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2a Bateman - Phase 2a MASTER DECK > Gastrointestinal and Liver > Flashcards

Gastrointestinal and Liver Flashcards

1
Q

WHAT IS HEPATITIS?

A

Hepatitis refers to an inflammatory condition of the liver. It’s commonly caused by a viral infection, but there are other possible causes of hepatitis. These include autoimmune hepatitis and hepatitis that occurs as a secondary result of medications, drugs, toxins, and alcohol

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2
Q

What are common hepatitides for each of these hepatitis?

Hepatitis A

Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E

Yellow fever

A

Epstein-Barr V

Cytomegalovirus

Toxoplasma

Influenza

Adenoviruses

Coxsackie B

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3
Q

What is the route of transmission for each of the hepatitis’?

A

A Faeco-oral.

B blood/ sexual.

C Blood/ sexual.

D Blood/ sexual

E Faeco-oral.

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4
Q

Is there chronic infection in each of the hepatitis’?

A

A No

B Yes

C Yes

D Yes

E No

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5
Q

How can you prevent each of the hepatitis’?

A

A Pre and post-exposure immunisation.

B Pre and post-exposure immunisation. Behaviour modification.

C Blood donor screening. Behaviour modificationtion.

D HBV immunisation. Behaviour modification.

E Clean drinking water.

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6
Q

What are the symptoms of acute hepatitis?

A

Malaise

Myalgia

Fever

Nausea/vomiting

Jaundice

RUQ pain.

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7
Q

What are the different levels of these in acute hepatitis?

AST

ALT

Alk Phos

Albumin.

Bilirubin.

A

AST (aspartate transaminase) raised

ALT (alanine transaminase) raised

Alk Phos same or raised

Albumin lower or same

Bilirubin raised.

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8
Q

What is a typical case history for hep A?

A

Travelled to Malaysia for

  • stayed in hostels, local food
  • ‘sea-food banquet’

Unwell 3 weeks after return to UK

  • headache
  • lethargy
  • aching all over
  • poor appetite
  • hot and cold 10/7

later notices eyes/skin yellow

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9
Q

What is the name for hep A?

A

PicoRNAvirus.

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10
Q

Where is hepatitis A found?

A

Contaminated food or water.
Shellfish
Travellers.
Infected food handlers.

Close personal contact.
Household.
Sexual.
Childcare groups.

Blood - IVDU.

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11
Q

When does ALT and AST rise in hep A? When do they return back to normal?

A

Within 1 month. 2 months.

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12
Q

When does IgM anti-HAV show an increase in hep A? When is IgG detectable?

A

2-4 months. For life.

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13
Q

What is the hep A vaccination?

A

Inactivated hepatitis A virus

Grown in human diploid cells

Dose - 0.5ml im - repeat at 6-12 months - booster every 10 years

HAV immunoglobulin - post exposure prophylaxis.

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14
Q

When do you notice a rise in IgM anti-HBc in hep B?

A

From 8-24 weeks.

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15
Q

What is a typical case for Hep B?

A

Divorced

  • new partner for last 8/12
  • Egyptian

Feeling tired ‘long time’
Noticed eyes yellow 5 days ago
Skin very yellow last 24 hours
Urine ‘dark orange’

Afebrile (no fever)
Tender hepatomegaly
Mild pitting oedema of ankles
Arthralgia (pain in joints) and urticaria (skin rash) are commoner.

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16
Q

What would be found out from the investigations for hep B?

A

USS abdo:

  • enlarged liver, bright echogenic texture
  • no focal abnormality
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17
Q

When do anti-HBs start being produced in hepatitis B? What antigens are produced when?

A

After 32 weeks.

HBSAg (surface antigen) is present 1–6 months after exposure.

HBeAg (e antigen) is present for 11⁄2–3 months after acute illness and implies high infectivity.

HBSAg persisting for >6 months defines carrier status.

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18
Q

What are the serology results for acute hepatits B?

A
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19
Q

What would you find in a chronic hep B sufferer?

A

A high hep B surface antigen (HBsAg) (Australian antigen).

Total anti-HBc is also high.

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20
Q

What is the serology for a chronic hepatitis B suferer?

A
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21
Q

What is Hep B called?

A

Hepadnavirus.

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22
Q

Where does hep B replicate?

A

Hepatocytes.

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23
Q

What happens in a hep B infection?

A

incubation 6 week to 6 months

May be asymptomatic - esp <5 yrs

Symptoms can last 6-12 weeks

>90% adults will clear infection

<50% children <5 yrs will clear infection

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24
Q

What are the facts of chronic hep B infection?

A

<50% adults develop chronic infection
- HBsAg >6/12

Highly infectious
- HBeAg +ve

2% carriers / year clear infection and develop natural immunity
- female>male

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25
Q

What is the hep B vaccine types?

A

Inactivated HBsAg

Recombinant DNA (biosynthetic)

Dose: 1ml

  • 3 doses at 0, 1 and 6/12
  • booster every 5 years
  • accelerated course 0, 1, 2/12

HBV immunoglobulin - post-exposure prophylaxis

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26
Q

What is the hep B treatment?

A

Alpha Interferons

Nucleoside Analogues

Tenofovir

Entecavir

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27
Q

What are the different serologies for acute, previous, chroic low infectious and chronic high infectious?

HBcAb

HBsAb

HBeAb

HBsAg

HBeAg

A
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28
Q

What is the typical case for hep C?

A

Intravenous drug use for 12 yrs

  • heroin +/- crack cocaine
  • often shared ‘works’
  • smokes cannabis ‘occasionally’

In rehab for 6/12

  • not injected 5/12
  • attended for health check
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29
Q

What would you find on examination of Hep C patient? Also Serology?

A

Underweight
Scars both arms and groins
Not jaundiced
Afebrile
Tender liver edge.

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30
Q

What are the tests for hep C?

A

LFT (AST:ALT <1:1 until cirrhosis develops)

anti-HCV antibodies confirms exposure;

HCV-PCR confirms on-going infection/chronicity;

liver biopsy if HCV-PCR +ve to assess liver damage and need for treatment.

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31
Q

What is hep C called?

A

Flavivirus (RNA).

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32
Q

What happens in hep C patients, what percentage have acute and chronic?

A

Acute hepatitis ~20% patients

  • majority asymptomatic
  • incubation 2-26/52

Chronic hepatitis ~ 80%

cirrhosis 15%

hepatocellular carcinoma 5%

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33
Q

How is Hep C characterised in the liver?

A

Lymphocytic inflammation.

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34
Q

What is the serology like in a hep C patient?

A
  • *HCV Ab**
  • in all patients
  • appears up to 4/52 after infection
  • *HCV RNA**
  • detected by PCR
  • present in chronic infection

No vaccine available.

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35
Q

What is the hep C treatment?

A

Pegylated Interferons
Weekly injections

Ribavirin
Tablets

Newer drugs (eg Sofofbuvir)

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36
Q

How can you prevent hep C?

A

Screening blood products

Lifestyle modification - needle exchanges etc

Universal precautions - for handling all bodily fluids

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37
Q

What is hep D?

A

Co-infection with acute HBV
- increased severity of infection

Super-infection in patients with chronic HBV

  • 2o acute hepatitis
  • increases risk of fulminant hepatitis
  • increased progression of liver disease
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38
Q

What are the tests and treatments for hep D?

A

Anti-HDV antibody

As interferon-alpha has limited success, liver transplantation may be needed.

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39
Q

What is hep E?

A

Small RNA virus

Similar to Hep A

  • acute hepatitis
  • no chronic disease

Less infectious

Increased mortality 1-2%
- pregnant women 10-20%

now endemic in UK

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40
Q

What one of the hepatitis’ is DNA?

A

Hepatitis B

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41
Q

WHAT DOES THE LIVER DO?

A

Glucose and fat metabolism.

Detoxification and excretion.

  • bilirubin
  • ammonia
  • drugs / hormones / pollutants

Protein synthesis.

  • albumin
  • clotting factors

Defence against infection.

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42
Q

How is the liver arranged? How does the blood flow through it?

A

Regular way (acing or lobular models).

Blood enters via the portal vein and hepatic artery, which lie together with a small bile duct within the portal tract.

Blood flows into a system of sinusoids which bathe the liver cells arranged in plates, with blood, before exiting via the hepatic vein.

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43
Q

How many zones does the liver have?

A

Three, each receiving progressive less oxygenated blood.

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44
Q

What are the types of liver injury? What can they lead to?

A

Acute and chronic.

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45
Q

What does acute liver injury lead to?

A

Results in damage to and loss of cells.

Cell death may occur by necrosis (associated with neutrophils).

Or apoptosis.

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46
Q

What does chronic liver injury lead to?

A

Leads to fibrosis, termed cirrhosis in severest form.

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47
Q

What can cause acute liver injury?

A

Viral (A,B, EBV).

Drug.

Alcohol.

Vascular.

Obstruction.

Congestion.

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48
Q

What can cause chronic liver injury?

A

Alcohol.

Viral (B,C).

Autoimmune.

Metabolic (iron, copper).

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49
Q

How does acute liver injury present?

A

malaise, nausea, anorexia, jaundice

rarer:

  • confusion
  • bleeding
  • liver pain
  • hypoglycaemia
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50
Q

How does chronic liver injury present?

