X-ray features of osteoarthritis

A

LOSS

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

258
Q

What nodes are seen in osteoarthritis?

A

Heberden’s nodes on DIP

Bouchard’s nodes on PIP

259
Q

Crystal type in gout

A

Urate crystals
Needle shaped
Negatively birefringent crystals

260
Q

Crystal type in pseudogout

A

Calcium pyrophosphate crystals
Rhomboid shaped
Positively birefringent crystals

261
Q

How does fracture repair occur?

A
  1. Organisation of haematoma (pro-callus)
  2. Formation of fibrocartilaginous callus
  3. Mineralisation of fibrocartilaginous callus
  4. Remodelling of bone along weight bearing lines
262
Q

Which organisms are most likely to cause osteomyelitis in the following groups?

a) adults
b) sickle cell patients
c) children

A

a) Staph aureus
b) Salmonella
c) Haemophilus influenza, Group B strep

263
Q

Compare bones affected in osteomyelitis between adults and children

A

Adults

  • vertebrae
  • jaw (secondary to dental abscess)
  • toes (secondary to diabetic skin ulcer)

Children
- long bones

264
Q

X-ray changes in osteomyelitis

A

Early changes
- sub-periosteal new bone formation

~10 days post-onset
- lytic destruction of bone

265
Q

Rare causes of osteomyelitis

A

TB
- immunocompromised patients

Syphilis
- congenital or acquired

266
Q

Diseases affecting the glomerulus that present with nephrotic syndrome

A

Primary

  • Minimal change disease
  • Membranous glomerular disease
  • Focal segmental glomerulosclerosis

Secondary

  • diabetes
  • amyloidosis
  • SLE
267
Q

Diseases affecting the glomerulus that present with nephritic syndrome

A 
Acute post-infections (post-strep)
IgA nephropathy (Berger disease)
Rapidly progressive
Alport's syndrome (hereditary) 
Thin basement membrane disease (benign familial haematuria)
268
Q

Diseases affecting the tubules and interstitium

A

Acute tubular necrosis

Tubulointerstitial nephritis

269
Q

Diseases affecting the blood vessels of the renal system

A

Thrombotic microangiopathies

  • haemolytic uraemic syndrome (HUS)
  • thrombotic thrombocytopenic purpura (TTP)
270
Q

Proteinuria
Hypoalbuminaemia
Hyperlipidaemia
Oedema

Which syndrome is this?

A

Nephrotic syndrome

271
Q

Proteinuria
Haematuria
Hypertension

Which syndrome is this?

A

Nephritic syndrome

- also see oliguria

272
Q

Features of nephrotic syndrome

A 
Proteinuria (frothy urine)
Hypoalbuminaeima 
Oedema (periorbital)
Hyperlipidaemia 
Thrombotic disease
273
Q

Features of nephritic syndrome

A 
Proteinuria 
Haematuria 
Azootemia 
Red cell casts
Oliguria 
Hypertension
274
Q

Compare pathology of nephrotic and nephritic syndrome

A

NephrOtic
- pOdocyte damage leading to glomerular change-barrier disruption

NephrItic
- Inflammation disrupting glomerular basement membrane

275
Q

Acute changes in asthma

A

Bronchospasm
Oedema of mucosa
Hyperaemia
Inflammation

276
Q

Chronic change in asthma

A

Muscular hypertrophy
Airway narrowing
Mucus plugging

277
Q

Condition results in smooth muscle cell hyperplasia, excess mucus, and inflammation

What histological features would you see?

A

ASTHMA

Curschmann’s spirals (whorls of shed epithelium)
Eosinophils and mast cells
Goblet cell hyperplasia
Charcot-Leyden crystals (eosinophilic protein buildup)
Blood vessel dilation

278
Q

Condition results in dilatation of the airways and excess mucus production

What histological features would you see?

A 
CHRONIC BRONCHITIS
Dilated airways
Mucus gland hyperplasia 
Goblet cell hyperplasia 
Mild inflammation
279
Q

Condition results in airspace enlargement and wall destruction

What histological features would you see?

A

EMPHYSEMA
Loss of alveolar parenchyma distal to the terminal bronchiole
Centrilobular (centred on bronchiole) damage if caused by smoking
Panacinar (diffuse loss of alveolae) damage if caused by alpha-1 antitrypsin deficiency

280
Q

Condition results in airway dilatation and scarring

What histological features would you see?

A

BRONCHIECTASIS

Permanent dilatation of the bronchi

281
Q

Inflammatory causes of bronchiectasis

A 
Post-infectious/inflammatory
Abnormal host defence
- hypogammaglobulinemia
- chemotherapy, NG 
Obstruction 
Secondary to bronchiolar disease and interstitial fibrosis 
Systemic disease
Asthma
282
Q

Congenital causes of bronchiectasis

A

Cystic fibrosis
Primary ciliary dyskinesia
Hypogammaglobulinemia
Young’s syndrome = rhinosinusitis, azoospermia, bronchiectasis

283
Q

Most common CF mutation

A

Delta F508

- chromosome 7q3 = CFTR gene

284
Q

Stages of lobar pneumonia

A
  1. Consolidation
    - hyperaemia and intra-alveolar fluid
  2. Red hepatisation
    - hyperaemia, intra-alveolar neutrophils
  3. Grey hepatisation
    - intra-alveolar connective tissue (fibrosis vibes)
  4. Resolution
    - restoration of normal tissue architecture
285
Q

Interstitial pneumonitis pneumonia describes a…

A

…n atypical pneumonia

286
Q

Patchy bronchial/peri-bronchial distribution pneumonia describes a…

A

…bronchopneumonia

287
Q

Fibrinosuppurative consolidation pneumonia describes a…

A

…lobar pneumonia

288
Q

Owl’s eye inclusions

A

Big, eosinophilic viral inclusion seen in CMV infections

289
Q

Steps of atherosclorosis

A

Endothelial injury
LDL enters and converted into oxidised LDL causing inflammation
Macrophages eat it up and become foam cells
Apoptosis of foam cells create cholesterol core of plaque
Adhesion molecules attract more macrophages and T cells into plaque
Vascular smooth muscle cell forms fibrous cap

290
Q

Which part of the aorta is more affected by atherosclerosis?

