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YEAR 2 GI > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Where is cholesterol synthesised?

A

In the liver

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2
Q

Is the liver an endocrine organ?

A

Yes eg produces hormones like angiotensin

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3
Q

Where is the main detoxification unit in the body?

A

The liver

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4
Q

Where does urea production happen?

A

In the liver

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5
Q

What is urea

A

Urea nitrogen is a waste product, it develops when your body breaks down the protein in the foods you eat. Travels from liver to the kidneys

We like urea, indicates kidney function.

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6
Q

Where can insulin and hormones be broken down?

A

The liver

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7
Q

When does jaundice occur?

A

Excess bilirubin in the bloodstream

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8
Q

6 common causes of jaundice as

A

1) liver conditions eg cirrhosis, hepatitis, alcoholic liver disease

2) haemolytic anemia = body destroys red blood cells quickly

3) bile duct obstruction eg due to hall stones of pancreatic cancer

4) medications

5) infections of the liver eg hepatitis

6) newborn jaundice (immature liver)

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9
Q

What’s phototherapy got to do with jaundice?

A

Phototherapy May be used to help the body break down bilirubin more effectively

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10
Q

Use the mnemonic LIVER BMN to remember the causes of jaundice

A

Liver conditions
Infections
Viral hepatitis
Excessive haemolysis
Red blood cell conditions
Bile duct obstruction
New born jaundice

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11
Q

So we know that bilirubin is conjugated by hepatocytes in the liver, after leaving the spleen. Why is it conjugated?

A

To make it water soluble. Goes to bile / intestines, and then Either back to blood stream (Pee) or modified by gut bacteria (bm)

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12
Q

Mnemonic for function of liver =
VIP SLIM-PR

(The liver is a vip, so is slim shady???? idek at this point lol)

A

Vitamin and mineral storage
Immune system support
Protein synthesis
Storage of glycogen and lipids
Lipid metabolism
Iron storage
Metabolism of carbs (regulate blood sugar levels)
Processing and detox of drugs and toxins
Regulation of blood clotting

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13
Q

How does the liver regulate blood sugar levels?

A

Metabolism of carbs

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14
Q

Think about why the liver might obviously be an immune organ?

A

Because it’s the first port of entry from the gut!!

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15
Q

Zinc is stored throughout the body, but what organ plays a role in regulating zinc levels?

A

Liver

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16
Q

Zinc deficiency can lead to weight loss, t or f

A

T

Zinc plays a role in metabolism, so low zinc = inefficient use of nutrients. Also zinc deficiency can lead to weakened immune system = illness leads to weight loss.
Chronic inflammation can lead to catabolic state = weight loss

Also zinc is needed for digestion.

Zinc deficiency can lead to loss of appetite

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17
Q

What happens when the liver stops working

A

Jaundice
Ascites (fluid in abdomen)
Variceal bleeding (mainly from oesophagus)
Hepatic encephalopathy (confusion due to toxin build up)

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18
Q

What’s the 3 way classification of jaundice

A

Pre hepatic
Hepatic
Post hepatic

All to do with bilirubin remember

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19
Q

History of anemia eg dyspnoea, fatigue, chest pain, is what classification of jaundice?

A

Pre hepatic

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20
Q

If bilirubin is conjugated and can come out in the urine, then it’s either which two classifications of jaundice?

A

Hepatic or post-hepatic

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21
Q

Risk factors for liver disease like drug intake and also, decompensation like ascites, variceal bleed, encephalopathy is what classification of jaundice

A

Hepatic

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22
Q

Abdominal pain, pale stools and high coloured urine suggests what type of jaundice?

A

Post hepatic

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23
Q

A palpable hall bladder suggests what

A

Post hepatic jaundice, as obstruction below level of cystic duct

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24
Q

What’s the most important test to figure out where the jaundice is coming from?

A

Ultrasound

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25
Q

Most important screening test for liver

A

Prothrombin time

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26
Q

What enzyme is raised (liver screening test) of alcohol abuse?

