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Path Laz (condensed) > Histopath > Flashcards

Histopath Flashcards

1
Q

Describe the appearance of neutrophils.

A

Multilobed nuclei with lots of granules

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2
Q

In what states might you see an abundance of lymphocytes?

A

Chronic inflammation

Lymphoma

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3
Q

Describe the appearance of eosinophils.

A

Bi-lobed nucleus with red granules

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4
Q

List three conditions that could cause an eosinophilia.

A

Allergic reactions

Parasitic infections

Hodgkin’s lymphoma

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5
Q

Describe the appearance of the oesophagus in eosinophilic oesophagitis.

A

Horizontal striae are seen within the oesophagus (feline oesophagus)

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6
Q

Describe the appearance of mast cells.

A

Large cells containing a lot of granules

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7
Q

Describe the appearance of macrophages.

A

Large cells with lots of cytoplasm

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8
Q

In what states do macrophages tend to appear?

A

Late acute inflammation (macrophages clear up the debris)

Chronic inflammation (become secretory rather than phagocytic)

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9
Q

Define granuloma.

A

Organised collection of activated macrophages

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10
Q

Describe the appearance of macrophages in granulomas.

A

Epithelioid macrophages – they have a lot of cytoplasm making them look like epithelial cells

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11
Q

What cytological feature is suggestive of a good sputum sample?

A

Pigmented macrophages – this suggests that they have come from the alveoli

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12
Q

What do macrophages in granulomas fuse together to form?

A

Langerhans giant cells

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13
Q

List some causes of granulomas.

A

TB

Leprosy

Cat scratch fever

Fungal infections

Sarcoidosis

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14
Q

List three types of carcinoma.

A

Squamous cell carcinoma

Adenocarcinoma

Transitional cell carcinoma

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15
Q

What are two key features of squamous cell carcinomas?

A

Keratin production

Intercellular bridges

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16
Q

What are two key features of adenocarcinomas?

A

Mucin production

Glands

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17
Q

Which stain is used for melanin?

A

Fontana stain

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18
Q

Which stain is used for iron?

A

Prussian blue

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19
Q

Which stain is used for amyloid?

A

Congo Red

When viewed under polarised light, it produces apple green birefringence

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20
Q

What is a key immunological lymphoid marker?

A

CD45

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21
Q

What is a classic histological feature of HSV infection?

A

Cells with multiple nuclei

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22
Q

Outline some presenting features of neoplastic bone disease.

A

Pain

Swelling

Deformity

Fracture

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23
Q

What type of biopsy is often used for diagnosing neoplastic bone disease?

A

Needle biopsy using a Jamshidi needle under CT or US guidance

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24
Q

List some tumour-like conditions of the bone.

A

Fibrous dysplasia

Metaphyseal fibrous cortical defect/non-ossifying fibroma

Reparative giant cell granuloma

Ossifying fibroma

Simple bone cyst

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25
Q

What is fibrous dysplasia?

A

Condition in which fibrous tissue develops in place of normal bone tissue

Can occur in any bone but ribs and proximal femur is most common

Tends to affect patients < 30 years

Causes soap bubble osteolysis on X-ray

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26
Q

Which eponymous syndrome is characterised by polyostotic fibrous dysplasia?

A

McCune Albright Syndrome – polyostotic fibrous dysplasia + endocrine problems + rough border café-au-lait spots

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27
Q

Describe the histological appearance of fibrous dysplasia.

A

The marrow is replaced by fibrous stroma with rounded trabecular bone (‘Chinese letters’)

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28
Q

Describe the X-ray appearance of fibrous dysplasia of the femoral head.

A

Shepherd’s crook

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29
Q

List three types of cartilaginous benign bone tumour.

A

Osteochondroma

Enchondroma

Chondroblastoma

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30
Q

List three types of bone-forming benign bone tumour.

A

Osteoid osteoma

Osteoma

Osteoblastoma

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31
Q

What are osteochondromas and which bones tend to be affected?

A

A benign overgrowth of cartilage and bone that tends to happen at the ends of long bones

They mimic normal tubular bone as they have a cartilaginous surface overlying normal trabecular bone

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32
Q

What is an enchondroma and which bones tend to be affected?

A

A cartilaginous proliferation within the bone

Most tend to be found in the hands and can cause pathological fractures

X-ray may show popcorn calcification

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33
Q

What are two macroscopic features of benign bone tumours?

A

Well demarcated

May erode through the cortex of bone but does not burst through the cartilaginous surface

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34
Q

What are giant cell tumours? Where do they tend to be found and what is their histological appearance?

A

Benign tumour of the bone characterised by the presence of lots of osteoclasts (giant cells)

They tend to be found at the ends of long bones

It has a lytic appearance on X-ray

Histology shows many osteoclasts on a background of spindle/ovoid cells

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35
Q

What is the most common type of malignant bone tumour?

A

Metastases

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36
Q

Which cancers in adults tend to spread to the bone?

A

Breast

Prostate

Lung

Kidney

Thyroid

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37
Q

Which cancers in children tend to spread to the bone?

A

Neuroblastoma

Wilm’s tumour

Osteosarcoma

Ewing’s sarcoma

Rhabdomyosarcoma

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38
Q

List three types of malignant bone tumour.

A

Osteosarcoma

Chondrosarcoma

Ewing’s sarcoma/PNET

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39
Q

What is an osteosarcoma?

A

Malignant bone-forming tumour of the bone that mainly occurs at the ends of long bones

Tends to occur at age 10-30 years

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40
Q

Describe the X-ray appearance of osteosarcoma.

A

Usually metaphyseal

Lytic

Elevated periosteum (Codman’s triangle)

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41
Q

Describe the histological appearance of osteosarcoma.

A

There are lots of malignant mesenchymal cells with or without bone and cartilage formation

NOTE: this can be stained for using ALP

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42
Q

How can osteosarcoma be classified?

A

Site within the bone (intramedullary, intracortical, surface)

Degree of differentiation

Multicentricity

Primary or secondary

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43
Q

What is a chondrosarcoma?

A

Malignant cartilage producing tumour

Tends to occur in patients aged > 40 years

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44
Q

Describe the X-ray appearance of chondrosarcoma.

A

Lytic with fluffy calcification

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45
Q

List the histological subtypes of chondrosarcoma.

A

Conventional (myxoid or hyaline)

Clear cell (low grade)

Dedifferentiated (high grade)

Mesenchymal

NOTE: myxoid = composed of clear, mucoid substance

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46
Q

What is an Ewing’s sarcoma?

A

Highly malignant small round cell tumour

Occurs in people < 20 years old

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47
Q

Describe the X-ray appearance of Ewing’s sarcoma.

A

Onion skinning of the periosteum

Lytic with or without sclerosis

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48
Q

Describe the histological appearance of Ewing’s sarcoma.

A

Sheets of small round cells

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49
Q

Which genetic abnormality is associated with Ewing’s sarcoma?

A

Chromosomal translocation 11:22 (EWSR1/FLI1) (q24:q12)

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50
Q

List three types of soft tissue tumour.

A

Liposarcoma

Spindle cell sarcoma

Pleomorphic sarcoma

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51
Q

Outline the coding used by cytopathologists when assessing breast aspirates.

A

C1 = inadequate

C2 = benign

C3 = atypia, probably benign

C4 = suspicious of malignancy

C5 = malignant

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52
Q

Define duct ectasia. Describe its presentation.

A

Inflammation and dilatation of large breast ducts

Typically presents with a breast lump and nipple discharge

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53
Q

Describe the histology of duct ectasia.

A

The duct will be distended and full of proteinaceous material

Foamy macrophages will also be present

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54
Q

Which organism is usually responsible for acute mastitis?

A

Staphylococci

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55
Q

Describe the cytological appearance of acute mastitis.

A

Lots of neutrophils

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56
Q

Describe the cytological appearance of fat necrosis.

A

Fat cells surrounded by macrophages

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57
Q

Define fibrocystic disease.

A

A group of alterations in the breast which reflect normal, albeit exaggerated, responses to hormonal influences

On histology, the ducts are usually dilated and calcified

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58
Q

Define fibroadenoma.

A

Benign fibroepithelial neoplasm of the breast

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59
Q

Describe the histology of fibroadenoma.

A

Consists of lots of glandular and stromal cells

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60
Q

Define Phyllodes tumour.

A

A group of potentially aggressive fibroepithelial neoplasms of the breast.

NOTE: the majority are benign

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61
Q

Describe the histology of Phyllodes tumours.

A

Cells do not form uniform layers

Whether it is benign or malignant depends on the cellularity of the stroma

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62
Q

Define intraductal papilloma.

A

A benign papillary tumour arising within the duct system of the breast

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63
Q

What are the two different types of intraductal papilloma

A

Peripheral papilloma – arises in small terminal ductules

Central papilloma – arises in large lactiferous ductules

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64
Q

Describe the histology of intraductal papillomas.

A

Histology will show a large dilated duct with a polypoid mass in the middle

The mass tends to have a fibrovascular core

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65
Q

What is a radial scar?

A

A benign sclerosing lesion characterised by a central zone of scarring surrounded by a radiating zone of proliferating glandular tissue

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66
Q

How do radial scars present?

A

Seen as stellate masses on mammograms

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67
Q

Describe the histological appearance of radial scars.

A

Central stellate area with proliferation of ducts and acini in the periphery

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68
Q

Describe the appearance of usual epithelial hyperplasia.

A

Irregular lumens

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69
Q

What is flat epithelial atypia/atypical ductal hyperplasia?

A

May be the earliest precursor to low grade DCIS

There are multiple layers of epithelial cells and the lumens become more regular

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70
Q

List some risk factors for invasive breast carcinoma.

A

Early menarche

Late menopause

Obesity

Alcohol

OCP

Family history

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71
Q

Which histological grading system is used for invasive breast carcinoma?

A

Nottingham modification of the Bloom-Richardson system

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72
Q

What is histological grading dependent on?

A

Tubule formation

Nuclear pleomorphism

Mitotic activity

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73
Q

Which three receptors are all invasive breast cancers assessed for?