A

Abdominal > thoracic

291
Q

Complications of MI

A 
Contractile dysfunction
Congestive heart failure
LV infarct
Cardiac rupture of ventricular wall, septum, papillary muscle
Ventricular aneurysm
Arrhythmias 
Pericarditis 
Pericardial effusion
Dressler's syndrome
Fibrinous pericarditis
Mural thrombus embolisation
292
Q

Common cause of sudden death post-MI

A

Ventricular fibrillation

293
Q

What histological changes do you see 24 hours post-MI?

A

under 6 hours

  • normal by histology
  • CK-MB normal

6-24 hours
- loss of nuclei, homogenous cytoplasm, necrotic cell death

294
Q

What histological changes do you see between 1-10 days post-MI?

A

1-4 days
- infiltration of polymorphs then macrophages (clear up debris)

5-10 days
- removal of debris

295
Q

What histological changes do you see weeks post-MI?

A

1-2 weeks
- granulation tissue, new blood vessels, myofibroblasts, collagen synthesis

Weeks-months
- strengthening, decellularising scar tissue

296
Q

Common causes of heart failure

A 
Ischaemic heart disease
Valve disease
Myocarditis
Hypertension
Dilated cardiomyopathy
Arrhythmias
297
Q

Complications of heart failure

A

Sudden death
Systemic emboli
Arrhythmias
Deep vein thrombosis and pulmonary embolism

298
Q

What causes fluid overload in heart failure?

A

Cardiac damage -> decreased CO -> activates RAS -> salt and water retention

This compensatory mechanism to maintain perfusion eventually leads to fluid overload

299
Q

What causes dilatation and poor contractility in heart failure?

A

Cardiac damage -> decreased stroke volume -> activation of sympathetic nervous system via baroreceptors (low BP)

This mechanism to maintain perfusion eventually leads to increased total peripheral resistance -> increased afterload -> LVH and increased EDV -> dilatation and poor contractility

300
Q

What ix are done for heart failure?

A

BNP
CXR
ECG
ECHO

301
Q

LVHF signs

A

Dyspnoea, orthopnoea, PND, wheeze, fatigue

*pooling of blood in pulmonary circulation -> decreased peripheral BP and flow

302
Q

RVHF signs

A

Engorgement of systemic and portal venous systems: peripheral oedema, ascites, facial engorgement

*chronic severe pulmonary HTN/secondary to LVF

303
Q

What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

A

Myocyte loss with fibrofatty

replacement typically affecting the right ventricle

304
Q

What is Hypertrophic obstructive cardiomyopathy (HOCM)?

A

Septal hypertrophy resulting in an
outflow tract obstruction

Cause of sudden death in young people

305
Q

Histology of hypertrophic cardiomyopathy

A

Myocyte disarray

- arrhythmogenic

306
Q

Which mutation causes hypertorphic cardiomyopathy?

A

beta-MHC gene

  • autosomal dominance
  • affects sarcomeric proteins

MYBP-C and Trop-T gene mutations

307
Q

What are the mechanisms of the following patterns of cardiomyopathy?

a) dilated
b) hypertrophic
c) restrictive

A

a) dilated - systolic dysfunction
b) hypertrophic - diastolic dysfunction
c) restrictive - diastolic dysfunction

308
Q

What are the causes of the following patterns of cardiomyopathy?

a) dilated
b) hypertrophic
c) restrictive

A

a) dilated
- IHD, valvular heart disease, HTN, congenital HD
b) hypertrophic
- HTN, AS
c) restrictive
- pericardial constriction

309
Q

What does acute rheumatic fever affect?

A

Heart: pancarditis i.e. endocarditis, myocarditis, pericarditis
Joints: arthritis and synovitis
Skin: Erythema marginatum, subcutaneous nodules
CNS: Encephalopathy, Sydenham’s chorea

310
Q

What criteria is used to diagnose acute rheumatic fever?

A 
Jones' Major Criteria: 
Carditis
Arthritis
Sydenham's chorea
Erythema marginatum
Subcutaneous nodules
Minor: 
Fever
Raised ESR or CRP
Migratory arthralgia
Prolonged PR interval
Previous rheumatic fever
Malaise
Tachycardia
311
Q

Which valve is affected by rheumatic fever?

A

Mitral 70%

Mitral & aortic 25%

312
Q

Main pathogen causing rheumatic fever

A

Lancefield group A strep

313
Q

Histology seen in rheumatic fever

A 
Beady fibrous vegetations
- verrucae
Aschoff bodies
- small giant-cell granulomas
Antischkov myocytes
- regenerating myocytes
314
Q

What immunological mechanism results in rheumatic fever?