A

Ascites

Oedema

Haematemesis (varices)

Malaise

Anorexia

Wasting

Easy bruising

Itching

Hepatomegaly,

Abnormal LFTs rarer: - jaundice - confusion

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51
Q

What are some serum ‘liver function tests’?

A

Serum bilirubin, albumin, prothrombin time:

Serum liver enzymes:
- cholestatic: alkaline phosphatase, gamma-GT
- hepatocellular: transaminases (AST, ALT)
(give no index of liver function)

(give some index of liver function)

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52
Q

What are the different types of jaundice? Where are they seen?

A

•Unconjugated - “pre-hepatic”

  • Gilberts, Haemolysis

•Conjugated – “cholestatic”

  • Liver disease “hepatic”
  • Bile duct obstruction “post hepatic”
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53
Q

Compare pre hepatic and hepatic or post hepatic for these. Urine. Stools. Itching. Liver tests.

A

Urine. Normal Dark.

Stools. Normal May be pale.

Itching. No Maybe.

Liver tests. Normal Abnormal.

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54
Q

What are some causes of liver disease?

A

Hepatitis - Viral - Drug - Immune - Alcohol

Ischaemia

Neoplasm

Congestion (CCF).

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55
Q

What are some causes of obstruction?

A

Gallstone

  • Bile duct
  • Mirizzi

Stricture

  • Malignant
  • Ischaemic
  • Inflammatory

Blocked stent

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56
Q

What liver tests would tell you which jaundice it is? What further tests could be done?

A

Liver enzymes: Very high AST/ALT suggests liver disease, some exceptions

Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound

Need further imaging:
CT
Magnetic resonance cholangioram MRCP
Endoscopic retrograde cholangiogram ERCP

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57
Q

What are the different types of drug induced liver injury?

A

Hepatocellular.

Cholestatic.

Mixed.

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58
Q

What drugs are known to have drug induced liver injury?

A

Antibiotics.

CNS drugs.

Immunosuppresents.

Analgesics/musculoskeletal.

Gastrointestinal drugs.

Dietary supplements.

Multiple drugs.

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59
Q

WHAT HAPPENS IN PARACETAMOL POISONING?

A

Paracetamol conveyed by Cy P450 into reactive intermediate and then into cellular macromolecules which causes cellular necrosis.

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60
Q

What is needed to help paracetamol poisoning? What does it do?

A

Start N-acetylcystine.

Increases Reactive intermediate to stable metabolite conversion.

Increases glutathione transferase activity.

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61
Q

What does N-acetylcystine correct?

A

coagulation defects

  • fluid electrolyte and acid base balance
  • renal failure
  • hypoglycaemia
  • encephalopathy
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62
Q

What are some paracetamol induced liver failure poor prognosis indicators?

A

Late presentation

Acidosis

Prothrommbin time > 70 sec

Serum creatinine ≥ 300 µmol/l

Consider emergency liver transplant - otherwise 80% mortality

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63
Q

WHAT ARE GALLSTONES MADE UP OF?

A

70% cholesterol, 30% pigment(mainly bilirubin) +/- calcium.

Pigment stones:
Small.
Causes: haemolysis.

Cholesterol stones:
Large.
Causes: gender, age, obesity

Mixed stones: Faceted (calcium salts, pigment, and cholesterol).

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64
Q

What is the prevalence of gallstones?

A

8% of those over 40yrs.

90% remain asymptomatic.

Risk factors for stones becoming symptomatic: smoking; parity.

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65
Q

What are some risk factors for gallstones?

A

Female

Fat

Forty

Fertile.

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66
Q

WHAT IS CHOLECYSTITIS?

A

Stones or sludge in the neck of the gallbladder or cystic duct.

Causing inflammation of the gall bladder.

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67
Q

What happens when somebody eats some food containing a lot of fat?

A

The small intestine secretes CCK which travels in the blood to cause the gallbladder to contract and release bile.

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68
Q

What is the pathology of cholecystitis?

A

Stone stuck in cystic duct

Causes stretching out of gall bladder

Irritates nerves around the gall bladder (pain)

Bile stays in gall bladder causing release of mucus and inflammatory mediators

Results in inflammation and pressure increase

Bacteria start to build up

Pressure builds up and bacteria go through wall causing peritonitis (rebound tenderness)

Immune system starts response with neutrophils

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69
Q

What things can happen with a stone in the cystic duct?

A

Stone falls back out the cystic duct back into the gall bladder

OR

Stone stays stuck causing ballooning of gall bladder
Pressure on blood vessels and gangrenous cell death
Could rupture

OR

Stone gets stuck further down
Bile backs up into liver
Bile forces between tight junctions into blood
Increase in serum conjugated bilirubin
Jaundice
ALP from bile cells leaks because they die

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70
Q

What bacteria start to build up in the gut?

A

E. Coli

Enterococci

Bacteriodes fragilis

Clostridium

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71
Q

What are the symptoms of cholecystitis?

A

Right midepigastric pain at first

Then RUQ pain (referred to the right shoulder)

Vomiting

Fever

Local peritonism, or a GB mass.

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72
Q

What is a classic sign of peritonitis?

A

Rebound tenderness

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73
Q

What are the tests for cholecystitis?

A

Ultrasound
Thick-walled
shrunken GB (also seen in chronic disease),
pericholecystic fluid, stones, CBD (dilated if >6mm),

MRCP
Dye injected

HIDA cholescintigraphy
Radioactive tracer into vein, should show in gallbladder within 1 hour. BLOCKED.

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74
Q

What is Murphy’s sign?

A

Lay 2 fingers over the RUQ; ask patient to breathe in. This causes pain & arrest of inspiration as an inflamed GB impinges on your fingers. It is only +ve if the same test in the LUQ does not cause pain.

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75
Q

What is the treatment for cholecystitis?

A

Laparoscopic cholecystectomy

Pain relieft
NSAIDs

Antibiotics
Cefuroxime IV

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76
Q

WHAT IS BILIARY COLIC?

A

Gallbladder attack or gallstone attack, is when pain occurs due to a gallstone temporarily blocking the bile duct.

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77
Q

Compare gallstones for the gallbladder and bile duct locations?

Biliary pain.

Cholecystitis.

Obstructive jaundice.

Cholangitis.

Pancreatitis.

A

Gallbladder Bile Duct

Biliary pain. Yes Yes

Cholecystitis (inflammation of gall bladder). Yes No

Obstructive jaundice. Maybe Yes

Cholangitis (infection of bile duct). No Yes

Pancreatitis. No Yes

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78
Q

What is Leuconychia?

A

White spots on fingernails.

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79
Q

What is spider naevus? Why is it important?

A

Swollen blood vessels below the skin. Extensive could indicate liver disease.

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80
Q

WHAT IS ASCENDING CHOLANGITIS?

A

Gallstone is stuck in the CBD (choledocholithiasis)

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81
Q

What happens in ascending cholangitis?

A

The flow of bile prevents intestinal bacteria from migrating up the biliary tree and this process is stopped due to the gallstone

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82
Q

What are the common bugs for ascending cholangitis?

A

E. coli

Klebsiella

Enterococcus (group D strep)

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83
Q

What are the symptoms for ascending cholangitis?

A

Charcot’s Triad

Fever, RUQ pain, Jaundice

Reynold’s Pentad

Hypotension + confusion

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84
Q

What tests can you do for ascending cholangitis?

A

USS abdomen

MRCP (Magnetic resonance cholangiopancreatography)
Locate stone

LFTS

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85
Q

What are the treatment options for ascending cholangitis?

A

ERCP (Endoscopic Retrograde Cholangio-Pancreatography)
Remove stone

Surgery

Antibiotics for bacterial cholangitis.

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86
Q

WHAT IS ASCITES?

A

Abnormal accumulation of fluid in the abdominal (peritoneal) cavity

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87
Q

What are the causes of ascites?

A

Portal hypertension
liver cirrhosis

Neoplasia (ovary, uterus, pancreas…)

Congestive heart failure

Advanced kidney failure

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88
Q

What is the pathogenesis of ascites?

A

Increased intrahepatic resistance leads to portal hypertension which leads to ascites. Systemic vasodilation leads to portal hypertension and also secretion of - Renin-angiotensin - Noradrenaline - Vasopressin This then leads to fluid retention. Low serum albumin also contributes to ascites.

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89
Q

What are the symptoms of ascties?

A

Abdo pain

Discomfort

Bloating

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90
Q

What are the investigations for ascites?

A

Physical examination

FBC

Paracentesis to look at fluid

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91
Q

What is the managent of ascites?

A

Treat cause

Limit dietary sodium intake

Diuretics

Therapeutic paracentesis

Surgical shunts

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92
Q

WHAT IS ALCOHOLIC LIVER DISEASE?

A

Liver manifestations of alcohol overconsumption, including

Fatty liver

Alcoholic hepatitis

Fibrosis or cirrhosis

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93
Q

What are the three pathways for alcohol after it enters the liver?

A

Alcohol dehydrogenase
In cytosol

Catalase
Peroxisomes

Cytochrome P450 2E1

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94
Q

What do all three pathways lead to the formation of?

A

Acetaldehyde

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95
Q

What does ADH need to convert alcohol to acetaldehyde?

A

NAD+

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96
Q

What does the levels of NAD have to do with liver disease?

