malignancies Flashcards

(38 cards)

1
Q

AN APPROACH TO LIVER TUMOURS
* Non-neoplastic versus neoplastic:
 Non-neoplastic lesions can mimic neoplasms
 – , — , — tumour-like
lesions, — : US, CT, MR + context
diagnostic
* Benign versus malignant neoplasms:
* Primary versus secondary malignancies
* Consider different types of primary neoplasm
 Depending on tissue type of origin, e.g. for
malignancies: carcinoma, possibly of different
types, sarcomas of different types, lymphoma etc.
* But focus/highlight commoner entities

A

Cysts, haemangiomas, regenerative, abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

PRIMARY LIVER TUMOURS
Benign
* — (= liver cell adenoma, anabolic — and oral — pill (OCP))
* — adenoma (rare)
* —
Malignant
* Hepatocellular — (=liver cell carcinoma, — , – )
* Intrahepatic — (=intrahepatic bile duct adenocarcinoma)
* — (textbook rarity)

A

hepatic adenoma
anabolic steroids and oral contraceptive pills
bile duct adenoma
haemagioma
carcinoma
hepatoma , HCC
Intrahepatic cholangiocarcinoma
Haemangiosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SECONDARY TUMOURS/LIVER
METASTASES
* — ‘liver tumour’ in Europe/N America
* Carcinoma - primary in – , — , –
* Other malignancies can infiltrate liver e.g. – , —
* Metastases may obstruct —
 Early: few symptoms/effects, Alk Phos —
 Late: rising — , —
* Generally poor —
* Identify primary site of origin for —–
* — for isolated colorectal metastases

A

commonest
GI tract , lung , breast
lymphoma and leukaemia
bile flow
raised
rising bilirubin , jaundice
poor prognosis
treatment
surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

— IS USED IN LIVER METASTASIS HISTOLOGY
* CK20, CDX2 : —
* TTF1 : —
* S100, Melan A, HMB, SOX10 : —

A

immunohistochemsity
large intestine
lung
melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Multiple pale deposits are —
(don’t confuse with cirrhosis, not diffuse change)

A

metastases
( check slide 8 for pic )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HEPATOCELLULAR CARCINOMA
* Europe/North America relatively uncommon
* East and SE Asia/Africa common
* Associated with — / — (>90%)
* Can occur in non-cirrhotic fibrotic — livers
* — mass or — , may have vascular —
* — not as usual as in some other tumour types
* Presentation:
High incidence areas - co-presents with or precedes — , in relatively — patients
Low incidence areas : — of cirrhosis, 3% HCC/yr, vague/changing symptoms

A

cirrhosis/chornic hepatitis
hbv
single or multifocal
vascular invasion
metastases
cirrhosis
young
decompression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HEPATOCELLULAR CARCINOMA
Diagnosis:
* Radiology: US, specific contrast-enhanced — and/or — protocols
* Assessment of nodules in cirrhosis, >1cm or enlarging
* Alpha-fetoprotein (AFP): ‘— ’
* — rarely necessary
Screening:
* High risk patients ( — cirrhosis), every —
* US
* AFP blood test – alone not specific/sensitive enough
Prevention
* Treatment of cause of underlying chronic liver disease?
* Prevention of chronic liver disease (HBV — )

A

CT , MRI
tumour marker
biopsy
compensated cirrhosis
6/12
HBV vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HEPATOCELLULAR CARCINOMA
Treatment
* — if early
* OLT
* Local ablative treatments: — , arterial —
Prognosis– depends on:
* –
* Degree of — impairment
* —
* Typically poor but in selected cases 5 year survival of 50%
Aetiology:
* — (HBV/HCV/HFE > other causes cirrhosis?)
* Chronic — directly oncogenic?
* — - fungal contaminants of food stores
- important info in microscopic appearance of HCC:
Tumour cells resemble hepatocytes but show –

A

resection
radio frequency , arterial chemo-embolisation
stage
liver function
co-morbidity
cirrhosis
HBV
aflatoxin
polymorphism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CHOLANGIOCARCINOMA
* – arising from – epithelium
 — or — location
* Commonest site at — of –
 — tumour = obstructing bifurcation of CHD
* Intrahepatic cholangiocarcinoma a minority of primary
liver malignancy (10%)
* Associations: —
 Rare: chronic fluke infestation, congenital biliary
abnormalities
* Diagnosis – and often – , outcome —
* Selected cases – surgical —
* Typically, — obstruction with — placement

