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BPT Flashcards > Gastro > Flashcards

Gastro Flashcards

1
Q

Classification of HCV

A

RNA enveloped virus
Flaviviridae

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2
Q

Characteristics of HCV acute phase

A

Increase in HCV RNA (first to increase)
Increase in HCV Ag (positive after 1 month)
Rise in Anti-HCV Ab (positive within 12 weeks and remains positive for life)

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3
Q

Definition of successful viral eradication in HCV

A

Eradication of HCV RNA 12 weeks after treatment

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4
Q

Examples of NS3/4A

A

All the ones that end with -previr
Glecaprevir
Simeprevir/Telaprevir
Boceprevir
Paritaprevir
Voxilaprevir

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5
Q

Examples of NS5A

A

All the ones that end with - svir
Velpatasvir
Pibrentasvir
Elbasvir
Daclatasvir
Lediapasvir
Omhitasvir

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6
Q

Examples of NS5B

A

All the ones that end with -buvir
Sofosbuvir
Dasabuvir

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7
Q

First line therapies for HCV

A

Sofosbuvir (NS5B) + Velpatasvir (NS5A)
Glecaprevir (NS3A/4A) + Pibrentasvir (NS5A)

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8
Q

Spontaneous clearance of HCV more likely in

A

Women, younger patients, and patients with symptoms, high ALT levels, or IL-28 CC genotype

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9
Q

Extrahepatic manifestations of HCV

A

B-NHL (primarily DLBCL)
Mixed cryoglobulinemic vasculitis
Sicca symptoms
Higher cardiovascular events
Vasculitis
Porphyria cutanea tarda
Lichen planus
Membrano-proliferative GN

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10
Q

High risk features of HBV requiring surveillance

A

Anyone with cirrhosis
Anyone with first degree relative
Asian men > 40 yrs
Asian women > 50 yrs
ATSI > 50 yrs
African men and women > 20 yrs

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11
Q

Classification of HBV

A

DNA virus – partially double stranded

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12
Q

Pathology of immune tolerant phase

A

High level HBV RNA
HbeAg positive
Normal LFTs

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13
Q

Pathology of immune clearance phase

A

High HBV DNA
Abnormal LFTs
HbeAg positive

High risk progression of HCC and cirrhosis

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14
Q

Pathology of immune control phase

A

Low HBV DNA
Normal LFTs
HbeAg negative
Anti-Hbe positive

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15
Q

Pathology of immune escape phase

A

Occurs due to mutation of virus

High HBV DNA
Abnormal LFTs
HbeAg negative
Anti-Hbe positive

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16
Q

Pathology of acute HBV

A

Positive HbsAg
Positive Anti-Hbc IgM
Positive HbeAg
HBV-DNA +++

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17
Q

Pathology of chronic HBV

A

Positive HbsAg
Could have positive or negative HbeAg
Positive Anti-Hbc
HBV-DNA +++
Generally Anti-Hbc IgM not positive

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18
Q

Pathology of vaccinated against HBV

A

Positive Anti-HbS
Otherwise everything else negative

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19
Q

Pathology of cleared HBV

A

Positive Anti-HBs
Positive Anti-HBc

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20
Q

Treatment of HBV

A

Entecavir
Tenofovir disoproxil fumarate
Peg-IFN alpha 2a
Tenofovir alafenamide - not listed for monotherapy but is PBS listed for co-infections

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21
Q

Difference between tenofovir disoproxil fumarate with alafenamide

A

Alafenamide has less issues with bone mineral density and renal disease

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22
Q

Entecavir vs tenofovir

A

Entecavir
- Preferred over tenofovir for patients with renal and bone disease

Tenofovir
- Preferred over entecavir for pregnant patients and those with prior exposure to nucleoside analogues i.e lamuvudine

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23
Q

Guidelines of treatment for HBV

A
  • For patients HBeAg positive chronic hepatitis, anti-viral therapy indicated when HBV DNA > 20,000 IU/ml and ALT persistently elevated or evidence of fibrosis
  • For patients HBeAg negative chronic hepatitis, anti-viral therapy indicated when HBV DNA > 2,000IU/mL and ALT persistently elevated, or evidence of fibrosis
  • All patients with cirrhosis and any detectable HBV DNA, regardless of ALT levels
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24
Q