A

ER

PR

Her2

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74
Q

Describe the receptor phenotype of Low grade invasive breast cancer

A

ER/PR positive

Her2 negative

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75
Q

Describe the receptor phenotype of High grade invasive breast cancer

A

ER/PR negative

Her2 positive

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76
Q

Describe the receptor phenotype of Basal-like carcinoma

A

Triple negative

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77
Q

What is the most important prognostic factor in invasive breast cancer?

A

Status of axillary lymph nodes

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78
Q

Which age group is screened in the NHS breast screening programme?

A

47-73 year olds (every 3 years)

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79
Q

Describe the histology of gynaecomastia.

A

Epithelial hyperplasia with finger-like projections extending into the duct lumen

Periductal stroma is often cellular and oedematous

Similar to fibroadenoma

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80
Q

What types of cell are the anterior and posterior pituitary made up of?

A

Anterior = epithelial cells

Posterior = nerve cells

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81
Q

What is the blood supply to the anterior pituitary?

A

Pituitary portal system

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82
Q

Where do the nerves that make up the posterior pituitary originate?

A

Supraoptic nucleus and paraventricular nucleus

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83
Q

Outline the clinical features of prolactinoma.

A

Amenorrhoea

Galactorrhoea

Loss of libido

Infertility

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84
Q

What disease is caused by corticotroph cell adenomas?

A

Cushing’s disease

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85
Q

List some causes of hypopituitarism.

A

Non-secreting pituitary adenoma

Ischaemia

Iatrogenic (e.g. surgery, radiotherapy)

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86
Q

List some clinical features of hypopituitarism.

A

Pituitary dwarfism

Gonadotrophin deficiency – amenorrhoea, infertility, impotence, loss of libido

Hypothyroidism and Hypoadrenalism

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87
Q

Which hormones are produced by the posterior pituitary?

A

ADH and oxytocin

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88
Q

List some consequences of the local mass effect of pituitary tumours.

A

Bitemporal hemianopia (optic chiasm)

Headaches (raised ICP)

Obstructive hydrocephalus

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89
Q

Describe the histological appearance of the thyroid gland.

A

Arranged into follicles with a small amount of stromal tissue between them

They are lined by epithelial cells and have a large amount of colloid in the middle

Parafollicular cells are found between the follicles

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90
Q

Which hormone do parafollicular cells produce?

A

Calcitonin – this promotes the absorption of calcium by the skeletal system

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91
Q

What is the most common cause of non-toxic goitre?

A

Iodine deficiency

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92
Q

List some causes of thyrotoxicosis that are not associated with the thyroid gland.

A

Struma ovarii – ovarian teratoma with ectopic thyroid hormone production

Factitious thyrotoxicosis – exogenous thyroid hormone intake

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93
Q

List some primary causes of hypothyroidism.

A

Post-ablative

Autoimmune (Hashimoto’s)

Iodine deficiency

Congenital biosynthetic defect

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94
Q

Describe the histology of Hashimoto’s thyroiditis.

A

There are lots of lymphoid cells with germinal centres

The epithelial cells become large with lots of eosinophilic cytoplasm (Hurthle cells)

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95
Q

List some features of a thyroid lump that would be suggestive of neoplasia.

A

Solitary rather than multiple

Solid rather than cystic

Younger patients

Male more than female

Less likely to take up radioiodine

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96
Q

List some features of adenomas of the thyroid gland.

A

Usually solitary

Well circumscribed

Well-formed capsule

Small proportion will be functional

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97
Q

List the four types of thyroid cancer in order of decreasing prevalence.

A

Papillary (80%)

Follicular (15%)

Medullary (5%)

Anaplastic

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98
Q

What is the diagnosis of papillary thyroid cancer based on?

A

Nuclear features

· Optically clear nuclei

· Intranuclear inclusions (Orphan Annie eye)

There may also be psammoma bodies (little foci of calcification)

Usually non-functional

On histology, they have a papillary structure (central connective tissue stalk with surrounding epithelium)

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99
Q

Where does papillary thyroid cancer tend to metastasise to?

A

Cervical lymph nodes

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100
Q

Where does follicular thyroid cancer tend to metastasise?

A

Lungs, bone and liver (via the bloodstream)

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101
Q

Which cells are medullary thyroid cancers derived from?

A

Parafollicular C cells

NOTE: 80% are sporadic, 20% are familial

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102
Q

What tends to happen to the calcitonin produced by tumour cells in medullary thyroid cancer?

A

It is broken down and deposited as amyloid within the thyroid

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103
Q

List the actions of PTH.

A

Activates osteoclasts

Increased renal absorption of calcium

Increases activation of vitamin D

Increases urinary phosphate excretion

Increases intestinal calcium absorption

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104
Q

Describe the histological appearance of a parathyroid adenoma.

A

Very cellular tissue with no fat (whereas the normal parathyroid gland is quite fatty)

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105
Q

What bone change is seen in hyperparathyroidism?

A

Osteitis fibrosa cystica – caused by bone resorption with thinning of the cortex

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106
Q

What is the most common cause of secondary hyperparathyroidism?

A

Renal failure

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107
Q

List some clinical features of hypoparathyroidism.

A

Neuromuscular irritability

Cardiac arrhythmias

Fits

Cataracts

(CATs go NUMB)

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108
Q

Which cells types constitute the cortex and medulla of the adrenal gland?

A

Cortex = epithelial

Medulla = neural

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109
Q

What are the layers of the adrenal cortex and which hormones do they produce?

A

Glomerulosa – aldosterone

Fasciculata – glucocorticoids

Reticularis – sex steroids

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110
Q

What is the most common cause of Cushing’s syndrome?

A

Administration of exogenous corticosteroids (leads to adrenal atrophy)

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111
Q

What are the causes of hyperaldosteronism?

A

35% adenoma (Conn’s syndrome)

60% bilateral adrenal hyperplasia

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112
Q

List the two main clinical features of hyperaldosteronism.

A

Hypertension

Hypokalaemia

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113
Q

Describe the pathophysiology of congenital adrenal hyperplasia.

A

Autosomal recessive

Hereditary defect in an enzyme involved in cortisol synthesis leads to cortisol deficiency

This leads to increased ACTH release from the pituitary gland

ACTH stimulates androgen synthesis from the adrenal gland

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114
Q

List three causes of acute primary adrenal failure.

A

Haemorrhage

DIC associated with sepsis (Waterhouse-Friderichson syndrome)

Sudden withdrawal of corticosteroid treatment

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115
Q

List some causes of chronic primary adrenal failure.

A

Autoimmune (90%)

TB

HIV

Metastatic tumour

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116
Q

What are the two types of tumours of the adrenal medulla?

A

Phaeochromocytoma

Neuroblastoma

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117
Q

What are the main features of SLE?

A

Serositis

Oral ulcers

ANA

Photosensitivity

Bloods (low counts)

Renal (proteinuria)

Arthritis

Immunological (anti-dsDNA)

Neurological (psychiatric, seizures)

Malar rash

Discoid rash

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118
Q

List three autoantibodies found in SLE. Which is most specific?

A

Anti-dsDNA

Anti-smith (against ribonucleoproteins) – most specific but low sensitivity

Anti-histone – drug-related (e.g. hydralazine)

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119
Q

Describe the appearance of skin histology in SLE.

A

Lymphocytic infiltration of the dermis

Vacuolisation (dissolution of the cells) of the basal epidermis

Extravasation of blood causes a rash

Immunofluorescence will show immune complex deposition at the epidermis-dermis junction

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120
Q

Describe the appearance of renal histology in SLE.

A

Glomerular capillaries are thickened (wire-loop capillaries) due to immune complex deposition

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121
Q

What is the name of non-infective endocarditis associated with SLE?

A

Libman-Sacks endocarditis

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122
Q

What is scleroderma?

A

A condition characterised by excess collagen in the skin and fibrosis

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123
Q

What are the two types of scleroderma? Name the antibodies that they are associated with.

A

Diffuse – involves the trunk (anti-Scl70 antibodies (aka anti-topoisomerase))

Limited – only affects distal to the elbows and knees (anti-centromere)

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124
Q

What are the main features of limited cutaneous systemic sclerosis?

A

Calcinosis

Raynaud’s phenomenon

Oesophageal dysmotility

Sclerodactyly

Telangiectasia

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125
Q

Describe the vascular histology in scleroderma.

A

Intimal proliferation gives an onion skin appearance

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126
Q

What is a major consequence of this vascular change (in scleroderma)?

A

Renal hypertensive crisis

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127
Q

What pattern of ANA immunofluorescence is seen in scleroderma?

A

Nucleolar

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128
Q

What ANA immunofluorescence pattern is seen in mixed connective tissue disease?

A

Speckled

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129
Q

What is dermatomyositis?

A

A condition characterised by proximal muscle pain and weakness, high CK and skin changes (e.g. Gottron’s papules – purple rash across the knuckles)

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130
Q

List some features of sarcoidosis.

A

Arthritis

Lupus pernio

Erythema nodosum

Bilateral hilar lymphadenopathy

Pulmonary fibrosis

Lymphadenopathy

Inflammation of layers of the heart

Uveitis

Meningitis

Hepatitis, cirrhosis

Bilateral parotid enlargement

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131
Q

What is the pathological hallmark of sarcoidosis?

A

Non-caseating granuloma

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132
Q

Which investigations are useful in sarcoidosis?

A

Hypergammaglobulinaemia

High ACE

Hypercalcaemia (due to activation of vitamin D by macrophages)

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133
Q

What is polyarteritis nodosa? What are its main features?

A

A necrotising arteritis which is focal and sharply demarcated

It heals by fibrosis and mainly affects the renal and mesenteric vessels

May present with gut ischaemia or renal impairment

It produces a rosary beads appearance on angiography due to multiple aneurysms

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134
Q

Which condition is polyarteritis nodosa associated with?

A

Hepatitis B

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135
Q

What is a characteristic feature of vasculitis?

A

Palpable purpuric rash

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136
Q

How is temporal arteritis diagnosed and treated?

A

High ESR

High dose prednisolone

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137
Q

What will be seen on temporal artery biopsy in temporal arteritis?

A

Lymphocytic infiltration of the tunica media

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138
Q

What are the main features of granulomatosis with polyangiitis?