A

adenocarcinoma
bile duct
intahepatic or extra hepatic
him of liver
klatskin
PSC
difficult , late , poor
surgical resection
palliate , stent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PANCREAS
* — location
* — components, — distinct
* Exocrine 98%: makes — enzymes
* Endocrine: — , —
* Exocrine composed of glandular — grouped into —
* Exocrine secretions drain via — , joining to form—

A

retroperitoneal
2
embryologically
digestive enzymes
islets of Langerhans, hormones
acini
lobules
ducts
pancreatic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

histology of normal pancreas:
Small pancreatic duct (centre) surrounded by — pancreatic glandular — .
— collection of cells (left centre) is islet of Langerhans

A

exocrine
acini
pale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PANCREATIC TUMOURS
Exocrine pancreas:
* Malignant: pancreatic (ductal) —
* Other less common tumours, sometimes —
* May be – or have — behaviour
* Some recognised as precursors to pancreatic —
Endocrine:
* Pancreatic — tumours rare
* Behaviour difficult to —
* Classified by — type produced
* Hormone may cause — symptoms
* Association with — and — in inherited — syndrome

A

adenocarcinoma
cystic
bengin
intermediate
pancreatic ca
neruoendocrine
predict
hormone
clinical
h parathyroid hyperplasia and pituitary adenomas
MEN type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PANCREATIC CARCINOMA
* — , arising from —
* Common: 5th/6th by rank of cancer deaths
* M — F, 80% >60 years
* 60-70% from — , rest from — &—
* Spread:
 Direct local: — (vessels, nerves),
duodenum, CBD = ‘ — advanced’
 Lymph nodes or to liver (50% — at diagnosis)
* Risk factors (relatively weak)
 Smoking, DM, chronic pancreatitis
 Family history (5%)

A

adenocarcinoma
pancreatic duct
m > f
head , body , tail
peritoneum
locally advanced
metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PANCREATIC CARCINOMA
Symptoms
* Typically symptomatic only with — disease
* Easily missed
* — , —
* — obstructive — (tumours in — )
* Vague abdominal pain, may radiate to —
* Rare: palpable mass, thrombotic tendency
 Migratory thrombophlebitis = — sign
Diagnosis:
* — serum marker for pancreatico-biliary cancer
 Not useful in diagnosis, used for — / — assessment
* Imaging (US, CT, EUS), FNA cytology via EUS
* Avoid unnecessary invasive investigation in majority

A

advanced
anorexia , weight loss
painless obstructive jaundice
head
back
Trousseau’s
CA 19-9
response/relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PANCREATIC CARCINOMA
Prognosis
* 5 year survival <3%, most patients die <1 year
* 10-20% suitable for surgery
* 10-20% 5yr survival in these selected patients
Treatment:
* Pancreatico-duodenectomy ( — procedure)
* Chemotherapy ( — ), modest benefit
* Majority: —
 Stenting, analgesia
* Painless extrahepatic cholestasis/obstructive
jaundice a/w weight loss: suspect —
malignancy

A

Whipple
adjuvant
palliation
pancreatico-biliary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

NORMAL GALL BLADDER
* — and – bile (not vital)
* Anatomical variants (— , — )
* Bile contents:
 — and — ( — action for digestion of fats)
 Excretory: – , — , — , —
* Cholesterol remains in solution by forming — with — – often may be an — solution

A

stores and concentrates
cystic duct and vessels
bile salt and phospholipid
detergent
bilrubin , cholesterol , calcium salts and copper
micelles
bile salt
unstable

17
Q

GALLSTONES
* Common, easily identified with —
* Formed from — (+/- — )
 Predominantly — >90%, may be mixed
 Predominantly — <10%
 10% only are — (+ calcium) on plain x ray
* Cholelithiasis = stones in —
* Choledocholithiasis = stones in —-
 Typically, pass from — to — via —
 Less commonly, form primarily in CBD
* Significant part of workload for general surgeons

A

ultrasound
bile constituents ( calcium )
cholesterol
bilrubin
radio-opaque
gall bladder
common bile duct
gall bladder to CBD to cystic duct

18
Q

WHO GETS GALLSTONES?
Predisposing factors:
* — (16% of US women vs 9% US men)
* Increasing age
* Obesity, high fat/low fibre
* High lipids, type —
* Geography and race (Native Americans, Hispanic)
* High does — : pregnancy, ?Pill, ?HRT
* Gall bladder – / — : rapid weight loss (bariatric surgery), fasting, TPN
* Bilirubin (pigment) stones: bile salt — (Crohn’s ileitis, ileal surgery), — , — , —

A

females
type 2 DM
osterogen
hypo motility/stasis
depletion
cirrhosis , haemolytic , parasite