Treatment of acute hepatitis B

A
  • Supportive care
  • Antiviral therapy generally not indicated unless severe or fulminant disease (coagulopathy, marked protracted jaundice, acute liver failure etc.)
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25
Q

Indications for treatment of chronic hepatitis B

A
  • Cirrhosis or advanced fibrosis
  • Acute liver failure
  • Immune active phase – ALT >/ 2 ULN + significantly elevated HBV DNA level, with or without HBeAg
  • Immunosuppression in HBV positive patients
  • Coinfection with HCV or HIV
  • Family history of HCC
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26
Q

Indication of HBV for pregnant women

A

Pregnant women with high viral load (>200,000) should be offered tenofovir from 28th week of pregnancy - reduces perinatal transmission of hepatitis B

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27
Q

Treatment of neonate with mothers positive for HBV

A

All infants should receive HBIg and hepatitis B vaccination as soon as possible after birth

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28
Q

Genotypes of HAV and HEV that affect humans

A

Genotypes 1-4

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29
Q

Transmission of HAV/HEV

A

HAV and HEV mostly spread via faecal-oral route
HEV genotype 3 and 4 are zoonotic viruses. Can be spread foodborne.

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30
Q

Prognosis for HAV and HEV

A

Both are self-limiting infections and do not require treatment

Risk of chronic HEV in immunosuppressed patients

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31
Q

Characteristics of HDV

A

Caused by small, defective RNA virus
Requires HBsAg for transmission

Co-infection of HBV and HDV associated with more severe acute hepatitis and higher mortality
- 50-70% of patients with chronic HBV/HDV co-infection develop cirrhosis

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32
Q

Treatment of HDV

A

Peginterferon alfa - at least 48 week course weekly SC injections
Bulevirtide 2mg SC/daily

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33
Q

Difference between all the stages of HBV infection

A

Immune tolerant
- Immune system does not recognise virus as foreign resulting in high levels of viral replication due to minimal immune pressure and no reaction
- High levels of virus
- Normal LFTs and minimal liver damage done at this stage
- E antigen positive

Immune clearance
- Immune pressure on HBV, causing decrease in viral loads and increase in ALT levels (due to immune reaction)
- Suppression of virus causing formation of e antibodies
- Tissue damage at this stage

Immune control
- Suppression of virus –> nil further replication and improvement in LFTs

Immune escape
- Due to mutations of virus, immune escape can occur
- Increase in viraemia and ALT
- E Antigen would be negative
- Tissue damage at this stage

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34
Q

Drugs that may induce autoimmune hepatitis

A

Minocycline
Nitrofurantion
Isoniazid
Prophylthiouracil
Methyldopa

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35
Q

Treatment for autoimmune hepatitis

A

1st line
- Budesonide + azathioprine
- Prednisone +/ azathioprine

Refractory disease
- High dose prednisone + azathioprine
- Calcineurin inhibitor

Azathioprine intolerance
- Mycophenolate mofetil

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36
Q

Diagnostic findings on primary biliary cholangitis

A

Increase IgM
Increase lipids
Positive AMA (in 95% of patients)
Positive ANA
If AMA negative, may have positive anti-GP210 or anti SP100

Nil need for liver biopsy if strong clinical suspicion

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37
Q

Management of PBC

A

Ursodeoxycholic acid - reduces rate of liver decompensation and transplantation

Management of pruritus with cholestyramine, antihistamines, rifampicin

Treatment other complications: OP, fat soluble vitamin deficiency, lipid issues, autoimmune conditions

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38
Q

Diagnosis of primary sclerosing cholangitis

A

Cholestatic LFT picture + MRCP findings (strictures of intra and extrahepatic bile ducts)

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39
Q

Management of PSC

A

Minimal therapies to improve long term effects
Ursodeoxycholic acid can improve LFTs, but nil effects on long term outcomes

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40
Q

Prognosis of PSC

A

Increased rate of bowel cancer and liver cancer
Requires annual assessment of liver with MRCP, liver US and colonoscopy

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41
Q

Histology findings on PSC

A

Bile duct inflammation and fibrosis

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42
Q

Histology findings on PBC

A

Bile duct damage
Granulomas within portal tract

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43
Q

Most frequent extra-pancreatic manifestation of type 1 AIP

A

IgG4 related AIP
IgG4 related sclerosing cholangitis is most frequent extrapancreatic manifestation