A

As NADH levels increase and NAD+ levels decrease

Higher NADH
More fatty acids

NAD+
less fatty acid oxidation

More fat production

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97
Q

What happens at this fatty liver stage?

A

Patients don’t have symptoms or have high levels of neutrophils in the blood

More yellow due to fat deposits

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98
Q

What is the buildup of fat in the liver called?

A

Stenatosis

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99
Q

What is also a product of ADH? What do these cause?

A

ROS
Hydrogen peroxide
Hydroxyl radical
Superoxide anion

React with different components of hepatocyte

Cause damage to cells

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100
Q

What can acetaldehyde do?

A

Bind to macromolecules and other compounds

When they bind they inihibt the molecule

Acetyaldhyde adducts

Recognised as foreign

Send neutrophils

Neutrophils destroy hepatocytes

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101
Q

What happens as the liver cells become inflammed and damaged?

A

Patient develops alcoholic hepatitis

Mallory bodies appear on histology
Damaged intermediate fillaments
Cytoplasm of hepatocytes

Most commonly seen here

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102
Q

What are the symptoms of alcoholic liver disease?

A

Abdominal (tummy) pain
Loss of appetite
Fatigue
Feeling sick
Diarrhoea
Feeling generally unwell
Jaundice
Oedema
Ascites
Fever

Unusually curved fingertips and nails (clubbed fingers)

Blotchy red palms

Weakness and muscle wasting

Increased sensitivity to alcohol and drugs (because the liver can’t process them)

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103
Q

What does the progression of ALD look like?

A

Alcoholic hepatitis coming and going whilst fat and fibrosis rise.

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104
Q

What is the diagnosis for alcoholic liver disease?

A

Hepatomegaly

Neutrohpilic leukocytosis
increased amount in blood

Perivenular fibrosis

ALT increase
AST incease more
ALP increase
GGT increase

Platelet low

Low blood sugar

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105
Q

What is the treatment of alcoholic liver disease?

A

Stop drinking

Corticosteroids to suppress immune system

Diazapam for alcohol withdrawal

Could lead to cirrhosis or liver failure

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106
Q

WHAT ARE THE CAUSES OF PORTAL HYPERTENSION?

https://www.youtube.com/watch?v=Cox6Z5pqMBo

A

Cirrhosis

Fibrosis

Portal vein thrombosis

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107
Q

What is the pathology of portal hypertension?

A

Increased hepatic resistance

Increased splanchnic blood flow

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108
Q

What are the consequences of portal hypertension?

A

Varices (oesophageal, gastric…)

Splenomegaly

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109
Q

How are varices formed from cirrhosis and portal hypertension?

A

Cirrhosis occurs which means less blow flow can get into liver

Pressure builds up in the veins and causes portal hypertension

Anastomosing vien take the path of lowest resistance

Flow towards the heart straight away rather than portal system

Smaller vein dilate causing varices

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110
Q

WHAT IS PRIMARY BILIARY CIRRHOSIS?

https://www.youtube.com/watch?v=CQtHOMzLzwU&t=1s

A

Excess bile and cholesterol in the blood

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111
Q

What happens in primary biliary cirrhosis?

A

Immune damage is directed towards the small bile ducts inside the liver sinusoids.

Granulomas

Eventually, this will result in the destruction of the bile duct branch.

This will cause cholestasis (reduced bile flow).

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112
Q

What is the cause of PBC?

A

Unknown environmental triggers

+ Genetic predisposition (IL12A)

Leading to loss of immune tolerance to self-mitochondrial proteins.

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113
Q

What is the epidemology of PBC?

A

50 Years olds.

Female more than Men.

0.004% incidence

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114
Q

What is characteristic of PBC?

A

Antimitochondrial antibodies

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115
Q

How does primary biliary cirrhosis present?

A

Asymptomatic
Detected in routine check up

Liver failure
Ascites
Jaundice
​Itching and/or fatigue (pruritus)

Cholsesterol
Xanthelasma
Hyperpigmentation
Xeropthalmia (dry eyes)
Corneal arcus

Joint pain

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116
Q

What are the differential diagnosis of PBC?

A

Hepatitis

Alcoholic liver disease

Primary sclerosing cholangitis

Non-alcoholic fatty liver disease

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117
Q

What are the tests for primary biliary cirrhosis?

A

Blood: increased Alk phos, increased gammaGT, and mildly increased AST & ALT.

Late disease: increased bilirubin, decreased albumin, increased prothrombin time.

AMA

Immunoglobulins
IgM

TSH & cholesterol increased or same

Ultrasound
Excludes extrahepatic cholestasis.

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118
Q

What is the treatment of primary biliary cirrhosis?

A

Pruritus
Colestyramine

Fat-soluble vitamin prophylaxis
Vitamin A, D, E and K.

Ursodeoxycholic acid (UDCA)
Decease cholsterol

Liver transplantation

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119
Q

WHAT IS PRIMARY SCLEROSIS CHOLANGITIS?

https://www.youtube.com/watch?v=ycDfF0EJssY

A

Fibrosing of intra-hepatic and extra-hepatic duct

No continous

Onion skin fibrosis

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120
Q

What is PSC associated with?

A

Complication of cholangiocarcinoma

Correlation with ulcerative colitis

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121
Q

What happens in PSC?

A

Autoimmune destruction of cells lining bile duct

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122
Q

What autoanitbody is PSC associated with?

A

pANCA

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123
Q

How does PSC present?

A

Leads to strictures (areas of narrowing) ± gallstones

Presents

Itching

Pain ± rigors

Jaundice

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124
Q

What are the tests for PSC?

A

Blood: increased Alk phos, increased gammaGT, and mildly increased AST & ALT.

Late disease
Increased bilirubin, decreased albumin, increased prothrombin time.

Immunoglobulins
pANCA and IgM

TSH & cholesterol increased or same

Ultrasound
Excludes extrahepatic cholestasis.

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125
Q

What is the treatment for PSC?

A

Colestyramine for pruritus

Vitamin ADEK supplementation since they are fat soluble

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126
Q

WHAT IS HAEMOCHROMATOSIS?

https://www.youtube.com/watch?v=T7ybRVFXRD0

A

Increased intestinal iron absorption

Iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin.

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127
Q

What is the cause of haemochromatosis?

A

Genetic disorder

Autosomal recessive

90% have mutations in HFE gene

Chromosome 6

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128
Q

What does the excess iron cause to happen?

A

Produces ROS which damage the cells they are in

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129
Q

What are the symptoms of haemochromatosis?

A

DM
‘bronze diabetes’ from iron deposition in pancreas

Dilated cardiomyopathy

Slate-grey skin pigmentation

Tiredness

Arthralgia

Signs of chronic liver disease

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130
Q

How can you diagnose haemochromatosis?

A

Transferrin saturation
Increased

Serum ferritin
Increased

HFE genotyping

Liver biopsy

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131
Q

What is the treatment for haemochromatosis?

A

Venesect (removing blood)

Deferoxamine
Binds iron and excretes in urine

Low iron diet

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132
Q

WHAT IS NON-ALCOHOLIC FATTY LIVER DISEASE?

A

Results from fat deposition in the liver not from alcohol

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133
Q

What are the risk factors for non-alcoholic liver?

A

Obesity

Hypertension

Diabetes

Hypertriglyceridemia

Hyperlipidaemia

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134
Q

How does non-fatty liver disease cause damage?

A

Production of ROS

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135
Q

What are the symptoms of non-alcoholic liver?

A

Usually no symptoms;

Fatigue malasie

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136
Q

What investigations can you do for non-alcoholic liver?

A

LFTs Usually ALT; Alk phos, GGT often normal

Fat, sometimes with inflammation, fibrosis (NASH)

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137
Q

How can you treat non-alcoholic liver?

A

Still no effective drug treatments

Wt loss works- the more the better

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138
Q

WHAT IS ALPHA-1 ANTITRYPSIN DEFICIENCY?

A

Genetic condition when alpha-1 antitryspin is absent

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139
Q

What is the pathology of alpha-1-antitrypsin deficiency?

A

Misfolded alpha-1 antitrypsin builds up in hepatocytes

Leading to cirrhosis

Results in inability to export alpha1-antitrypsin from liver

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140
Q

What are the symptoms of alpha-1 antitrypsin?

A

Cirrhosis

Cholestatic jaundice

Inability to make coagulation factors

Buildup of toxins

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141
Q

What are the investigations for alpha-antitrypsin deficiency?

A

Serum alpha1-antitrypsin (1AT) levels lower

Liver biopsy
Periodic acid Schi (PAS) +ve

Diastaise resistant

Liver ultrasound

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142
Q

What is the treatment for anti-1-antitrypsin deficiency?

A

Lactulose

Liver transplant

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143
Q

WHAT IS WILSON’S DISEASE?

https://www.youtube.com/watch?v=Cr8R_bnKAtk

A

Too much copper (Cu) in liver and CNS

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144
Q

What type of gene disease is Wilson’s disease?

A

Autosomal recessive

Chromosome 13

Codes for a copper transporting ATPase

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145
Q

What is the pathology of Wilson’s disease?

A

In the liver, copper is incorporated into caeruloplasmin.

Copper incorporation into caeruloplasmin in hepatocytes
and its excretion into bile are impaired.

