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Sera's MBBS > Histopath > Flashcards

Histopath Flashcards

1
Q

which cells are associated with acute inflammation v chronic inflammation (histpaht)

A

neutrophils - acute

Lymphocytes and plasma cells - chronic

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2
Q

Bilobed nucleus with red granulocytes

A

Eosinophils

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3
Q

Eosinophils are associated with (3)

A

Allergic reactions
Parasitic infections
Tumours e.g. Hodgkin’s - they are reactive processes to tumourgenesis

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4
Q

Cell with very large granules containing inflammatory mediators

A

mast cells

associated with allergic reactions

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5
Q

Lots of cytoplasm, associated with late acute and chronic inflammation

A

Macrophages

primary role is to phagocytose debris
secondary role to secrete the inflammatory mediators

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6
Q

A true sputum sample will contain macrophages - T/F

A

T

Even in non-smokers, because marcophages are need to clear up any inhaled pollutants including industrial fumes and especially cigarette smoke

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7
Q

2 features of squamous cell carcinomas

A

Keratin production + intracellular bridges

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8
Q

2 features of adenocarcinomas

A

Glands and mucin production

You can stain for mucin using special stains which cause goblet cells to appear bright blue

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9
Q

Name the stain for melanin

A

Fontana stain - chemical reaction with melanin that makes it more pigmented (appears black)

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10
Q

histochemical stians v immunohistochemical stains?

name examples (*2-3 each)

A

histochemical is based on CHEMICAL reaction between stain and tissue e.g. H&E, Prussian blue for iron, congo red for amyloid

immuno stain is based on antigen and antibody interaction e.g. immunofluorescence or immunoperoxidases e.g .CD45 (pan-lymphocyte stain), cytokeratin (stain for ketarin used in SCC)

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11
Q

Staining for amyloid (2)

A

Congo red + apple green birefringence under polarised light

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12
Q

Sheets of plasma cells

A

Lymphoma

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13
Q

Langerhan type giant cell

A

Granulomas formed by activated macrophages

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14
Q

Resembles both stratified squamous and stratified cuboidal depending on degree of organ stretch

A

Transitional epithelium

Seen in bladder, ureters and part of urethra, allows the bladder to expand and contract when needed

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15
Q

Smokers cancer type

A

Squamous cell carcinoma (also the most common lung cancer overall)

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16
Q

Non-smoker lung ca

A

Adenocarcinoma (more peirpheral)

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17
Q

Smoking is most associated with these 2 types of lung ca

A

SCC and small cell carcinoma

*Adenocarcinoma is more in non-smokers

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18
Q

Types of histology samples for a ?lung Ca

A
  1. Biopsy at bronchoscopy
  2. Per-cutaneous CT guided biopsy for peripheral tumours
  3. Mediastinoscopy and lymph node biopsy for staging
  4. Open biopsy at time of surgery
  5. Resection specimen - confirm full excision and staging
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19
Q

Pathogenesis of lung SCC

A

Normal epithelium -> hyperplasia -> squamous metaplasia -> dysplasia -> carcinoma in situ -> invasive carcinoma

  • Tends to arise from proximal airways
  • Smoking irritates epithelium which undergoes hyperplasia in response
  • No cilia on the airways and deposits of carcinogens from cigarettes stays there
  • Metaplasia is characterised by instability which increases risk of accumulating mutations → dysplastic changes
  • Stopping smoking can reverse these genetic changes
  • But when threshold of mutations reached, cells form carcinoma in situ
  • Breakthrough of basement membrane → invasive carcinoma
  • Hirsch et al 2001, at each stage, there is accumulation of specific genetic mutations
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20
Q

Clinical features of lung SCC

  • who gets it
  • Risk factors
  • site
  • behaviour
A

Smokers
Usually centrally located, arising from bronchial epithelium
Local spread, mets late

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21
Q

This specific type of lung Ca shows prominent capillary loops underneath dysplastic epithelium
- there is keratinisation and intercellular bridges

A

angiosqaumous SCC

specific type of SCC, sen in high risk smokers, clinical significance is uncertain

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22
Q

Histology of SCC

A

Keratinisation

intercellular ‘prickles’ representing desmosome

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23
Q

Adenocarcinoma clinical features

  • who gets it
  • Risk factors
  • site
  • behaviour

*BONUS QN: what is a new targetted therapy for adenoCa

A

Non-smoker, usually females, far east

site: peripheral and often multi-centric, specifically arises from terminal alveoli wall
behaviour: mets early and common, especially extra-thoracic, 80% present with mets

Tarceva (anti-EGFR) which is the most common mutation in adneoCa for non-smoker.
*smoker version of kras, p53 = useless

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24
Q

precursor cells of lung adenoCa

what is the pathogenesis

A

Atypical adenomatous hyperplasia

Normal terminal alveoli wall lined by type 1 pneumocytes -> develop atypically into type 2-like pneumocytes with large nuclei -> these abnormal cells then grow like a caterpillar along the alveoli wall (adenoCa in situe) -> acquires invasive phenotype to break through basement membrane by destroying elastin

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25
Q

Histological features of adenoCa lung

A

Desmoplasia with angular glands and single cell infiltration - acinar pattern
(desmoplasia is stained pink)

Glandular differentiation+ mucin production

In medicine, desmoplasia is the growth of fibrous or connective tissue. Desmoplasia may occur around a neoplasm, causing dense fibrosis around the tumor, or scar tissue (adhesions) within the abdomen after abdominal surgery.

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26
Q

Cytological lung adenoCa

A

Mucin vacuoles

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27
Q

Molecular pathways of adenoCa (2)

A

Smokers
- kras -> DNA methylation -> p53

Non-smokers
- EGFR amplication/mutation

The two are mutually exclusive

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28
Q

large cell carcinoma lungs

  • who gets it
  • Risk factors
  • site
  • behaviour
A

Rare, poorly differentiated tumours

Site: peripheral or central
Behaviour: poor prognosis

no idea what is the original cell, histology shows no differentiation into squamous (keratin) or adeno (glands + mucin).