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44
Q

Presentation of IgG4 cholangitis

A

Cholestatic liver disease
Usually steroid responsive

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45
Q

Diagnosis of MAFLD

A

Hepatic steatosis with overweight/obesity + T2DM –> MAFLD

Hepatic steatosis with lean/normal weight + at least 2 metabolic risk abnormalities –> MAFLD

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46
Q

Metabolic risk abnormalities associated with MAFLD

A

Waist circumference >102/88 in Caucasian men and women (or >90/80 in Asian men and women)

Blood pressure >130/85mmHg or treatment

Plasma triglycerides >/ 1.70 or treatment

Plasma HDL < 1.0 mmol/L for men or 1.3mmol/L for women

Prediabetes

Homeostasis model assessment of insulin resistance score >/ 2.5

Plasma high sensitivity CRP > 2

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47
Q

Management of MAFLD

A

Weight loss
Evidence of Mediterranean diet
Pharmacology TBD - some vidence with pioglitazone, obeticholic acid, GLP1 analogues

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48
Q

High risk patients of HCC requiring surveillance

A

Non-cirrhotic HBV
- Asian men > 40 yrs
- Asian women > 50 yrs
- Sub-saharian > 20 yrs
- Indigenous and Torres Strait > 50 yrs

All cirrhosis pts

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49
Q

Requirements for surveillance of HCC

A

6 monthly US +/- AFP

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50
Q

Evaluation of HCC

A

If < 10mm lesion –> repeat liver US +/- AFP in 3 months

If > 10mm lesion –> evaluate lesion with multiphase CT or MRI

Liver biopsy/alternative imaging/repeat imaging if indeterminate findings

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51
Q

Management of HCC

A

If solitary nodule </ 2cm –> Ablation or resection

If solitary nodule > 2cm or 2-3 nodules –> resection/transplant/ablation

If multiple nodules –> chemoembolisation

If metastatic disease –> systemic therapy

If non-transplant candidate –> supportive care

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52
Q

Transplant criteria for HCC

A

Single lesion </ 50-65mm
2-3 tumours, all </ 30mm/45mm

No macrovascular invasion, no regional nodal disease, no distant metastases

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53
Q

First line immunotherapy for HCC

A

Atezolizumab (PDL-1 inhibitor)
Bevacizumab (VEGF inhibitor)

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54
Q

Side effects of atezolizumab and bevacizumab

A

Atezolizumab –> AI related problems
Bevacizumab –> bleeding and thrombosis

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55
Q

Gene associated with alcoholic cirrhosis

A

PNPLA3 gene
Located on chromosome 12

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56
Q

Mechanism of hepatic fibrosis in alcoholic liver disease

A

Hepatic degradation of ethanol to acetyl-CoA by alcohol dehydrogenase results in NADH excess → ↑ NADH drives the formation of glycerol 3-phosphate (G3P) from dihydroxyacetone phosphate (DHAP) → ↑ in both G3P and fatty acids causes increased triglyceride synthesis in the liver and accompanying inflammation → steatohepatitis → chronic inflammation leads to hepatic fibrosis and sclerosis → portal hypertension and eventually cirrhosis

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57
Q

Histology of alcoholic hepatitis

A

Steatosis and degeneration of cells
Mallory’s hyaline cells ceens

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58
Q

Management of alcoholic hepatitis

A

Alcohol cessation
Prednisone may be used in subset of pts

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59
Q

Risk factors for paracetamol toxicity

A
  • Prolonged fasting or dehydration
  • Chronic under nutrition
  • Chronic, excessive alcohol use
  • Severe hepatic impairment
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60
Q

Paracetamol toxicity management

A

NAC infusion until
- ALT or AST decreasing
- INR < 2.0
- Pt clinically well

FFP if active bleeding

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61
Q

Considerations of liver transplant

A

INR > 3 at 48 hours, or >4.5
Oliguria or Cr > 200
Persistent acidosis or lactate > 3
Systolic hypotension despite resuscitation
Hypoglycaemia, severe thrombocytopenia or encephalopathy
Any alteration of consciousness

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62
Q

Immunotherapy with highest rates of side effects

A

Anti- PD-1/PDL-1 - pembrolizumab, nivolimuab, atezolizumab, avelumab
Anti-CTLA4 - ipilimumab