A

Antigenic mimicry

- cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens

315
Q

Tx of rheumatic fever

A

Benzylpenicillin

Erythromycin if allergic

316
Q

Small, warty vegetations found along the
lines of closure of valve leaflet -
‘verrucae’

Dx?

A

Rheumatic heart disease

317
Q

Large, irregular masses on valve cusps,
extending into the chordae

Dx?

A

Infective endocarditis

318
Q

Small, bland vegetations attached to
lines of closure. Formed of thrombi

Dx?

A

Non-bacterial thrombotic endocarditis (marantic)

319
Q

Small (up to 2mm), warty vegetations
that are sterile and platelet-rich

Dx?

A

Libman-Sacks endocarditis

- associated with SLE and anti-phospholipid syndrome

320
Q 
Narrowed 
aortic valve 
high velocity, 
high pressure 
flow

Causes?

A

Aortic stenosis

  • calcification (old age)
  • congenital bicuspid valve
321
Q

Incompetent aortic
valve blood flows
back into LV after
systole

Causes?

A

Aortic regurgitation

  • infective endocarditis
  • aortic aneurysm
  • LV dilation
  • connective tissue disorder (Marfan’s, ank spond)
322
Q 
Narrowed mitral 
valve high 
velocity, high 
pressure flow. 
Back pressure 
in left atrium 
dilatation

Causes?

A

Mitral stenosis

- rheumatic fever

323
Q

Incompetent mitral
valve blood flows
back into left atrium
during systole

Causes?

A

Mitral regurgitation

  • infective endocarditis
  • connective tissues disease
  • post-MI
  • rheumatic fever
  • left ventricular dilatation (functional MR)
324
Q

Middle aged woman presents with SOB and chest pains

O/E Mid systolic click and late systolic murmur

Dx?

A

Mitral valve prolapse

325
Q

Causes of pericarditis

A 
Fibrinous
- MI, uraemia
Purulent
- Staphylococcus
Granulomatous
- TB
Haemorrhagic
- tumour, TB, uraemia
Fibrous
- constrictive
326
Q

What causes pericardial effusion?

A

Chronic heart failure

- serous fluid in pericardial sac

327
Q

Myocardial rupture from myocardial infarction or trauma

A

Haemopericardium

328
Q

3 main types of renal stones

A

Calcium oxalate 75%
Magnesium ammonium phosphate 15%
Uric acid 5%

329
Q

Staghorn calculi cause

A

Magneisum ammonium phosphate

Commonly due to urease producing organisms which alkanise urine
promoting precipitation of magnesium ammonium phosphate salts

330
Q

Histology seen for BPH

A

Nodule formation

Prostatic epithelial ducts with duct spaces

331
Q

Tx for BPH

A

TURP

5-alpha reductase inhibitors

332
Q

Most common prostate cancer

A

Adenocarcinoma

- develops from PIN

333
Q

Grading system for prostate cancer

A

Gleason system

334
Q

30 yo with testicular mass. Radiosensitive.

Which tumour?

A

Seminoma

335
Q

18 yo with testicular mass. Chemosensitive. Markers presents are AGP, HCG and LDH.

Which tumour?

A

Teratoma

336
Q

Germ cell testicular tumours

A 
Seminoma
Embryonal carcinoma
Yolk sac tumour
Choriocarcinoma
Teratoma
337
Q

Predisposing factors to germ cell testicular tumours

A

Cryptochordisim
Testicular dysgenesis
Genetic factors
- Klinefelter’s, testicular feminisation

338
Q

Non germ cell testicular tumours

A 
Leydig (from stroma)
Sertoli cell (from sex cord)
339
Q

Most common bladder tumour

A

Transitional cell (urothelial)

90% cases, 3:1 M:F

340
Q

Bladder tumour associated with schistosomiasis

A

Squamous cell carcinoma

341
Q 
Renal biopsy of tumour:
- Bland epithelial cells 
growing in a papilliary or 
tubopapilliary pattern
- Well circumscribed 
cortical nodules

What is it?

A

Papillary adenoma

  • benign
  • < 5mm
342
Q 
Renal biopsy of tumour: 
- Macroscopic: 
mahogany brown
- Microscopic: sheets of 
cells, pink cytoplasm, 
form a nest of cells

What is it?

A

Oncocytoma

- benign

343
Q

Renal biopsy of tumour:
- Fat spaces, thick blood vessels and spindle cell components

What is it?

A

Angiomyolipoma

- mesenchymal benign tumour composed of fat, blood vessels, and muscle

344
Q 
Renal biopsy of tumour: 
Microscopic –
1. Small round blue 
cells (very 
undifferentiated) 
2. Epithelial 
component – cells 
trying to differentiate 
and form primitive 
renal tubules

What is it?

A

Nephroblastoma

- childhood renal malignancy

345
Q 
Renal biopsy of tumour: 
- Macroscopic: golden yellow with 
haemorrhagic areas
- Microscopic: nests of epithelium 
with clear cytoplasm

What is it?

A

Clear cell renal cell carcinoma

  • epithelial tumour
  • 70% cases
346
Q

Renal biopsy of tumour:

  • macroscopic: friable brown tumour
  • microscopic: papillary/tubopapilliary growth pattern

What is it?

A

Papillary renal cell carcinoma

- 15% cases

347
Q

Renal biopsy of tumour:

  • macroscopic: solid brown tumour
  • microscopic: sheets of large cells, distinct cell borders

What is it?