Electron microscopy may show some glandular/squamous differentiation.Thought to be due to very poorly differentiated adenoCa or SCC

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29
Q

Small cell carcinoma lungs

  • who gets it
  • Risk factors
  • site
  • behaviour
A

SMOKERS

site; central bronchi (as with SCC)

behaviour: abysmal prognosis, 80% present with BULKY primary and mets. Even when treated (small cell is chemosensitive) tend to recur

ASSOCIATED WITH PARANEOPLASTIC SYNDROMES (ESP SIADH)

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30
Q

Lung Ca + SIADH

A

small cell carcinoma lungs

two of the most common are humoral hypercalcemia of malignancy (HHM) in squamous cell carcinoma and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in small cell lung cancer

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31
Q

Lung Ca + hyperCa

A

SCC with PTHrP

two of the most common are humoral hypercalcemia of malignancy (HHM) in squamous cell carcinoma and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in small cell lung cancer

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32
Q

Mutations in small cell Ca of lungs (2)

A

p53 and RB1

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33
Q

Lung Ca that can be treated with chemo

A

small cell lung Ca

But even so, Ca tend to recur and abysmal outcome

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34
Q

Lung ca with ERCC1 has good prognosis - T/F

A

F

ERCC-1 is a predictor for poor response to chemo. Cancers with high ERCC1 proteins are able to remove drug-DNA adducts caused by chemo and hence is chemo resistant

*Chemo is only effect for small cell lung Ca

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35
Q

young female with lung Ca, non-smoker

what type of Ca and what new drug can treat it

A

Likely adenoCa with EGFR mutation cos non-smoker

Drug is TKI (tyrosine kinase inhibitor) that reduces EGFR activity and dramatically shrink tumours.

Drug name is Tarceva.

but 60-70% of patients acquire resistance to TKI by 790M mutation in EGFR

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36
Q

never smoker adenoCa with EML4-ALK mutation

A

EML4-ALK mutation found in adenoCa which causes gain of function for Alk gene and ALKinase

Therefore although adenoCa, no benefit from Tarceva (TKI) due to no EGFR mutation.

Solid and signet ring patterns

New targeted therapy - ALKinase inhibitor

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37
Q

SVC syndrome in lung Ca

A

head and arm oedema
oncology emergency
leads ultimately to circulatory collapse

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38
Q

Lymphangitis carcinomatosa

A

Complication of lung Ca whereby there is diffuse lymphatic spread within the lung

presents with SOB, poor prognostic feature

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39
Q

Paraneoplastic syndromes with lung Ca

A 
SIADH - small cell 
Cushing's - small cell (ACTH) 
PTHrP - squamous cell 
Coagulation defects 
Myasthenia gravis like picture
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40
Q

Mesothelioma

  • who gets it
  • Risk factors
  • site
  • behaviour
  • histology (2)
A

Asbestos exposure
site: pleura
behaviour: fatal
Long lag time between exposure and disease but dismal prognosis

Histology

  1. Epithelioid type
  2. Sarcomatoid type

Both are poor prognosis

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41
Q

Explain the pathology behaviour pulmonary oedema and iron-laden macrophages

A

Pulmonary oedema is usually caused by LVF or alveolar injury e.g. inhalation of fumes.

because of the damage from fumes, poteineous fluid leaks into the alveolar spaces (where the air usually goes).

In the case of LVF, there is backpressure into the lungs, leading to haemorrhage into the alveolar spaces.

The red cells in the alveolar is mopped up by macrophages which become iron rich (staining blue)

therefore presence of iron-laden macrophages in the lungs are also know nas heart-failure cells

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42
Q

Common point between adult ARDS and infant RDS

A

Infant RDS = hyaline membrane dx of the newborn

BOTH CAUSES DIFFUSE ALVEOLAR DAMAGE although by diff mechanism

Adult due to cytokine activities destroying the alveolar lining
infants due to insufficient surfactant from prematurity

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43
Q

Macroscopic and microscopic pathology of diffuse alveolar damage

A

Macroscopic

  • expanded, firm solid lungs
  • plum colour, airless
  • weight >1kg

Microscopic

  • proteinaceous fluid in alveolar spaces which impairs gas exchange
  • exudate becomes organised and lung tries to repair itself by forming granuloma tissue
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44
Q

Outcomes of diffuse alveolar damage

A

40% death
superimposed infection
Health and recovery but with permanent fibrosis and residual scarring (in infants known as bronchopulmonary dysplasia)

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45
Q

histological features of acute asthma + correlate these to clinical features of acute asthma

A

histology

  1. dilated blood vessels - hyperaemia
  2. increase number of goblet cells
  3. oesinophilia

Clinical

  1. leaky capillaries & airway oedema
  2. increased mucus production
  3. bronchospasm
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46
Q

histological features of chronic asthma + correlate these to clinical features of acute asthma

A

Histology

  1. airway smooth muscle hyperplasia + remodelling
  2. mucus plug
  3. epithelial damage!

Clinical

  1. SOB
  2. SOB
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47
Q

Def chronic bronchitis

A

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

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48
Q

Reid index

A

Defined as ratio of thickness of submucosal mucus secreting glands:thickness between epithelium and cartilage

<0.4 is normal
> suggest bronchitis

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49
Q

histological features of chronic bronchitis

A

goblet cell hyperplasia + permanently dilated airways

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50
Q

Causes of emphysema (4)

A
  1. smoking
  2. alpha-1 anti-trypsin def (blocks elastase, in def, overactive elastase destroy alveolar walls)
  3. IVD
  4. marfans
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51
Q

patterns of emphysema in smoking v alpha1 anti-trypsin deficiency

A

Smoking -> centrilobular (loss centered around bronchiole, not so much alveolar terminal air sacs)
Alpha1 anti-trypsin -> panacinar (diffuse loss)