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63
Q

Treatment of immunotherapy hepatotoxicity

A

Grade >/ 2 (AST and/or ALT >3-5x ULN or bili >1.5-3x ULN)
- Corticosteroid
- withhold immunotherapy
- monitor changes in liver function

Grade 3 (AST and/or ALT >5x ULN or bili > 3x ULN)
- Corticosteroid
- Permanent discontinuation

64
Q

Role of FIB-4

A

Identifies risk of liver disease
Low risk (<1.3) –> follow up in GP
High risk –> follow up with specialist, consider fibroscan, liver biopsy

65
Q

Definition of portal HNT

A

Portal hypertension is defined as a hepatic venous pressure gradient (HVPG) of ≥ 6 mm Hg.

HVPG > 10 mm Hg is clinically significant and > 12 mm Hg is associated with complications.

66
Q

Aetiology of portal HTN

A

Prehepatic
- Portal vein thrombosis
- Splenic vein thrombosis

Intrahepatic
- Cirrhosis including fibrous proliferation (most common cause of portal hypertension in the US)
- Hepatosplenic schistosomiasis
- Massive hepatic metastases
- Hepatic sinusoidal obstruction syndrome (SOS; previously called hepatic veno-occlusive disease)

Posthepatic
- Budd-Chiari syndrome
- Right-sided heart failure
- Constrictive pericarditis

67
Q

Management of portal HTN

A

Non-selective B blocker - carvedilol is choice

Portal systemic shunts:
Transjugular intrahepatic portosystemic shunt (TIPS or TIPSS) for
- Persistent, recurring, or treatment-resistant upper gastrointestinal bleeding resulting from portal hypertension, e.g., from esophageal varices
- Refractory ascites
- Acute thrombosis of portal vein
- Patients with hepatorenal syndrome who are not eligible for or are awaiting liver transplantation

Total portosystemic shunts

Selective portosystemic shunts

68
Q

Principles of acute liver failure

A

Hypothermia
Hypernatraemia
Hypocapniea
Haemofiltration

69
Q

Pathophysiology of hepatic encephalopathy

A

Cirrhosis → ↓ hepatic metabolism and portosystemic shunt → accumulation of neurotoxic metabolites, including ammonia (NH3) → excess glutamine and swelling produced by astrocytes → cerebral edema and ↑ intracranial pressure → neurological deterioration

Metabolic effects:
Hypokalemia → shift of K+ ions out of the cells → shift of H+ ions into the cells to maintain electroneutrality → intracellular acidosis → tubular cells produce more ammonia → neurological deterioration
Metabolic alkalosis → decreased H+ ion availability → decreased conversion of ammonia to ammonium (NH4+) → increased levels of ammonia → diffuses freely through the blood-brain barrier → neurological deterioration

70
Q

Management of hepatic encephalopathy

A

Lactulose - a synthetic disaccharide laxative
- First-line treatment for hepatic encephalopathy
- Improves symptoms of hepatic encephalopathy by decreasing the absorption of ammonia in the bowel
Rifaximin: a broad-spectrum, nonabsorbable oral antibiotic (off-label)
- Reduces the number of ammonia-producing intestinal bacteria
May be added to lactulose if recurrent episodes occur

71
Q

MOA of lactulose for HE

A

Lactulose is converted to lactic acid by intestinal flora → acidification in the gut → conversion of ammonia (NH3) to ammonium (NH4+) → ammonium is excreted in the feces → decreased blood ammonia concentration

72
Q

Pregnancy related liver disease

A
  • Severe preeclampsia and eclampsia
  • HELLP syndrome
  • Acute fatty liver of pregnancy
73
Q

Features of severe pre-eclampsia and eclampsia

A

Occurs after gestational week 22
High BP
Proteinuria
Oedema
Seizure
Renal failure
Pulmonary oedema

74
Q

Features of HELLP syndrome

A

Late second trimester to early postpartum
Abdominal pain
Nausea/vomiting

Haemolysis
Elevated liver enzymes
Low platelet

75
Q

Features of acute fatty liver of pregnancy

A

Third trimester
Abdominal pain
Nausea/vomiting
Jaundice
Hypoglycaemia
Hepatic failure