A

Chromophobe renal cell carcinoma

- 5% cases

348
Q

Conditions that cause nephrotic syndrome

A

Primary

  • minimal change disease
  • membranous glomerular disease
  • focal segmental glomerulosclerosis

Secondary
- diabetes, amyloidosis, SLE

349
Q

Conditions that cause nephritic syndrome

A 
Acute post-infectious (post-strep)
IgA nephropathy (Berger)
Rapidly progressive
Alport's syndrome (hereditary nephritis)
Thin basement membrane disease (benign familial haematuria)
350
Q

Proteinuria
Hypoalbuminaemia
Oedema

What this?

A

Nephrotic syndrome

- may also see hyperlipidaemia, thrombotic disease

351
Q

Child comes in with swelling around their eyes and frothy urine

Renal biopsy would show loss of podocyte foot processes and no immune deposits

Pt responds to steroids

What this and mx?

A

Minimal change disease
- common in children

Mx

  • Steroids
  • Cyclosporin 2nd line

*generally AVOID renal biopsy in children

352
Q

Pt comes in with swollen feet and frothy urine

Renal biopsy shows loss of podocyte foot processes and spikey deposits as well as Ig deposits along entire GBM

No response to steroids

What this and mx?

A

Membranous glomerula disease
- spikey deposits = subepithelial deposits

Mx

  • steroids
  • ACEi/ARB for BP
353
Q

Pt comes in with swollen feet and frothy urine

Renal biopsy shows loss of podocyte foot processes and Ig and complement in scarred areas

Partial response to steroids

What this and mx?

A

Focal segmental glomerulosclerosis

Mx

  • steroids
  • ACEi/ARB control BP
  • calcineurinin inhibitors 2nd line
354
Q

When do you see Kimmelstiel Wilson nodules?

A

Nephrotic syndrome cause by diabetes due to diffuse glomerular basement membrane thickening with mesangial matrix nodules

355
Q

Which renal syndrome do you see red cell clasts in?

A

Nephritic syndrome

- in urine as red cells clumped together and leaked out into tubules

356
Q

When does acute post-infectious glomerulonephritis occur and why?

A

1-3 weeks after strep throat infection or impetigo due to immune complex deposition damaging glomeruli

357
Q

When does IgA nephropathy present and why?

A

1-2 days after URTI with frank haematuria due to deposition of IgA immune complexes in glomeruli

358
Q

Most aggressive form of glomerulonephritis and how does it present

A 
Rapidly progressive (cresenteric) glomerulonephritis
- oliguria and renal failure more pronounced in this nephritic syndrome presentation
359
Q

Types of rapidly progressive GN

A

Type 1
- anti-GBM antibody (Goodpasture’s)

Type 2
- immune complex mediated

Type 3
- pauci-immune/ANCA-associated

360
Q

Pt presents with nephritic syndrome, sensorineural deafness and cataracts at age 18

What is this caused by?

A

ALPORT’S SYNDROME

  • X-linked recessive disorder
  • Mutation in type IV collage alpha 5 chain
  • eye disorders: lens disolcation, cataracts
361
Q

Pt comes in and + blood found on dipstick

Tells GP dad has same problem

What is this?

A

Thin basement membrane disease/benign familial haematuria

362
Q

What causes benign familial haematuria?

A

Diffuse thinning of GBM due to mutation in type IV collage alpha 4 chain

  • autosomal dominant
  • renal function typically unaffected
  • chill vibes, no woz, usually asx
363
Q

Ddx if pt presents with asx haematuria

A
  1. Benign familial haematuria
    - more likely microscopic haematuria
  2. IgA nephropathy
    - more likely frank haematuria, Cr raised, happens in Asians
  3. Alport syndrome
    - well rare, deafness & eye problems too
364
Q

Renal biopsy shows necrosis of short segments of tubules

What this?

A

Acute tubular necrosis

365
Q

Causes of acute tubular necrosis

A

Hypovolaemia

  • ischaemic of nephrons
  • despite cured hypovolaemia pt may present with persistent acute renal failure

Nephrotoxins

  • aminoglycosides, NSAIDs
  • radiographic contrast agents
  • myoglobin
  • heavy metals
366
Q

Renal tumour biopsy shows well differentiated transparent cells

A

Clear cell carcinoma

367
Q

Renal tumour in pt with dialysis-associated cystic disease

A

Papillary carcinoma

368
Q

Renal tumour biopsy shows pale, eosinophilic cells

A

Chromophobe renal carcinoma

369
Q

Renal histology shows wire loop capillaries and GBM has a lumpy-bumpy granular fashion

What this and how would it present?

A

Lupus nephritis

  • immune complex deposition in capillaries and GBM cause this
  • present with renal failure, nephrotic syndrome, urinary abnormalities
370
Q

Chronic renal failure stages GFRs

A
  1. > 90
  2. 60-89
  3. 30-59
  4. 15-29
  5. <15 or treated with renal replacement therapy
371
Q

Which mutations cause adult polycystic kidney disease and how is it inherited?

A

Autosomal dominant

  • PKD1, chr16
  • PKD2, chr14
372
Q

Clinical features of adult polycystic kidney disease

A 
MISHAPES
abdominal Mass
Infected cysts & Increased BP
Stones
Haematuria
Aneurysms (berry)
Polyuria & nocturia
Extra-renal cysts
Systolic murmur (mitral valve)
373
Q

What causes acute interstitial nephritis?

