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Gastro Flashcards

1
Q

What is the characteristic endoscopy finding in Gastric Antral Vascular Ectasia?

A

Watermelon stomach - longitudinal rows of flat, reddish stripes radiating from the pylorus into the antrum that resemble the stripes on a watermelon

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2
Q

Are there any conditions associated with GAVE?

A

It is usually an isolated condition but may be associated with cirrhosis or systemic sclerosis

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3
Q

What patient demographic is GAVE most commonly found in?

A

Older (>70yo) women (80%)

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4
Q

How do you diagnose Gastric Antral Vascular Ectasia?

A

Based on classical endoscopic appearance.

Diagnosis may be confirmed by endoscopic biopsy, endoscopic ultrasound, tagged red blood cell scan, or computed tomography (CT) scan

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5
Q

What are the histopathological characteristics of GAVE?

A

vascular ectasia, spindle cell proliferation, and fibrohyalinosis

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6
Q

How might GAVE present?

A

Usually as chronic GI bleed causing iron deficiency anaemia.

However it may present with an acute upper GI bleed

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7
Q

How do you treat GAVE?

A

Periodic blood transfusions

+

Endoscopic coagulation with a heater probe, bipolar probe, argon plasma coagulator, laser therapy, or radiofrequency ablation - these can obliterate the vascular ectasia and decrease the degree of bleeding

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8
Q

Does portal decompression with TIPS reduce bleeding in GAVE?

A

No, underscoring the uncertain relationship between GAVE and portal hypertension

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9
Q

Other than endoscopic therapies, what other treatments can be tried for refractory GAVE?

A

Combination oestrogen-progesterone therapy

Or

Antrectomy

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10
Q

What is Zollinger-Ellison syndrome?

A

ZE refers to the syndrome of gastric acid hypersecretion by a duodenal or pancreatic neuroendocrine tumour (which secretes gastrin - ie a gastrinoma) that results in severe acid-related peptic disease and diarrhoea

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11
Q

Is Zollinger-Ellison syndrome more common in males or females?

A

Males
Commonly diagnosed between age 20-50

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12
Q

What autosomal dominant predisposition to tumors is associated with Zollinger-Ellison syndrome?

A

Multiple endocrine neoplasia type 1 (MEN1)
It is classically associated with the “3 Ps”
- parathyroid glands
- pituitary gland (anterior)
- pancreatic endocrine cells
But many other types of cancers recognised to be increased in this condition

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13
Q

What are the 3 Ps of Multiple Endocrine Neoplasia type 1 (MEN1)?

A

Refers to classical tumour location that patients with MEN1 are predisposed to:

  1. Parathyroid gland
  2. Pituitary gland (anterior)
  3. Pancreatic endocrine cells
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14
Q

What percentage of Zollinger-Ellison syndrome is linked to MEN1?

A

20-30%
The rest are sporadic

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15
Q

What percentage of gastrinomas arise in the pancreas?

A

20-25%
The rest are in the duodenum - mostly D1

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16
Q

What are some of the differences between duodenal and pancreatic gastrinomas?

A

Duodenal gastrinomas tend to be:
- small (<1cm)
- multiple
- less likely to have metastasised to liver at diagnosis

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17
Q

In what percentage of patients with gastrinomas do the gastrinomas arise from sites other than the pancreas or duodenum? Where may they arise?

A

5-15%
Can arise from stomach, peripancreatic lymph nodes, liver, bile duct, ovary, heart, small cell lung ca

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18
Q

How are neuroendocrine tumours arising from the digestive system classified by the WHO?

A

Based on the extent to which they resemble their normal non-neoplastic counterparts

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19
Q

If a neuroendocrine tumour stains for gastrin and secretes gastrin but does not produce symptoms of Zollinger-Ellison syndrome, is it a gastrinoma?

A

No - the designation of the tumor as a gastrinoma is based upon the presence of a clinical syndrome that results from tumor production and secretion of gastrin, and not by its morphologic appearance or the presence of gastrin in the secretory granules

In many cases, whilst the tumour may secrete gastrin, the hormone is not processed to biologically active gastrin

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20
Q

What is the pathophysiology of Zollinger-Ellison syndrome?

A

In ZE syndrome, gastrinomas secrete excessive gastrin which results in high gastric acid output due to the trophic actions of gastrin on parietal cells and histamine-secreting enterochromaffin-like cells

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21
Q

Why do patients with Zollinger-Ellison syndrome experience chronic diarrhoea?

A

The high volume of gastric acid secreted cannot be fully reabsorbed in small and large intestines

It also exceeds the neutralising capacity of pancreatic bicarbonate secretion resulting in exceptionally low intestinal pH which inactivates digestive enzymes and the emulsification of fat as well as damaging intestinal epithelial cells and villi resulting in malabsorption

The high serum gastrin concentration also inhibits sodium and water reabsorption by the small intestine leading to a component of secretory diarrhoea

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22
Q

What are the main clinical manifestations of Zollinger-Ellison syndrome?