A

ENT – nosebleeds, sinusitis, saddle nose

Lungs – haemoptysis, SOB

Kidneys – haematuria

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139
Q

Which antibody is associated with granulomatosis with polyangiitis?

A

cANCA – against proteinase 3

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140
Q

What are the main features of Churg-Strauss syndrome?

A

Asthma

Eosinophilia

Vasculitis

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141
Q

Which antibody is associated with Churg-Strauss syndrome?

A

pANCA – against myeloperoxidase

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142
Q

What feature of high-risk HPV viruses are responsible for the carcinogenic effects of HPV?

A

E6 protein – inactivates p53

E7 protein – inactivates retinoblastoma

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143
Q

In which type of epithelium does CIN occur?

A

Usually squamous

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144
Q

Which staging system is used for cervical cancer?

A

FIGO staging

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145
Q

What are the two HPV vaccines that are currently available?

A

Bivalent = 16 + 18

Quadrivalent = 6 + 11 + 16 + 18

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146
Q

What is a leiomyoma? Outline its key features.

A

A benign smooth muscle cell tumour in the uterus (MOST COMMON uterine tumour)

Present in > 20% of women > 35 years

Often multiple

Usually asymptomatic

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147
Q

What are the three types of leiomyoma?

A

Intramural

Submucosal

Subserosal

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148
Q

What are the key features of type I endometrial carcinoma?

A

Younger patients

Oestrogen-dependent

Often associated with atypical endometrial hyperplasia

Low-grade tumours that are superficially invasive

Genetic mutations: PTEN, P13KCA, K-Ras, CTNNB1, FGFR2, p53

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149
Q

What are the key features of type II endometrial carcinoma?

A

Older patients

Less oestrogen-dependent

Arise in atrophic endometrium

High grade, deeper invasion and higher stage

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150
Q

Which genetic mutations are associated with the two types of type II endometrial carcinoma?

A

Endometrial Serous Carcinoma

· P53 (90%)

· P13KCA (15%) Her2 amplification

Clear Cell Carcinoma

· PTEN

· CTNNB1

· Her2 amplification

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151
Q

List some prognostic factors in endometrial carcinoma.

A

Type

Grade

Stage

Tumour ploidy (diploid has a better prognosis)

Hormone receptor expression

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152
Q

What is choriocarcinoma?

A

Rare (1 in 20,000) rapidly invasive and widely metastasising tumour

Responds well to chemotherapy

50% arise in moles

25% arise in patients with previous abortion

22% arise in normal pregnancy

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153
Q

List two types of non-neoplastic functional cysts.

A

Follicular and luteal cysts

Endometriotic cyst

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154
Q

List three types of primary specific ovarian tumour.

A

Surface epithelial tumours

Sex cord stromal tumours

Germ cell tumours

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155
Q

List some risk factors for ovarian cancer.

A

Nulliparity

Early menarche

Late menopause

Genetic predisposition (MOST SIGNIFICANT)

Infertility

Endometriosis

HRT

Inflammation (PID)

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156
Q

Outline the classification of epithelial ovarian tumours.

A

Type 1

· Low grade

· Relatively indolent and arise from well characterised precursors (benign tumours) and endometriosis

· Mutations: K-Ras, B

Type 2

· HIGH GRADE

· Aggressive

· P53 mutation in 75% of cases

· NO precursor lesion

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157
Q

List some benign ovarian tumours.

A

Serous cystadenoma

Cystadenofibroma

Mucinous cystadenoma

Brenner tumour

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158
Q

What are the key features of serous tumours?

A

MOST COMMON type of ovarian tumour

Usually cystic

30-50% bilateral

Benign tumours are lined by bland epithelium

Borderline tumours have a more complex, atypical epithelial lining with papillae but no invasion through the basement membrane

Malignant tumours are invasive with a poor prognosis

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159
Q

What are the key features of mucinous tumours?

A

10-20% of ovarian tumours

Composed of mucin-secreting epithelium (may resemble endocervical or GI epithelium)

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160
Q

What are the key features of endometrioid tumours?

A

10-24% of ovarian tumours

10-20% associated with endometriosis

Better prognosis than mucinous and serous

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161
Q

What are the key features of clear cell tumours?

A

Strong association with endometriosis

NOTE: called clear cell because the cytoplasm contains a lot of glycogen

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162
Q

List four types of sex cord stromal tumours.

A

Fibroma

Granulosa cell tumour (may produce oestrogen)

Thecoma (may produce oestrogen (rarely androgens))

Sertoli-Leydig cell tumour (may be androgenic)

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163
Q

What are the key features of germ cell tumours?

A

20% of ovarian tumours

95% are benign

Mainly occur in < 20 years

Classified based on how they differentiate

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164
Q

What are the four main types of germ cell tumour?

A

Dysgerminoma – no differentiation

Teratoma – from embryonic tissues

Endodermal sinus tumour – from extraembryonic tissue (e.g. yolk sac)

Choriocarcinoma – from trophoblastic cells which would form the placenta

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165
Q

What are the key features of an immature teratoma?

A

Indicates presence of embryonic elements (most commonly neural tissue)

Malignant tumour that grows rapidly, penetrates the capsule and forms adhesions

Spreads within peritoneal cavity and metastasises to the lymph nodes, lungs, liver and other organs

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166
Q

Name two secondary ovarian tumours.

A

Krukenberg Tumour – bilateral metastases composed of mucin-producing signet ring cells (usually from breast or gastric cancer)

Metastatic colorectal cancer

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167
Q

List some specific genetic associations for serous, mucinous and endometrioid carcinoma.

A

Serous – BRCA

Mucinous and endometrioid - HNPCC

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168
Q

What is lichen sclerosus?

A

Thinning of the vulval epithelium with a layer of hyalinisation underneath

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169
Q

List some other types of malignant tumour of the vulva.

A

Squamous cell carcinoma (85%)

Paget’s disease (adenocarcinoma in situ)

Adenocarcinoma

Malignant melanoma

BCC

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170
Q

What are the most common sites for atheromatous plaques within the coronary circulation?

A

First few centimetres of the LAD and left circumflex

Entire length of right coronary artery

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171
Q

Which arteries tend to be involved in myocardial infarction (in order of most to least frequent)?

A

LAD – 50%

RCA – 40%

LCx – 10%

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172
Q

List some causes of aortic regurgitation.

A

Rigidity (rheumatic, degenerative)

Destruction (endocarditis)

Disease of the aortic valve ring (dilatation, dissection, Marfan’s, syphilis, ankylosing spondylitis)

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173
Q

Which valves are most commonly affected by endocarditis?

A

Left-sided valves (unless you are an IVDU)

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174
Q

What is the role of stellate cells and what could happen to them when activated?

A

Storage of vitamin A

When activated, they become myofibroblasts that lay down collagen (this is responsible for scarring in liver disease)

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175
Q

Describe how these arrangements change in liver disease.

A

Kupffer cells become activated (inflammatory response)

Endothelial cells stick together so blood finds it more difficult to get into the space of Disse

Stellate cells become activated and secrete basement membrane-type collagens into the space of Disse

Hepatocytes lose their microvilli

All these changes make it difficult for blood to be exposed to hepatocytes

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176
Q

List some complications of cirrhosis.

A

Portal hypertension

Hepatic encephalopathy

Hepatocellular carcinoma

NOTE: cirrhosis may be reversible

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177
Q

What is a common histological feature of all acute hepatitis?

A

Spotty necrosis

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178
Q

List some histological features of alcohol hepatitis.

A

Ballooning – cell swell and may contain pink deposits within cells (Mallory Denk bodies/Mallory hyaline)

Apoptosis

Pericellular fibrosis

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179
Q

In which part of the liver do the histological features of alcoholic hepatitis tend to be seen and why?

A

Zone 3

Alcohol is not toxic, but acetaldehyde is toxic

Zone 3 cells contain the most alcohol dehydrogenase thereby producing the most acetaldehyde

Furthermore, by the time blood reaches zone 3 (after passing zones 1 and 2) it is relatively hypoxic making the cells in zone 3 even more vulnerable to damage

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180
Q

Describe the histological appearance of non-alcoholic fatty liver disease.

A

Looks like alcoholic hepatitis

NOTE: caused by insulin resistance associated with a raised BMI and diabetes

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181
Q

What is primary biliary cholangitis?

A

Autoimmune conditions characterised by bile duct loss associated with chronic inflammation (with granulomas)

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182
Q

What is the diagnostic test for PBC?

A

Anti-mitochondrial antibodies (AMA)

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183
Q

What is the histological appearance of PBC?

A

Bile ducts surrounded by epithelioid macrophages, suggestive of chronic granulomatous destruction of bile ducts

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184
Q

What is primary sclerosing cholangitis?

A

Autoimmune condition characterised by periductal bile duct fibrosis leading to loss of bile ducts

NOTE: in PBC, bile duct loss is caused by inflammation, whereas in PSC it is caused by fibrosis

NOTE: PSC is associated with ulcerative colitis and is associated with an increased risk of cholangiocarcinoma

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185
Q

What is the diagnostic test for PSC?

A

Bile duct imaging

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186
Q

What causes haemochromatosis and which gene is implicated?

A

Caused by increased gut iron absorption

HFe gene on chromosome 6

NOTE: women tend to present later because they have naturally lower iron levels

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187
Q

What is haemosiderosis?

A

Type of iron overload characterised by the accumulation of iron in macrophages

Usually occurs as a result of receiving blood transfusions

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188
Q

How does Wilson’s disease lead to movement disorders?

A

Accumulation of copper in the lentiform nucleus of the basal ganglia leads to movement disorders

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189
Q

How is autoimmune hepatitis diagnosed?

A

Anti-smooth muscle antibodies (ASMA)

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190
Q

How is autoimmune hepatitis treated?

A

Steroids (usually responds well)

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191
Q

Describe the levels of alpha-1 antitrypsin in the blood and liver in a patient with alpha-1 antitrypsin deficiency.

A

The mutation means that the protein cannot fold properly and cannot exit hepatocytes

This leads to alpha-1 antitrypsin forming globules within hepatocytes which causes damage leading to chronic hepatitis

An inability to exit the liver leads to a deficiency of alpha-1 antitrypsin elsewhere in the body which leads to an increased risk of emphysema

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192
Q

List some causes of hepatic granulomas.