Therefore, copper accumulates in liver, and later in other organs.

ROS made and damage liver

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146
Q

What are the manifestations of Wilson’s disease?

A

Kayser–Fleischer (KF) rings
Copper in iris

Neurological signs
Due to copper in CNS

Liver failure

Hepatosplenogmegaly

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147
Q

What are some tests for Wilson’s disease?

A

Urine: Copper high

Serum copper: LOW

Serum caeruloplasmin LOW

Molecular genetic testing can confirm the diagnosis.

Liver biopsy: increase Hepatic copper

MRI: Degeneration of brain

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148
Q

What is the management of Wilson’s disease?

A

Penicillamine
Bind copper, easier to excrete

Zinc
Decrease copper reabsorption

Liver transplantation
If severe

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149
Q

WHAT IS HELIOCBACTER PYLORI?

A

Gram negative, curved motile rod, microaerophilic.

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150
Q

What is heliocbacter pylori’s key biochemical feature?

A

Urease positivity-used in testing.

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151
Q

How is heliocbacter pylori spread?

A

Oro-fecal or oral-oral.

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152
Q

What is the pathogenesis of heliocbacter pylori?

A

Adapted to living in gastric mucus Colonises over gastric but not intestinal epithelium.

Induces inflammation

Stimulates increased gastrin

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153
Q

Why is heliocbacter pylori adapted to live in gastric mucus?

A

Microaerophilic, motile, urease generates ammonium to buffer acidity.

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154
Q

How does heliocbacter pylori stimulate gastrin?

A

Increased parietal mass but also may modulate gastric acid production.

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155
Q

What are the usual symptoms of heliocbacter pylori?

A

Acquisition usually asymptomatic but may cause nausea and epigastric pain.

Chronic diffuse superficial gastritis

Followed by a period of achlorrydria.

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156
Q

How does heliocbacter pylori alter the production of gastrin and what does this result in?

A

In Antrum: H.pylori reduces somatostatin release by D cells. This leads to loss of inhibition of gastrin release.

G cells now produce increased gastrin levels in the stomach

Increased gastrin levels increases basal acid output

In duodenum: Increased aciditiy leads to gastric metaplasia, H.pylori is then able to colonise duodenum and causes further mucosal damage.

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157
Q

What are some disease associations with heliocbacter pylori?

A

Ulcers.

In the absence of NSAIDS or Zollinger-Ellison syndrome.

Gastric cancer.

Gastric lymphoma.

Oesophageal disease.

Barrett’s oesophagus.

Others.

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158
Q

What is gastric cancer associated with? Why is this strange? HP?

A

Reduced gastric acid, strange because in some patients H.pylori reduces gastric acid in some patients.

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159
Q

What is the spectrum of gastric acid due to in HP?

A

Bacterial strain. Genetics. Diet.

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160
Q

What investigations can you do for HP?

A

Serology

Stool antigen

Urea breath test

Endoscopy with urease test

Histology ± culture

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161
Q

What is the treatment for HP?

A

Omeprazole

Amoxicillin

Clarithromycin

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162
Q

WHAT IS APPENDICITIS?

https://www.youtube.com/watch?v=r9amif1DQMc

A

Inflammation of the appendix

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163
Q

Where is the appendix?

A

Connected to the cecum

Also known as veriform appendix (worm shaped)

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164
Q

What is the funciton of the appendix?

A

Uknown

Maybe gut flord hideout

Lymphatics

Vestigial organ

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165
Q

What is the epidemology of appendicits?

A

10% of people get it

Most common surgical emergency

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166
Q

What are the causes of appendicits?

A

Obstruction
From

Feacalith

Undigested seeds

Pinworm infection

Lymphoid follicle growth
Collection of lymphocytes become maximum size in adolesence

Viral infection caues follicle growth

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167
Q

What happens when the appendix tube is blocked?

A

Continues to secrete mucus

This causes it to swell

Presses on the afferent visceral nerve fibres

Causing pain

Flora and bacteria become trapped

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168
Q

What bacteria become trapped and what happens as a result?

A

E.Coli
Bacteriodes fragilis

Immune cells calls WBC

Pus builds up in appendix

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169
Q

What happens if the appendix continues to swell?

A

Blood vessels get compressed

No oxygen

Walls become ischaemic

They die

Bacteria can now invade wall

Can lead to rupture

Caused peritonitis with rebound tenderness

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170
Q

What are the symptoms of appendicits?

A

Right lower quadrant pain
Mcburney’s point

Fever

Nausea

Vomiting

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171
Q

What are the signs of peritonitis from appendicitis?

A

Rebound tenderness

Abdominal guarding

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172
Q

What is the treatment for appendicitis?

A

Appendectomy

Antibiotics

Drain abscess

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173
Q

WHAT IS PERITONITIS?

A

Inflammation of peritoneum.

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174
Q

What are the causes of peritonitis?

A

Perforation of GI tract i.e. trauma

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175
Q

What are the symptoms of peritonitis?

A

Pain

Rebound tenderness

Guarding reflex

Fever

Increase in WBC

Shoulder tip pain in sepsis

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176
Q

What are the investigations of peritonitis?

A

Erect CXR - air under diaphragm.

USS/CT

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177
Q

How can you treat peritonitis?

A

IV fluids

antibitoics

Electrolytes

Surgery laparotomy

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178
Q

WHAT IS THE DEFINITION OF INTESTINAL OBSTRUCTION?

A

Blockage to the lumen of gut Intestinal

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179
Q

What are some causes of bowel obstruction?

A

Adhesions

Hernias

Tumour

Crohn’s

Volvulus

Gallstone Ileus

180
Q

How is bowel obstruction classified?

A

According to site

Extent of luminal obstruction

Mechanical / True ( intraluminal / extraluminal)

Paralytic (Pseudo obstruction)

Simple Closed loop Strangulation Intussusception

181
Q

What is adhesions?

A

Sticking together abdominal structures to one another, bowel loops or omentum, other solid organs, abdominal wall.

182
Q

What is intesusspition?

A

Telescoping one hollow structure into its distal hollow structure

183
Q

What are the two types of intesusspition?

A

idiopathic enteroenteral intussusception (jejunojejunal, jejunoileal, ileoileal), Associated with special medical situations HSP, cystic fibrosis, hematologic dyscrasias

184
Q

What is the mechanism of intesusspition?

A

an imbalance in the longitudinal forces along the intestinal wall. a mass acting as a lead point or disorganized pattern of peristalsis The invaginating portion - the intussusceptum) the receiving portion - the intussuscipiens.

185
Q

What happens if the mesentery of the intesusspition is lax?

A

The progression is rapid The intussusceptum - prolapse out the anus. Invagination causes the classic pathophysiologic process of any bowel obstruction.

186
Q

What is atresia?

A

Absence of opening or failure of development of hollow structure.

187
Q

What is gallstone ileus?

A

Huge gallstone in gall bladder, inflamed, sticks onto small bowel and erodes through

188
Q

WHAT IS A VOLVULUS?

A

A twist / rotation of segment of bowel

189
Q

What are the types of volvulus?

A

Sigmoid (most common)

Cecal

Midgut

190
Q

What is the cause of a sigmoid volvulus?

A

Pregnancy

Middle aged and eldery constipation

Adhesions

191
Q

What can cause a cecal volvulus and what can cause a midgut volvulus?

A

Same as sigmoid, mesenteric join loose

Abnormal fetal development for midgut

192
Q

What can happen to a volvulus?

A

Can twist and stop blood flow to that part

Can release bacteria into body

193
Q

What are the symptoms of a volvulus?

A

Colicky abdominal pain

Vomiting (earlier with small bowel)

Constipation (earlier with large bowel).

Distension and tinkling bowel sounds.

194
Q

What are the tests for a volvulus?

A

Abdo X-ray

Barium enema
Bird’s beak

195
Q

What is the treatment for a volvulus?

A

Sigmoidoscopy

Endoscopy

Surgery

196
Q

WHAT IS A HERNIA?

A

Protrusion of organ or tissue out of the body cavity in which it normally lies

197
Q

What are some causes of hernias?

A

Age

Chronic cough

Trauma damage

Failure of abdo wall to close properly in womb

Constipation

Heavy weight lifting

Pregnancy

198
Q

What are the different meanings for these?

Irreducible

Reduction

Incarceration

Obstructed

Strangulated

A

Irreducible= hernia cannot be pushed back into the right place

Reduction = pushing tissue/organ back into place

Incarceration = contents of hernialsac are stuck inside by adhesions

Obstructed = bowel contents cannot pass through them

Strangulated = if ischaemic occurs

199
Q

What are the different types of hernia?

A

Hiatal

Inguinal

Femoral

Incisional (after surgery)

Umbilical (<6m, normally corrects itself)

200
Q

What is the most common hernia and why?

A

Inguinal hernia

70%

More common in MEN because after testicles descend through canal after birth the canal doesn’t always close properly so is weakened

201
Q

What is a direct hernia?

A

Protrudes DIRECTLY into inguinal canal

Medial to inferior epigastric vessels

202
Q

What is an indirect hernia?

A

Protrudes through internal inguinal ring

Lateral to inferior epigastric vessels

203
Q

What is a hiatal hernia?

