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Medicine > Histopathology UoB > Flashcards

Histopathology UoB Flashcards

1
Q

Intra tubular germ cell neoplasia

A

In situ stage
Proliferation of neoplasticism germ within seminiferous tubules
80% oh GCT show ITGCN in the adjacent tube
Sometimes seen in the biopsy for infertility and cryptorchidism

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2
Q

Classic seminoma

A

Commonest sub-type
Peak at the 4th decade
M/S sheets of rounded cells with clear cytoplasm and variable lymphocytic infiltrate in the stroma

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3
Q

Spermatocytic seminoma

A

3-5% of all seminomas
Older age group
M/S mixed population of small,intermediate and giant cells with increased mitosis rate
Excellent prognosis

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4
Q

Embryonal Carcinoma

A 
20-30yrs 
More aggressive than seminoma
M/S the cells are anaplastic and arranged in glandular, alveolar, solid, or papillary growth patterns.
Associated with other germ cell tumours
Pure form only 3%
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5
Q

Yolk sac tumour

A

Pure form in children
Most common GCT in infants and children up to 3yrs
In adults associated w/ embryonal carcinoma
Variable morphology
Schiller-Duval bodies by peri-vascular layer of tumour cells
AFP raised
Neoplasticism cells positive for AFP

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6
Q

Choriocarcinoma

A

0.3% pure, 1.5% in other NSGCT
Both cyto and syncitiotrophoblasts
Highly malignant
Raised HCG

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7
Q

Teratoma

A

Can differentiate into any of the three germ cell layers
They can have mature tissue TD or immature (foetal) tissue
Pure teratoma TD 2nd most common in children - good prognosis
In adults pure form rarely
Treated as malignant as it has metastatic potential

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8
Q

Testicular tumour staging

A 
1 cancer contained in testes
2 nearby lymph nodes in pelvis abdomen
2A LN <2cm, 2B LN 2-5cm, 2C >5cm
3A distant LN or lungs, S0, S1
3B near LN and S2, or lungs/distant LN S2
3C as 3B but S3 or spread to brain/liver
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9
Q

Prostate cancer

A

Aetiology: hormones, 1q24-25, 1st degree relatives, far consumption, lycopene reduces risk
M/S adenocarcinoma, small glandular structures w/ single layer of cells
Grading - Gleason’s score
Staging: A; not palpable, B; palpable, confined, C;extra-capsular, D; metastatic

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10
Q

Minimal change disease/glomerulopathy

A

Commonest cause in nephrotic syndrome in childhood
No detectable immune deposit but immune basis
Strong association with respect. infection and immunisation
Diffuse effacement of foot processes (fused)

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11
Q

Focal segmental glomerulosclerosis

A

Primary or secondary
Some glomeruli (foci) show partial (segmental) hyalinisation
Unknown pathogenesis
Poor prognosis

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12
Q

Membranous glomerulonephritis

A

Deposition of anti-glomerular basal membrane antibodies
Thickened GBM and subepithelial deposits/spikes
Commonest cause of nephrotic syndrome in adults
85% idiopathic, 15% association with malignant tumours, SLE, drugs, chronic infection

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13
Q

Acute proliferative glomerulonephritis

A

Major cause of acute nephritis in childhood
Follows beta-haemolytic streptococcal infection
Endocapillary hypercellularity with numerous neutrophils and closure of glomerular vessels
Glomeruli increase in size and cellularity

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14
Q

Membranoproliferative glomerulonephritis

A 
Crescenting or rapidly progressing
Increase in mesangial substances
Localised capillary wall thickening 
Increased cellularity
Pronounced lobulation
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15
Q

Acute tubular necrosis

A

Focal necrosis
Desquamation of cells in tubular lumen
Causes: ischaemia, toxic injury, DIC, urinary obstruction

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16
Q

Acute pyelonephritis

A

Fever
Elevated creatinine
Acute inflammatory infiltrate in interstitium and tubular lumina

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17
Q

Chronic pyelonephritis

A 
Kidney surface: irregular, depressed, scarred, bulging
Can affect both kidneys at the same time
Scarring is asymmetrical
Dilated, blunted, deformed calyces
Dilated colloid - filled tubules
Thyroidisation of the kidney
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18
Q

Hypertensive kidney

A 
Benign nephrosclerosis
Some degree present with increased age
HTN and DM can increase severity
Fine, granular surface
Fibrous intimal thickening
NB: Malignant HTN &amp; accelerated nephrosclerosis
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19
Q