A

Gamma GT

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27
Q

As diagnostic procedures, MRCP and ERCP, which is the therapeutic option (perhaps with radiation)?

A

ERCP (more invasive)

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28
Q

What’s important for the definitive diagnosis of certain conditions eg autoimmune hepatitis?

A

Liver biopsy

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29
Q

What are varices? (Which can occur in the digestive tract due to portal hypertension)

A

Enlarged and fragile blood vessels

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30
Q

Portal hypertension can lead to ascities, what is this

A

Abdominal fluid accumulation

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31
Q

What’s hepatic encephalopathy

A

Brain dysfunction due to liver disease

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32
Q

How might congestive heart failure cause portal hypertension?

A

Affects right side of heart, can lead to increased pressure in the portal vein due to blood backing up in the liver

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33
Q

How might liver cirrhosis lead to portal hypertension?

A

Portal vein thrombosis

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34
Q

What is the most common cause of portal hypertension?

A

Cirrhosis

Leads to distortion of liver architecture, making it difficult for blood to flow through the liver, leading to increased pressure in the portal vein

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35
Q

Risk factors (2) non alcoholic fatty liver disease?

A

Obesity
Diabetes

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36
Q

Biggest drug to cause cirrhosis?

A

Methotrexate

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37
Q

For cirrhosis, what’s a compensated version? (Investigations)

A

When it’s only picked up on liver function test, so no like hepatic encephalopathy, or ascites or variceal bleeding…

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38
Q

What’s happens in ascites?

A

Gradual sodium retention
Water retention
Renal vasoconstriction

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39
Q

Ascites, apart from liver cirrhosis, can also be caused by what:

A

Heart failure, kidney disease, cancer

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40
Q

What does a high SAAG (serum albumin ascites gradient) of ascites fluid suggest?

A

Portal hypertension

We basically do a SAAG to find out if the ascites is due to portal hypertension or not

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41
Q

How is the SAAG test for ascites patients calculated, as in the gradient?

A

albumin concentration of the blood serum - Albumin concentration of the ascital fluid -

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42
Q

Why would a high SAAG in ascites fluid suggest portal hypertension?

A

Increased portal hypertension = albumin leaks out of vessels into peritoneal cavity.

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43
Q

Why would you treat ascites with diuretics?

A

Promotes removal of excess salt and water from the body, therefore symptom relief. (E.g. pressure of diaphragm) = prevents risk of hernia, symptom relief etc.

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44
Q

What are aquaretics?

A

Medications that promote the secretion of excess water from the body without significantly affecting the excretion of sodium and potassium

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45
Q

Difference between aquaretics and diuretics?

A

Aquaretics is only targeting water retention

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46
Q

Link between ascites and hepatorenal syndrome?

A

Ascites often precedes the development of hepatorenal syndrome , as circulatory changes and worsening liver function = development of hepatorenal syndrome

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47
Q

What is hepatorenal syndrome?

A

Sudden development of kidney dysfunction specifically alongside liver dysfunction or cirrhosis.

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48
Q

Why would we expand blood volume with albumin in hepatorenal syndrome due to portal vein hypertension?

A

1) portal hypertension = vasodilation of the splenic vasculature
2) so the body feels the the blood volume effect is less
3) RAAS kicks in, adrenaline released. To raise blood pressure
4) increased vasoconstriction, so less renal blood flow I.e. hypovolemia

So must expand blood volume with albumin

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49
Q

How does portal hypertension cause variceal haemorrhage?

A

It can cause alternative blood routes

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50
Q

How do you treat variceal haemorrhage of the esophageal?

A

Endoscopic band ligation

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51
Q

What drug do you give for oesophageal variceal haemorrhage? To reduce pressure in the veins

A

Terlipressin

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52
Q

Why might ammonia build up in the brain in liver disease, causing hepatic encephalopathy?

A

Toxins from the gut are converted (especially in the colon) into ammonia, by bacteria. Liver can’t handle this ammonia, so escapes to the brain.

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53
Q

What are the risk factors for hepatocellular carcinoma?