A

Peptic ulcer disease
Heartburn
Diarrhoea
Weight loss
Complications of acid hypersecretion including bleeding, stricture fistulisation

In <10% - especially those with metastatic disease or MEN1 - may have symptoms due to second hormonal syndrome eg VIPoma

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23
Q

What percentage of gastrinomas are malignant?

A

60-90%

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24
Q

Are there any features on endoscopy that may raise suspicion for Zollinger-Ellison syndrome?

A

Ulcers are more likely to be refractory to PPI therapy and more likely to recur than in patients with sporadic ulcer disease

Ulcers often occur in unusual locations e.g. beyond the first or second fold of the duodenum

90% of patients with Zollinger-Ellison syndrome have prominent gastric folds

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25
When should you suspect Zollinger-Ellison syndrome?
In patients with: 1) Multiple or refractory peptic ulcers 2) Ulcers distal to duodenum 3) Peptic ulcer disease and diarrhoea 4) Enlarged gastric folds 5) MEN1 or FHx of MEN1 6) Diarrhoea responsive to PPI
26
How do you confirm the diagnosis of Zollinger-Ellison syndrome?
By demonstrating an elevated serum gastrin concentration (typically fasting level) and low gastric pH If not diagnostic then consider secretin stimulation test Finally, if still suspicious but negative consider calcium gluconate IV infusion test
27
What other tests are considered helpful in establishing a diagnosis of Zollinger-Ellison syndrome and why?
- Gastric antral/body biopsy demonstrating a lack of atrophic gastritis - The absence of parietal cell and intrinsic factor antibodies As there are several causes of "appropriate" hypergastrinemic conditions that are more common (eg atrophic gastritis, PPI use, renal failure, vagotomy, pangastritis-associated H pylori infection)
28
How does the Secretin stimulation test work in Zollinger-Ellison syndrome?
Secretin is administered by rapid IV infusion over one minute with baseline fasting serum gastrin measured twice then at 2, 5 and 10 minutes.  Secretin stimulates the release of gastrin by gastrinoma cells, and patients with ZES tumors have a dramatic rise in serum gastrin. In contrast, normal gastric G cells are inhibited by secretin. Therefore a significant increase in gastrin levels = positive test. Achlorhydria can lead to false positives and PPI use can lead to false negatives
29
After Zollinger-Ellison syndrome has been diagnosed, how can you localise the tumour?
UGIE Triple phase contrast CT or MRI Somatostatin receptor based PET imaging (DOTATATE) Laparotomy
30
What other testing should you consider in a patient diagnosed with Zollinger-Ellison syndrome?
Biochemical screen for MEN1 eg parathyroid hormone, ionised calcium, prolactin levels
31
What is the first test you should order in a patient with suspected Acute Intermittent Porphyria?
A spot urine test for рοrрhοbilinοgеn (with paired urine creatinine)
32
What percentage of newly diagnosed colorectal cancer cancers are due to Lynch syndrome?
2-3%
33
What is Lynch syndrome?
The most common inherited colorectal cancer susceptibility syndrome - autosomal dominant disorder - results from germline mutations in one of the DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2) or EPCAM gene
34
What is the most prevalent mutation in Lynch syndrome?
PMS2 (note these mutations tend to have lower penetrance than the others and confer comparatively smaller CRC and endometrial ca risk than others + are not associated with increased risk of other cancers
35
Which mutations confer the highest risks of colorectal cancer in Lynch syndrome?
MLH1 and MSH2
36
What is the characteristic feature of loss of mismatch repair in tumours?
DNA mismatches commonly occur in regions of repetitive nucleoside sequences called microsatellites Therefore, in Lynch-associated cancers, you typically see expansion or contraction of microsatellite regions in the tumour (compared to normal tissue) - which is termed microsatellite instability (MSI) MSI may affect genes that control cell growth, regulate apoptosis and some of the DNA MMR genes themselves - the accumulation of mutations in these cancer-related genes is through to drive the process of carcinogenesis in Lynch syndrome
37
In patients with Lynch syndrome, which mismatch repair mutation confers the highest risk of urothelial cancer?
MSH2
38
What is the lifetime risk of CRC in patients with Lynch syndrome?
8.5-56% depending on sex, mismatch repair gene mutation and penetrance of the mutation in the patient and family - highest in males with MLH1 and MSH2 Note age of onset of CRC tends to vary by genotype but usually occurs at a younger age than patients with sporadic CRC
39
How are colorectal cancers in patients with Lynch syndrome different from those with sporadic CRC?