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52
Q

Type 1 v type 2 respiratory failure

A

type 1 is hypoxia with hypercapnia

Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected

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53
Q

COPD blue bloaters, v pink puffers

A

blue bloaters = chronic bronchitis

pink puffers = empysema

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54
Q

Bronchopneumonia v lobar pneumonia

  • who gets each type
  • causative organism
  • histological features
A

bronchopneumo

  • elderly pt, underlying COPD
  • low virulence organisms e.g. staph, haemophilus, strep, pneumoccocus
  • fairly extensive dx but localised around the airways
  • histology: patchy peribroncho distribution usually in lower lobes

lobar pneumonia

  • young, fitter pit
  • high virulence organism e.g. S.pnaeumonia
  • histology; widespread, fibrinosuppurative consolidation
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55
Q

Congestion, red hepatization, grey hepatization, resolution

A

progress of lobar pneumonia

initially congestion with hyperaemia/intra-alveolar lfuid

red hepatization - neutrophils in alveolar

grey hepatisation - connective tissue

resolution - fibrosis or completely repair

Rare nowadays with antibiotics

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56
Q

histology of atypical pneumonia

A

not lobar or bronchopneumo

INTERSTITIAL inflammation

  • no alveolar inflammation
  • inflamamtion within the septa with oedema +/- viral inclusion bodies on histology (if viral cause e.g. influenza, CMV)
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57
Q

Define granuloma

A

Collection of macrophages +/- multinucleate giant cells

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58
Q

Lung histology of this pt shows discrete epithelial and giant cell granulomas, mostly in the upper zones.

Granulomas are non-caseatin gand also found in the lymph nodes.

Diagnosis + what investigation?

A

Sarcoidosis
- idiopathic grnaulmatous disease

diagnose by biopsy - non-necrotising granulomas + elevated ACE

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59
Q

Classify the causes of pulmonary HTN

A

Pre-capillary

  • vasoconstrictive
  • embolic

Capillary
- pulmonary fibrosis causing mechanical vascular distortion and chronic hypoxia

post-capillary
- left-sided heart disease

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60
Q

Def pulmonary HTN

A

mean pulmonary arterial pressure >25mmhg at rest

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61
Q

Abstesto affects the upper/lower lobes of the lungs

Inorganic dust e.g. coal workers lung and silicosis affects the upper/lower lobes of the lungs

A

Abstesto affects the LOWER lobes of the lungs

Inorganic dust e.g. coal workers lung and silicosis affects the UPPER lobes of the lungs

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62
Q

young’s syndrome

A

Rhinosinusitis
azoospermia
bronchiectasis

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63
Q

a) Cryptogenic Fibrosing Alveolitis / Idiopathic Pulmonary Fibrosis

A

● M>F
● Causative agents unknown
● Histological pattern of fibrosis = Usual Interstitial Pneumonia, required for diagnosis
(also seen in connective tissue disease, asbestosis and EAA)
o Progressive patchy interstitial fibrosis with loss of normal lung architecture and
honeycomb change, beginning at periphery of the lobule, usually sub-pleural o Hyperplasia of type II pneumocytes causing cyst formation – honeycomb
fibrosis.
● Can have inflammatory cause e.g. RA, SLE, systemic sclerosis
● Clinical presentation: increasing exertional dyspnoea and non-productive cough. 40- 70y at presentation, with hypoxaemia 􏰁 cyanosis and pulmonary HTN +/- cor pulmonale, and clubbing.
● Rx: steroids, cyclophosphamide, azathioprine, but little impact on survival

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64
Q

b) Pneumoconiosis

A

Typically an occupational lung disease; a non-neoplastic lung reaction to inhalation of mineral dusts or inorganic particles. The majority of pneumoconioses affect the upper lobe. e.g. coal worker’s pneumoconiosis, silicosis, asbestosis.
NB: asbestosis can cause benign pleural lesions (plaques, fibrosis) but can also cause malignant lesions (adenocarcinoma, mesothelioma). Asbestosis tends to affect the lower lobe.

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65
Q 
Paraneoplastic syndromes: 
ADH → 
ACTH → 
PTH/ PTHrP →
Calcitonin →
Serotonin → 
Bradykinin →
A

Paraneoplastic syndromes:
ADH → SIADH
ACTH → Cushing’s syndrome
PTH/ PTHrP → primary hyperparathyroidism, hypercalcaemia and bone pain
Calcitonin → hypercalcaemia
Serotonin → carcinoid syndrome (flushing + diarrhoea + bronchoconstriction)
Bradykinin → cough

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66
Q

Day 1 post MI histo + cardiac enzymes

A

Microscopic histo:

  • coagulation necrosis, loss of nuclei and striations
  • neutrophils

Gross histo: no changes

Enzymes
- high CK, high trop, normal myoglobin (normal by 24 hours)

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67
Q

Day 3 post MI histo + cardiac enzymes

A

Microscopic histo:

  • neutrophils predominant, still coagulation necrosis, loss of nuclei and striations but now there is also necrotic cell death
  • beginnings of macrophage infiltrate to clear up debris, beginning of angioblast infiltration, myofibroblast and collagen synthesis
  • muscle fibres at its weakest because there is new vessel formation between the wall (DAY4-5 is highest risk of myocardial rupture)

Gross pathology will show pale, oedematous tissue with inflammation

Enzymes
- high trop but normal CKMB. CKMB falls by day 3

68
Q

Day 10 post MI histo + cardiac enzymes

up until first month post MI

A

Microscopic histo:

  • macrophages clear up the debris from neutrophilic inflammation and form granulomas (debris cleared by day 10)
  • Angiogenesis with angioblasts, and scarring with myofibroblasts and collagen synthesis continues

Gross histology
- formation of THIN granulomas

Enzymes

  • Trop is still high at end of first week but normal by day 10
  • all other enzymes normal
69
Q

3 months post MI histo + cardiac enzymes

A

Microscopic histo:
- dense scar tissue with fibroblasts and collagen (non-contractile)

Scar is resistant against contractions of surrounding fibres

all cardiac enzymes normals

The histology will look the same with a 3 month old MI and a 3 year old MI

70
Q

Name the 4 types of thyroid cancer fro most common to least common

A

PFMA

Papillary
Follicular
Medullary
Anaplastic

71
Q

Papillary carcinoma of the thyroid- what are the nuclear features on histology

A

May have papillary architecture

But diagnosis is based on nuclear features

  • Optically clear nuclei
  • Intranuclear inclusions
  • May be psammomas bodies (focus of calcifications)
72
Q

how does papillary thyroid carcinoma present?