ADPKD

A

1/500
Middle age
Haematuria, UTI, abdo mass, HTN, assoc. cerebral aneurysm
Rx: supportive, HTN, dialysis/transplant

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20
Q

ARPKD

A 
1/20000
Large abdominal mass at birth
Possible “potter” appearance
Liver abnormalities
Evolves into: death, renal failure, HTN, portal hypertension
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21
Q

Wim’s tumour

A

Benign
Papillary adenomas
Fibroma

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22
Q

Renal cell carcinoma

A

Risk factors: smoking, HTN, obesity, heavy metals, Von hippel lindau syndrome (naemangioblastoma of cerebellum, retina, renal cyst, bilateral RCC)
Haematuria
Backpain
Palpable mass
Paraneoplastic
Histotypes: clear cell, papillary and chromophobe
High power view: clear cytoplasm, sharply outlined cell membrane

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23
Q

Bladder carcinomas

A 
Papillary (1%), benign
Urothelial carcinoma
RFs:
Smoking
Industrial exposure to arylamines
Previous irradiation
Long term use analgesia
Cyclophosphamide
Schistosoma (SCC)
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24
Q

Haemangioma

A

Benign vascular tumour
Most common benign tumour
Incidental pick up
Rarely rupture

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25
Q

Bile duct malformation

A 
Common
Incidental finding
Often misinterpreted as metastasis
Benign
Along with bile duct adenoma
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26
Q

Liver cell adenoma

A

More common in women
Associated with OCP
Multiple subtypes
Some more likely to bebecome malignant

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27
Q

FNH

A

Tumour like malformation
Central scar
Can become very large
More common in women

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28
Q

Hepatocellular carcinoma

A

Most common primary malignant tumour
More common in men
5th most common malignancy in men
Huge regional variance

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29
Q

Causes of HCC

A 
Cirrhosis
Hep B/C
ASH/NASH
Autoimmune hepatitis
Chronic biliary disease
Much less common: haemochromatosi, A1AT- deficiency, wilson’s disease
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30
Q

Fibrolamellar HCC

A

Occurs in younger people
No background cirrhosis
Better prognosis

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31
Q

Hepatoblastoma

A 
Occurs on children under 5
Most frequent liver tumour in children
Most are male
AFP often raised
Lobulated appearence
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32
Q

Angiasarcoma

A

Rare but most common sarcoma of liver
Throrotrast, arsenic, anabolic steroids, vinyl chloride
More often in older men

33
Q

Cholangiocarcinoma

A

Often aggressive with poor prognosis

Associated with chronic inflammation of bile ducts (PSC, parasites, pyogenic cholangitis)

34
Q

Primary sclerosing cholangitis

A 
Often in young/middle aged males
Common in patients with ulcerative
Progressive inflammation and fibrosis of large intra and extrahepatic bile ducts
Can lead to secondary biliary cirrhosis
Increased risk of CC 
AMA negative
Can be p-ANCA +
35
Q

Primary biliary cirrhosis

A

Middle aged females
AMA+, IgM+, Alk Phos raised
Affects small bile ducts
Can lead to cirrhosis

36
Q

Wilson’s Disease

A

Autosomal recessive Ch 13
Aberrant storage of copper in many organs including the liver
Leads to liver failure
Often presents in childhood

37
Q

Haemochromatosis

A

Autosomal recessive HFE gene on Ch 6
Leads to increased iron absorption and storage in the liver
Leads to cirrhosis
Increased risk of HCC

38
Q

Alpha-1-antitrypsin deficiency

A

Mutation in the A1AT gene on Ch 14
Abnormal protein leeds to accumulation in the liver
Leads to fibrosis and cirrhosis
Increased risk of HCC

39
Q

Fibroadenoma

A 
Commonest benign breast tumour
20-35yrs
Increased in size during pregnancy
Decrease in size with age
M/S composed of both proliferating ducts and connective tissue stroma
40
Q

Phylloides tumour

A

4th-5th decade
M/S composed of epithelial and mesenchymal elements
Mesenchymal component is malignant and can produce metastasis through haematogenous route
Rx wide local excision
Recurrence is common

41
Q

Carcinoma of the breast

A

Hormonal factors
Genetic factors: BRAC 1 (ch 17 ovaries and breast), BRAC2 (ch 13)
Environmental influence