A

Part of stomach herniates through oesophageal hiatus of diaphragm

204
Q

How does a hiatal hernia occur?

A

Sliding
GO junction slides through hiatus and lies above diaphragm

Para-oesophageal hernia
Gastric fundus rolls up through hiatus alongside oesophagus, GO junction remains below diaphragm

205
Q

What are the symptoms of a sliding hernia?

A

None unless gastric oesophageal reflux occurs

206
Q

What are the symptoms of a para-oesophageal hernia?

A

Serious risk of complications (gastric volvulus, bleeding)

207
Q

What are the investigations for a hernia?

A

Made clinically with history and examination

208
Q

What are the treatments for hernias?

A

May require surgical repair

Reducing the hernia can prevent strangulation from occurring

209
Q

WHAT IS DIVERTICULOSIS?

https://www.youtube.com/watch?v=TL9_WKuNfu0

A

Little pouches at the side of the gut

210
Q

What is diverticular caused by?

A

High pressure within the lumen pushes part of the intestine out

211
Q

Where can diverticulosis happen?

A

Any hallow structure in the body

212
Q

What are the types of diverticulosis?

A

True diverticulitis
All layers - mucosa to serosa

False (pseudo) diverticulitis
No muscle layer

213
Q

What is thought to happen when the smooth muscle contracts?

A

Unequal pressure inside the lumen

The contractions are abnormal and exaggerated

Unclear why

214
Q

What is laplace’s law?

A

Pressure inside a vessel is inversely proportional to the diameter

Decrease in diameter increases pressure

215
Q

Where do most diverticulums occur?

A

Sigmoid colon

216
Q

What part of the lumen is more affect by diverticulosis?

A

Where the blood vessels traverse the muscle layer

217
Q

By what part of the gut layer is the divericulum seperated by?

A

Mucosa

Subject to injury and rupture

Haematochezia
Blood in stools

218
Q

What causes incresed risk of diverticulosis?

A

Low fiber foods leads to constipation

Fatty foods and red meat

Marfan’s syndrome

Ehlers-danlos syndrome

219
Q

WHAT IS DIVERTICULAR DISEAESE?

A

Diverticula + complications e.g. infection, hemorrhage, infection

220
Q

What is the symptoms of diverticular disease

A

Usually no symptoms

Sometimes stomach pain and bleeding

221
Q

What can happen if a outpouching ruptures?

A

Can form a fistula

Connection between it and another organ

Most commonly the bladder

222
Q

What is the tests for diverticular disease?

A

Flexible sigmoidoscopy

Barium enema

223
Q

What are the treatment options for diverticular disease?

A

Diet more fibre

Smooth muscle relaxants

224
Q

WHAT IS DIVERTICULITIS?

A

Inflammation of diverticula

225
Q

How can a diverticulosis become a diverticulitis?

A

Inflammation

Through high pressures erroding the wall
OR
Lodged fecalith

226
Q

What are the symptoms of diverticulitis?

A

LIF pain

Fever

Abdoguarding

Tachycardia (similar to appendicitis but on the left)

227
Q

What are the tests for diverticulitis?

A

USS

Bloods (ESR, CRP)

Sigmoidoscopy

228
Q

What is the treatment of diverticulitis?

A

Antibiotics

High fiber

Surgical removal

229
Q

WHAT DOES GRAPHS OF COLORECTAL CANCER SHOW?

A

Environmental causes.

230
Q

What do older people have?

A

Polyps in colon.

231
Q

What causes a predisposition to cancer?

A

polyps.

232
Q

What can happen with cancer in the colon?

A

Go to a dysplastic epithelium but not to cancer.

233
Q

What is the normal progression of the colon into cancer?

A

Normal epithelium. Adenoma. Colerectal adenocarcinoma.

234
Q

What is a genetic condition that can predispose to colorectal cancer?

A

familial adenomatous polyposis

235
Q

How does familial adenomatous polyposis cause cancer?

A

APC bound GSK suppose to break down beta catenin, APC ascent in FAP, beta catenin builds up and causes epithelial proliferation.

236
Q

What is hereditary nonpolyposis colorectal cancer HNPCC?

A

Two hits of DNA repair protein. No DNA repair.

237
Q

What are the reasons for identifying HNPCC cancers?

A

risk of further cancers in index patient and relatives possible implications for therapy tolerance of 5-FU etc. do not recognise DNA damage apoptosis not activated.

238
Q

Where is the most common site for cancer?

A

Rectum.

239
Q

What is colorectal cancer called?

A

Adenocarcinoma.

240
Q

What is important is cancers?

A

Can do staging, using whether it has spread to lymph nodes, how big tumour is.

241
Q

What is the resection margin?

A

Area around a tumour that has been cut out which is not cancerous.

242
Q

What are the different resection coding?

A

R0 - tumour completely excised locally R1 - microscopic involvement of margin by tumour R2 - macroscopic involvement of margin by tumour.

243
Q

Why should you stage a tumour?

A

To give prognosis and see life expectancy.

244
Q

How does staging of tumour work?

A

As it progresses it goes higher.

245
Q

What are the Duke stage prognosis?

A

A 95% 5 year survival B 75% 5 year survival C 35% 5 year survival D 25% 5 year survival.

246
Q

What are Dukes classification?

A

Duke A in gut. Duke B just outside gut. Duke C lymph node. Duke D high tie lymph node.

247
Q

How do you treat normal epithelium going to adenomas?

A

prevention. Low dose aspirin.

248
Q

How do you treat an adenoma?

A

endoscopic resection

249
Q

How do you treat a colorectal adenocarcinoma?

A

surgical resection.

250
Q

How do you treat a metastatic colorectal adenocarcinoma?

A

chemotherapy and palliative care

251
Q

What does Duke’s classification not take into account?

A

Peritoneum.

252
Q

WHAT ARE THE CAUSES OF DIARRHOEAL DISEASES?

A

Infective causes and non-infective.

253
Q

What are some non-infective causes of diarrhoea?

A

Neoplasm. Hormonal. Inflammatory. Radiation. Irritable bowel. Chemical. Anatomical.

254
Q

What are the infective causes of diarrhoea?

A

Non-bloody and bloody (dysentery)

255
Q

What are some different types of transmission?

A

Direct Direct route. STIs Faeco-Oral route. Viral GE Indirect Vector-bourne Malaria Vehicle-bourne Viral GE Airborne Respiratory route TB

256
Q

27 year old student just returned from backpacking holiday around South Asia. Presents with frequent bouts of diarrhoea, flatulence, nausea and abdominal discomfort. What is this a case of?

A

Vibrio cholerae

257
Q

2 year old child presents with loose stools for 2 days. Miserable. Loss of appetite but drinking ok. No fever. Attends nursery and playgroup. Recently been to a petting zoo. What is this a case of?

A

Escherichia coli

258
Q

87 year old resident of a care home presents with confusion, altered consciousness, dehydration and a history of diarrhoea. What is this a case of?

A

Norovirus

259
Q

What is the norovirus?

A

Major cause of “Winter Vomiting” Mainly occurs in the winter Mainly causes vomiting May cause diarrhoea, nausea, cramps headache, fever, chills, myalgia Lasts 1-3 days Immunity is short lived

260
Q

36 year old man presents with bouts of low volume bloody stools. He works in a take-away. What is the a case of?

A

Shigella.

261
Q

84 year old patient at the Northern General Hospital presents with diarrhoea. She is recovering from a surgical operation a few days ago. What is the a case of?

A

Clostridium difficile.

262
Q

What is clostridium difficile associated with?

A

Associated with antibiotic use Especially broad spectrum antibiotics In hospitalized patients cause Antiobitic-associated diarrhoea Antibiotic-associated colitis Pseudomembranous colitis Mortality high Especially as patients tend to be elderly and ill

263
Q

What is the epidemiology of clostridium difficile?

A

Asymptomatic carriage occurs in 2-3% of healthy adults, 2/3 of babies ~36% of hospital patients Spread by faeco-oral route directly or through spores in the environment. Asymptomatic carriers without diarrhoea unlikely to spread it. 80% of symptomatic cases in persons > 65 years Causes 20% of antibiotic-associated diarrhoea

264
Q

How can you prevent clostridium difficile?

A

Clostridium difficile produces spores highly resistant to chemicals (spores) Alcohol hand rubs will not destroy the spores. Hand washing using soap and water will remove the microorganisms (including spores) from the hands.

265
Q

What is SIGHT?

A

S uspect C diff as a cause of diarrhoea I solate the case G loves and aprons must be worn H and washing with soap and water T est stool for toxin.

266
Q

How do you manage a clostridium difficile patient?

A

Control antibiotic usage Esp. Ampicillin, amoxicillin & cephalosporins Standard infection control procedures Surveillance & case finding Any patient with diarrhoea Isolate Enteric precautions Test stool samples Environmental cleaning Treat cases with metronidazole or vancomycin

267
Q

What do you test for clostridium difficile?

A

Test stool samples for the toxin Can also culture it (in order to identify which strain it is) Tissue samples (histology) obtained at sigmoidoscopy Don’t need to screen or treat asymptomatic carriers

268
Q

WHAT IS A PEPTIC ULCER?

https://www.youtube.com/watch?v=26Rdx2EiBaA

A

Having one or more sores in the stomach, gastric ulcers or duodenum, duodenal ulcers

269
Q

What does the normal gut look like?