19
Q

HOW DO GALLSTONES FORM?
Pathogenesis:
* Altered bile composition (“ — bile”), precise mechanism typically unexplained (cholesterol
supersaturation?)
* Gall bladder —
* Phases of accelerated — and —
(sluggish/static gall bladder) in stone formation
* Stones form in — episodes over — period
* Lithogenic bile may cause – and bile — , as well as or instead of stones
* — not a primary event in pathogenesis of stones

A

lithogenic bile
hypomotility
nucleation and growth
sequential
long
microlithiasis and bile sludge
infection

20
Q

SYMPTOMATIC GALLSTONES & BILIARY COLIC
* — most common symptom related to gall stones
– may be difficult to confidently diagnose
 Pain will recur in 70%
 1-2% with biliary colic get complications of gallstones
* — RUQ/epigastric pain, > — minutes, < — hours
 May radiate to – , —
 Usually — pattern/persistent
 — pain due to distension of GB following transient obstruction of —
 No fever/raised WCC/tenderness
 Moderately severe pain: differential diagnosis –
dyspepsia, PUD, acute pancreatitis, oesophageal
pain, MI

A

biliary colic
steady
30
4 hrs
back , right shoulder
crescendo
visceral
cystic duct

21
Q

ASYMPTOMATIC GALLSTONES
Most gallstones — / —findings
* Only 20% cause symptoms if followed up x 15yrs
* Biliary pain (biliary colic) develops in 1-4% annually
* If asymptomatic, treatment not indicated
* Other symptoms – vague abdominal pain, dyspepsia,
fatty food intolerance – are they due to gallstones?
* Distinction between asymptomatic and symptomatic can be difficult
* Will patients benefit from cholecystectomy?

A

asymptomatic/incidental

22
Q

COMPLICATIONS OF GALLSTONES
* Acute cholecystitis and its complications
* Common bile duct —- if stone moves into CBD (or forms there)
 Obstructive —- (—– cholestasis)
 Ascending cholangitis
 Acute pancreatitis
* Gall bladder adenocarcinoma (rare, low overall risk)
* Complications: approx. 1% risk if gallstones, higher if
biliary colic

A

obstruction
jaundice
extra hepatic

23
Q

ACUTE CHOLECYSTITIS
* Nearly always (>90%) a/w —
* — obstruction (sustained), causing:
 — in gall bladder
 — infection
 Small % — (i.e. without stone)
* Fever, nausea, vomiting, pain RUQ x days
* RUQ tenderness, Murphy’s sign +ve
* High WCC, US findings characteristic
* No — (exception: rare Mirizzi syndrome)
* Fluid, analgesia, antibiotics
* Cholecystectomy

A

gallstones
cystic duct
stasis
2ndary infection
small acalculus
no jaundice

24
Q

COMPLICATIONS OF ACUTE
CHOLECYSTITIS
Occur in 10-20%
* — (chronically obstructed, ongoing active
inflammation)
* — (chronically obstructed, sterile)
* — inflammation with risk of perforation
* Pericholecystic abscess or generalised biliary peritonitis
(very rare, high mortality)
* — to duodenum with cholecysto-duodenal —
* Fistula followed by risk of — (small intestinal obstruction due to stone)