76
Q

Definition of haemochromatosis

A

Iron overload of genetic origin and related to relative hepciden deficiency

77
Q

Pathophysiology of haemochromatosis

A

HFE gene defect (homozygous) → defective binding of transferrin to its receptor → ↓ hepcidin synthesis by the liver → unregulated ferroportin activity in enterocytes → ↑ intestinal iron absorption → iron accumulation throughout the body → damage to the affected organs

78
Q

Aetiology of haemochromatosis

A

Primary (hereditary) haemochromotosis -
- Classical and most frequent form: adult hemochromatosis type I
- Homozygous or heterozygous for the HFE gene defect
- Located on chromosome 6
- Most commonly affects C282Y and H63D
- Associated with HLA-A3 genotype
- Inheritance: autosomal recessive with incomplete penetrance

Further forms: Hemochromatosis types II–IV are also hereditary, but significantly less frequent.

Secondary haemochromatosis -
- Caused by iron overload
- Transfusion-related (e.g., in individuals with beta-thalassemia major or other forms of chronic anemia requiring chronic transfusion)
- Ineffective erythropoiesis
- Thalassemia
- Sickle-cell anemia
- Sideroblastic anemia (e.g., hereditary sideroblastic anemia; anemia of chronic disease)
- Excessive alcohol consumption

79
Q

Clinical findings of haemochromatosis

A

Fatigue/impotence
Arthropathy
Bronze skin
Liver disease
Signs of DM

80
Q

Management of haemochromatosis

A

Phlebotomy - aiming serum ferritin < 50
Iron chelation
Dietary changes
PPIs
Family screening

Liver transplantation indicated if:
- Decompensated cirrhosis
- Hepatocellular carcinoma

81
Q

Presentation of Wilson’s disease

A

Young patient
Kayser Fleischer rings
Moderately elevated ALT
High bili:ALP ratio
Coombs negative haemolytic anaemia and encephalopathy

Panda sign on MRI
Low ceroplasmin
Elevated 24 hr urine copper

82
Q

Genetic mutations of Wilson’s disease

A

Autosomal recessive disorder
Caused by mutations in ATP7B gene

ATP7B is coppy transporting transmembrane protein

83
Q

Management of Wilson’s disease

A

Chelating agents (D-penicillamine)
Zinc agents
Liver transplant if acute liver failure

84
Q

Use of Maddrey’s DF

A

Determine prognosis and use of steroid in alcohol hepatitis

Maddrey’s DF > 32 - poor prognosis, should have corticosteroids

85
Q

Montreal classification of Crohn’s disease

A

Age, disease location, disease behaviour

86
Q

Montreal classification of UC

A

Age and extent

87
Q

Histology of IBD

A

Crypt architectural distortion and lymphoplasmic infiltrate within lamina propria

88
Q

Genetic factors of IBD

A

NOD2 gene
HLA B27 association

89
Q

Relevance of NOD2 in CD

A

Associated with fibrostenotic complications and increased surgery rates in CD

90
Q

Environmental exposures and IBD

A

Smoking associated with CD but protective for UC
High fat/proteun diet
Poor hygiene
Antibiotics

91
Q

Classification of UC

A

Proctitis - E1
Left sided - E2
Pancolitis - E3

92
Q

Risk factors for colon cancer in UC

A
  • Increased duration and extent of disease
  • Primary sclerosing cholangitis
  • Co-existent FHx
  • Disease activity
93
Q

Surveillance guidelines for IBD

A

Annual
- Active disease
- PSC
- FHx of colorectal cancer in first degree relative < 50 yrs
- Colonic stricture, multiple pseudopolyps
- Previous dysplasia

3 yearly
- Inactive UC
- Crohn’s colitis
IBX and FHx of CRC in first degree relative > 50y/o

5 yearly
- Two previous normal colonoscopies

94
Q

Risk factors for severe CD

A
  • Steroids at diagnosis
  • Age < 40 yrs
  • Perianal disease
  • Smoking
  • Strictures
  • Upper GI disease
  • Deep ulcers in colon
  • High titre ASCA
  • NOD2, ATG16L1, MDR1 genes
95
Q

Treatment targets for IBD

A

Therapeutic drug levels
Mucosal healing
Normal calprotectin

96
Q

Risk factors for severe UC

A

Age < 40 yrs
Extensive disease
Primary sclerosing cholangitis
Deep ulcers
High titre pANCA