A

Hypersensitivity reaction to drugs

- abx, NSAIDs, diuretics

374
Q

Histology seen in acute interstitial nephritis

A

Inflammatory infiltrate with tubular injury, eosinophils & granulomas

375
Q

HUS features

A

TRIAD

  • MAHA
  • thrombocytopenia
  • renal failure
376
Q

TTP features

A

PENTAD

  • MAHA
  • thrombocytopenia
  • renal failure
  • fever
  • neurological sx: confusion, seizures, headaches
377
Q

Cells that make up oesophagus

A 
Squamous epithelium (proximal 2/3 - bottom bit)
Columnar epithelium (distal 1/3 - top bit)

Joined by squamo-columnar junction/Z-line

378
Q

Most common cause of oesophagitis and its complications

A

GORD

  • ulceration
  • haemorrhage
  • haematemesis/melaena
  • Barrett’s oesophagus
  • stricture
  • perforation
379
Q

Tx for GORD

A

Stop smoking
Weight loss
PPI/H1 antagonists

380
Q

How does oesophageal adenocarcinoma occur?

A
  1. Metaplasia of squamous -> columnar (Barrett’s)
  2. Dysplasia
  3. Cancer rip

RFs: smoking, obesity, prior radiation therapy

381
Q

Pt presents with progressive dysphagia, odynophagia, anorexia, and severe wt loss

They are a known alcoholic and heavy smoker

What this?

A

Squamous cell carcinoma

- rapid growth usually found in middle

382
Q

What are squamous cell oesophageal carcinomas associated with?

A 
Alcohol, smoking
Achalasia of cardia
Plummer-Vinson syndrome
Nutritional deficiencies 
Nitrosamines
HPV
x6 more common in black people
M > F
383
Q

What causes varices?

A

Portal HTN leading to back pressure forming engorged dilated veins

384
Q

Cells of stomach

A

Lined by gastric mucosa, columnar epithelium (mucin secreting) and glands

385
Q

Epigastric pain that is worse with food

What ix needed?

A

Gastric ulcer

Biopsy for H pylori histology status (punched out lesion with rolled margins)

386
Q

RFs for gastric ulcers

A 
H pylori
Smoking
NSAIDs
Stress
Delayed gastric emptying
Elderly
387
Q

Tx for gastric lymphomas

A

Caused by H pylori due to chronic antigen stimulation so remove cause!

Triple therapy: PPI + clarithromycin + amox/metro

388
Q

Causes of acute gastritis

A

Neutrophil mediated

  • aspirin
  • NSAIDs
  • corrosives (bleach)
  • acute H pylori
  • severe stress (burns)
389
Q

Causes of chronic gastritis

A

Lymphocyte and plasma cell mediated

  • H pylori
  • pernicious anaemia
  • alcohol
  • smoking
390
Q

Epigastric pain worse at night and relieved by food and milk

What is this and its possible causes?

A

Duodenal ulcer

RFs:

  • H pylori
  • drugs (aspirin, NSAIDs, steroids)
  • smoking
  • acid secretion
391
Q

Gold standard ix for coeliac disease and its findings

A

Upper GI endoscopy and duodenal biopsy

  • villous atrophy
  • crypt hyperplasia
  • lymphocyte infiltrates
392
Q

Cancers associated with coeliac disease

A

Enteropathy-associated T cell lymphomas (duodenal)

Non-Hodgkin’s lymphoma

Adenocarcinoma of small intestine

393
Q

Which parts of the GI tract are most commonly affected by ischaemic colitis?

A

Splenic flexure
- SMA transition to IMA

Rectosigmoid
- IMA transition to internal iliac

394
Q

Histology seen in Crohn’s

A 
Skip lesions
Cobblestone appearance
Aphthous ulcer - rosethorn ulcers as they join to form serpentine ulcers
Non-caseating granulomas
Transmural inflammation
Fistula formation
395
Q

Histology seen in UC

A 
Continous involvement of mucosa
Backwash ileitis if severe
Superficial inflammation
No granulomas/fissures/fistulas
Pseudopolyps (can fuse to form mucosal bridges)
396
Q

Complications of Crohn’s

A

Strictures
Fistulae
Abscess formation
Perforation

397
Q

Complications of UC

A

Severe haemorrhage
Toxic megacolon
Colectomy
Adenocarcinoma

398
Q

Tx for Crohn’s

A

Mild
- prednisolone

Severe
- IV hydrocortisone, metronidazole

Additional

  • azathioprine
  • methotrexate
  • infliximab
399
Q

Tx for UC

A

Mild
- prednisolone + mesalazine (5 ASA)

Moderate
- prednisolone + 5-ASA + steroid enema bd

Severe
- admit, NBM, IV fluids, IV hydrocortisone, rectal steroids

Remission
- 5-ASA 1st line, azathioprine 2nd line

400
Q

Tx for C diff

A

Metronidazole or Vancomycin

401
Q

Complications of diverticular disease

A

Diverticulitis (fever, peritonism)
Gross perforation
Fistula
Obstruction (due to fibrosis)

402
Q

Carcinoid syndrome features

A

Serotonin release from enterochromaffin cell origins in tumours:

  • Bronchoconstriction
  • Flushing
  • Diarrhoea
403
Q

Carcinoid crisis features

A 
Life threatening vasodilation
Hypotension
Tachycardia
Bronchoconstriction
Hyperglycaemia
404
Q

Tx of carcinoid syndrome

A

Octreotide (somatostatin analogue)

405
Q

RFs for neoplastic polyps to become malignant

A

Large size
Degree of dysplasia
Increased villous component

406
Q

Which gene mutation causes neoplastic polyps?

A

APC gene

407
Q

Once APC gene first mutated in colon, which following genes being hit progress to carcinoma?