A

Specific: PBC, drugs

General: TB, sarcoidosis

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193
Q

List the main types of benign liver tumour. State which is most common.

A

Liver cell adenoma

Bile duct adenoma

Haemangioma (MOST COMMON)

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194
Q

What is the most common type of malignant liver tumour?

A

Secondary tumours

195
Q

What are some risk factors for cholangiocarcinoma?

A

PSC

Worm infections

Cirrhosis

196
Q

Describe the three main patterns of injury in acute pancreatitis and describe what they result from.

A

Periductal – necrosis of acinar cells near ducts (usually secondary to obstruction)

Perilobular – necrosis at the edges of the lobules (usually due to poor blood supply)

Panlobular – results from worsening periductal or perilobular inflammation

197
Q

Outline the pathway of inflammation in acute pancreatitis.

A

Activated enzymes à acinar necrosis à release of more enzymes

198
Q

What is saponification?

A

Lipases break down fats to release free fatty acids

Calcium binds to the free fatty acids forming soaps

199
Q

List some complications of acute pancreatitis.

A

Pseudocyst formation, abscesses

Shock

Hypoglycaemia

Hypocalcaemia

200
Q

List some causes of chronic pancreatitis.

A

Metabolic/Toxic: alcohol (80%), haemochromatosis

Duct obstruction: gallstones, abnormal anatomy, cystic fibrosis (mucoviscoidosis)

Tumours

Idiopathic

201
Q

Outline the pattern of injury in chronic pancreatitis.

A

Chronic inflammation with parenchymal fibrosis and loss of parenchyma

There will be duct strictures with calcified stones with secondary dilatations

202
Q

What is the characteristic feature of autoimmune pancreatitis?

A

Large numbers of IgG4 positive plasma cells typically found around the ducts

203
Q

How is autoimmune pancreatitis treated?

A

Steroids – usually responds well

204
Q

What are the two types of pancreatic cancer and which is more common?

A

Ductal (85%)

Acinar (15%)

205
Q

Name two types of dysplastic precursor lesion that ductal carcinoma can arise from.

A

Pancreatic intraductal neoplasia (PanIN)

Intraductal mucinous papillary neoplasm

206
Q

Which mutation is very common in pancreatic cancer?

A

K-ras (95%)

207
Q

Describe the macroscopic appearance of ductal carcinoma?

A

Gritty and grey

Invades adjacent structures

NOTE: tumours in the head of the pancreas present earlier

208
Q

Describe the microscopic appearance of ductal carcinoma.

A

Adenocarcinomas (secrete mucin and form glands)

Mucin-secreting glands are set in desmoplastic stroma

209
Q

What are the usual sites of metastasis of ductal carcinoma?

A

Direct: bile ducts, duodenum

Lymph nodes

Blood: liver

Serosa: peritoneum

210
Q

By what mechanism does pancreatic cancer cause migratory thrombophlebitis?

A

Circulating pancreatic cancer cells release mucous which activates the clotting cascade

211
Q

List some key features of pancreatic neuroendocrine neoplasms.

A

Usually non-secretory

Contains neuroendocrine markers (e.g. chromogranin – can be measured as a screening test for neuroendocrine tumours)

May be associated with MEN1

212
Q

What is the most common type of functional neuroendocrine tumour?

A

Insulinoma

213
Q

What are the two types of gallstone and what are their distinguishing features?

A

Cholesterol

· May be single

· Mostly radiolucent (NOT seen on AXR)

Pigment

· Often multiple

· Contain calcium salts of unconjugated bilirubin

· Mostly radio-opaque

214
Q

What is the term used to describe diverticula of the gallbladder? How do they form?

A

Rokitansky-Aschoff sinuses – form as a result of the gallbladder contracting against an obstruction

215
Q

Outline the presentation of polycystic kidney disease.

A

Hypertension

Haematuria

Flank pain

216
Q

What is the inheritance pattern of polycystic kidney disease and which genes are implicated?

A

Autosomal dominant (most of the time)

Genes: PKD1 and PKD2

NOTE: PKD is associated with an increased risk of berry aneurysms (and subarachnoid haemorrhage)

217
Q

List some causes of acute renal failure.

A

Pre-renal: failure of perfusion (shock, heart failure)

Renal: ATN, acute glomerulonephritis, thrombotic microangiopathy

Post-renal: obstruction

218
Q

What is the most common cause of acute renal failure?

A

Acute tubular injury

219
Q

How does acute tubular injury lead to reduced GFR?

A

Blockage of tubules by casts

Leakage from tubules into interstitial space

Secondary haemodynamic changes

220
Q

Describe the histological appearance of acute tubulo-interstitial nephritis.

A

Heavy interstitial infiltration with eosinophils and granulomas

221
Q

What causes crescents to appear in acute glomerulonephritis?

A

Occurs in severe glomerulonephritis due to proliferation of cells within Bowman’s capsule

222
Q

List some causes of acute crescentic glomerulonephritis.

A

Immune complex deposition

Anti-GBM disease (Goodpasture’s)

Pauci-immune (ANCA)

NOTE: these can rapidly lead to irreversible renal failure

223
Q

List some causes of immune complex-associated crescentic glomerulonephritis.

A

SLE

IgA nephropathy

Post-infectious glomerulonephritis

224
Q

What are the antibodies directed against in anti-GBM disease?

A

Against the C-terminal domain of type IV collagen

NOTE: these antibodies can cross-react with the alveolar basement membrane leading to pulmonary haemorrhage and haemoptysis

225
Q

Describe the immunohistochemistry picture produced in anti-GBM disease.

A

Linear deposition of IgG on the glomerular basement membrane

226
Q

What is thrombotic microangiopathy?

A

Damage to the endothelium in glomeruli, arterioles and arteries resulting in thrombosis

Red cells can be damaged by fibrin causing MAHA or HUS

227
Q

List some causes of thrombotic microangiopathy.

A

Diarrhoea-associated: E.coli – toxins can target the renal epithelium

Non-diarrhoea associated: defects in complement regulation, deficiency of ADAMTS13, drugs, radiation, hypertension, scleroderma, antiphospholipid syndrome

228
Q

List some causes of nephrotic syndrome.

A

Primary glomerular disease (non-immune complex mediated)

· Minimal change disease

· Focal segmental glomerulosclerosis

Primary renal disease (immune complex mediated)

· Membranous glomerulonephritis

Systemic disease

· SLE

· Amyloidosis

· Diabetes mellitus

229
Q

What is minimal change disease?

A

Most common cause of nephrotic syndrome in children

Glomeruli look normal on light microscopy, but electron microscopy shows loss of foot processes

Generally responds well to steroids and immunosuppression

230
Q

Describe the histological appearance of focal segmental glomerulosclerosis.

A

Some glomeruli are partially scarred

NOTE: this responds less well to immunosuppression

231
Q

What is membranous glomerulonephritis?

A

Common cause of nephrotic syndrome in adults

Characterised by immune deposits outside the glomerular basement membrane (subepithelial)

Primary disease is autoimmune

It can occur secondary to epithelial malignancy, SLE, drugs and infections

232
Q

Which antibodies are often found in primary membranous glomerulonephritis?

A

Antibodies against phospholipase A2 type M receptor (PLA2R)

233
Q

List and describe the stages of diabetic nephropathy.

A

Stage 1: thickening of the basement membrane on electron microscopy

Stage 2: increase in mesangial matrix, without nodules

Stage 3: nodular lesions/Kimmelstein-Wilson nodules

Stage 4: advanced glomerulosclerosis

234
Q

What are the two types of amyloidosis?

A

AA – derived from serum amyloid protein and associated with chronic inflammatory disease

AL – derived from immunoglobulin light chains usually as a result of multiple myeloma

235
Q

Name two causes of isolated microscopy haematuria.

A

Thin basement membrane

IgA nephropathy

236
Q

How can the cause of asymptomatic proteinuria be confirmed?

A

Renal biopsy (could be caused by several abnormalities)

237
Q

What is thin basement membrane disease and what causes it?

A

Basement membrane < 250 nm thickness

Caused by a hereditary defect in type IV collagen synthesis

Microscopic haematuria is the only consequence in most cases

238
Q

What is Alport syndrome?

A

X-linked disease caused by a mutation in the alpha-5 subunit of type IV collagen (some forms affect alpha-3 and alpha-4)

Leads to progressive damage resulting in renal failure in middle-age

Often accompanied by deafness and ocular disease

239
Q

What is IgA nephropathy?

A

Most common cause of glomerulonephritis

Caused by mesangial IgA immune complex deposition

NOTE: Henoch-Schonlein purpura is a type of IgA nephropathy

30% will progress to end-stage renal failure

240
Q

What are consequences of hypertensive nephropathy?

A

Shrunken kidneys with granular cortices

Nephrosclerosis on histology (arterial hyalinosis, arterial intimal thickening, ischaemic glomerular changes, segmental and global glomerulosclerosis)

241
Q

What is a key histological feature of the oesophageal mucosa?

A

Presence of submucosal glands

242
Q

What is the Z-line?

A

The point in the oesophagus at which the epithelium transitions from being squamous to being columnar

243
Q

Which part of the stomach tends to be affected by H. pylori-associated gastritis?

A

Pylorus and antrum

244
Q

What are the three layers of the gastric mucosa?

A

Columnar epithelium

Lamina propria

Muscularis mucosa

245
Q

What is the normal villous: crypt ratio?

A

2:1

246
Q

What does the presence of goblet cells in the stomach signify?

A

Intestinal metaplasia

NOTE: goblet cells are NOT normally seen in the stomach

247
Q

What is the characteristic histological feature of acute oesophagitis?

A

Presence of lots of neutrophils

This is usually caused by GORD

248
Q

Define Barrett’s oesophagus.

A

Metaplastic process by which the normal squamous epithelium of the lower oesophagus is replaced by columnar epithelium

NOTE: this is also known as columnar-lined epithelium (CLO)

249
Q

What further degree of metaplasia is associated with an even greater risk of cancer than Barrett’s oesophagus?

A

Intestinal metaplasia – goblet cells become visible

NOTE: metaplasia is reversible

250
Q

What is squamous carcinoma of the oesophagus associated with?