42
Q

Breast screening programme

A

All women aged between 50-69
Mammography
Every three years

43
Q

Crohn’s

A 
Involvement of both terminal ileum and caecum ~50%
Confined to the colon ~20
Skip lesions
Cobblestone appearance
Mesentery thickened and oedematous
Histopathology:
Transmural inflammation
Non-necrotising granulomas
Crypt abscess
Ulcers deep; abscess and fistulas
Healing of ulcers > fibrosis and strictures
44
Q

Crohn’s complications and Rx

A 
Inflammatory adhesions
Perforation
Perirectal disease  
Malabsorption
Small bowel carcinoma
Rx:
5-aminosalycilic acid (mesalazine)
Steroids
Immunosupressive drugs
Anti-TNFs infliximab
Surgery
45
Q

UC

A

Crypt abscesses with neutrophils in crypts, crypt wall and in lamina propria
Crypt architectural distortion, with gland branching, shortening and loss of normal parallel arrangement of glands
Complications: toxic megacolon, perforation, massive haemorrhage, colon cancer
Treatment: 5-ASA, steroids, immunosuppressive drugs, surgery

46
Q

Inflammatory pseudopolyps

A

In UC and Crohn’s
Macroscopically can look like adenomas
Microscopically: inflammatory tissue, hyper-plastic mucosa

47
Q

Hamartomatous polyps

A

Benign tumour-like lesion
Two or more differentiated tissue elements
Juvenile polyps: most common paeds GI polyp
Peutz-Jegher: GI polyps, pigmentation of oral polyps, lips, palsm, genitalia

48
Q

Juvenile polyp

A 
Cystic glands w/ normal or inflamed epithelium
Germ line SMAD4 mutation (18q21-22)
Children mean age 8
80% in rectum
Clinical: bleeding, prolapse
49
Q

Peutz-jeghers polyps

A 
Autosomal dominant
Occur throughout the GI tract
Small>large
Intussusception and partial or complete obstruction
Carcinoma develops from dysplastic foci
50
Q

Adenomas

A 
All dysplastic
Premalignant
Tubular; tubular growth
Tubo-villous adenoma; villi - elongated crypts, stalk
Villous adenoma; more than 75% villous
51
Q

Flat/depressed adenoma

A

High malignant potential
High incidence of severe dysplasia
Associated with HNPCC, or FAP

52
Q

Colon cancer screening

A

Colonoscopy: UC, FAP/HNPCC, adenomatous polyps
Faecal occult blood (false positives)
Flexible sigmoidoscopy
Genetic testing

53
Q

HNPCC

A 
Dominant
Carcinoma develops younger
Right sided
Multiple
5% of cases
4 mismatch repair
Amsterdam criteria
54
Q

FAP

A

Rare
No intervention > cancer
Multiple polyps (up to 1000s)
Polyps not present at birth

55
Q

Role of virus in Lymphoma

A

EBV - Burkitt, Hodgkin, post transplant and AIDS related lymphoma
HTLV1 - T Cell NHL
Hepatitis C - low grade B cell NHL
HHV 8 kaposi plasma cell malignancy

56
Q

Lymphoma diagnostic methods

A

Morphology, H + E (follicular lymphoma)
Immunochemistry
Flow cytometry
Molecular techniques - PCR, FISH (chromosomal abnormalities)

57
Q

Reflux oesophagitis

A

Risk factors: hiatus hernia, peptic ulcer, smoking & alcohol, excessive vomiting, pregnancy, diabetes, GOJ surgery

Complications: stricture, barret’s, neoplasia

58
Q

Achalasia

A

Aetiology unknown

Inflammatory destruction of myenteric ganglion cells

Long term complications: squamous cell carcinoma

59
Q

Oesophageal infection

A
  1. Candida
  2. Herpes simplex virus
  3. Trypanosomiasis: transmitted in faeces of blood sucking reduviid bug - via it’s blood
60
Q

Barret’s oesophagus

A

Metaplastic replacement of oesophageal lining by glandular mucosa
Aetiology: reflux
Normal squamous > Barret’s > dysplasia > adenocarcinoma 80% (20% SCC DXT +/- surgery)

61
Q

Chemical/reactive gastritis

A 
More frequently recognised
Commonest form of chronic gastritis
Bile reflux
Drugs: aspirin, NSAIDs
Alcohol
62
Q

H. Pylori

A

Gastritis
Ulcer
MALT lymphoma: eradication of HP with PPI Abx and bismuth > regression
Carcinoma: superficial gastritis > atrophic gastritis > intestinal metaplasia > dysplasia > carcinoma