A

Mucosa which contains

Epithelial cells
Absorbs and secretes digestive enzymes

Lamina propria
Blood and lymph vessels

Muscularis mucosa
Smooth muscle contracts/breaks

270
Q

What are the different regions of the stomach?

A

Cardia

Fundus

Body

Pylroic antrum

271
Q

What cells does the cardia have?

A

Fovelar cells

Water and glycoproteins

272
Q

What cells do the fundus and body have?

A

Parietal cells
Secrete HCL

Chief cells
Secrete pepsinogen

273
Q

What cells does the antrum have?

A

G cells
Secrete gastrin in repsonse to food entering

Also found in duodenum and pancreas

274
Q

What does gastrin do?

A

Triggers parietal cells to release HCL

Also stimulates growth of glands in epithelial layer

275
Q

What are brunner glands?

A

Found in duodenum and secrete mucus rich in bicarbonate into lumen

276
Q

What protects the stomach and duodenum?

A

Mucus and secretion of bicarboante ions to neutralise acid

277
Q

What is also brought in the blood to the stomach and duodenum?

A

Bicarbonate ions

278
Q

What gets secreted by epithelial cells in the stomach and duodenum, what do they do?

A

Prostaglandins

Stimulate mucus and bicarbonate secretion

Also dilation of nearby blood vessels
More blood to area

New epithelial cell growth

Inhibits acid secretion

279
Q

What are the causes of peptic ulcers?

A

H.pylori infection

NSAIDs

Zollinger-ellison syndrome

280
Q

Where is H.pylori most common? What type is it?

A

Low income settings

Gram negative bacteria

281
Q

Where do helicobacter live?

A

In the mucus layer in the stomach.

282
Q

What does helicobacter do?

A

Release adhesins which allow them to stick to fovelar cells

Secrete proteases which damage mucosal cells

Starts in antrum and spreads

Errodes deeper and deeper causing ulcers

283
Q

What can happen to the epithelial lining in helicobacter pylori?

A

Change from stomach epithelium to intestinal epithelium. Intestinal metaplasia.

284
Q

What do NSAIDs do?

A

Inhibit COX-2

Inhibit synthesis of prostaglandins

Gastric mucosa suseptable to damage

285
Q

How can you avoid COX-2 inhibition by aspirin?

A

Produce aspirin with enteric coat on it, therefore won’t dissolve in stomach but lower down in gut.

286
Q

What is zollinger-ellison syndrome?

A

Tumour called a gastrinoma

Neuroendocrine tumour

gastrin produced in excess

More HCL

Overwelms duodenum

Causing ulcers

287
Q

What do ulcers normally look like?

A

Smooth punched out holes

Like a dishwasher

288
Q

Where do ulcers normally appear?

A

Gastric in lesser curvature

Duodenum in first part
Brunner gland hypertrophy

289
Q

What can happen in ulceration to an artery?

A

Can eat into the artery and start haemorrhaging.

Stomach - will come straight up Intestine - black stools.

Coud lead to shock

Lesser curvature - left gastric artery

Posterior wall - gastroduodenal artery

290
Q

What can happen in ulceration to the muscle?

A

Ulceration through the muscle
Which allows free flow of contents in the peritoneum
Causing peritonitis.

Anterior part of duodenum
Trap air
Causing irritation of phrenic
Referred pain to shoulder

291
Q

What can ulceration lead to on the posterior side?

A

Erode through into the pancreas to give pancreatitis.

292
Q

What happens when the blood flow slows to the gut?

A

Cells break down as the buffer is not produced as much, the acid the attacks the cells and an ulcer forms.

293
Q

What can happen from a breach in the cells in the mucosa?

A

Acid attack adjacent cells.

294
Q

What are the symptoms of peptic ulcers?

A

Epigastric pain - aching in abdomen

Bloating

Belching

Vomiting

295
Q

When do symptoms improve for gastric and duodenal ulcers?

A

Gastric when not eating

Duodenal when eating

296
Q

What is the diagnosis of peptic ulcers?

A

Endoscopy

C13 Urea breath test
H pylori

Biopsy
Check for malignancy
H.pylori

297
Q

How could you treat peptic ulcers?

A

H.pylori
Antibiotics (Omeprazole, Metronidazole, Clarithromycin)

Acid lower medications

Proton pump inhibitors
Lansoprazole

H2 blocker
Rantidine

Surgery

298
Q

What makes gastric ulcers worse?

A

NSAIDs

Smoking

Caffiene

Alcohol

299
Q

WHAT IS GASTRITIS?

A

Irritation of stomach lining without an ulcer

300
Q

What are the causes of gastritis?

A

Excessive alcohol

NSAIDs

Spicy foods

Stress

301
Q

What are the symptoms of gastritis?

A

Epigastric pain

Loose stools

Vomiting

Haematemesis.

302
Q

How can you diagnose gastritis

A

Endoscopy + biopsy

303
Q

What is the differential diagnosis of gastritis?

A

Ulcerative collits

Chron’s

IBS

304
Q

What is the treatment for gastritis?

A

Ranitidine or PPI; eradicate H. pylori as needed.

Troxipide PO improves gastric mucus.

Endoscopic cautery may be needed.

305
Q

What is the treatment for H.pylori?

A

Lansoprazole, amoxicillin, and clarithromycin (LAC)

306
Q

WHAT IS THE STRUCTURE OF THE SMALL INTESTINE?

A

Villi and crypts.

Crypts provide new cells for the villi.

307
Q

What is located in the tips of the villi?

A

Lymphocytes.

308
Q

What are the different types of malabsorption?

A

Insufficient intake.

Defective intraluminal digestion.

Insufficient absorptive area.

Lack of digestive enzyme.

Defective epithelial transport.

Lymphatic obstruction.

309
Q

What can defective intraluminal digestion be caused by?

A

Pancreatic insufficiency
Pancreatitis
Cystic fibrosis

Defective bile secretion (lack of fat solubilisation)
Biliary obstruction
Ileal resection – decreased bile salt uptake

Bacterial overgrowth

310
Q

What is Giardia lamblia?

A

Giardia lamblia, also known as Giardia intestinalis, is a flagellated parasite that colonizes and reproduces in the small intestine, causing giardiasis.

The parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission.

311
Q

What is involved with small intestine resection or bypass?

A

procedure for morbid obesity Crohn’s disease infarcted small bowel

312
Q

What is involved with lack of digestive enzymes?

A

disaccharidase deficiency (lactose intolerance) bacterial overgrowth – brush border damage.

313
Q

What is involved with defective epithelial transport?

A

abetalipoproteinaemia primary bile acid malabsorption – mutations in bile acid transporter protein

314
Q

What is involved with lymphatic obstruction?

A

lymphoma tuberculosis

315
Q

What are the chronic idiopathic inflammatory bowel disease conditions? What are the other inflammatory conditions?

A

Crohn’s disease. Ulcerative colitis. Diverticulits. Ischameic colitis. Infective colitis - bacterial and protozoal.

316
Q

WHAT IS CROHN’S DISEASE?

A

Massive inflammation and associated ulcers.

Transmural granulomatous inflammation

317
Q

What is the cause of crohn’s?

A

Genetic

Family history likely to get it
Frameshift mutation in NOD2 gene
CARD15

Insertion

318
Q

Where is Crohn’s disease most common?

A

Terminal Ilieum.

319
Q

Where can ulceration/granulomatous inflammation be found in Crohn’s?

A

Whole length of the GI tract

PATCHY

Throughout the mucosa, submucosa, muscular propriety and fat of the gut.

320
Q

What type of disease is Crohn’s disease?

A

Immune related disease

321
Q

What are the bacteria thought to be responsible for Crohn’s?

A

Mycobacterium paratuberculosis

Pseudomonas

Listeria

322
Q

What happens in crohn’s?

A

Immune response occurs in reponse to pathogen but is wide and damages cell in GI tract

Defect in epithelial wall which lets bacteria in

323
Q

What happens when the bacteria comes in?

A

GI epithelial cell present bacteria on surface

T helper cells come along

They release inflammatory cytokines
Infereron gamma
Tumour necrosis factor alpha

These attract macrophages

324
Q

What do the macrophages release?

A

ROS

Proteases

Platelet-activating factor

325
Q

What is thought to happen in crohn’s disease?

A

The process of antigen presenting and macrophage attraction is dysfunctional

Leading to unregulated inflammation

Lots of proteases
Lots of ROS
Lots of platelet-activating factor

Destroying tissues

326
Q

What does all the immune cells in the GI wall cause?

A

Granulomas

327
Q

What is formed in both ulcerative colitis and crohn’s?

A

Ulcers

328
Q

Where do crohn’s ulcers extend?

A

All the way through muscle layer

Ulcerative colitis does not

329
Q

What are the symptoms of crohn’s?

A

Pain in assocaited areas

RLQ

Diarrhoea and blood in stool
If affecting large bowel

Malabsorption
If affect small bowel

330
Q

What are the test for crohn’s disease?

A

Acutely can sound like Appendicitis.

**_Barium Swallow_** 
COBBLESTONE APPEARANCE (may also have stricture formation and bowel shortening)

CT
Shows areas of wall thickening

Colonoscopy (and biopsy)
DIAGNOSITIC

331
Q

What does the histology look like for crohn’s?