A

Non-functional

Present as painless mass in neck or may preset with just mets in cervical lymph node (enlarged lymph nodes for no apparent reason, the adenoma in the thyroid is too small to be palpated)

10 year survival up to 90%

73
Q

Follicular thyroid carcinoma

A

Peak incidence in middle age
Follicular morphology
Histological looks just like normal thyroid with colloid and follicles
May be well demarcated with minimal invasion or clearly infiltrate
Usually mets via bloodstream to lungs, bone and liver

74
Q

Medullary thyroid carcinoma

A

Neuroendocrine neoplasm derived from parafollicular C cells - calcitonin Ca
80% sporadic - adults in 5-6th decade
20% familial - MENS2, seen in younger patients

Characteristic feature is amyloid deposits within the cancer
Can be visualised under polarised light with Congo Red stain (appears green)
Due to breaking down of the calcitonin produced by tumour into amyloid within the tumour

75
Q

Anaplastic thyroid carcinoma

A

Occurs in elderly patients
VERY aggressive
Likely to be very aggressive follicular Ca
Mets common - early and widely
Most cases death within 1 year due to local invasion

76
Q

Name the zones of an adrenal gland and the substance they secrete

A 
Zones of the adrenal gland
Glomerulosa: Aldosterone 
Fasiculata: Glucocorticoids 
Reticularis:Androgens and glucocorticoids 
Medullar: NA and A
77
Q

Causes of adrenal insufficiency

A 
Primary 
- Acute 
Sudden withdrawal of steroid therapy 
Haemorrhage into the adrenal (neonates) 
Sepsis with DIC (Waterhouse-Friderichson syndrome) 
- Chronic (Addison’s disease) 
Autoimmune (75-90%) 
TB 
HIV 
Mets (lung and breast particularly) 
Rarely amyloid fungal infections, haemochromatosis, sarcoidosis

Secondary to low ACTH

  • Non-functional pit adenomas compressing on ant.pit
  • Other lesions of pituitary and hypothalamus including infarction
78
Q

Adrenal adenomas v carcinomas

A

Adenomas are usually non-functional. If thy are functional, they tend to secrete cortisol or aldersterone causing Cushing’s or Conn’s

Carcinomas are rarer and usually large. They are functional and tend to secrete androgens and cause virilising syndromes

79
Q

name 2 cancers of adrenal medulla

A

Phaechromocytoma

Neuroblastoma

80
Q

Rule of 10s in phaeo

A

10% in association with familial syndrome e..g MEN 2A and 2B, von Hippel-Lindau disease and Struve-Weber syndrome
10% bilateral
10% malignant
10% of catecholamine-secreting tumours arise from outside the adrenal (paragangliomas)

81
Q

Men 1, 2a and 2b

A

MEN1 (3Ps): Pituitary, Pancreatic (e.g. insulinoma), Parathyroid (hyperparathyroidism)

MEN2a (2Ps, 1M): Parathyroid, Phaeochromocytoma, Medullary thyroid

MEN2b (1P, 2Ms): Phaeochromocytoma, Medullary thyroid, Mucocutaneous neuromas (& Marfanoid)

82
Q

Asymptomatic Haematuria

If this appears in an EMQ – the differentials include:

A
  1. THIN BASEMENT MEMBRANE DISEASE (Benign familial haematuria)
  2. IgA NEPHROPATHY (Berger disease)
  3. ALPORT SYNDROME

IgA and Thin basement membrane are more common causes of asymptomatic haematuria than of nephritic syndrome. Differentiation between thin basement membrane and IgA is clinically difficult.

If there are no histological findings included in the questions clinical differences include IgA being more likely to cause frank haematuria, more likely to cause a change in renal function Cr raised) and slightly more common in the Asian population.

83
Q
  1. THIN BASEMENT MEMBRANE DISEASE

what is the inheritance patter and mutation
what do they present with

A

● VERY RARELY A CAUSE OF NEPHRITIC SYNDROME – normally exclusively asymptomatic haematuria
● Diffuse thinning of GBM caused by mutation in type IV collagen alpha 4 chain
● Autosomal dominant
● Quite common – prevalence is ~5%
● Usually asymptomatic – incidentally diagnosed with microscopic haematuria
● Renal function usually normal

84
Q

Alports syndrome

what renal syndrome (nephrotic or nephritic) does it cause? what other symptoms and age of presentation

A
  1. HEREDITARY NEPHRITIS (ALPORT’S SYNDROME)
    ● Hereditary glomerular disease caused by mutation in type IV collagen alpha 5 chain
    ● X linked
    ● Nephritic syndrome + sensorineural deafness + eye disorders (lens dislocation,
    cataracts)
    ● Presents at 5-20yrs with nephritic syndrome progressing to ESRF
85
Q

Kimmelstiel Wilson nodules

A

Histological features of GN caused by diabetes - nephritic syndrome

Diffuse glomerular basement membrane thickening Mesangial matrix nodules – aka Kimmelstiel Wilson nodules

86
Q

Fluorescence Microscope (FM): granular/lumpy bumpy deposits of IgG and C3 in GBM

A

Immune complex mediated (Type 2) rapidly progressive crescentic glomerulonephritis

Causes

  • SLE
  • Post-strep GN (weeks after strep throat or impetigo)

If it is lumpy bumpy but IgA then can also be IgA nephropathy (days after URTI)

Other types of rapidly progressive crescentic GN

  • type 1 (Goodpasture’s, antiGBM)
  • type 2 (immune - SLE, post-strep GN and gA nephropathy
  • type 3 (pauci-immune e.g. ANCA wegener’s and MPA)
87
Q

Bowen’s disease

A

SCC in situ

88
Q

Does squamous cell carcinoma of the skin mets? and if so, how and where?