A

Smoking and alcohol

It tends to affect the middle/lower oesophagus

It is the most common type of oesophageal cancer in Africa

251
Q

What are the main histological features of squamous cell carcinoma of the oesophagus?

A

Cells produce keratin (normal oesophageal squamous epithelium is non-keratinised)

Intercellular bridges

252
Q

What is mucosa-associated lymphoid tissue and what is their presence indicative of?

A

Chronic gastritis caused by H. pylori infection induces lymphoid tissue in the stomach

The presence of lymphoid follicles in a stomach biopsy, is highly suggestive of H. pylori infection

This is important because it is associated with an increased risk of lymphoma

253
Q

Name a key virulence factor that enables H. pylori to cause chronic infection.

A

Cag-A positive H. pylori has a needle-like appendage that injects toxins into intercellular junctions allowing bacteria to attach more easily

254
Q

What must you do with all gastric ulcers?

A

They should all be biopsied to rule out malignancy

255
Q

What type of cancer is gastric cancer?

A

95% adenocarcinoma

5%: squamous cell carcinoma, lymphoma (MALToma), gastrointestinal stromal tumour (GIST), neuroendocrine tumours

256
Q

Name two types of diffuse adenocarcinoma of the stomach.

A

Linitis plastica

Signet ring cell carcinoma

257
Q

What is the overall survival rate of gastric cancer?

A

15%

258
Q

What is gastric lymphoma?

A

Lymphoma of the gastric mucosa that is driven by chronic inflammation (H. pylori gastritis)

Consists of lots of B lymphocytes (marginal zone)

NOTE: if H. pylori is also present, crypts may also contain neutrophils

259
Q

What causes duodenitis and duodenal ulcers?

A

Caused by increased acid produced in the stomach that spills into the duodenum

It can also occur due to chronic inflammation and gastric metaplasia with H. pylori infection

260
Q

List some histological features of malabsorption.

A

Villous atrophy

Crypt hyperplasia

Increased intraepithelial lymphocytes (> 20 per 100 enterocytes)

NOTE: the T cell response to gliadin in Coeliac disease is responsible for the damage to villi

261
Q

What is lymphocytic duodenitis?

A

When you get the inflammatory changes (increased intraepithelial lymphocytes) without architectural changes

Many people with this condition either have coeliac disease or will go on to develop coeliac disease

262
Q

How is coeliac disease diagnosed?

A

Antibodies: anti-tTG, anti-endomysial

Duodenal biopsy

NOTE: duodenal biopsy will be normal in people with coeliac disease who have been following a strict gluten-free diet

263
Q

Which other condition has very similar clinical and histological features to coeliac disease?

A

Tropical sprue

264
Q

What type of lymphoma is duodenal lymphoma?

A

T cell lymphoma

265
Q

How is palmar-plantar skin different from skin in other parts of the body?

A

There are no sebaceous glands

There is a very thick corneal layer

266
Q

List some different types of inflammatory reactions patterns in the skin.

A

Vesiculobullous – forms bullae

Spongiotic – becomes oedematous

Psoriasiform – becomes thickened

Lichenoid – forms a sheeny plaque

Vasculitic – associated with vasculitis

Granulomatous – associated with granulomas

267
Q

What is bullous pemphigoid? Describe the macroscopic appearance.

A

Vesiculobullous condition

Occurs in elderly patients on their flexor surfaces

Characterised by the formation of tense bullae

NOTE: it has a 10-20% mortality

268
Q

Outline the pathophysiology of bullous pemphigoid.

A

Autoimmune disorder driven by IgG and C3 which attack the basement membrane

They recruit eosinophils which release elastase which further damages anchoring proteins (anchoring lower keratinocytes to the basement membrane)

269
Q

How can bullous pemphigoid be definitively diagnosed?

A

Immunofluorescence will show IgG and C3 along the dermo-epidermal junction

270
Q

Describe the macroscopic appearance of pemphigus vulgaris.

A

Blisters are flaccid meaning that they rupture easily exposing a red raw surface underneath

271
Q

Describe the macroscopic appearance of pemphigus foliaceus.

A

You rarely see intact bullae because they are so thin and fragile

You are likely to see some flaky remnants of old bullae

272
Q

Describe the appearance of discoid eczema.

A

Very itchy and found on the flexural surfaces

Presents with discoid plaques

273
Q

What is hyperparakeratosis?

A

Thickening of the skin on the surface where the patient has been scratching

The epidermis gets thicker

274
Q

What type of inflammatory skin reaction is eczema?

A

Spongiotic because there is oedema between the keratinocytes

275
Q

What are the main immune mediators in eczema?

A

T-cell mediated

Eosinophils are also recruited

276
Q

Describe the typical presentation of plaque psoriasis.

A

This is a psoriasiform reaction pattern

Tends to present as silvery plaques on the extensor surfaces

277
Q

How is the keratinocyte turnover time different in psoriasis compared to normal skin?

A

Normal skin turnover = 50 days (time for a keratinocyte to go from the bottom of the epidermis to the top)

Psoriasis = 7 days

This leads to thickening of the epidermis and you get a layer of parakeratosis at the top

278
Q

Which layer of the epidermis disappears in plaque psoriasis and why?

A

Stratum granulosum – there is not enough time to form it

279
Q

What can neutrophil recruitment to the epidermis in plaque psoriasis cause?

A

Formation of Munro’s microabscesses

280
Q

What is lichen planus and what are its main features?

A

Lichenoid reaction pattern

T-cell mediated

Presents with papules and plaques that are slightly purplish in colour on the wrists and arms

In the mouth it presents as white lines (Wickham striae)

281
Q

Describe the histological appearance of lichen planus.

A

Distinction between dermis and epidermis is difficult to see due to lymphocyte-mediated destruction of the bottom layer of keratinocytes

There is band-like lymphocytic infiltration just under the epidermis

NOTE: this is also seen in mycosis fungoides

282
Q

What type of inflammatory skin reaction results in pyoderma gangrenosum?

A

Vasculitic

283
Q

Describe the appearance of a sebaceous/epidermal cyst.

A

Smooth surface

Non-mobile

Tend to have a punctum

Can get infected/rupture

Can smell really bad

284
Q

Describe the histological appearance of a sebaceous cyst.

A

Looks like the surface has become invaginated to form a cyst

Lined by squamous epithelium

285
Q

Describe the macroscopic appearance of a basal cell carcinoma.

A

Rolled, pearly edge with a central ulcer and telangiectasia

286
Q

Describe the histological appearance of a basal cell carcinoma.

A

Cancer arises from the keratinocytes along the bottom of the epidermis (basal cells)

They can infiltrate through the basement membrane

They are locally infiltrative but don’t metastasise

287
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ

288
Q

List the three main types of urinary tract calculi in order of prevalence.

A

Calcium oxalate (Weddelite) – 75%

Magnesium ammonium phosphate – 15%

Urate – 5%

289
Q

List some underlying conditions that can lead to the formation of calcium oxalate stones.

A

Absorptive hypercalciuria – excessive calcium absorption from the gut

Renal hypercalciuria – impaired absorption of calcium in the proximal renal tubule

Hypercalcaemia (e.g. hyperparathyroidism)

290
Q

Which patients are predisposed to the formation of urate stones?

A

Gout

Rapid cell turnover (e.g. chemotherapy)

NOTE: however, most patients with urate stones will not have these risk factors

291
Q

Where do urinary calculi stones tend to get stuck within the urinary tract?

A

Pelvi-ureteric junction

Pelvic brim

Vesico-ureteric junction

292
Q

Define papillary adenoma.

A

Benign epithelial kidney tumour composed of papillae and/or tubules

They must be < 15 mm in size

They tend to be well circumscribed

293
Q

What are the genetic associations of papillary adenomas?

A

Trisomy 7 and 17

Loss of Y chromosome

294
Q

What is a renal oncocytoma?

A

Benign epithelial kidney tumour composed of oncocytic cells

They are usually well-circumscribed and usually sporadic

NOTE: often an incidental finding

295
Q

Name a syndrome that is associated with renal oncocytoma.

A

Birt-Hogg-Dubé syndrome

296
Q

Describe the histological appearance of oncocytes.

A

Large cells with pink granular cytoplasm and a prominent nucleolus

297
Q

What is an angiomyolipoma?

A

Benign mesenchymal kidney tumour composed of thick-walled blood vessels, smooth muscle and fat

Derived from perivascular epithelioid cells

NOTE: often an incidental finding but may cause flank pain, haemorrhage and shock (if > 4 cm)

298
Q

Which hereditary condition is associated with angiomyolipoma?

A

Tuberous sclerosis

299
Q

How does renal cell carcinoma tend to present?

A

Painless haematuria

300
Q

Name the subtypes of renal cell carcinoma in order of prevalence.

A

Clear cell renal carcinoma (70%)

Papillary renal cell carcinoma (15%)

Chromophobe renal cell carcinoma (5%)

301
Q

Define clear cell renal carcinoma.

A

Epithelial kidney tumour composed of nests of clear cells set in a delicate capillary vascular network

Grossly appears golden-yellow with haemorrhagic areas

302
Q

What is a common genetic finding in clear cell renal carcinoma?

A

Loss of chromosome 3p

303
Q

Define papillary renal cell carcinoma.

A

Epithelial kidney tumour composed of papillae and/or tubules

By definition > 15 mm in size

NOTE: this is the malignant counter part of papillary adenoma. They appear grossly as a fragile, friable brown tumour

304
Q

Describe the histological appearance of the two types of papillary renal cell carcinoma.

A

Type 1: composed of a single layer of small and flat cells. You see a lot of islands of cells.

Type 2: there is stratification (multi-layering) of the cells

NOTE: type 2 tends to have a worse prognosis than type 1

305
Q

Define chromophobe renal cell carcinoma.

A

Epithelial kidney tumour composed of sheets of large cells that display distinct cell borders, reticular cytoplasm and a thick-walled vascular network

NOTE: grossly appears as a well-circumscribed solid brown tumour

306
Q

What grading system is used for clear cell and papillary renal cell carcinoma?

A

ISUP Nuclear Grade

307
Q

What risk progression index is used for clear cell carcinoma?

A

Leibovich risk model

308
Q

What is Nephroblastoma (Wilm’s tumour)?