A

KRAS, LOF mutations of p53

408
Q

Peutz-Jeghers syndrome features

A

Autosomal dominant - LKB1

= multiple hamartomatous polyps
= mucocutaenous hyperpigmentation
= freckles on mouth, palms, soles
= risk of intussusception and malignancy

409
Q

Most common type of colorectal cancer

A

Adenocarcinoma (98% cases)

410
Q

Compare right and left-sided colorectal cancer presentations

A

Right

  • iron deficiency anaemia
  • wt loss

Left

  • change in bowel habit
  • crampy LLQ pain
411
Q

Colorectal cancer staging

A

Duke’s staging

A: confined to mucosa (5yr survival >95%)
B1: extending into muscularis propria (5yr survival 67%)
B2: transmural invasion, no lymph nodes involved (5yr survival 54%)
C1: extending to muscularis propria, with LN metastases (5yr survival 43%)
C2: transmural invasion, with lymph node metastases (5yr survival 23%)
D: distant metastases (5yr survival <10%)

412
Q

Which chemotherapy is used for terminal colorectal cancer?

A

Fluorouracil

413
Q

Which familial syndromes increase the risk of colorectal cancer?

A

Familial adenomatous polyposis (FAP)

Gardners

Hereditary non-polyposis colorectal cancer/Lynch syndrome (HNPCC)

414
Q

What cancers is Lynch syndrome associated with?

A 
Colorectal
Endometrial
Ovarian
Small bowel
Transitional cell 
Stomach carcinoma
415
Q

What makes up a hepatic lobule?

A

Think of like hexagon

  • at the centre is hepatic vein = centrilobular vein
  • points of hexagon = portal tracts

Portal tracts made up of portal triad

  1. branches of bile ducts
  2. hepatic artery
  3. portal vein
416
Q

3 zones of the liver

A

Zone 1 (closest to portal triad)

  • periportal hepatocytes
  • more oxygen

Zone 2 (mid zone)

Zone 3 (closest to terminal hepatic vein)

  • perivenular hapetocytes
  • most mature and metabolically active
  • most liver enzymes
417
Q

Functions of the liver

A 
Metabolism
Protein synthesis
Storage
Hormone metabolism
Bile synthesis
Immune function
418
Q

Spotty necrosis of liver on histopathology with small foci of inflammation and infiltrates

Cause?

A

Acute hepatitis

419
Q

Histopathology of chronic hepatitis

A
  1. Portal inflammation
  2. Peicemeal necrosis (no clear border between portal tract and parenchyma)
  3. Lobular inflammation
  4. Bridging between portal vein to central vein which evolves into cirrhosis
420
Q

Histopathology of cirrhosis

A

Hepatocyte necrosis
Fibrosis
Nodules of regenerating hepatocytes
Disturbance of vascular architecture

421
Q

Major causes of cirrhosis

A
  1. Alcoholic liver disease
  2. Non-alcoholic fatty liver disease
  3. Chronic viral hep (B+/-D, C)
  4. Autoimmune
  5. Biliary (PBC, PSC)
  6. Genetic
  7. Drugs (methotrexate)
422
Q

Genetic causes of cirrhosis

A
  1. Haemochromatosis- HFE gene Chr 6
  2. Wilson’s disease- ATP7B gene Chr 13
  3. Alpha 1 antitrypsin deficiency (A1AT)
  4. Galactosaemia
  5. Glycogen storage disease
423
Q

Micronodular causes of cirrhosis

A

Alcoholic hepatitis

Biliary tract disease

424
Q

Macronodular causes of cirrhosis

A

Viral hepatitis
Wilson’s disease
Alpha 1 antitrypsin deficiency

425
Q

What score is used for cirrhosis?

A

Modified Child’s Pugh Score (ABCDE)

  • Albumin
  • Bilirubin
  • Clotting prothrombin time
  • Distention (ascites)
  • Encephalopathy

determines prognosis

426
Q

Large, pale, yellow and greasy liver with accumulation of fat droplets in hepatocytes

A

Hepatic steatosis (fatty liver)

427
Q

Large, fibrotic liver with hepatocyte ballooning and necrosis alongside Mallory Denk bodies

A

Alcoholic hepatitis

= seen acutely after heavy night of drinking

428
Q

Yellow-tan, fatty and enlarged liver that transforms into shrunken, non-fatty, brown sad boy

A

Alcoholic cirrhosis

- micronodular = small nodules & bands of fibrous tissue

429
Q

What are Mallory Denk bodies?

A

Cytoplasmic hyaline inclusions of hepatocytes

430
Q

NAFLD histology

A

Simple steatosis
- fatty infiltrates, relatively benign

NASH

  • steatosis + hepatitis
  • can progress to cirrhosis
431
Q

Types of autoimmune hepatitis

A

Type 1
- ANA, anti-SMA, anti-actin Ig, anti-soluble liver antigen Ig

Type 2
- anti-LKM Ig

Associated with HLA-DR3 all

432
Q

Autoimmune inflammatory destruction of medium sized intrahepatic bile ducts

What is this and what can it progress to?

A

Primary biliary cirrhosis

Leads to cholestasis and slow development of cirrhosis

433
Q

Inflammation and obliterative fibrosis of extrahepatic and intrahepatic bile ducts

What is this and what can it progress to?