A

Skip Lesions

Transmural inflammation

Increase in Goblet cells

Non-Caseating Granulomas

332
Q

What are the treatment option for crohn’s?

A

NSAIDs

Antibiotics
Reduce bacteria levels in intestine

Immunosuppresants
Corticosteroids

Surgical removal doesn’t cure disease

333
Q

What are some Crohn’s disease complications?

A

Malabsorption
-disease extent -surgical resections

Obstruction
-acute swelling -chronic fibrosis

Perforation
-acute abdomen

Fistula formation

Osteoporosis

Neoplasia
-colorectal cancer

334
Q

What different surgical resections are there?

A

Ileocolonic anastomosis

Jejunocolonic anastomosis

End-jejunostomy

335
Q

WHAT IS ULCERATIVE COLITIS?

A

Inflammation in the large intestine forming ulcers including colon and rectum

336
Q

What is the cause of ulcerative collitis?

A

Autoimmune

Stress and diet make it worse

337
Q

What are found in large amounts lining the colon?

A

Cytotoxic T cells

These destroy cells in the large intestine

338
Q

What do a large amount of people with ulcerative collitis have?

A

p-ANCAs
Thought to be due to bacteria mimicary

Increase in Sulfide gut bacteria

339
Q

What is the epidemology of ulcerative collits?

A

Family history positive

Women

30s

Caucasions and eastern europeans

340
Q

Where does ulcerative collitis start and what does it look like inside the lumen?

A

Rectum

Makes way round with no breaks

Circumfrential and continuous

341
Q

What can ulcerative colitis involve?

A

Inflammatory disorder of the colonic mucosa.

Does not involve the muscle

Forming ulcers

342
Q

What happens in flares and remission?

A

New ulcers forms

Ulcers heal

343
Q

How do you distinguish ulcerative colitis from Crohn’s disease?

A

Ulcerative colitis only involves mucosa whilst Crohn’s involves many layers of the gut.

344
Q

What is the pathology of ulcerative colitis?

A

Hyperaemic/haemorhagic granular colonic mucosa and maybe pseudo polyps formed by inflammation.

345
Q

What are the symptoms of ulcerative colitis?

A

Pain in LLQ

Episodic or chronic diarrhoea

Cramps abdominal discomfort

Bowel frequency relates to severity

Urgency/tenesmus.

Fever, malaise, anorexia, weight.

346
Q

What are some complications of ulcerative colitis in the skin?

A

Erythema nodosum

pyoderma gangrenosum

347
Q

What are some complications of ulcerative colitis in the colon?

A

Blood loss toxic dilatation

Colorectal cancer.

348
Q

What are some complications of ulcerative colitis in the liver?

A

fatty change chronic pericholangitis sclerosing cholangitis

349
Q

What are some complications of ulcerative colitis in the joints?

A

ankylosing spondylitis arthritis

350
Q

What are some complications of ulcerative colitis in the eyes?

A

iritis uveitis episcleritis

351
Q

What would show on histology for UC?

A

Continuous superficial inflammation

Crypt Abscesses

Goblet cell depletion

Ulcers

Only rectum affected (not proximal to ileocaecalvalve)

352
Q

What investigations can be done for ulcerative colitis?

A

Bloods

BARIUM SWALLOW
Loss of haustrations and drain pipe colon

XR
No faecal shadows; mucosal thickening/islands, colonic dilatation

Stools
Exclude bacteria

Colonoscopy
Look for inflammatory infiltrate; goblet cell depletion; glandular distortion; mucosal ulcers; crypt abscesses.

Sigmoidoscopy and biopsy - ***DIAGNOSTIC

353
Q

What are the principles of management for ulcerative colitis?

A

5-Aminosalicylic Acid

Inducing remission
Sulfasalazine
Mesalamine

Steroids - Prednislone.
Cyclosporine

Surgery
Colectomy

354
Q

WHAT IS THE OESOPHAGUS LINED BY?

A

Squamous epithelium.

355
Q

What is the stomach lined by?

A

Glandular epithelium.

356
Q

What happens in barrett’s oesophagus?

A

Change from squamous epithelium to glandular. Columnar lined lower oesophagus.

357
Q

What is metaplasia?

A

Change in differentiation of a cell from one fully- differentiated type to a different fully-differentiated type.

358
Q

What does reflux of acid into the oesophagus cause?

A

Destruction of the squamous cells and ulceration.

359
Q

What can cause acid reflux?

A

Obesity - increased intra-abdominal pressure.

360
Q

What can develop from this acid reflux and changing of cells?

A

Adenocarcinoma.

361
Q

What is the progression of cell type in Barrett’s oesophagus?

A

Normal Metaplasia Dysplasia Neoplasia. As a result of on going acid reflux.

362
Q

What are the different types of oesophageal cancers for different parts of the world and why?

A

China have squamous cancer by smoking and drinking. Europe has adenocarcinoma by acid reflux and obesity.

363
Q

What happens when a cancer grows in the oesophagus, at what point can you not remove it?

A

Could metastasise into the wall of the oesophagus, could move to far so that it comes into close contact with the superior vena cava and other major vessels.

364
Q

What is a risk factor for gastric cancer?

A

Eating certain foods such as pickled and smoked foods,. Asia.

365
Q

What can helicobacter pylori put you at a predisposition to? Why is this?

A

Gastric cancer. Due to intestinal metaplasia.

366
Q

What is limits plastica?

A

Cancer cells everywhere producing a plastic like feel.

367
Q

What is early gastric cancer?

A

Anything that doesn’t go into the muscular wall.

368
Q

What is late gastric cancer?

A

Into the muscular wall and lymph nodes.

369
Q

WHAT IS IBS?

A

Recurrent abdominal pain and abnormal bowel motility

370
Q

What are the symptoms of IBS?

A

Constripation and/or diarrhoea

Symptoms improve after voiding

Does not involve inflammation

371
Q

What is the cause of IBS?

A

Uknown

372
Q

What happens with visceral hypersensitivity in IBS?

A

Sensory nerve ending s

Abnormaly stong response to stimuli

When eating

Recurrent abdo pain

373
Q

How does increased bowel motitlity work with IBS?

A

Short-chain carbohydrates

Fructose and lactose act as solutes

Draw water into lumen

Stretch lumen causing pain

Smooth muscle spasm and diarrhoea

Gut flora metabolise short chain and produce gas

374
Q

What is the epidemology of IBS?

A

North america
Middle aged women

Other parts
Both sexes equally

375
Q

What are some risk factors for IBS?

A

Gastroenteritis
Norovirus
Rotovirus

Stress

376
Q

What is the treatment of IBS?

A

Diet modification
Avoid certain food, apples, beans and caulifflour

Constipation
Soluble fibre
Stool softeners
Laxatives

Spasms
Antimuscarinic

Manage stress

LOW FODMAP
Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols

377
Q

WHAT IS COELIACS DISEASE?

https://www.youtube.com/watch?v=nXzBApAx5lY

A

Autoimmune response which attacks the small intestine

378
Q

What is in wheat?

A

Individual wheat kernals

Inside each kernal is endosperm

For seeds embryos

This endosperm contains protein and starch

The protein is gluten

379
Q

What is the main culprit of coeliacs?

A

Gliadin found in gluten

380
Q

What happens when somebody eats food contain gluten?

A

Broken down in stomach in gliadin and other stuff

381
Q

What happens to gliadin after the stomach?

A

Gliadin resists break down

Gets to small intestine

Binds to secretory IgA
IgA normally protects enterocytes
Should normally be destroyed but isn’t

It then binds to transferrin receptor

Moves across cell into lamina propria

382
Q

What happens when the gliadin-IgA complex gets into the lamina propria?

A

Tissue transglutaminase cuts off amide group from protein

Deaminated gliadin eaten by macrophages

Displayed on MHC2

383
Q

What codes for MCHs?

A

HLA genes

384
Q

What genes do coeliac’s normally have?

A

HLA DQ2

HLA DQ8

385
Q

What happens when the macrophage presents gliadin to other immune cells?

A

T helper cell (CD4+)
Recognise gliadin
Release inflammatory cytokines
IFgamma
TNF
These destory epithelial cells in small intestine

T cells also activates B cells to secrete antibodies
Anti-gladin
Anti-tTG
Anti-endomyseal

T cells also activate cytotoxic T cells
These directly destory epithelial cells

386
Q

Why are antibodies produce to tTG moleucles in endomysium? Why are they helpful?

A

No symtpoms

Structual transglutaminase in lamina propria

Useful for diagnosis

387
Q

What screening tests can be used?

A

Anti-tTG and anti-endomyseal useful in severe cases

388
Q

What happens if a patient is IgA deficient?

A

Need to have an IgG screening test

389
Q

Which part of the intestine is mainly affected by coeliacs?

A

Duodenum

390
Q

What are the signs seen in the intestinal wall for coeliac’s?

A

Villi destoryed and flattened out
Villus atrophy

Crypts get longer
Crypt hyperplasia

Lymphocyte infiltration

391
Q

How does coeliac’s disease present?