A

Malignant triphasic kidney tumour of childhood:

· Blastema (small round blue cells)

· Epithelial

· Stromal

Typically present with an abdominal mass in children aged 2-5 years

NOTE: 95% have an excellent prognosis

309
Q

What are the major risk factors for urothelial carcinoma?

A

Smoking

Aromatic amines

310
Q

What are the three main subtypes of urothelial carcinoma?

A

Non-invasive papillary urothelial carcinoma

Invasive urothelial carcinoma

Flat urothelial carcinoma in situ

311
Q

List some treatment options for BPH.

A

5a-reductase inhibitors

Alpha-blockers

TURP

312
Q

How can BPH present?

A

LUTS (most common)

UTI

Acute urinary retention

Renal failure

313
Q

What is the precancerous lesion that prostate cancer arises from?

A

Prostatic intraepithelial neoplasia

314
Q

List some mutations that are implicated in prostate cancer.

A

PTEN

AMACR

P27

GST-pi

315
Q

What scoring system is used for prostate cancer? Explain how it is calculated.

A

Gleason score

Expressed as x + y = z

Calculated by adding the top two most common patterns/grades seen on histological grading

Higher scores are associated with a poorer prognosis

316
Q

List some risk factors for testicular germ cell tumours.

A

Undescended testicles

Low birth weight

317
Q

Which genetic factor is associated with testicular germ cell tumours?

A

Amplification of i12p

318
Q

List the five histological subtypes of testicular germ cell tumours.

A

Seminoma

Embryonal carcinoma

Post-pubertal teratoma

Yolk sac tumour

Choriocarcinoma

319
Q

How are testicular germ cell tumours treated?

A

They are highly sensitive to platinum-based chemotherapy

5-year survival: 98%

320
Q

Name three types of testicular non-germ cell tumours.

A

Lymphoma – more in older men, poor prognosis

Leydig cell tumour – may cause precocious puberty (if pre-pubertal)

Sertoli cell tumour – 90% benign

321
Q

What are the causes of epididymitis?

A

< 35 years = N. gonorrhoea and C. trachomatis

35+ years = E. coli

322
Q

List some describe a few types of benign penile diseases.

A

Lichen sclerosus/balanitis xerotica obliterans – inflammatory condition that causes phimosis

Zoon’s balanitis – inflammatory condition that causes red areas

Condylomas – HPV 6 and 11

Peyronie’ disease – scarring, inflammation and thickening of the corpus cavernosa

323
Q

List some risk factors for penile carcinoma.

A

HPV

Smoking

Lichen sclerosus

324
Q

In which part of a bone is the growth plate found?

A

Metaphysis

325
Q

What are the main features of cortical bones?

A

Long bones

80% of skeleton

Appendicular

80-90% calcified

Mainly mechanical and protective

326
Q

What are the main features of cancellous bones?

A

Vertebrae and pelvis

20% of skeleton

Mainly axial

15-25% calcified

Mainly metabolic

Large surface

327
Q

Which protein is important in regulating the action of osteoclasts?

A

Osteoblasts produce osteoprotegrin which blocks the RANK-RANKL interaction which prevents the differentiation of an osteoclast precursor into a fully functioning osteoclast

328
Q

Where is bone usually sampled from for histological analysis of bone in metabolic bone disease?

A

Iliac crest

NOTE: the sample must be processed and un-decalcified for histomorphometry

329
Q

Which static parameters are measured in the histological analysis of bone in metabolic bone disease?

A

Cortical thickness

Trabecular bone volume

Thickness, number and separation of trabeculae

330
Q

Which technique is used to measure histodynamic parameters when investigating metabolic bone disease?

A

Tetracycline labelling

331
Q

Which investigations may be used in a patient with suspected osteoporosis?

A

Serum calcium, phosphate and ALP (should be NORMAL)

Urinary calcium

Collagen breakdown products

Imaging

DEXA

332
Q

Which four organs are affected by PTH and have a role in calcium homeostasis?

A

Kidneys

Bone

Proximal small intestine

Parathyroid gland

333
Q

What two underlying abnormalities can cause osteomalacia?

A

Deficiency of vitamin D

Deficiency of phosphate

334
Q

What is the main histological feature of osteomalacia?

A

Reduced amount of mineralised bone compared to the amount of osteoid

335
Q

Name some radiological features of osteomalacia.

A

Bowing of the legs in Rickets

Horizontal pseudofractures in Looser’s zones

336
Q

Describe how the urine excretion of calcium and phosphate changes in primary hyperparathyroidism.

A

Both increase

337
Q

What skeletal change is seen in primary hyperparathyroidism?

A

Osteitis fibrosa cystica

338
Q

What histological feature is typically seen in hyperparathyroidism?

A

Brown cell tumour – several multinucleated giant cells on a background of fibrous stroma with haemorrhage

339
Q

What is Paget’s disease and what are its three phases?

A

Disorder of bone turnover

Three phases

· Osteolytic

· Osteolytic-osteosclerotic

· Quiescent osteosclerotic

NOTE: the combination of osteoblast and osteoclast activity results in new bone formation

NOTE: 85% are polyostotic

340
Q

Describe the histological appearance of Paget’s disease.

A

Lines will be seen between areas of new bone formation so it looks like a mosaic/jigsaw puzzle

341
Q

Which virus is associated with Paget’s disease?

A

Parvomyxovirus

342
Q

Describe the presentation of Paget’s disease.

A

Most lesions affect the skull and lumbar spine

Pain

Microfractures

Nerve compression

Skull changes (can put the medulla at risk leading to haemodynamic changes)

Sarcoma

Paget’s disease of the tibia can cause bowing

343
Q

What are the four stages of fracture repair?

A

Organisation of a haematoma at the site of the fracture (pro-callus)

Formation of a fibrocartilaginous callus

Mineralisation of the fibrocartilaginous callus

Remodelling of the bone along weight-bearing lines

344
Q

Which sites are most commonly affected by osteomyelitis?

A

Vertebra

Jaw (secondary to dental caries)

Toe

Long bones (usually metaphysis)

345
Q

Describe the typical presentation of osteomyelitis.

A

General – FLAWS

Local – pain, swelling, redness

346
Q

Which investigations may be used in suspected osteomyelitis?

A

Blood cultures (positive in 60%)

X-ray (will eventually show lytic areas)

NOTE: osteomyelitis is almost always bacterial

347
Q

Which organisms can cause osteomyelitis?

A

Staphylococcus aureus (90%)

E. coli

Klebsiella

Pseudomonas (IVDU)

348
Q

Which bacterium is associated with osteomyelitic in patients with sickle cell disease?

A

Salmonella

349
Q

Describe the X-ray changes seen in osteomyelitis.

A

Usually appear about 10 days after onset

Mottled rarefaction and lifting of periosteum

First week changes – irregular sub-periosteal new bone formation (involucrum – layer of new bone that forms around dead bone)

Later changes – irregular lytic destruction

Some areas of the necrotic cortex may become detached (sequestra). This takes 3-6 weeks

350
Q

What are the potential consequences of TB osteomyelitis of the vertebrae?

A

Aka Pott’s disease

May result in psoas abscess or skeletal deformity

NOTE: TB osteomyelitis tends to only occur in immunocompromised patients

NOTE: systemic amyloidosis may occur in some cases

351
Q

Describe the histological appearance of TB osteomyelitis.

A

Lots of inflammatory cells can be seen in between trabeculae

Langerhans-type giant cells (with a horse-shoe nucleus) will be seen

352
Q

What congenital skeletal lesions are associated with syphilis?

A

Osteochondritis

Osteoperiostitis

Diaphyseal osteomyelitis

353
Q

List some acquired skeletal lesions that are associated with syphilis.

A

Non-gummatous periostitis

Gummatous inflammation of joints and bones

Neuropathic joints (tabes dorsalis)

Neuropathic shaft fractures

354
Q

What is the organism and vector in lyme disease?

A

Organism: Borrelia burgdorferi

Vector: Ixodus dammini

355
Q

What is the skin rash that is classically associated with lyme disease?

A

Erythema chronicum migrans

356
Q

Describe the clinical features of lyme disease.

A

Early localised – rash (90%) often on thigh, groin or axilla, 1-50 cm in diameter

Early disseminated – affects many organs (musculoskeletal, heart, nervous system)

Late, persistent – dominated by arthritis

357
Q

Outline the treatment of lyme disease.

A

Aim for prevention

Antibiotics

No effective prophylaxis

Diagnosis is clinical

358
Q

What are the HLA associations of rheumatoid arthritis?

A

HLA DR4 and HLA DR1 (Chr6p21)

Other alleles: TFNA1P3, STAT4

359
Q

What is rheumatoid factor and what proportion of patient’s with rheumatoid arthritis are rheumatoid factor positive?

A

IgM antibody against IgG

80% positive

May be responsible for extra-articular disease

360
Q

Which sites tend to be affected by rheumatoid arthritis?

A

Small joints of the hand and feet (except DIP)

Wrists, elbows, ankles and knees

361
Q

List some characteristic deformities associated with rheumatoid arthritis.

A

Radial deviation of the wrist

Ulnar deviation of the fingers

Swan neck and Boutonniere deformity

Z-shaped thumb

362
Q

Describe the histological features of rheumatoid arthritis.

A

Proliferative synovitis with thickening of synovial membranes, hyperplasia of surface synoviocytes, intense inflammatory cell infiltrate and fibrin deposition and necrosis

A pannus can form (exuberant inflamed synovium)

363
Q

Which type of multinucleate giant cell may be seen in rheumatoid arthritis?

A

Grimley-Sokoloff cell (like a Langerhans cell but does not have horseshoe nuclei)

364
Q

What type of crystals cause gout?

A

Needle-shaped negatively birefringent urate crystals

NOTE: big toe is involved in 90% of cases

NOTE: a tophus is pathognomonic of gout

365
Q

Which crystals cause pseudogout?

A

Calcium crystals

Calcium pyrophosphate – mainly knees

Calcium phosphate (hydroxyapatite) – knees and shoulders

Rhomboid-shaped positively birefringent crystals

366
Q

Which tumours most commonly metastasise to the bone in adults

A

Breast

Prostate

Lung

Kidney

Thyroid

367
Q

Which tumours most commonly metastasise to the bone in children

A

Neuroblastoma

Wilm’s tumour

Osteosarcoma

Ewing’s

Rhabdomyosarcoma

368
Q

What are the key clinical and radiological features of osteosarcoma?