A

Yes
They tend to met to local lymph nodes and also can wrap around nerves to travel to distant sites.

SCC that wraps around nerves are likely to recur

89
Q

Elderly, cauliflower like lesion on the scalp

Diagnosis?
Histology will show?

A

Seborrheaic keratosis (Solar keratosis)

This is benign but can be surgically removed it becomes bulky/catches on clothing

Histology shows enlarged/thickend epidermis with keratin within cysts
but the growth is ORDERED

If this keratin growth becomes disordered = SCC in situ (Bowen’s dx)

90
Q

nests of melanocytes siting at the bottom of the epidermis
v
melanocytes that migrate down into the dermis
v
melanocytes that migrate upwards into the epidermis

A

Junctional naevus
- benign and common in young people

Compound naevus
- still benign, more common with old age

Malignant melanoma
- abnormal, melanocytes should normally be found sitting o the basement membrane with the other basal keratinocytes, they have finger like projections (dendrites) into the epidermis

91
Q

Behaviour of melanocytes in malignant melanomas

A

they migrate upwards into the epidermis (abnormal)

and they also migrate downwards to penetrate basement membrane on which non-cancerous melanocytes sit. The melanocytes in the dermis are poor differentiated with abnormal mitotic features

92
Q

What is Breslow thickness

A

Measurement of the thickness of melanocyte migration in malignant melanomas

(>4mm is the worst prognosis, ulcerated worsen prognosis)

50% in 5 year mortality if >4mm

93
Q

3 layers of filtration barrier in the kidney glomerular bowman’s capsule

A

Inside: endothelium (fenestrated, with holes)
Middle: Basement membrane made up type 4 collagen
Outside: Podocytes sitting outside the basement membrane (damage here = proteinuria, most important factor)

94
Q

What is the mesangium in the kidneys?

A

Mesangium contains a cluster of specialised cells (smooth muscle) that holds the capillary loops together in the glomerulus

The mesangium supports the capillaries

95
Q

compare the mesangium of the kidneys and mesentery of the gut

A

both are specialised smooth muscle cells

Difference is that the mesangium is branched while the mesentery is a single tube

96
Q

What is nephrin?

A

Nephrin is a protein in the slip diagram of podocytes. The slip diagram cover the gaps between podocytes. Mutation in this protein causes proteinuria in utero because it is so important

97
Q

What are glomerular crescents?

A

feature of v severe glomeruneprhtiis whereby there is accumulation of cells in the bowman’s space (where there should be no cells)

Neutrophils and macrophages release inflammatory mediators that destroy the basement membrane

The break in the basement membrane = cells leak out

generally irreversible and on recovery turns into a scar

If glomerular crescents are seen on biopsy, we have hours to days to do something about the aetiology. Else when majority/all of glomeruli are affected = irreversible kidney damage

98
Q

Causes of crescentic glomerulonephritis

A

Immune complex

  • Especially subepithelial deposits which affect the podocytes
  • Includes SLE, IgA nephropathy, post-infectious (post-strep)
  • Anti-GBM disease
  • Pauci-Immune
    Associated with anti-neutrophil cytoplasm antibodies (ANCA)
  • Called pauci because staining of glomerulus do not reveal immune complexes but is mediated by immune system

Crescentic glomerunephritis is also another term for rapidly progressive GN cos they will cause RF rapidly

99
Q

Antibodies to phospholipase A2 is associated with what form of GN?

A

Membraneous GN (presents with nephrotic syndrome)

100
Q

Causes of CKD by prevalence

list the top 5

A 
Causes of CKD by prevalence 
Diabetes (19.5%)
Glomerulonephritis (15.3%)
Hypertension and vascular disease (15%)
Chronic infection (pyelonephritis) associated with reflux nephropathy (9.5%) 
Polycystic kidney disease (9.4%)
101
Q

A few pts may have membranous GN associated with secondary causes
Give 3 examples of secondary causes

A

SLE
Infection
Drug
Malignancy - neoantigens against tumours

102
Q

Histological features of diabetes nephrotic syndrome kidney disease

A

Histologically characterised by mesangial expansion (Kimmelstiel Wilson nodules)→ glomerulus obliteration

Clinically characterised by microalbuminaemia → proteinuria/nephrotic syndrome

103
Q

Renal cause of AKI: Thrombotic microangiopathy

What is the name of the syndrome associated with this cause?

What are the two types of this syndrome

A

Syndrome referred to as HUS because

  • Damage to endothelium of glomeruli, arteriole and arteries leading to thrombosis
  • Red blood cells may become damaged by fibrin leading to haemolysis (mechanical damage) - MAHA

MAHA + low platelets + AKI

Two forms
- Diarrhoea assisted - especially E.Coli O157
Release toxin that targets the renal endothelium
Contaminated meat/burgers and petting zoos (faecal-oral)

  • Non-diarrhoea associated (or atypical HUS)
    Often associated with abnormalities of proteins that control activation of the complement pathway on endothelium
    May be familial
    There is effective treatment - antibodies that bind to C5 (very expensive)
104
Q

Chronic inflammation e.g RA + proteinuria/neprhotic syndrome. What is the cause of proteinuria?