A

Classical
Diarrhoea
Steatorrhoea
Weight loss
Failure to thrive

Non-classical
Irritable bowel type symptoms
Iron Deficiency
Anaemia
Osteoporosis
Chronic Fatigue
Dermatitis Herpitiformis
Ataxia
Peripheral neuropathy
Hyposplenism
Ammenorhoea Infertility

392
Q

What is Dermatitis Herpetiformis?

A

Rash common with coeliac disease patients.

Bumpy skin rash which pops up from IgA antibodies

Transglutaminase in dermal papillae

Neutrophils come by and start reaction

393
Q

What commonly happens with the presentation of coeliac’s disease?

A

More non-common presentations then common.

394
Q

How do you test for coeliac’s disease?

A

Serology
Tissue transglutaminase (tTG)
Anti-endomysial antibody (EMA)
Immunoglobulins.

Endoscopy + Duodenal biopsies.

Histology
Villous atrophy.

395
Q

What do patients need to do when undergoing testing for coeliac’s?

A

testing is accurate only if they follow a gluten-containing diet when following a gluten- containing diet they should eat some gluten in more than one meal every day for at least 6 weeks before testing they should not start a gluten- free diet until diagnosis is confirmed by intestinal biopsy

396
Q

What are the different stages of coeliac’s disease? 0. 1 2 3a 3b 3c

A
  1. Normal 1. Raised Intra epithelial Lymphocytes (IEL) >30/100 enterocytes 2. Raised IEL + Crypt Hyperplasia 3a. Partial Villous Atrophy (PVA) 3b. Subtotal villous atrophy (SVA) 3c .Total villous atrophy TVA)
397
Q

Where will a duodenal biopsy be taken from for coeliac’s?

A

1 x Duodenal bulb (new) 4 x D2 (traditional)

398
Q

How many duodenal biopsy’s should be taken to make sure the most severe lesion is identified?

A

5.

399
Q

How do you manage coeliac’s disease?

A

Gluten free diet – strict and lifelong

Dietician review

DEXA scan- osteoporotic risk

Coeliac UK info.

Prescription entitlement Inform 10% risk in 1st degree relatives.

400
Q

What happens if coeliac’s disease is left untreated?

A

Persistent symptoms

Osteoporosis

Subfertility

Cancer risk

Quality of life.

401
Q

What is the percentage of osteoporosis in coeliac’s disease?

A

40-60% of untreated adult CD Fracture risk Clinical, subclinical and silent affected Adherence improves BMD

402
Q

What is the associated cancer risk with coeliac’s disease?

A

2 fold increase in cancer and mortality compared with controls Small bowel lymphoma Oesophageal and ENT malignancies Lung and breast cancer LESS likely

403
Q

WHAT IS TROPICAL SPRUE?

https://www.youtube.com/watch?v=In1uajyiSxE

A

GI disease that results in malabsorption of nutrients in water

404
Q

What is the cause of tropical sprue?

A

Uknown

405
Q

What happens to the villi in tropical sprue?

A

Villi become flattened

406
Q

What is thought to be the pathology of tropical sprue?

A

Bacteria, virus or protazoa initially damage gut wall

Cause inflammation

Enteroglucagon released by enterocytes

Decreases intentinal motility

407
Q

What happens with this decreased intentinal motility?

A

Food lingers longer in intestine

More food means more resources

Change in bacteria flora

Bacteria overgrowth

One type of bacteria dominate flora

408
Q

What are the bacteria in tropical sprue?

A

Klebsiella

E.Coli

Enterobacter

409
Q

What does the bacteria in tropical sprue do?

A

Release toxic byproducts in fermention

Which causes more inflammation

Villi atrophy

410
Q

What does villi atrophy lead to?

A

Less surface area and enzymes for digestion

More food for bacteria

Depletion of B12 and folate

411
Q

What is folate needed for?

A

Needed to maintain integrity of mucosal wall

412
Q

What are the symptoms of tropical sprue?

A

Has flare ups

Diarrhoea

Abdominal pain

Fatigue

Weight loss

Dehydration

413
Q

What is a complication of tropcial sprue?

A

Megaloblastic anaemia

Large immature RBCs

414
Q

What is the diagnosis of tropical sprue?

A

Lived in tropics and have long standing GI symptoms

Fat malabsorption
72 hour stools test on prescribed diet

Carbohydrate malabsorption
D-xylose absorption test

Imaging techniques
Endoscopy
Villi atropy

Barium swallow
intestinal wall thickening

Tissue biopsy of jejenum

415
Q

What is the treatment for tropical sprue?

A

Antibiotics
Tetracycline

Nutrition
Folate
B12

416
Q

WHAT IS MALLORY-WEISS TEAR?

https://www.youtube.com/watch?v=YEaP_P5HrLQ

A

A longtitudinal tear in the mucosa lining at the gastroesophageal opening

417
Q

What is the cause of mallory-weiss?

A

Anyhting that causes a suddden rise in intragastric pressure

Normaly prolonged vomiting
Persistant retching
Intentse coughing
Alcholic binge drinking
Beluimic
Gastritis

418
Q

What are the symptoms of Mallory-Weiss?

A

Upper GI pain

Severe vomiting

Vomiting blood (Hematemisis)

Bloody or black stools (Melena)

419
Q

How can you diagnose Mallory-weiss?

A

Pateint history and presenting complaint
Binge drinking?
Bulimic?

Upper GI endoscopy
See tear in mucosa

FBC
Low RBC

420
Q

What are the treatment options for Mallory-weiss?

A

Most of the time it heals itself

IV fluid

Oesophagus balloon tamponade

Oesophageal clips

Proton pump inhibitors

Sclerotherapy (medications close off vessel)

Coagulation therapy

421
Q

WHAT ARE OESOPHAGO-GASTRIC VARICES?

https://www.youtube.com/watch?v=06nBQxYro8s&t=37s

A

The dilated veins that are in the distal oesophagus

422
Q

What causes varices?

A

Increase in portal venous system

423
Q

What happens when these veins rupture?

A

Cause mass amount of bleeding

424
Q

What diseases cause varices?

A

Liver cirhosis

Alcoholics

425
Q

How does liver cirrhosis cause varices?

A

progressive liver fibrosis + regenerative nodules produce contractile elements in the liver’s vascular bed

Portal hypertension

Causes veins in oesophagus to become engorged and serpentine

426
Q

What happens when the pressure in the veins becomes more than 12?

A

The varices can rupture

427
Q

What are the symptoms of varices?

A

History
Alcoholic

Upper GI bleeding
More than Mallory Weiss

428
Q

How do you diagnose varices?

A

Endoscopy

FBC

PT

PTT

LFT

429
Q

What is the treatment for varices?

A

Octreotide IV
Decreases blood flow
Inhibits vasodilation

Non-selective beta blockade
Propanalol

Endoscopic banding
Put rubber band around enlarged veins

TIPS
Transjugular, intrahepatic portosystemic shunting
Bypass between portal and hepatic venous circulations

430
Q

WHAT IS ACHALASIA?

https://www.youtube.com/watch?v=Ck5Xhre-UZU&t=1s

A

Lower esopahgeal sphincter does not relax

Esophagus dilates

431
Q

What is the cause of achalasia?

A

Loss of LOS nerve innervation

Loss of ganglion cells

432
Q

What are the features of achalasia?

A

Impaired of peristalsis

Lack of relaxation of LOS

Increased pressure

433
Q

What are the symptoms of achalasia?

A

Dysphagia - difficulty swallowing

Patinet will regurgitate food at night

Cough

Pulmonary aspiration

Weight loss

434
Q

What is the diagnosis of achalasia?

A

Oesophageal monometry - catheter down esophagus
Assess peristalsis
100% failed peristalsis

Function of LOS
Incomplete relaxation
Increased pressure

Barium swallow
Fluid stuck in esophagus
Bird’s beak

435
Q

What is the treatment for achalasia?

A

Try to open LOS

Decrease pressure at LOS

Surgical myotomy
Cut muscles of LOS

Balloon dilation
Then proton pump inhibitors

436
Q

WHAT IS SCLERODERMA?

A

Collagen deposition in skin and other organs

437
Q

What is the epidemology of scleroderma?

A

30-50 years

Women more than men

438
Q

What is the cause of scleroderma?

A

Uknown agent causes disease in suseptable host

439
Q

What is thought to be the cause of scleroderma?

A

Viruses

Chemicals

HLA genes

440
Q

What are the cells affected?

A

Fibroblasts
Excess of collagen in skin

Endothelium
Contriction of arteries

Immune cells
Dysregulated production of cytokines and antibodies

441
Q

What can the antibodies do?

A

Complex with self antigens forming immune complexes

Immune complexes and cytokines

Damage blood cells

Produce more collagen

442
Q

What antibody is involved with scleroderma?

A

Limited: Anticentromere

Diffuse: Antitopoisomerase-1

443
Q

What are the symptoms of scleroderma?

A

CREST

Raynaud’s phenomenom

Skin develops hard texture
Cannot be wrinkled

Face is expressionless

Claw like fingers

444
Q

How is scleroderma involved with GI?

A

Esophagus loses elasticity and becomes firm

Difficulty in swallowing

445
Q

What is the diagnosis of sclermoderma?

A

Radiography
Diffuse widening of peridontal ligament space

Microscopy
Excess collagen in stroma of organ involved

446
Q

What is the cure of scleroderma?

A

No cure

Immunosuppresants
Cyclophosphamide

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