A

Liver disease e.g. cirrhosis
Also hepatitis b and c

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54
Q

Hepatocellular carcinoma might present as either decompensated liver disease? Or compensated?

A

Decompensated

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55
Q

Why might propranolol be prescribed to patients with cirrhosis and esophageal varices?

A

Prophylactic/preventative, lower risk of bleeding.
It slows down heart rate

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56
Q

Which viral hepatitis is self limiting?

A

A and e
Others chronic

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57
Q

Which vital hepatitis strains are enteric?

A

Only a and e actually

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58
Q

Meaning of hepatitis

A

Inflammation of the liver

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59
Q

Which hepatitis (viral) strains can be prevented through vaccination?

A

A and B

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60
Q

Which viral hepatitis has asymptomatic children?

A

A

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61
Q

Which is the most common drug to induce liver injury?

A

Paracetamol

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62
Q

Which drug treats paracetamol overdose?

A

N-acetylcysteine

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63
Q

For screening for hepatitis B, we test for: HBcAb, HBsAg, and HBeAg. Which is for previous infection, active infection, or acute phase of infection showing how infectious

A

HBcAb = previous infection
HBsAg = active infection
HBeAg = infectivity / acute phase

To remember, think
C = I can ‘see’ the past clearly, think s is like an active snake, and e for me, how infectious am I

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64
Q

Who do we treat for HBV?

A

Just those with high viral loads

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65
Q

Hepatitis E- has it got a vaccine?

A

No

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66
Q

Oral contraceptives can affect the hepatic system how?

A

Cholestasis

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67
Q

What’s cholestasis?

A

Slowing or stalling of bile flow through your biliary system. Bilirubin accumulates in blood rather than going out in urine.

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68
Q

Non alcoholic fatty liver disease is the umbrella term for what three things

A

Simple steatosis
Non alcoholic steatohepatitis
Fibrosis and cirrhosis

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69
Q

What’s non alcoholic steatohepatitis?

A

Accumulation of fat, therefore causing inflammation

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70
Q

Fatty liver causes steatohepatitis, = inflammation. What might this lead to if it’s chronic

A

Fibrosis and cirrhosis

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71
Q

Fibrosis Vs cirrhosis, what’s the difference?

A

Cirrhosis is irreversible

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72
Q

How is fatty liver disease diagnosed?

A

Through ultrasound

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73
Q

How do we diagnose fatty liver disease?

A

Through ultrasound and also liver biopsy

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74
Q

What does Fib-4 score?

A

How advanced the fibrosis is

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75
Q

Biggest three autoimmune liver diseases?

A

1) autoimmune hepatitis
2) primary biliary Cholangitis
3) primary sclerosing Cholangitis

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76
Q

For autoimmune hepatitis, is it male or female dominant d

A

Female

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77
Q

T or f, autoimmune hepatitis is high IgG?

A

True

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78
Q

What does autoimmune hepatitis respond well to?

A

Steroids
(A lot of inflammation, lots of like lymphocytes, plasma cells, other inflammatory cells)

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79
Q

What immunoglobulin is raised in primary biliary cholangitis?

A

IgM elevated

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80
Q

What specifically is inflamed in primary biliary cholangitis? (Think biliary)

A

Predominantly bile ducts that are involved
And therefore blockage of bike within the liver causing cholestasis

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81
Q

Is primary sclerosis cholangitis male or female predominant?

A

Make

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82
Q

What is primary sclerosis cholangitis

A

Stricturing of the bile ducts

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83
Q

Primary sclerosis cholangitis patients present with what?

A

Recurrent cholangitis and jaundice

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84
Q

Would active extrahepatic malignancy be a contraindication for liver transplant?

A

Yes

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85
Q

What score is used to decide who gets prioritised for liver transplantation?

A

UKELD score

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86
Q

What is steatosis?

A

Fatty liver

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87
Q

What is steatohepatitis? (3)

A

Fatty liver with inflammation, Neutrophil infiltration and fibrosis/cirrhosis (build up of scar tissue)

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88
Q

Initial physical findings of liver disease?

A

Majority no physical findings

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89
Q

Signs of chronic liver disease?