A

Primary sclerosing cholangitis

Leads to multi-focal stricture formation with dilation of preserved segments

Increased incidence of cholangiocarcinoma in the long-term

434
Q

Ix findings in primary biliary cirrhosis

A

Increased serum ALP, cholesterol, IgM, bilirubin (late)

Anti-mitochondrial antibodies

US: no bile duct dilatation

435
Q

Ix findings in primary sclerosing cholangitis

A

Increased serum ALP, associated with auto-Ig (p-ANCA)

Associated with UC

US: bile duct dilatation

ERCP: beading of bile ducts (strictures)

436
Q

Compare histology of PBC and PSC

A

PBC
- bile duct loss with granulomas

PBS
- onion skinning fibrosis (concentric fibrosis)

437
Q

Benign tumours in the live

A

Hepatic adenoma
- associated w OCP

Haemangioma
- most common

438
Q

Most common malignant liver lesion

A

Metastasis

- secondary tumours from GI tract, breast or bronchus

439
Q

Causes of hepatocellular Ca

A

Chronic liver disease

  • viral hep
  • alcoholic
  • haemochromatosis
  • NAFLD
  • aflatoxin
  • androgenic steroids
440
Q

Ix for hepatocellular Ca

A

alpha-fetoprotein

USS

441
Q

Causes of cholanigiocarinoma

A 
Primary sclerosing cholangitis
Parasitic liver disease
Chronic liver disease
Congenital liver abnormalities
Lynch syndrome type II
442
Q

Highly invasive liver cancer affecting the vascular epithelium

A

Haemangiosarcoma

443
Q

Liver cancer that originates from immature liver precursor cells seen in children

A

Hepatoblastoma

444
Q

How are the following genetic causes of cirrhosis inherited?

a) Haemochromatosis
b) Wilson’s diease
c) Alpha 1 antitrypsin deficiency

A

a) autosomal recessive
b) autosomal recessive
c) autosomal dominant/codominant

445
Q

Periodic acid Schiff detects which liver disease?

A

Alpha 1 antitrypsin deficiency

= intracytoplasmic inclusions of A1AT stained by it

446
Q

What are the intracytoplasmic inclusions of alpha 1 antitrypsin stained by?

A

Periodic acid Schiff

447
Q

Features of haemochromatosis

A 
Skin bronzing (melanin deposition)
Diabetes
Hepatomegaly with micronodular cirrhosis
Cardiomyopathy
Hypogonadism
Pseudogout
448
Q

Features of Wilson’s disease

A

Liver disease: acute hepatitis, fulminant liver
failure or cirrhosis
Neuro disease: parkinsonism, psychosis,
dementia (basal ganglia involvement)
Kayser Fleischer rings: copper deposits in
Descemet’s membrane in cornea

449
Q

Features of alpha 1 antitrypsin deficiency

A

Kids: neonatal jaundice
Adults: emphysema and chronic
liver disease

450
Q

Tx of haemochromatosis

A

Venesection

Desferrioxamine

451
Q

Tx of Wilson’s disease

A

Lifelong penicillamine

May require liver transplant

452
Q

Breast Ca monoclonal antibody if HER2 receptor present (poor prognosis)

A

Trastuzumab

453
Q

Tram track opacities in lung

A

Bronchiectasis

454
Q

Fitz Hugh Curtis syndrome features

A

Complication of PID:

  • RUQ pain from peri-hepatitis
  • Violin string peri-hepatic adhesions
455
Q

Histological findings in endometriosis

A

Macro

  • red-blue to brown nodules = powder burns
  • chocolates cysts in ovaries

Micro
- endometrial glands and stroma

456
Q

Sharply circumscribed, discrete, round, firm, gray-white tumour found in the uterus containing bundles of smooth muscle cells

A

Leiomyoma (fibroid)

457
Q

Which system is used to stage endometrial Ca?

A

FIGO

458
Q

Endometrial Ca types

A

Endometrioid
- peri-menopausal, related to E2
= ADENOCARCINOMA

Non-endometrioid
- post-menopausal, not related to E2
= PAPILLARY, SEROUS, CLEAR CELL

459
Q

HPV associated with VIN

A

HPV-16

460
Q

What cell type is Paget’s of the vulva?

A

Adenocarcinoma in situ

461
Q

Normal vulva hsitology

A

Squamous epithelium

462
Q

Epithelial ovarian tumours

A

Serous cystadenoma
Mucinous cystadenoma
Endometrioid
Clear cell

463
Q

Germ cell ovarian tumours

A

Dysgerminoma (female testicular seminoma)
Teratoma
Choriocarcinoma

464
Q

Sex cord/stroma ovarian tumours

A

Fibroma
Granulosa-theca cell tumour
Sertoli-Leydig cell tumour

465
Q

Metastatic ovarian tumour and its histology

A

Krukenberg tumour

= signet ring cells from gastric/colonic cancer

466
Q

Psammoma bodies and columnar epitherlium of ovarian tumour

A

Serous cystadenoma

- most common type of epithelial tumour

467
Q

Ovarian tumour that causes pseudomyxoma peritonei

A

Mucinous cystadenoma

- 75% K-ras mutation

468
Q

Abundanct clear cytoplasm and hobnail appearance of ovarian tumour

A

Clear cell

- poor prognosis

469
Q

What do the following ovarian tumours produce?

a) teratoma
b) chroriocarcinoma
c) granulosa-theca cell tumour
d) sertoli-leydig cell tumour

A

a) teratoma = AFP
b) chroriocarcinoma = hCG
c) granulosa-theca cell tumour = E2
d) sertoli-leydig cell tumour = androgens

470
Q

Which ovarian tumour is associated with Meig’s - and what is it?