97
Q

Approach to UC therapy

A

Treatment according to disease extent and severity

  • 5-ASAs oral and rectal
  • Steroids if inadequate control with 5 ASA but taper
  • Thiopurines - if requiring steroids > x1/year
  • Anti-TNFs - infliximab > adalimumab, golimumab
  • Vedolizumab
  • JAK inhibitors - tofacitinib
98
Q

Approach to CD therapy

A

Symptoms dependent on location and phenotype
Step up vs top down approach
Stop smoking

99
Q

Indications for rapid step up therapy

A

Active disease
Extensive disease
Complicated disease (if fistula –> use TNF inhibitor)
Not reaching treatment target

100
Q

Biologics used in IBD

A

Anti-TNFs - Infliximab, adalimumab, golimumab
(works better in CD > UC)

Anti-integrin - Vedolizumab
(works better in UC > CD)

Anti-IL12/23 - Ustekinumab

101
Q

Use of steroids in IBD

A

Effective as induction but not maintenance agents

Budesonide used in mild ileocolonic CD or UC

102
Q

MOA of azathioprine

A

Azathioprine > non-enzymatic conversion to 6-MP > 6-TIMP > 6-MMPR (mercaptopurine) and 6-TGN (thioguanine)

6-MMPR > hepatotoxicity

6-TGN > T cell apoptosis

103
Q

Measuring thiopurine metabolites

A

Low/absent 6-TGN + Low/absent 6-MMP –> Non compliance

Low 6-TGN/Low 6-MMP –> underdosing

Low 6-TGN/High 6-MMP –> Thiopurine resistance

High 6-TGN/High 6-MMP –> Thiopurine refractory

104
Q

Adverse events of azathioprine

A

Myelosuppression
Hepatitis
Pancreatitis
Nausea/vomiting
Flu-like symptoms
Hypersensitivity syndrome
Infection
Lymphoma
Non-melanoma skin cancer

105
Q

Anti-TNFa agent classification

A

Chimeric - Infliximab
Human - Adalimumab
Humanised Fab’ PEG - certolizumab
Human recombinant receptor/Fc fusion - Etanercept

106
Q

Adverse effects of Anti-TNF

A

Infection - Tuberculosis, invasive fungal infections, viral infections, bacterial sepsis
Lymphoma
Melanoma risk doubled
Demyelinating disorders
Drug-induced lupus like syndrome
Congestive heart failure
Abnormal LFTs

107
Q

MOA of vedolizumab

A

Gut specific
Blocks a4B7-MAdCAM –> T cell adhesion –> causes T cell migration –> inflammatory cytokines (IL-17, IFN-y) produced by T cells

108
Q

MOA of ustekinumab

A

Blocks IL-12/23 via p40 subunit
Effective for moderate disease but not severe

109
Q

Use of JAK inhibitors in IBD

A

Highly effective however significant toxicity
Used for UC, but not available for CD

110
Q

MOA of Tofacitinib

A

JAK 1/3 inhibitors

111
Q

MOA of upadacitinib

A

Blocks JAK1 predominantly

112
Q

MOA of ozanimod

A

S1P modulator
Traps lymphocytes within lymphatic tissues
Reduces lymphocytes in circulation

113
Q

Side effects of ozanimod

A

Bradycardia and cardiac conduction delays
Macular oedema

114
Q

Management of acute severe UC

A

IV hydrocortisone
Flexible sigmoidoscopy and biopsy
Salvage therapy vs Surgery

115
Q

Management of fistula

A

Antibiotics
Surgery
Anti TNF

116
Q

IBD medications contraindicated in pregnancy

A

MTX
Thalidomide

Inadequate data for
- Allopurinol
- Tofacitinib
- Upadacitinib
- Ozanimod

117
Q

Role of parietal cell

A

Releases H+ acid
Activated by Ach (released from distension of stomach) and H2
Inhibited by SSR (from paracrine, D cell) and CCK (gastrin)

118
Q

Role of ECL cell

A

Releases Histamine –> H2
Activated by ACh and M3 (from enteric nervous system), and somatostatin (from D cell)