A

Spider naevi
Loss of axillary and pubic hair
Ascites
Encephalopathy
Red hands I.e. palmar erythema
Moobs on men I.e gynecomastia
Jaundice
Muscle wasting

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90
Q

Why does spider naevi occur in liver disease?

A

Well spider naevi are abnormal capillaries near the skin’s surface
But liver disease can lead to increased pressure in the blood vessels that supply the liver (portal hypertension) = capillaries dilate

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91
Q

How might spider naevi be formed in liver disease apart from due to portal hypertension?

A

Accumulation of toxins in the blood stream affects blood vessels
Also affected by hormonal imbalances (liver involved in metabolising hormones)

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92
Q

What stage finding is jaundice for liver disease?

A

Late

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93
Q

What would an ultrasound show in liver disease? (Think about what happens to the liver)

A

Fatty liver

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94
Q

What blood tests for liver diseases that’s suggestive of alcohol?

A

Aspartate amino transferase (AAT) > alanine amino transferase (ALT)
If AAT is more than twice the ALT, then it’s alcohol

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95
Q

When alcohol affects the liver, we see thrombocytopenia, what is this

A

Low platelets
This can affect your bone marrow

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96
Q

Really severe hepatic encephalopathy leads to what

A

A coma

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97
Q

Hepatic encephalopathy presents late stage liver disease patients with underlying what

A

Infection
So we screen for that

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98
Q

Why might constipation cause hepatic encephalopathy?

A

Bowel can’t clear toxins eg ammonia, which can cross blood brain barrier

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99
Q

Why would internal GI bleed lead to hepatic encephalopathy?

A

Blood into bowel, has lots of proteins, this gets broken down and this releases ammonia

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100
Q

Treatment of hepatic encephalopathy?

A

Bowel clear out
Antibiotics- everyone, even if infection isn’t immediately obvious
Airway support- because depressed conscious level

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101
Q

Hepatic encephalopathy- conscious level too depressed for medications?

A

Give medications through nasogastric tube into the stomach

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102
Q

Ascites will often present endstage liver disease. Ie spontaneous bacterial peritonitis. What’s the complication here that could occur?

A

Excess fluid could get infected, so abdominal pain

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103
Q

Spontaneous bacterial peritonitis, signs?
Of the liver

(Think: it’s an infection. What complication could be infected, what might you see in a normal infection?)

A

Abdominal pain because ascites is infected
Fever, rigors
Renal impairment as kidneys infected
Signs of sepsis, tachycardia, temperature

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104
Q

How do we diagnose spontaneous bacterial peritonitis?

A

Tap some fluid from the abdomen, send away for protein levels and glucose levels
And culture to see which bacteria

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105
Q

Proteins in spontaneous bacterial peritonitis is high or low?

A

Low

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106
Q

Someone looks like they have spontaneous bacterial peritonitis. We need to make sure that it isn’t actually caused by what

A

Surgical causes, so we do a CT scan

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107
Q

Treatment for bacterial peritonitis?

A

High dose broad spectrum antibiotics, usually given intravenously

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108
Q

Why do we give albumin intravenously when ascites?

A

Because it creates oncotic pressure

1) so helps retain fluid within the blood vessels and prevent it from leaking.
2) Also draws fluid back into the bloodstream

I.e. reduce volume of ascitic fluid and increase vascular volume.

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109
Q

Why might ascites occur in liver cirrhosis?

A

Albumin production by liver reduced. Oncotic pressure lost and fluid leaks

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110
Q

Where is albumin primarily synthesised

A

The liver

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111
Q

What’s delirium tremens?

A

Medical emergency of alcohol withdrawal.

Psychosis?
Heart arrhythmias, severe dehydration, seizures etc
Tremors
Agitation
Profuse sweating and fever
Tachycardia and high blood pressure

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112
Q

Treatment for delirium tremens

A

Benzodiazepines

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113
Q

Purpose of benzodiazepines for delirium tremens

A

They enhance the effects of neurotransmitter GABA, to calm the individual

Helps agitation, tremors, hallucinations, calm central nervous system.