63
Q

Adenocarcinoma of the stomach

A

M:F = 3:1
7th commonest cancer killer in the UK
Risk factors: diet (high salt, low dairy products), H. pylori

64
Q

GIST

A

Rare
Stomach>SI>oesophagus and large bowel
Mutation in tyrosine kinase genes (KIT)
Rx: surgery +/- TKI inhibitors imatinib

65
Q

Coeliac disease

A

Malabsorption (anaemia, low albumin)
Autoimmune (anti-tTG)
Abnormal immunological reaction to gluten
Improvement on gluten-free diet
Flat mucosa
Reduction of normal villous height to crypt depth ratio from 5:1 to <3:1
Crypt hyperplasia
Increased intra-epithelial lymphocytes
Infiltration of the lamina propria by plasma cells and lymphocytes

66
Q

Coeliac complications

A

Refractory sprue - non responsive to gluten restriction
Ulcerative jejunitis
Neoplasia: enteropathy-associated T-cell lymphoma (EATL), small intestinal adenocarcinoma

67
Q

Giardiasis

A

Giardia lamblia
Commonest SI protozoal infection worldwide
Contaminated water (orofeacal)
Immunocompromised more likely to get infected
SI mucosal may be normal or inflamed

68
Q

SI neoplasia

A 
Adenomas: duodenal (FAP)
Adenocarcinoma - rare (coeliac, crohn’s, FAP)
Lymphoma: Burkitt’s, EATL
GIST
Neuroendocrine tumours
69
Q

Pr-eclamsia

A

Unknown cause
Maternal high BP + protein in urine
Autopsy: Asymmetrical IUGR
Placenta pathology

70
Q

Common pathological findings in perinatal autopsy

A

Maceration; skin slippaged post mortem in stillborn
Intra ventricular haemorrhage
Anecephaly; absence of brain and skull vault
Spina bifida (neural tube defect)
Hydrops; generalised oedema of the foetus
Atresia of bowel
Single palmar crease (trisomy 21)
Findings in oligohydramnios (wrinkled glove like skin and potter facies)

71
Q

Placenta pathology

A

Pre-eclampsia

Acute choriomanionitis: common after PROM, ascending infection

72
Q

Hirschsprung’s disease

A

Developmental disorder with absence of ganglion cells in distal rectum
Aganglionic part of variable length
Due to failure of neuronal crest cells migration during development of enteric nervous system
Delayed meconium passage
Abdominal distentions
Bilious vomiting

73
Q

Cystic fibrosis

A

Autosomal recessive mutation of CTFR
Lung involvement: mucus plugging of airways, severe suppurative lung disease, bronchiectasis
Bowel involvement: bowel lumen filled with inspissated meconium, interstitial atresia, rectal prolapse
Characteristic mucus extends deep into crypts

74
Q

Coeliac disease

A

T-cell response in small intestine
Inflammatory reaction to gliadine
Seen in T1DM, trisomy 21
Breastfeeding protective
Young children: failure to thrive, malabsorption, abdo pain
Older children: abdo pain
Long term complications: osteoporosis, intestinal T-lymphoma
Anti-gliadine and anti-tissue transglutaminase Ab - AGA and TGA
Villous atrophy
Increased intraepithelial lymphocytes
Increased lamina inflammatory cells

75
Q

Polycystic kidney disease

A

Autosomal recessive - PKHD1 (stillbirths and early neonatal death)
Autosomal dominant: 30-50

76
Q

Effects of ischaemia on myocytes

A 
Onset of ATP depletion - seconds
Loss of contractility - <2min
ATP reduced: to 50% - 10min, to 10% 40min
Irreversible injury - 20-40min
Microvascular injury - >1h
77
Q

Gross changes of MI

A

None to occasional mottling ( up to 12 hours)
Dark mottling (12-24h)
Central yellow tan with hyperaemic border (3-7 days)
Grey white scar (2-8wks)

78
Q

Microscopic changes of MI

A

Early coagulation necrosis and oedema; haemorrhage
Pyknosis of nucleic, hypereosinophilia, early neutrophilic infiltrate
Coagulation necrosis, interstitial infiltrate of neutrophils
Dense collagenous scar

79
Q

Lab detection of MI

A

CK (MB isozyme)
Lactate dehydrogenase
Troponin - I and T

Medicine (4 decks)

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