Histo Flashcards
what do neutrophil polymorphs indicate
acute inflammation
what do lymphocytes indicate
chronic inflammation
lymphocytes + neutrophils =
acute on chronic
what is the loss of surface epithelium +/- lamina propria with muscularis in tact
erosion
what is the loss of surface epithelium with depth of tissue loss beyond the muscularis mucosae
ulcer
ulcer with element of fibrosis
chronic ulcer
what is dysplasia
cytological and histological features of malignancy, basement membrane in tact
what are the two roads to GI cancer
metaplasia-dysplasia pathway (oesophageal)
adeno-carcinoma pathway (colorectal cancer)
features of adenocarcinoma
gland forming
mucin secreting
features of squamous cell carcinoma
make keratin
inter-cellular bridges
what is the squamo-columnar junction called in oesophagus
Z line
what subtype of barrett’s oesophagus carries greater risk
goblet cell positive(intestinal type columnar epithelium)
stain to highlight intestinal type columnar epithelium
methylene blue
most common oesophageal malignancy worldwide
upper/mid oesopahgeal SCC
alcohol/ cigarettes
most common oesophageal malignancy UK
distal adenocarcinoma (columnar epithelium transformation)
GORD/ oesophagitis
oesophageal varices cause
portal HTN: cirrhosis, portal vein thrombosis, IVC obstruction
oesophageal varices presentation
upper gi bleed, melaena
oesophageal varices management
fluid resuscitate, terlipressin, scope, PPI infusion
should goblet cells be seen in stomach?
NO - indicates intestinal type metaplasia
what do chief cells produce
pepsin
what do parietal cells produce
intrinsic factor
HCl
causes of acute gastritis
alcohol consumption, NSAIDs, H. pylori, stress
causes of chronic gastritis
autoimmune (pernicious anaemia), H. pylori, bile reflux, NSAIDs, CMV if immunosuppressed, crohn’s
H. pylori eradication therapy
PPI
clarithromycin
amoxicillin or metronidazole
h pylori under microscope
gram negative curved rod
what is H pylori associated with
MALT, B cell marginal lymphoma
what is the main type of gastric cancer
adenocarcinoma (95%)
other 5% are SCC, lymphoma, GIST
what are the two types of gastric adenocarcinoma
intestinal - well-differentiated, mucin producing, gland forming
diffuse - sinlge-cell architecture, no gland formation, signet-ring cells
what are signet ring cells associated with
diffuse type gastric adenocarcinoma
usual type of stomach cell
columnar epithelium
most common cause of duodenal ulcers
H pylori
coeliac disease changes on biopsy
villous atrophy, crypt hyperplasia
lymphocytic duodenitis villous structure
NORMAL
examples of non-neoplastic polyps
hyperplastic polyps
inflammatory pseudo-polyps
hamartomatous polyps
examples of neoplastic polyps
tubular adenoma
tubulovillous adenoma
villous adenoma
polyps with increased risk of cancer
higher villous component, dysplastic features
pathology of liver fibrosis
kupferr cells activated
stellate cells activated –> myelofibroblasts
basement membrane secreted
collagen in space of disse
features of liver cirrhosis
whole liver fibrosis with nodules of regenerating hepatocytes and distortion of vascular architecture
alcoholic hepatitis features
ballooning of cells
mallory denk bodies
apoptosis
pericellular fibrosis
hypoxic zone 3
relatively irreversible
most common cause of liver cancer
secondary metastatic disease
primary tumours of the liver
hepatocellular carcinoma
hepatoblastoma
cholangiocarcinoma
haemangiosarcoma
peri-ductal injury in acute pancreatitis suggests what cause
obstructive cause
peri-lobular injury in acute pancreatitis suggests what cause
vascular cause
acute pancreatitis pathology
reflux enzymes –> acinar necrosis –> release of more enzymes
release of lipases –> fat necrosis –> soaponification with calcium
acute pancreatitis complications
haemorrhagic pancreatitis
hypoglycaemia, hypocalcaemia
pesudocyst, abcess
chronic pancreatitis features
fibrosis, duct strictures, loss of paenchyma
main cause = alcohol
main type of pancreatic carcinoma
ductal (85%)
other type = acinar
other types of pancreatic cancer
cystic neoplasms: - serous cystadenoma
- mucinous cystic neoplasm
neuroendocrine tumours
pancreatic neuroendocrine tumour features
associated with MEN1 (pituitary, pancreas and parathyroid)
most commonly in tail
most commonly non-secretory
most common type if secretory = insulinoma
pancreatic ductal carcinoma features
95% associated with K-ras mutations
most common in head (60%)
nephrotic syndrome triad
hypoalbuminaemia
proteinuria
oedema
primary causes of nephrotic syndrome
minimal change disease
membranous glomerular disease
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis
secondary causes of nephrotic syndrome
SLE
diabetes
amyloidosis
minimal change disease on electron microscopy
loss of podocyte foot processes
minimal change disease management
oral prednisolone
most common cause of adult nephrotic syndrome
membranous glomerular disease
membranous glomerular disease auto-antibody
anti-phospholipase A2 receptor
membranous glomerular disease light microscopy
diffuse GBM thickening
membranous glomerular disease electron microscopy
loss of podocyte foot processes
spikey subendothelial deposits
membranous glomerular disease management
ACEi/ ARB, Bp control
focal segmental glomerulosclerosis light microscopy
focal and segmental scarring, hyalinosis
focal segmental glomerulosclerosis electron microscopy
loss of podocyte foot processes
focal segmental glomerulosclerosis management
ACEi/ ARB, BP control
50% respond to steroids
nephritic syndrome features
proteinuria
haematuria
azootemia (high urea and creatinine)
red cell casts
oliguria
HTN
nephritic syndrome causes
acute post-infectious GN
IgA nephropathy (berger’s disease)
rapidly progressive GN (cresentic)
Alport’s syndrome (hereditary nephritis)
thin basement membrane disease (benign familial haematuria)
acute post infectious GN features
1-3 weeks after strep throat or impetigo
acute post infectious GN bloods
high antistreptlysin O titer (ASOT)
low C3
acute post infectious GN light microscopy
increased cellularity of glomeruli/ mesangium
acute post infectious GN electron microscopy
subendothelial humps
acute post infectious GN immunofluorescence
granular deposition of IgG + C3
acute post infectious GN management
supportive
IgA nephropathy features
most common cause of GN worldwide, east/ south asian patients
days after URTI/ GI infection
frank haematuria
deposition of IgA immune complexes
can progress to ESRF
IgA nephropathy bloods
high igA
IgA nephropathy immunofluorescence
granular deposition of IgA and C3 in mesangium
IgA nephropathy rule of thirds
1/3 asymptomatic
1/3 CKD
1/3 progressive ckd –> dialysis/ transplantation
rapidly progressive GN features
ESRF within weeks, most aggressive GN
rapidly progressive GN type 1 association
anti-GBM antibody
rapidly progressive GN type 2 association
immune complex mediated
rapidly progressive GN type 3 association
ANCA associated, pauci-immune