119
Q

Role of D cell

A

Releases somatostatin and SSR
Activated by ACh and M3

120
Q

Role of G cell

A

Releases gastrin

Activated by vagus nerve (via gastrin-releasing peptide and GRP released from presynaptic terminals of postganglionic fibers), amino acids and peptides,
Decreased acidity and distention of the stomach

Inhibited by somatostatin

121
Q

Role of D cells

A

Releases somatostatin

Inhibits gastrointestinal secretions
↓ Gastric acid
↓ Gastrin
↓ Pepsinogen
↓ Cholecystokinin
↓ Secretin
↓ Pancreatic secretions (VIP, glucagon, insulin)
↓ Gastric inhibitory polypeptide
- Inhibits gall bladder contraction
- Decreases motility of the stomach and intestine
- Causes splanchnic vasoconstriction
- Decreases growth hormone and TSH secretion

Activated by postprandial - gastric acid, fatty acids, and amino acids entering the duodenum

Inhibited by vagus nerve (ACh)

122
Q

Role of GLP1

A

Secreted by L cells in duodenum and colon
Proglucagon cleavage product

Short acting effects - slows gastric emptying
Long acting effects - increase insulin, reduces glucagon
Adverse effects - pancreatitis, nausea, tachycardia

123
Q

Role of GIP

A

Released by K cells in small intenstine

Glucose dependent insulin secretion

124
Q

Side effects of PPI

A

Hypergastrinaemia
- Prolonged acid inhibition
- Atrophic gastritis –> pernicious anaemia, H pylori
- Gastrin secreting tumours
- Renal failure
- Hypercalcaemia
Pneumonia
Gastroenteritis
Osteoporosis
Hypomagnesaemia
Interstitial nephritis
Microscopic colitis

125
Q

Features of MEN1

A

Hyperparathyroidism
Pituitary and pancreatic cancer
1/3rd pts present with Zollinger Ellison syndrome

Autosomal dominant

126
Q

Diagnosis of gastropancreatic neuroendocrine tumours

A

Urinary 5HIAA - 90% sensitivity
Ki-67 index to review severity

127
Q

Motility disorders associated with loss of interstitial cells of Cajal

A

Slow transit constipation
Chronic idiopathic constipation
Achalasia
Gastroparesis
Afferent loop syndrome
Megacolon and megaduodenum
Paraneoplastic dysmotility
Crohn’s disease
Chaga’s disease

128
Q

Chronic pancreatitis definition

A

Permanent structural damage and impaired exocrine + endocrine function
Leading to malabsorption and malnutrition

129
Q

Presentation of chronic pancreatitis

A

Abdominal pain, worse post-prandially
Pancreatic insufficiency
- Fat malabsorption –> steatorrhoea, B12 deficiency
- glucose intolerance/overt diabetes

130
Q

Complications of chronic pancreatitis

A

Pseudocysts
Bile duct/duodenal obstruction - from fibrosis of pancreatic head or compressive effects of pseudocyst
Pancreatic ascites/pleural effusions

131
Q

Diagnosis of chronic pancreatitis

A

72 hour quantitative faecal fat –> diagnostic for malabsorption
Faecal elastase
Abdominal XR - review for calcification of pancreatic duct
CT Abdomen - review for pancreatic atrophy, duct dilatation, parenchymal and intraductal calcifications
MRCP

132
Q

Management of chronic pancreatitis

A

Pancreatic enzyme supplementation
Fat soluble vitamin supplementation
Restrict fat intake
Lipase supplementation

133
Q

Inherited causes of pancreatitis

A

Disorders with trypsin:
- PRSS gene - trypsinogen
- SPINK1 mutation

Pancreatic ductal secretion abnormalities:
- CF gene mutations
- viarant common chymotrypsin C

134
Q

Features and management of IgG4 AI pancreatitis

A

Mild recurrent attacks
Raised serum IgG4
Very responsive to steroids

135
Q

Management of fluid collections

A

If acute fluid/necrotic collection –> delay
If pseudocyst –> drain
If walled off necrosis –> debridement

136
Q

Definition of ABCB4

A

Transmembrane fioppase protein
Transports phosphatidylcholine into bile duct

137
Q

ABCB4 disease

A

Heterozygous disease
Causes
Intrahepatic cholestasis of pregnancy
Isuses with gallstones
Can be treated with ursodeoxycholic acid