A

Think amyloidosis as cause of nephrotic syndrome

rheumatoid arthritis, chronic infections (TB) – causes AA protein deposition

Clinical clues of amyloidosis - Macroglossia, heart failure, hepatomegaly

105
Q

Clinical clues of amyloidosis in a SBA qn

A

Clinical clues of amyloidosis - Macroglossia, heart failure, hepatomegaly

106
Q

Compare HUS and TTP

A

HUS usually affects children, TTP affects adults

TTP has neurological symptoms because the thrombi occurs throughout the circulation but in HUS mostly limited to kidneys

Both will show MAHA, AKI and low platelets. But in TTP also neurlogical signs and fever

In bloods, both will show

  • low Hb, low platelets
  • haemolysis: increased bilirubin, increased LDH, increased reticulocytes
  • blood film will show fragments RBC/schistocytes (SHEEEEEEAR)
  • Coomb’s test negative (as this is not autoimmune AIHA)
107
Q

Compare mucosa of gastric body and duodenum

A

Gastric body

  • columnar epithelium (mucin secreting)
  • specialised glands e.g. parietal and chief cells
  • NO goblet cells

Intestional/duodenum

  • glandular epithelium with GOBLET CELLS
  • villous architecture (villous:crypt 2:1)
108
Q

Difference between mucosa of stomach antrum v stomach fundus/body

A

Important to note the specialised mucosa (parietal cell and chief cells) in the body/fundus and non-specialised mucosa in the antrum

Chief cells secrete pepsinogen and chymosin
Parietal cells secrete HCl and intrinsic factor

109
Q

What is the Z line of the oseophagus

A

Z-line

  • Also known as squamo-columnar junction or gastric-oesophageal junction
  • Sharp transition from the stratified squamous epithelium to the columnar epithelial of the stomach
  • Because the oesophagus is squamous epithelium, any pathology that affects squamous epithelium e.g. pemphigus, pemphigoid can sometimes affect the oesophagus.
110
Q

acute oesphagitis what will histology show

A

Neutrophil infiltration and oedema around individual squamous cells of the oesophagus

111
Q

patient has acid reflux) GORD. what are the 3 outcomes?

A
  1. Acute inflammation
  2. Ulceration
    Must goes through the muscularis mucosa (deep), if it doesn’t, it is just an erosion (superficial)
    Necrotic slough
    Inflammatory exudate
    Granulation tissue
  3. Fibrosis
    Once there is fibrosis, this is defined as a chronic ulcer
    It is not the depth of ulcer that defines chronicity
112
Q

Complications of GORD

A

Haemorrhage (if ulcer goes through a blood vessel)
Perforation
Stricture (due to fibrosis)
Barret’s oesophagus

113
Q

Name the two types of metaplasia in Barrett’s oesophagus

A

Metaplasia from stratified squamous to

  • Just columnar = gastric metaplasia (UK definition of Barrett’s)
  • Columnar + goblet = intestinal metaplasia (US definition of Barrett’s)
    Rmb that normal stomach do not normally have goblet cells!!!
    Intestinal metaplasia is more likely to become cancerous
114
Q

Where does adenocarcinoma of oesophagus typically occur?

A

Near the z line where the metaplasia in Barretts would be

Typical progression of metaplasia → dysplasia → adenocarcinoma

115
Q

What are common causes of squamous cell carcinoma of oesophagus and where is this cancer normally found?

A

Associated with alcohol and smoking (as with all head and neck cancer)

Typically Mid/lower oesophagus with signs of ulceration

Histology will show the cancer making keratin bridges as per usual for all squamous cell carcinomas

116
Q

Why does oesophageal varices bleed so easily?

A

Lower oesophageal-stomach varices are the most common

Do not take much ulceration (e.g. GORD, H.plyori) to make these varices bleed

117
Q

Oeosinophilic oesophagitis

A

Associated with allergic reaction
Spasms of the muscle of the oesophagus leading to dysplasia
Treated by steroids or removing allergen (e.g. food)

118
Q

Causes of acute gastritis (neutrophil predominant)

A

Alcohol
Chemical: NSAIDS, aspirin, corrosives
Shock causing hypo perfusion of stomach
Infection: Helicobacter pylori

119
Q

Causes of chronic gastritis (lymphocytes +/- neutrophils (acute on chronic)

A

H.pylori associated
Chemical (antrum): NSAIDS, bile reflux
Alcohol
Autoimmune (body): auto-antibodies e.g anti-parietal
- NB because specialised gland e.g. parietal cells and chief cells are only found in the body and fundus, NOT in the antrum

120
Q

You do not see lymphoid follicles in the stomach UNLESS you have H.plyori infection T/F

A

T
H.plyori induce the lymphoid follicles, initially polyclonal but can become monoclonal and hence H.plyori can cause lymphomas

121
Q

Metaview about the two pathways to cancers in the GI Tract

- flat v polyp pathway

A

Flat pathway is typically in upper GI cancers e.g. gastric cancer

  • chronic gastritis → intestinal METAPLASIA → dysplasia → cancer
  • at any stage, they can also form ulcers
  • hence BIOPSY all ulcers to check for malignancy

Polyp pathway is typically in lower GI cancers e.g. colorectal cancer
- polyp (excess epithelial proliferation) → adenomas → carcinomas

122
Q

Describe the cag-A toxin in H.pylori

A 
cag-A-positive H.pylori have needle like appendage that injects toxin into intercellular junctions allowing he bacteria to attach more easily 
The toxin (Cag-A) blocks apoptosis → pathway to cancer 
This strain is associated with more chronic inflammation
123
Q

What is the most common type of cancer of the stomach? what are the 2 morphological subtypes of this cancer?

A

> 95% of all malignant tumours in stomach are adenocarcinomas

Split morphologically into

  1. Intestinal - well differentiated
    - Evolve from pts with intestinal metaplasia
  2. Diffuse - poorly differentiated (Linitis plastica), signet ring cell carcinoma

Remaining 5% of gastric cancers are:
- Squamous cell carcinoma
- MALToma from H pylori→ progress to form large cell lymphoma (Early MALToma can be reversed by treating H.pylori infection)
- Gastrointestinal stromal tumour (GIST): Spindle cell tumour, derived from interstitial cells
- Neuroendocrine tumours: anywhere in the GI possible
Small bowel, stomach and appendix very common

124
Q

H.pylori in the duodenum

A

Continuation of what happens in the stomach
Increased acid production in the stomach which spills over into duodenum
Chronic inflammation and gastric metaplasia (lost of goblet cells) with H.pylori infection