A

Fibroma

Meig’s = ascites + pleural effusion + ovarian tumour

471
Q

FIGO ovarian staging system

A

Stage I: limited to ovaries (75-90%)
Stage II: limited to pelvis (45-60%)
Stage III: limited to abdomen (including regional LN metastases) (30-40%)
Stage IV: distance metastases outside abdominal cavity (<20%)

472
Q

Most common type of cervical carcinoma

A

Squamous cell carcinoma

473
Q

FIGO cervical staging system

A

Stage 0: CIN
Stage I: limited to cervix (80-95%)
Stage II: extended beyond uterus but not to pelvic side wall or lower 1/3 vagina
(75%)
Stage III: extension to pelvic side wall and/or lower 1/3 vagina (50%)
Stage IV: extension beyond true pelvis or involvement of bladder/bowel mucosa
(20-30%)

474
Q

What is the transformation zone of the cervix?

A

Area where columnar epithelium transforms into squamous cells

  • normal physiological process
  • susceptible to
    malignant change
475
Q

Which HPV strains cause CIN?

A

HPV 16 & 18

476
Q

CIN histology findings

A

CIN 1 = dysplasia confined to lower 1/3 of epithelium
CIN 2 = lower 2/3
CIN 3 = full thickness, but basement membrane intact

477
Q

Most common cause of strokes

A

Atherosclerosis

478
Q

Most common artery affected in strokes

A

Middle cerebral artery

479
Q

Most common vascular territories affected by TIA

A

Embolic atherogenic debris from carotid artery travels to ophthalmic branch of internal carotid

480
Q

Contralateral leg paresis, sensory loss, cognitive deficits

Which vascular territory affected?

A

Anterior cerebral artery

481
Q

Contralateral weakness and sensory loss of face and arm, cortical sensory loss, aphasia

Which vascular territory affected?

A

Middle cerebral artery

482
Q

Contralateral hemianopia/quadrantanopia, CN III and IV palsy, hemiparesis, sensory loss, amnesia, decreased level of consciousness

Which vascular territory affected?

A

Posterior cerebral artery

483
Q

Impaired extraocular muscles, vertical nystagmus, reactive miosis, hemi/quadriplegia, dysarthria, locked-in syndrome, coma

Which vascular territory affected?

A

Proximal basilar artery (usually thrombosis)

484
Q

Somnolence, memory and behaviour abnormalities, oculomotor deficit

Which vascular territory affected?

A

Distal basilar artery (usually emoblic)

485
Q

Lateral medullary syndrome

A

Ipsilateral

  • ataxia
  • Horner’s
  • facial sensory loss

Contralateral
- limb impairment of pain temperature, sensation

Nystagmus
N&V
Dysphagia, dysarthria
Hiccups

486
Q

Contralateral hemiparesis that is facial sparing, contralateral impaired proprioception and vibration sensation, ipsilateral tongue weakness

Which vascular territory affected?

A

Medial medullary infarct (anterior spinal artery assoc w anterior cord infarct also)

487
Q

What would you see with lacunar infarcts?

A
  1. Pure motor hemiparesis (posterior limb of internal capsule): contralateral arm, leg,
    and face
  2. Pure sensory loss (ventral thalamic): hemisensory loss
  3. Ataxic hemiparesis (ventral pons or internal capsule): ipsilateral ataxia and leg
    paresis
  4. Dysarthria-clumsy hand syndrome (ventral pons or genu of internal capsule):
    dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness
488
Q

Skull fracture → rapid arterial bleed → lucid interval → LoC

A

Extradural haemorrhage

489
Q

History of minor trauma → damaged bridging veins with slow
venous bleed → fluctuating
consciousness

A

Subdural haemorrhage

490
Q

Which artery is commonly affected in extradural haemorrhages?

A

Middle meningeal artery (superficial)

491
Q

Who’s at risk of subdural haemorrhages?

A

Elderly
Alcoholics
Associated w brain atrophy

492
Q

When does subacute sclerosing panencephalitis occur?

A

Post-measles infection

493
Q

Most common form of adult brain tumour

A

Metastatic lesions

- come from lung, breast, malignant melanoma

494
Q

Primary brain tumour in pt with neurofibromatosis type II

A

Meningioma

495
Q

Primary brain tumour affecting the ventricles and causing hydrocephalus

A

Ependymoma

496
Q

Primary brain tumour presenting in a child with an indolent presentation

A

Pilocytic astrocytoma

497
Q

Primary brain tumour that is soft, gelatinous, and calcified

A

Oligodendroma

498
Q

Most common types of nervous system tumours

A

Astrocytomas
Meningiomas
Pituitary adenomas
Metastatic tumours (small cell, breast)

499
Q

Tumours seen in Von Hippel-Lindau syndrome

A 
Haemangioblastoma of cerebellum
Brainstem and spinal cord
Retina
Renal cysts
Phaeochromocytomas
500
Q

Tumours seen in tuberous sclerosis

A

Giant cell astrocytoma
Cortical tuber
Supependymal nodules
Calcifications on CT

501
Q

Tumours seen in neurofibromatosis type I

A

Optic glioma

Neurofibroma astrocytoma

502
Q

Tumours seen in neurofibromatosis type II

A

Vestibular schwannoma
Meningioma
Ependymoma
Astrocytoma

503
Q

Tumours seen in multiple endocrine neoplasia type I affecting the CNS

A

Pituitary adenoma

Year 5 Pathology (6 decks)

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