A

Peak in adolescence

60% around the knee

X-ray: usually metaphysial, lytic, permeative, elevated periosteum (Codman’s triangle)

369
Q

Describe the histological appearance of osteosarcoma.

A

Malignant mesenchymal cells with or without bone and cartilage formation

370
Q

What are the main clinical, radiological and histological features of chondrosarcoma?

A

Malignant cartilage producing tumour

Affects axial skeleton, proximal femur and proximal tibia

X-ray: lytic with fluffy calcification

Histology: malignant chondrocytes with or without chondroid matrix

371
Q

What are the main clinical, radiological and histological features of Ewing’s sarcoma?

A

Highly malignant small round cell tumour

Occurs in < 20 years

Mainly affect diaphysis and metaphysis of long bones

X-ray: onion skinning of the periosteum, lytic with or without sclerosis

Histology: sheets of small round cells

372
Q

Which chromosomal translocation is associated with Ewing’s sarcoma?

A

11;22 (ESWR1:Fli1)

373
Q

What is a volvulus?

A

Twisting of a loop of bowel at the mesenteric base around a vascular pedicle

374
Q

Which part of the intestines tend to be affected by volvulus in children and the eldery?

A

Children – small bowel

Elderly – sigmoid colon

375
Q

What can cause pseudomembranous colitis?

A

Exotoxins by C. difficile

376
Q

How is pseudomembranous colitis treated?

A

Metronidazole or vancomycin

377
Q

Where in the intestines does ischaemic colitis tend to occur?

A

Watershed zones (e.g. splenic flexure, rectosigmoid)

378
Q

List some characteristic features of Crohn’s disease.

A

Can occur anywhere from mouth to anus

Skip lesions

Transmural inflammation

Non-caseating granulomas

Sinus/fistula formation

Mostly affects large bowel and terminal ileum

Thick rubber hose-like wall

Cobblestone mucosa

Narrow lumen

379
Q

List some extra-intestinal features of inflammatory bowel disease.

A

Arthritis

Uveitis

Stomatitis/cheilitis

Skin lesions (pyoderma gangrenosum, erythema multiforme, erythema nodosum)

380
Q

List some characteristic features of ulcerative colitis.

A

Involves rectum and colon in a continuous fashion

May see backwash ileitis (involvement of the terminal ileum)

Inflammation is confined to the mucosa

Bowel wall is normal thickness

381
Q

List some complications of ulcerative colitis.

A

Severe haemorrhage

Toxic megacolon

Adenocarcinoma (20-30 x increased risk)

382
Q

Which liver condition is associated with UC?

A

Primary sclerosing cholangitis

383
Q

List some features of an adenoma that are associated with increased risk of becoming a carcinoma.

A

Size of polyp (> 4 cm = 45%)

Proportion of villous component

Degree of dysplastic change within a polyp

384
Q

List some familial syndromes that are characterised by intestinal polyps.

A

Peutz-Jegher’s syndrome

FAP (Gardner’s, Turcot)

HNPCC

385
Q

What is the inheritance pattern of FAP?

A

Autosomal dominant

386
Q

Which gene is mutated in FAP?

A

APC gene – chromosome 5q21

NOTE: almost 100% will develop cancer in 10-15 years

387
Q

What is Gardner’s syndrome?

A

Same features of FAP but with extra-intestinal manifestations: multiple osteomas of the skull and mandible, epidermoid cysts, desmoid tumours and supernumerary teeth

388
Q

What is the inheritance pattern of HNPCC?

A

Autosomal dominant

389
Q

Where do carcinomas in HNPCC tend to occur?

A

Proximal to the splenic flexure

NOTE: poorly differentiated and mucinous cancers are more common. Polyps do not necessarily precede the cancer

390
Q

Outline Dukes’ staging of colorectal cancer.

A

A – confined to bowel wall

B – through the bowel wall

C – lymph node metastases

D – distant metastases

391
Q

Describe the radiological classification of brain tumours.

A

Extra-axial (coverings) – tumours of the bone, meninges and metastatic deposits

Intra-axial (parenchyma) – derived from normal cell populations of the CNS (e.g. glia, neurones, vessels) or derived from other cell types (e.g. lymphomas, metastases)

392
Q

What is the most common genetic syndrome associated with brain tumours?

A

Neurofibromatosis

393
Q

What is the inheritance pattern of neurofibromatosis?

A

Autosomal dominant

394
Q

Where are the genes that cause neurofibromatosis located?

A

NF1 – 17q11

NF2 – 22q12

395
Q

List some manifestations of brain tumours that are supratentorial

A

Focal neurological defect

Seizures

Personality changes

396
Q

List some manifestations of brain tumours that are subtentorial

A

Cerebellar ataxia

Long tract signs

Cranial nerve palsy

397
Q

Outline the management options for brain tumours.

A

Surgery – aim for maximal safe resection with minimal damage to the patient. Debulking may be performed and biopsies may be taken.

Radiotherapy – used for gliomas and metastases

Chemotherapy – mainly for high-grade gliomas

398
Q

Outline the meaning of the different WHO grades for brain tumours.

A

Grade I = benign, long-term survival

Grade II = death in > 5 years

Grade III = death in < 5 years

Grade IV = death in < 1 year

NOTE: grades I and II are low grade

399
Q

What is the most common type of primary brain tumour?

A

Glial tumours

400
Q

How are the types of glial tumours seen in children and adults different?

A

Diffuse Infiltration – mainly seen in adults, become more malignant with time, can either be astrocytomas or oligodendrogliomas

Circumscribed Gliomas – mainly seen in children, tend to be low-grade, rarely undergo malignant transformation

401
Q

Which genetic mutations are associated with gliomas in adults and in children?

A

Diffuse infiltration (adults) – IDH1/2

Circumscribed gliomas (children) – MAPK (BRAF)

402
Q

List some examples of circumscribed gliomas.

A

Pilocytic astrocytoma (MOST COMMON)

Pleiomorphic xanthoastrocytoma

Subependymal giant cell astrocytoma

403
Q

List some key features of pilocytic astrocytoma.

A

Usually grade I

Mainly occurs in children

Associated with NF1

Often cerebellar

BRAF mutation in 70% of cases

404
Q

What is the hallmark histological feature of pilocytic astrocytoma?

A

Piloid (hairy) cell

Often see Rosenthal fibres and granular bodies

Slow-growing with low mitotic activity

405
Q

List some key features of astrocytoma.

A

Usually Grade II-IV

Cerebral hemispheres are the most common site in adults

Can progress to become a higher grade (malignant progression)

IDH2 mutation in 80% of cases

Mitotic activity and vascular proliferation is absent

406
Q

What can astrocytomas eventually become?

A

Glioblastoma (after 5-7 years)

407
Q

What is the most aggressive and most common type of glioblastoma?

A

De novo glioblastoma (stage IV)

408
Q

List some key features of glioblastoma multiforme.

A

Grade IV

Most patients > 50 years

High cellularity and high mitotic activity

Microvascular proliferation and necrosis

409
Q

What does glioblastoma multiforme tend to arise from?

A

90% occur de novo and have wildtype IDH

10% occur secondary to astrocytoma and have IDH mutation

410
Q

List some key features of oligodendrogliomas.

A

Grade II-III

Tends to present with a long history of neurological signs (usually seizures)

Slow-growing

Better prognosis than astrocytoma (better response to chemotherapy and radiotherapy)

411
Q

What is a characteristic histological feature of oligodendroglioma?

A

Round cells with clear cytoplasm (fried egg)

412
Q

Which gene mutations are associated with oligodendroglioma?

A

IDH1/2

Co-deletion of 1p/19q

413
Q

What is the second most common primary intracranial tumour after gliomas?

A

Meningioma

414
Q

List some key features of meningioma.

A

Mainly low grade (I and II)

Can be multiple (e.g. in NF2)

Can cause focal symptoms (e.g. seizures, compression)

415
Q

Which histological feature of a meningioma is important in determining grade?

A

Mitotic activity (number of mitoses per 10 high power fields)

Grade 1 < 4

Grade 2: 4-20

Grade 3 > 20

NOTE: brain invasion is also an important thing to assess (presence of brain invasion makes it grade II)

416
Q

How does the grade of meningioma affect the management options?

A

Grade II and III requires radiotherapy as well as surgery

417
Q

What is a medulloblastoma?

A

Embryonal tumour originating from neuroepithelial precursors of the cerebellum and dorsal brainstem

They are always found in the cerebellum

418
Q

Describe the histological appearance of medulloblastoma.

A

Small blue round cell tumour with expression of neuronal markers (very little differentiation)

NOTE: synaptophysin is an example of a neuronal marker

419
Q

What histological feature is suggestive of partial neuronal differentiation?

A

Homer-Wright rosettes

420
Q

Which tumours most commonly metastasise to the brain?

A

Lung

Breast

Melanoma

421
Q

What radiological appearance is characteristic of cerebral oedema?

A

Loss of gyri

422
Q

Name and describe the two types of hydrocephalus.

A

Non-communicating – caused by obstruction of CSF flow (usually in the cerebral aqueduct)

Communicating – caused by reduced reabsorption of CSF into the venous sinuses (this could be caused by infection (e.g. meningitis))

423
Q

What is the normal range for ICP?

A

7-15 mm Hg

424
Q

Name and describe the three sites of brain herniation.

A

Subfalcine – the cortex is pushed under the falx cerebri

Transtentorial (uncal) – the posterior cranial fossa is covered by the tentorium cerebelli which has a rigid opening for the brainstem. Supratentorial pressure can result in herniation of the medial temporal lobe over the rigid end of the opening of the tentorium cerebelli

Tonsillar – herniation of the cerebellar tonsils through the foramen magnum (this can put pressure on the medulla and kill)

425
Q

What is a non-traumatic intraparenchymal haemorrhage?

A

Haemorrhage into the substance of the brain (parenchyma) due to rupture of small intraparenchymal vessels

426
Q

Where do non-traumatic intraparenchymal haemorrhages tend to occur most frequently?