125
Q

histology of coeliacs

A

Villous atrophy
Crypt hyperplasia
Increased intraepithelial lymphocytes (>20 lymphocytes/100 enterocytes)

126
Q

Original cells in gastric MALToma v duodenal MALTomas

A

MALTomas associated with coeliac is found in the duodenum and is T-cell origin
(vs B cell marginal zone in the stomach caused by H.pylori)

127
Q

Most oesophageal and gastric cancers arise from pre-existing adenomas T/F

A

F

This is the adenoma carcinoma pathway which is more common in lower GI cancers. Upper GI is from the flat pathway

128
Q

Pts with coeliacs on a diet containing gluten, what is the histological change in the duodenum

A

Villous atrophy with increased intraepithelial lymphocytes. → Very classic
Villous atrophy without increased intraepithelial lymphocytes if they recently stopped but villous atrophy damage hasn’t recovered

129
Q

Which of the following is not a cause of chronic gastritis

  • Autoimmunity - e.g. pernicious anaemia
  • Infection
  • Drug
  • Metabolic disease i.e diabetes etc
A
  • Metabolic disease i.e diabetes etc. There has been association but likely related to socio-economical class and diet
130
Q

C.diff has a distinct histology. Describe

A

Mucopurulent exudate erupts out of crypts to form a mushroom-like cloud with a linear configuration of karyorrhectic (destructive fragmentation of the nucleus in a dying cell) debris and neutrophils that adheres to surface
Looks like little volcanoes erupting

131
Q

C.diff abx

A

Therapy: Metronidazole or vancomycin

PO

132
Q

IBD with erythema multiforme which IBD?

A

Crohn’s

133
Q

IBD with myositis. Which IBD?

A

UC

134
Q

IBD + PSC. Which IBD?

A

UC

135
Q

Gardner’s syndrome

A

Familial adenopolypoptosis + distinctive extra-intestinal manifestations

  • Multiple osteomas of skull and mandible
  • Epidermoid cysts
  • Desmond tumours
  • Dental caries, unerupted supernumerary teeth
  • Post-surgical mesenteric fibromatoses
136
Q

Inheritance pattern of FAP/APC

A

Autosomal dominant - average onset is 25 years old
Mutation at chromosome 5q21, APC tumour suppressor gene
Virtually 100% will develop cancer within 10-15 years, 5% periampullary Ca

137
Q

HNPCC

A

Uncommon autosomal dominant disease
Onset of colorectal cancer at early age
High frequency of carcinoma proximal to splenic flexure
Poorly differentiated and mucinous carcinoma more frequent
Multiple synchronous cancers
Presence of extra-clonic cancers (endometrium, prostate, breast, stomach)
Due to DNA mismatch

138
Q

Staging system for colorectal Ca

A 
Duke’s staging = spread 
A = confined to wall of bowel 
B = through the wall of bowel 
C = lymph nodes metastases 
D = distant metastases

Stage is more important than grade (level of differentiation)

139
Q

Function of Stellate cells in the liver

A

Store Vit A

140
Q

Function of Stellate cells in the liver

A

Store Vit A

Found in the space of Disse

141
Q

Histological changes when there is liver damage

A

Loss of hepatocyte microvilli
Stellate cells activation and multiply within the space of Disse (between hepatocyte and endothelial cell wall of blood vessel)
Deposition of scar matrix (collagen) in the space of Disse
Loss of fenestration in the endothelial cells (normally endothelial cells in the liver do not sit on basement membranes and have gaps between them to allow ease of access of blood to the hepatocytes)
Kupffer cells becomes activated

From path guide
● Chronic inflammation causes activation of stellate cells that are usually quiescent in the space of Disse.
● They become myofibroblasts that initiate fibrosis by deposition of collagen in the space of Disse.
● Myofibroblasts contract constricting sinusoids and increasing vascular resistance.
● Undamaged hepatocytes regenerate in nodules between fibrous septa.

142
Q

Histology of chronic hepatitis

  • Severity of inflammation = grade
  • Severity of fibrosis = stage
A

Inflammation (grade) can occur at 3 locations

  • Portal inflammation (at the portal triad)
  • Interface hepatitis/“piecemeal necrosis” (between the portal train and liver parenchymal)
  • Lobular inflammation

Fibrosis (stage)

  • Bridging from portal tract to hepatic vein (shortcut)
  • Bypass the sinusoid and healthy hepatocytes
143
Q

Evolution of Hep C infection

A

(begins from acute hepatitis → chronic hepatitis → fibrosis → cirrhosis → liver cancer
Applies to Hep B too

144
Q

Alcoholic hepatitis

A

Acetaldehyde (breakdown of alcohol) is toxic to the liver
Binds to lysine residues and cross links them
If this happens to intermediate filaments in hepatocytes,
Affect transport system - hepatocytes accumulate protein and water → swell up - Ballooning of hepatocytes
Clumping of cytoskeleton to form Mallory-Denk bodies (also known as Mallory haline)

145
Q

Balloon of hepatocytes and Mallory-Denk (Mallory saline) bodies

A

alcoholic hepatitis

hepatocytes accumulate protein and water → swell up - Ballooning of hepatocytes
Clumping of cytoskeleton to form Mallory-Denk bodies (also known as Mallory haline)

146
Q

Micronodular cirrhosis

A

Micronodular cirrhosis is always due to alcohol

Nodules are spots of liver regeneration in response to liver injury. Often surrounded by fibrotic tissue and chronically can lead to liver Ca

147
Q

Non-alcoholic fatty live disease (NAFLD) including non-alcoholic steatohepatitis (NASH)

A

Histologically looks like alcoholic liver disease
Due to insulin resistance associated with raised BMI and diabetes
Differentiate according to clinical history
Becoming very common

148
Q

Anti-mitochondrial antibodies

A

Primary biliary cirrhosis (PBC)

149
Q

Histology of Primary biliary cirrhosis (PBC)

A

On histology, there is absent bile duct in the portal triad because it has been destroyed by inflammation
Bile duct associated with chronic inflammation (with granulomas)

150
Q

PBC v PSC

A

Primary biliary cirrhosis (PBC) v Primary sclerosing cholangitis (PSC)

Both shows loss of bile duct

but PBC is due to inflammation with granulomas. PSC is due to fibrosis choking off the bile duct.