In Lynch syndrome tend to have: - high rates of synchronous and metasynchronous CRC - more right sided CRC than sporadic disease - may progress rapidly from adenomas (tend to be flatter, larger, high-grade dysplasia, villous histology) - may bypass adenoma development and develop directly from microscopic colonic mucosal crypts - demonstrate high MSI and loss of mismatch repair protein expression on immunohistochemistry
40
Other than colorectal cancer, what other cancers are patients with Lynch syndrome more prone to?
Endometrial ca Ovarian ca Stomach ca Small bowel ca Pancreatobiliary ca Genitourinary ca incl TCC + prostate ca Gliomas (brain ca) Sebaceous neoplasms Keratoacanthomas
41
What is the most common extracolonic tumour in Lynch syndrome?
Endometrial ca
42
What type of brain tumours are most commonly associated with Lynch syndrome (compared to Familial adenomatous polyposis)?
Gliomas FAP = medulloblastomas Old name for association between familial CRC and brain tumours = Turcot syndrome
43
What is the Amsterdam (family-history-based) criteria for identifying individuals with Lynch syndrome?
Can be remembered by the "3-2-1" rule 3 affected members (on same side of family) 2 generations 1 under age 50
44
When should you suspect Lynch syndrome in patients with CRC?
If synchronous or metachronous CRC or endometrial ca before the age of 50 OR multiple Lynch associated cancers OR familial clustering of Lynch-assoc ca OR patients with tumours found to have deficient MMR on micosatellite instability or immunohistochemistry testing
45
What are some clues someone may have cirrhosis?
Thrombocytopenia Nodularity on USS Low albumin/high bilirubin/high INR High ARFI/fibroscan/SWE Stigmata of CLD
46
What other causes may result in high liver stiffness measurements?
High ALT Congestion Steatosis
47
What features make up Child-Pugh score?
Encephalopathy Ascites INR Albumin Bilirubin
48
What are the features of Model for End Stage Liver Disease (MELD +Na) score?
Creatinine Bilirubin INR Na Haemodialysis
49
How is HCC different to other cancers?
Mostly diagnosed radiologically - rarely need tissue biopsy - (arterial enhancement, portal vein washout on quad-phase CT) Limited symptoms Traditional chemotherapy has shown no benefit Underlying liver function most important factor 90% of cases assoc with CLD (cirrhosis, HBV, aflatoxin)
50
What strain of Aflatoxin is considered most toxic?
Aflatoxin-B1 (AFB1) - produced by aspergillus
51
What other conditions may be associated with AFP elevation besides HCC?
HCV Untreated HBV Testicular cancer Pregnancy
52
What groups of patients are recommended to undergo HCC surveillance?
Cirrhotic patients with Child-Pugh A, B or C Non-cirrhotic HBV carries with active hepatitis or family hx of HCC Non-cirrhotic HCV and advanced liver fibrosis F3 High risk start in men >40yo, women >50yo; african px >20yo
53
Should patients with seroconverted HBV undergo HCC surveillance?
Yes
54
What treatment is best for patients with stage 0 or A HCC (on Barcelona grading)
Ablation or resection with curative intent
55
What treatment is indicated for HCC (BCLC stage B)?
If ECOG <1, CP-A, nil portal HTN: -> TACE (palliative intent)
56
What treatment is indicated for HCC BCLC stage C? (ie tumour vascular invasion, met disease, multifocal disease)
Lenvatinib (slightly more effective, better tolerated eg less hand and feet syndrome than Sorafenib) Atezolizumab + Bevacizumab
57
What is the most sensitive and specific laboratory finding for the diagnosis of cirrhosis?
Thrombocytopenia
58
In what patients with chronic liver disease may you give vitamin K to (in the setting of asymptomatic lab changes eg prolonged INR)?
In those with suspected Vit K deficiency ie suspected poor nutrition and сirrhοsis, as well as those with cholestatic disease, diarrheal illness, or antibiotic use
59
How might you differentiate DIC from the haemostatic abnormalities of liver disease?
Factor VIII activity - reduced in DIC vs normal/increased in liver disease
60
Is it worth administering FFP or cryoprecipitate to correct the PT/INR value prior to a procedure in a patient with chronic liver disease?
No - studies have shown no clear benefit + additional risks/disadvantages incl transfusion reactions, volume overload (which increases portal pressure) and infection
61
WHat are the risk factors for portal vein thrombosis in individuals with cirrhosis?
Greater disease severity ie CP-C HCC Inherited thrombophilia e.g. factor V Leiden
62
What is the treatment of portal vein thrombosis?
In non-cirrhotics - treat underlying condition + anticoagulate In cirrhotics - treat underlying condition + individual decision re anticoagulation (must balance benefits vs risks; may consider in those awaiting liver transplant; but usually not in those who are asymptomatic, Plt count <50, hepatic encephalopathy + evaluate for varices
63
What anticoagulant would you use for portal vein thrombosis?
LMWH initially then transition to VKA (eg warfarin) for at least 6 months If chronic thrombotic condition OR thrombosis involving mesenteric veins - may continue anticoagulation indefinitely Alternatively can use DOAC

BPT (11 decks)

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