A

Basal ganglia

NOTE: hypertension is implicated in > 50% of bleeds

427
Q

What is an arteriovenous malformation?

A

A malformation where blood bypasses quickly from artery to vein without going through a normal capillary network

They can occur anywhere in the CNS and they can rupture

As they occur under high pressure, they tend to cause massive bleeds

428
Q

Define cavernous angioma.

A

Well-defined malformative lesion composed of closely-packed vessels with no parenchyma interposed between vascular spaces

NOTE: it is similar to an arteriovenous malformation but there is no brain substance wrapped up amongst the vessels

NOTE: these tend to bleed at lower pressure causing recurrent small bleeds

429
Q

Describe the appearance of cavernous angiomas on MRI.

A

Shows target sign

430
Q

What causes subarachnoid haemorrhages?

A

Rupture of a berry aneurysm

NOTE: berry aneurysms are congenital

431
Q

Where are berry aneurysms typically found?

A

80% at the internal carotid bifurcation

20% within the vertebro-basillar circulation

NOTE: highest risk of rupture if diameter of 6-10 mm

432
Q

Where is atherosclerosis most commonly found within the cerebral vasculature?

A

Carotid bifurcation

Basilar artery

433
Q

Which part of the cerebral vascular tends to be affected by infarcts resulting from emboli?

A

Middle cerebral artery branches

434
Q

What are the consequences of base of skull fractures?

A

The fracture may pass through the middle ear or anterior cranial fossa

It can cause otorrhoea or rhinorrhoea

Increased risk of infection

NOTE: battle sign and raccoon eyes are manifestations of basal skull fractures

435
Q

With regards to brain injury, what is a laceration?

A

Bruising of the brain that causes rupture of the pia mater

436
Q

What is the term used to describe rebound injury to the opposite side of the brain?

A

Contrecoup injury

437
Q

What is diffuse axonal injury?

A

Occurs at the moment of injury

Shear and tensile forces causes damage to the axons

This is the most common non-bleed related cause of coma

Midline structure are particularly affected (e.g. corpus callosum)

Some people suffer cognitive and behavioural changes further down the line

438
Q

What are prion diseases?

A

Proteinaceous infections only

They are transmissible diseases that have no DNA or RNA

439
Q

List some examples of prion diseases.

A

Creutzfeldt-Jakob disease

Gerstmann-Straussler-Sheinker syndrome

Kuru

Fatal familial insomnia

440
Q

Describe the histological appearance of brains affected by prion diseases.

A

The tissue is full of vacuoles (spongiform encephalopathies)

441
Q

What are the key features of new variant CJD?

A

Sporadic neuropsychiatric disorder occurring in mainly younger patients (< 45 years) and associated with BSE

Clinical features include cerebellar ataxia and dementia

442
Q

Which part of the brain is often affected by cortical atrophy in Alzheimer’s disease?

A

Inferior horn of the lateral ventricles where the hippocampus is found (this is responsible for loss of short term memory)

443
Q

Describe the Braak stages of Alzheimer’s disease

A

Stage 1: tau pathology in the transentorhinal cortex

Stage 2: posterior hippocampus

Stage 3: immunostaining is visible by eye, affects substantia nigra

Stage 4: superior temporal gyrus

Stage 5: peristriate cortex

Stage 6: striate cortex

NOTE: clinically, symptoms tend to arise in stage 3 or 4

444
Q

Outline the main histological features of Parkinson’s disease.

A

Characterised by the presence of Lewy bodies which are intracellular accumulations of alpha-synuclein

Parkinson’s disease is caused by abhorrent metabolism of alpha-synuclein

NOTE: this was discovered because mutations in the alpha-synuclein gene are associated with rare familial forms of Parkinson’s disease

445
Q

What is the diagnostic gold standard for Parkinson’s disease?

A

Alpha-synuclein immunostaining

446
Q

What are some non-extrapyramidal symptoms of Parkinson’s disease?

A

Sleep disorders

Depression

Anosmia

447
Q

What are three important differentials to consider in a patient with Parkinson’s disease?

A

Multiple system atrophy

Corticobasal degeneration

Progressive supranuclear palsy

448
Q

What is multisystem atrophy?

A

It is an alpha-synucleinopathy like Parkinson’s disease which targets glial cells

It presents similarly to Parkinson’s disease

It mainly affects the cerebellum so the patients are more likely to present with falls

449
Q

What are the main histological features of Pick’s disease?

A

Marked gliosis and neuronal loss

Balloon neurones

Tau-positive Pick bodies

NOTE: mutations in tau are associated with a fronto-temporal dementia phenotype often associated with Parkinson’s disease

NOTE: there are 17 autosomal dominant syndromes resulting from mutations in tau

450
Q

What is a characteristic feature of frontotemporal dementia associated with progranulin mutations?

A

Atrophy tends to be unilateral

451
Q

What type of epithelium lines the airways?

A

Ciliated respiratory epithelium

452
Q

Which types of cells line the alveoli?

A

Type 1 pneumocytes

453
Q

What is the main histological feature of pulmonary oedema?

A

Intra-alveolar fluid

454
Q

Describe the appearance of the lungs on post-mortem examination in a patient who died from ARDS.

A

Plum-coloured

Heavy

Airless

455
Q

Describe the main histological features of asthma.

A

Lots of eosinophils and mast cells

Goblet cell hyperplasia

Mucus plugs within airways

Thickening of bronchial smooth muscle and dilatation of blood vessels

456
Q

Define chronic bronchitis.

A

Chronic cough productive of sputum presents for most days for at least 3 months over 2 consecutive years

457
Q

List some histological features of chronic bronchitis.

A

Dilated airways

Mucus gland hyperplasia

Goblet cell hyperplasia

Mild inflammation

458
Q

Describe how the pattern of alveolar damage is different with smoking compared to alpha-1 antitrypsin deficiency.

A

Smoking – centrilobular damage

Alpha-1 antitrypsin deficiency – panacinar (throughout the lungs)

459
Q

Define bronchiectasis.

A

Permanent abnormal dilatation of the bronchi with inflammation and fibrosis extending into adjacent parenchyma

460
Q

Which part of the lungs tends to be affected most frequently in idiopathic bronchiectasis?

A

Lower lobe

461
Q

List some causes of bronchiectasis.

A

Infection (MOST COMMON)

· Post-infectious (e.g. CF)

· Abnormal host defence (e.g. chemotherapy, immunodeficiency)

· Ciliary dyskinesia

Obstruction

Post-inflammatory (aspiration)

Interstitial disease (e.g. sarcoidosis)

Asthma

462
Q

Where is the CFTR gene found?

A

7q3

463
Q

What is the most common mutation associated with CF?

A

Delta F508

464
Q

List some clinical manifestations of CF.

A

GI – meconium ileus, malabsorption

Pancreas – pancreatitis

Liver – cirrhosis

Male reproductive system – infertility

Recurrent chest infections

465
Q

List some causes of community-acquired bacterial pneumonia.

A

Streptococcus pneumoniae

Haemophilus influenzae

Mycoplasma

466
Q

List some causes of hospital-acquired bacterial pneumonia.

A

Gram-negatives (Klebsiella, Pseudomonas)

467
Q

What is bronchopneumonia?

A

Infection is centred around the airways

Tends to be associated with compromised host defence (mainly the elderly) and is caused by low virulence organisms (e.g. Staphylococcus, Haemophilus, Pneumococcus)

It will show patchy bronchial and peribronchial distribution often involving the lower lobes

468
Q

What is lobar pneumonia?

A

Infection is focused in a lobe of the lung

90-95% caused by S. pneumoniae

Widespread fibrinosuppurative consolidation

469
Q

What are the histopathological stages of lobar pneumonia?

A

Stage 1: congestion (hyperaemia and intra-alveolar fluid)

Stage 2: red hepatisation (hyperaemia, intra-alveolar neutrophils)

Stage 3: grey hepatisation (intra-alveolar connective tissue)

Stage 4: resolution (restoration of normal tissue architecture)

470
Q

Describe the histological appearance of atypical pneumonia.

A

Interstitial inflammation (pneumonitis) without accumulation of intra-alveolar inflammatory cells

NOTE: causes include Mycoplasma, viruses, Coxiella and Chlamydia

471
Q

What is a long term consequence of repeated small pulmonary emboli?

A

Pulmonary hypertension

472
Q

What are the main types of lung cancer?

A

Non-small cell carcinoma

· Squamous cell carcinoma (30%)

· Adenocarcinoma (30%)

· Large cell carcinoma (20%)

Small cell carcinoma (20%)

473
Q

Which types of lung cancer are most strongly associated with smoking?

A

Squamous cell carcinoma

Small cell carcinoma

474
Q

Which type of lung cancer tends to occur in non-smokers?

A

Adenocarcinoma

475
Q

What feature of squamous epithelium makes it vulnerable to undergoing malignant changes?

A

It does not have cilia leading to a build-up of mucus

Within the mucus carcinogens accumulate

476
Q

Where do squamous cell carcinomas tend to arise?

A

Centrally – arising from the bronchial epithelium

NOTE: there is an increasing incidence of peripheral squamous cell carcinomas (possibly due to deeper inhalation of modern cigarette smoke)

477
Q

Which mutations are associated with adenocarcinoma in smokers?

A

Kras

Issues with DNA methylation

P53

478
Q

Which mutation is associated with adenocarcinoma in non-smokers?

A

EGFR

479
Q

What is large cell carcinoma of the lung?

A

Poorly differentiated tumour composed of large cells

There is no evidence of squamous or glandular differentiation

It has a poor prognosis

480
Q

Where does small cell lung cancer tend to arise?

A

Central – around the bronchi

NOTE: 80% present with advanced disease and it carries a poor prognosis

481
Q

List some common mutations seen in small cell lung cancer.

A

P53

RB1

482
Q

What is the difference in the chemosensitivity of small cell lung cancer and non-small cell lung cancer?

A

Small cell – sensitive

Non-small cell – not very chemosensitive

483
Q

Which molecular changes are important to test for in adenocarcinoma?

A

EGFR (responder or resistance)

ALK translocation

Ros1 translocation

Path Laz (condensed) (5 decks)

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