PSC is associated with US and increased risk of cholangiocarcinoma

151
Q

Haemochromatosis v Haemosiderosis

A

Haemochromatosis (overall, SYSTEMIC high iron due to high gut iron absorption due to genetics) - Parenchymal damage to all organs secondary to iron deposition (bronzed diabetes, adrenals, seminiferous tubules)

  • human bodies do not excrete iron well
  • bronzed refer to skin due to melanin deposits

Haemosiderosis (accumulation of iron ONLY IN MACROPHAGES/KUPFFER CELLS, no systemic involvement, macrophages handles extra iron very well). Typically due to blood transfusions

152
Q

Kayser-Fleischer rings

A

Wilson’s disease (Copper)

KFC - C for copper

153
Q

Iron (haemachromatosis) do not require special stains (however you can use Prussian blue if you want) What stain is needed for Wilsons disease (copper)?

A

Rhoadnine stain - Stains copper-associated protein a golden-brown colour against the blue counterstain

154
Q

Haemchormatosis is due to increased gut absorption of iron. Wilsons is due to

A

Accumulation of copper due to failure of excretion by hepatocytes

155
Q

In haemachromatosis, the excess iron is deposited into every organ of the body e.g. pancreas, adrenals, liver. Where primarily does excess copper deposit in Wilson’s disease?

A

Accumulates in the liver and the CNS (hepato-lenticular degeneration)
Deposits particularly in the basal ganglia

156
Q

Alpha-1 antrypsin deficiency commonly causes lung problems? What lung problem does this cause? and how is the liver involved?

A

Role of alpha1-antitrypsin in the lung is to protect the lungs from neutrophil elastase. When this is deficient in the lungs, you get neutrophil breakdown of alveoli walls and early onset emphysema at a young age. PT MUST NOT SMOKE because cigarette smokes further inactivates A1AT

The liver is involved because the liver synthesises alpha-1 anti-trypsin. In A1AT deficiency, the A1AT is synthesised but fails to be excreted. Hence low levels in the blood but the liver is stuffed full of alpha-one antitrypsin

A1AT is toxic to the liver and causes intra-cytoplasmic inclusion → hepatitis and cirrhosis

A liver biopsy in such cases will reveal PAS-positive, diastase-resistant granules. Unlike glycogen and other mucins which are diastase sensitive (i.e., diastase treatment disables PAS staining), A1AT deficient hepatocytes will stain with PAS even after diastase treatment - a state thus referred to as diastase resistant.

157
Q

Causes of hepatic granulomas

A 
Specific causes 
- PBC 
- Drug 
General causes 
- TB 
- Sarcoid etc
158
Q

Which hepatitis is associated with fatty change in the liver?

A

hep C

NOT HEP B

159
Q

Most common liver cancer

A

Mets

In terms of primaries,

  • Hepatocellular carcinomas
  • Hepatoblastoma (foetal variant)
  • Cholangiocarcinoma
  • Haemangiosarcoma (blood vessels)
160
Q

RET proto-oncogene Cr10+

A

Hirschsprung’s disease

161
Q

Causes of MACRONODULAR (nodules > 3mm). Variable nodule size in the liver

A

Caused by: viral hepatitis, Wilson’s disease, alpha1 antitrypsin deficiency

162
Q

Causes of MICRONODULAR (nodules < 3mm). Uniform liver involvement

A

Caused by: alcoholic hepatitis, biliary tract disease

163
Q

Modified Child’s Pugh score

A

Used to indicate prognosis in liver cirrhosis

  • ascites
  • encephalopathy
  • bilirubin
  • albumin
  • PT

Total Score <7 = Child’s Pugh A (45% 5yr survival)
Total Score 7-9 = Child’s Pugh B (20% 5yr survival)
Total Score 10+ = Child’s Pugh C (<20% 5yr survival)

164
Q

In wilsons disease, will these be high or low?

  • serum caeruloplasmin
  • serum copper
  • urinary copper
A

LOW serum caeruloplasmin
LOW serum copper
HIGH urinary copper

Wilsons is a disease of copper EXCRETION.
the copper usually is excreted by the liver via BILE into the gut or via blood to circulate via binding to ceruloplasmin (blood transporter for copper).

In wilsons, both are affected. Copper is STUCK in the liver, cannot go into bile or blood as there is LOW ceruloplasmin. Hence serum copper is PARADOXICALLY low.

No carrier and no way to excrete copper in bile, the liver releases FREE COPPER into the serum. This free copper precipitates throughout the body but particularly in the kidneys, eyes and brain (hence the eye signs and neuro signs, copper in hepato-lenticular. The lentilcular nucleus of the CNS comprises of basal ganglia, particularly in the putamen and globus pallidus where copper mostly deposits).

The kidney filters these FREE Copper and hence high URINARY COPPER.

Wiki: In children, the penicillamine test may be used. A 500 mg oral dose of penicillamine is administered, and urine collected for 24 hours. If this contains more than 1600 μg (25 μmol), it is a reliable indicator of Wilson’s disease.[clarification needed] This test has not been validated in adults.[12]

Gold standard test is obv liver biopsy.

165
Q

Treatment for Wilson’s disease

A

Generally, penicillamine is the first treatment used. This binds copper (chelation) and leads to excretion of copper in the urine.

Good prognosis with early treatment but any neuro damage is permanent and may require liver transplant

166
Q

List in order of the most common cancers that mets to bones in adults

A 
Breast 
Prostate 
Liver 
Kidney 
Thyroid

BP LKT

167
Q

List is order of the most common bone cancers in children

A 
Neuroblastoma 
Wilm's 
Osteosarcoma 
Ewing's sarcoma 
Rhadomyosarcoma

Sera's MBBS (12 decks)

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