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Histopathology UoB Flashcards

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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
Bile duct malformation
``` Common Incidental finding Often misinterpreted as metastasis Benign Along with bile duct adenoma ```
26
Liver cell adenoma
More common in women Associated with OCP Multiple subtypes Some more likely to bebecome malignant
27
FNH
Tumour like malformation Central scar Can become very large More common in women
28
Hepatocellular carcinoma
Most common primary malignant tumour More common in men 5th most common malignancy in men Huge regional variance
29
Causes of HCC
``` Cirrhosis Hep B/C ASH/NASH Autoimmune hepatitis Chronic biliary disease Much less common: haemochromatosi, A1AT- deficiency, wilson’s disease ```
30
Fibrolamellar HCC
Occurs in younger people No background cirrhosis Better prognosis
31
Hepatoblastoma
``` Occurs on children under 5 Most frequent liver tumour in children Most are male AFP often raised Lobulated appearence ```
32
Angiasarcoma
Rare but most common sarcoma of liver Throrotrast, arsenic, anabolic steroids, vinyl chloride More often in older men
33
Cholangiocarcinoma
Often aggressive with poor prognosis | Associated with chronic inflammation of bile ducts (PSC, parasites, pyogenic cholangitis)
34
Primary sclerosing cholangitis
``` 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
Primary biliary cirrhosis
Middle aged females AMA+, IgM+, Alk Phos raised Affects small bile ducts Can lead to cirrhosis
36
Wilson’s Disease
Autosomal recessive Ch 13 Aberrant storage of copper in many organs including the liver Leads to liver failure Often presents in childhood
37
Haemochromatosis
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
Alpha-1-antitrypsin deficiency
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
Fibroadenoma
``` 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
Phylloides tumour
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
Carcinoma of the breast
Hormonal factors Genetic factors: BRAC 1 (ch 17 ovaries and breast), BRAC2 (ch 13) Environmental influence
42
Breast screening programme
All women aged between 50-69 Mammography Every three years
43
Crohn’s
``` 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
Crohn’s complications and Rx
``` Inflammatory adhesions Perforation Perirectal disease Malabsorption Small bowel carcinoma Rx: 5-aminosalycilic acid (mesalazine) Steroids Immunosupressive drugs Anti-TNFs infliximab Surgery ```
45
UC
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
Inflammatory pseudopolyps
In UC and Crohn’s Macroscopically can look like adenomas Microscopically: inflammatory tissue, hyper-plastic mucosa
47
Hamartomatous polyps
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
Juvenile polyp
``` Cystic glands w/ normal or inflamed epithelium Germ line SMAD4 mutation (18q21-22) Children mean age 8 80% in rectum Clinical: bleeding, prolapse ```
49
Peutz-jeghers polyps
``` Autosomal dominant Occur throughout the GI tract Small>large Intussusception and partial or complete obstruction Carcinoma develops from dysplastic foci ```
50
Adenomas
``` All dysplastic Premalignant Tubular; tubular growth Tubo-villous adenoma; villi - elongated crypts, stalk Villous adenoma; more than 75% villous ```
51
Flat/depressed adenoma
High malignant potential High incidence of severe dysplasia Associated with HNPCC, or FAP
52
Colon cancer screening
Colonoscopy: UC, FAP/HNPCC, adenomatous polyps Faecal occult blood (false positives) Flexible sigmoidoscopy Genetic testing
53
HNPCC
``` Dominant Carcinoma develops younger Right sided Multiple 5% of cases 4 mismatch repair Amsterdam criteria ```
54
FAP
Rare No intervention > cancer Multiple polyps (up to 1000s) Polyps not present at birth
55
Role of virus in Lymphoma
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
Lymphoma diagnostic methods
Morphology, H + E (follicular lymphoma) Immunochemistry Flow cytometry Molecular techniques - PCR, FISH (chromosomal abnormalities)
57
Reflux oesophagitis
Risk factors: hiatus hernia, peptic ulcer, smoking & alcohol, excessive vomiting, pregnancy, diabetes, GOJ surgery Complications: stricture, barret’s, neoplasia
58
Achalasia
Aetiology unknown Inflammatory destruction of myenteric ganglion cells Long term complications: squamous cell carcinoma
59
Oesophageal infection
1. Candida 2. Herpes simplex virus 3. Trypanosomiasis: transmitted in faeces of blood sucking reduviid bug - via it’s blood
60
Barret’s oesophagus
Metaplastic replacement of oesophageal lining by glandular mucosa Aetiology: reflux Normal squamous > Barret’s > dysplasia > adenocarcinoma 80% (20% SCC DXT +/- surgery)
61
Chemical/reactive gastritis
``` More frequently recognised Commonest form of chronic gastritis Bile reflux Drugs: aspirin, NSAIDs Alcohol ```
62
H. Pylori
Gastritis Ulcer MALT lymphoma: eradication of HP with PPI Abx and bismuth > regression Carcinoma: superficial gastritis > atrophic gastritis > intestinal metaplasia > dysplasia > carcinoma
63
Adenocarcinoma of the stomach
M:F = 3:1 7th commonest cancer killer in the UK Risk factors: diet (high salt, low dairy products), H. pylori
64
GIST
Rare Stomach>SI>oesophagus and large bowel Mutation in tyrosine kinase genes (KIT) Rx: surgery +/- TKI inhibitors imatinib
65
Coeliac disease
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
Coeliac complications
Refractory sprue - non responsive to gluten restriction Ulcerative jejunitis Neoplasia: enteropathy-associated T-cell lymphoma (EATL), small intestinal adenocarcinoma
67
Giardiasis
Giardia lamblia Commonest SI protozoal infection worldwide Contaminated water (orofeacal) Immunocompromised more likely to get infected SI mucosal may be normal or inflamed
68
SI neoplasia
``` Adenomas: duodenal (FAP) Adenocarcinoma - rare (coeliac, crohn’s, FAP) Lymphoma: Burkitt’s, EATL GIST Neuroendocrine tumours ```
69
Pr-eclamsia
Unknown cause Maternal high BP + protein in urine Autopsy: Asymmetrical IUGR Placenta pathology
70
Common pathological findings in perinatal autopsy
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
Placenta pathology
Pre-eclampsia | Acute choriomanionitis: common after PROM, ascending infection
72
Hirschsprung’s disease
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
Cystic fibrosis
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
Coeliac disease
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
Polycystic kidney disease
Autosomal recessive - PKHD1 (stillbirths and early neonatal death) Autosomal dominant: 30-50
76
Effects of ischaemia on myocytes
``` 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
Gross changes of MI
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
Microscopic changes of MI
Early coagulation necrosis and oedema; haemorrhage Pyknosis of nucleic, hypereosinophilia, early neutrophilic infiltrate Coagulation necrosis, interstitial infiltrate of neutrophils Dense collagenous scar
79
Lab detection of MI
CK (MB isozyme) Lactate dehydrogenase Troponin - I and T

Medicine (4 decks)

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