Homozygous disease causes neonatal cholestasis

138
Q

Features of serous cystadenoma

A

Located at head of pancreas
Imaging - Honeycombed, microcystic
Central stellate scar with calcification
Histology - glycogen-rich cuboidal cells

Generally not premalignant

139
Q

Features of IPMN

A

Located at head of pancreas
Imaging - Dilated main or branch duct
Histology - columnar mucin-producing cells

Premalignant

140
Q

Features of MCN

A

Affects mostly women
Located at body, tail of pancreas

Imaging - septated cyst, calcification in cyst wall

Histology - ovarian like stroma

Premalignanct

141
Q

High risk features of pancreatic findings

A

Size > 3cm
Main duct dilatation
Solid component

142
Q

Risk factors for pancreatic cancer

A

Smoking
Chronic pancreatitis
Cystic fibrosis
BRCA1, BRCA2
Lynch syndrome
FAMMM
Hereditary pancreatitis
Peutz-Jeghers syndrome

143
Q

Indications for testing in H pylori

A

Active peptic ulcer disease or history of PUD
Low grade gastric mucosa-associated lymphoid tissue lymphoma or history of endoscopic resection
Uninvestigated dyspepsia
Long term aspirin use
Long term NSAID use
Unexplained IDA
ITP in adults
Completion of H. pylori treatment

144
Q

H pylori treatment

A

2 week course of
Amoxicillin/Tetracycline/Bismuth
Otherwise levofloxacin/moxifloxacin

145
Q

Symptoms of eosinophilic oesophagitis

A

Dysphagia
Food impaction
Chest pain
Heart burn
Abdominal pain
Refractory “GORD”

146
Q

Diagnostic findings of eosinophilic oesophagitis

A

Scope - multiple ridges down oesophagus
Histology - esophageal oesinophilia, basal zone hyperplasia, dilated intercellular spaces

147
Q

Management of eosinophilic oesophagitis

A

PPIs
Topical steroids (fluticasone, budesonide, ciclosonide)
Elimination and elemental diets
Dilation
Antihistamines, immunosuppressants, immunomodulators

148
Q

Features of achalasia

A

Inadequate relaxation of the lower esophageal sphincter (LES) and nonperistaltic contractions in the distal two-thirds of the esophagus due to the degeneration of inhibitory neuron

149
Q

Management of achalasia

A

Low surgical risk -
Pneumatic dilation
- The success rate at one month is ∼ 85%; perforation risk is ∼ 2%.

LES myotomy (Heller myotomy): a surgical procedure in which the lower esophageal sphincter is incised longitudinally to re-enable passage of food or liquids to the stomach.

Peroral endoscopic myotomy: An endoscopy-guided myotomy of the inner circular muscular layer of the lower esophageal sphincter (the longitudinal muscle layer is preserved)
- May be considered in other esophageal motility disorders (e.g., diffuse esophageal spasm) as well, in which case the myotomy incision may need to be extended into the esophageal body

High surgical risk:
Botulinum toxin injection in the LES
- A good choice for patients who are poor surgical candidates
- More than 50% of patients require treatment again within 6–12 months.
If other measures are unsuccessful: nitrates or calcium channel blockers

150
Q

Vitamin B12 deficiency causes

A

Diet
Atrophic gastritis: H pylori, pernicious anaemia
Gastrectomy
Bacterial overgrowth
Pancreatic insufficiency
Crohn’s disease
Blocking agents (i.e. neomycin)
Drugs - PPI, metformin, colchicine

151
Q

Histology of coeliac disease

A

Villous atrophy
Lymphocytosis

152
Q

Disease associations with coeliac disease

A

Dermatitis herpetiformis
Autoimmune conditions
- IDDM
- Hypothyroidism
- IgA deficiency
Down syndrome
Turner syndrome
Liver disease

153
Q

Investigations for coeliac disease

A

TTG Antibody + IgA
Serology
Biopsy

154
Q

Definition of Barrett’s oesophagus

A

> 1cm of columnar metaplasia in distal oesophagus

155
Q

Risk factors for Barrett’s oesophagus

A

Reflux symptoms > 5yrs
Male gender
Tobacco smoking
Central obesity
Caucasian

156
Q

Risk of cancer for Barrett’s oesophagitis

A

Low risk

BPT Flashcards (32 decks)

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