A

empyema
mucocole
necrotising inflamamtion
adhesion
fistula
gallstone ileus

25
CBD OBSTRUCTION A/W GALLSTONES Stones move to or form in CBD, may cause: * --- * ---- pain (intermittent), elevated Alk Phos/GGT, dilated ducts (US), risk of infection * Ascending cholangitis * Obstruction with secondary infection * Acute pancreatitis
obstructive jaundice cloicky pain
26
CHRONIC CHOLECYSTITIS * --- finding rather than clinical entity * Pathological description of findings in most gall bladders removed at surgery * Always associated with gallstones * No specific/reliable correlation with symptoms * Gall bladder shows chronic response to repeated --- / --- * Fibrotic, --- gall bladder with stones * --- muscle, --- mucosa, ---
histopathological findings obstruction/inflammation shrunken thickend atrophied diverticula
27
GALL BLADDER ADENOCARCINOMA * <1% of those with gallstones * >80% of cases a/w are ---- gallstones * (Gallstones very common, gall bladder adenocarcinoma ---) * --- > --- , older age group * Presents late, vague symptoms, outlook poor * Clinical problem: gall bladder “ ---” often identified at US  Question is: could they be neoplasms of the gall bladder (adenomas or carcinomas)?  If small/non-progressive, likely to be harmless non- neoplastic cholesterol “polyps”
long standing female more than male polyps
28
CAUSES OF EXTRAHEPATIC BILE DUCT OBSTRUCTION * Gallstones in common bile duct * Tumour  Adenocarcinoma of pancreas  Extra-hepatic bile duct adenocarcinoma * Benign stricture (post-operative or PSC) * Mass outside CBD/CHD compressing duct  Mirizzi syndrome ( --- compression from stone in --- /--- of GB)  Primary tumour or metastases in lymph nodes
external compression neck/cystic duct
29
ASCENDING (ACUTE) CHOLANGITIS * Infection in --- , obstructed bile * High --- , --- , --- = Charcot’s triad * Add --- , altered --- = Reynolds’ pentad * Requires urgent ---
static fever , pain , jaundice hypotension , mental state decompression
30
HEPATIC ABSCESS * Biliary tract disease a/w --- infection commonest cause * Seeding from --- may sometimes be the cause * Historically, common cause was spread via --- from --- * -- and -- * ( -- abscess)
ascending systemic sepsis portal vein intra abdominal sepsis drain and antibiotic amoebic abscess
31
ACUTE PANCREATITIS * Acute inflammation of pancreas * 10-20/million, mortality ?5% (higher if severe) * --- or --- attacks * Pathogenesis  --- (intra-pancreatic) --- of pancreatic enzymes  Once initiated, --- cascade (----)  May trigger systemic inflammatory response syndrome (SIRS) if --- * Obstructing stone at lower end CBD causes --- of bile/concentration of pancreatic juices * -- direct toxic effect
single or recurrent premature activation irreversible auto digestion severe reflux alcohol
32
SEVERITY OF ACUTE PANCREATITIS Mild acute pancreatitis (80% cases): * --- disease * Interstitial --- acute pancreatitis on imaging, is --- Severe acute pancreatitis (20% cases): * --- inflammation of pancreas andsurrounding tissue (peri-pancreatic fat)
self limiting oedematous non necrotizing necrotising
33
EFFECTS OF SEVERE ACUTE PANCREATITIS * Systemic inflammatory response syndrome  Hypovolaemia, hypotension, ARDS, acute renal failure, disseminated intravascular coagulation (DIC) * Hypocalcaemia, hyperglycaemia, ileus * Local complications:  Extensive --- (acute necrotic collection), risk secondary infection  Later: -- , --- * Mortality a/w acute pancreatitis two phases  First week (50%) a/w --- and ---  Second week (50%) a/w --- , ---
necrosis pseudocyst and fistula SIRS , complication necrosis , sepsis
34
CAUSES OF ACUTE PANCREATITIS * ---– 50% men and women * ---– a very common case also * Post-ERCP (5%) * Idiopathic (10%) - biliary microlithiasis * Miscellaneous uncommon causes (5%)  Trauma, ischaemia, major surgery  Drugs, viral  Hypercalcaemia, hyperlipidaemia  Hereditary pancreatitis
gallstones alcohol
35
DIAGNOSIS OF ACUTE PANCREATITIS Symptoms * --- pain, may radiate into --- * ‘--- ’, seen by surgeons * If severe: differential diagnosis ---- , ruptured --- , perforated or ischaemic abdominal organ Blood tests: * Blood --- higher than 3X normal * Amylase short half life * Lipase used in future? * If equivocal, ?radiology * Try and identify cause, avoid immediate laparotomy
epigastric back acute abdomen MI , AAA amylase
36
CHRONIC PANCREATITIS * --- , irreversible -- , ongoing --- * Pancreatic function impaired ( --- > --- ) * Distortion of --- system  Strictures, dilatation and cysts behind strictures, pancreatic ductal stones Causes: * Alcohol * Idiopathic * Childhood causes including --- * CF more typically a/w pancreatic insufficiency due to damage but without clinical ‘chronic pancreatitis’
patchy irreversible fibrosis ongoing inflammation exocrine ? endocrine ductal cystic fibrosis
37
CHRONIC PANCREATITIS Symptoms: * Pain (dull, epigastric, radiating to back) * Weight loss * Steatorrhoea and malabsorption * Secondary diabetes mellitus Treatment: * Analgesia ( --- ), enzyme supplements Diagnosis: * Difficult, sometimes diagnosis of exclusion * Amylase not useful * Tests of pancreatic function not routine * Imaging in advanced disease
opaites
38
PANCREATIC PSEUDOCYST * Collection of --- in disrupted tissue in or adjacent to pancreas * Defined wall but not a true --- (no epithelial lining) * Causes: acute or chronic pancreatitis, pancreatic surgery or trauma * Complications: pain/pressure, infection, erosion with fistula or blood vessel damage * --- or --- by endoscopy or surgery
pancreatic fluid no cysts aspirate or drain