They also prevent seizures

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114
Q

For alcoholic hepatitis, treatment?

A

Mainly supportive
Treat infections (common)
And
Treat encephalopathy
Acid reducing meds

M

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115
Q

How to diagnose alcoholic hepatitis?

A

Raised bilirubin
Alcohol history
Exclude other causes

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116
Q

There is inflammation in alcoholic hepatitis, so why wouldn’t we use steroids or prednisone?

A

It increases the risk of GI bleeding

(Possibly use in very very severe alcoholic hepatitis)

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117
Q

What percentage of patients with alcoholic hepatitis are malnourished?

A

100%

= there’s an awful lot of death
If they remain malnourished, only 15% will survive two years

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118
Q

Korsakoff’s encephalopathy will occur after being malnourished (alcoholic hepatitis-please fact check this)
What vitamin do you need to replenish to do that?

A

Thiamine
Vitamin B

Otherwise permanent brain damage

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119
Q

Why would you pass a nasogastric tube into someone with alcoholic hepatitis?

A

They have high energy requirements that they can’t meet, malnourished

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120
Q

Prognosis for alcoholic hepatitis is linked to what

A

Alcohol cessation

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121
Q

Is there treatment for non alcoholic fatty liver disease?

A

No just lifestyle

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122
Q

Non alcoholic fatty liver disease can progress to what

A

Non-alcoholic steatohepatitis and cirrhosis

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123
Q

Difference between primary sclerosis cholangitis and primary biliary cholangitis?

A

Bile ducts: sclerosing = inside AND outside the liver, Vs biliary which is only small bile ducts in the liver

Sclerosing is associated with increased risk of bile duct cancer and colon cancer- not for biliary though

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124
Q

Itching, fatigue and abdominal pain- are these symptoms of primary biliary cholangitis, or primary sclerosing cholangitis

A

Both

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125
Q

What is primary biliary cholangitis?

A

Bile ducts in the liver become injured and inflamed and eventually destroyed.
Eventually bile builds up and destroys the live r

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126
Q

Why should we be worried about gallbladder polyps?

A

Because they could turn into gallbladder cancer
So remove if big like at least 1cm or more

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127
Q

Risk factors for gallstones? (4 Fs mnemonic)

A

Fat
Fair
Female
Forty

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128
Q

Gall stones present how?

A

Biliary colic:
Severe, colicky epigastric or right upper quadrant pain
Associated with nausea and vomiting
Often triggered by meals especially high fat

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129
Q

Why might patients with gall stones be advised to avoid fatty foods?

A

Fat entering the digestive system causes CCK secretion from the duodenum. CCK triggers contraction of the gall bladder

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130
Q

Why would hall stones lead to obstructive jaundice

A

If stones block the duct then it blocks where bilirubin drains (from liver through bile ducts). Raised bilirubin = jaundice

Bilirubin goes from spleen to hepatocytes in the liver to be conjugated (made water soluble)

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131
Q

A raised ALP (enzyme originating from places incl. liver) alongside right upper quadrant pain and/or jaundice, is consistent with what

A

Biliary obstruction

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132
Q

Aminotransferases (ALT and AST)- they are enzymes produced where

A

Liver

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133
Q

Aminotransferases (ALT and AST)- if they are high compared to ALP level, indicates what

A

Problem inside the liver

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134
Q

Which screening test for gall stones?

A

It’s ultrasounds

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135
Q

Patients with symptoms or complications of gall stones are treated with what

A

Cholecystectomy = surgical removal of the gallbladdrr

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136
Q

What is the composition of gallstones?

A

Cholesterol mainly

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137
Q

Gall stones are usually symptomatic or not?

A

Asymptomatic

If they’re symptomatic, then it’s bilary colic

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138
Q

What has empyema got to do with hall stones?

A

Could get pus in the gallbladder- and then gallbladder might perforate = surgical emergency

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139
Q

Perforated gall bladder due to stones requires what

A

Draining the gall bladder

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140
Q

Why would pancreatitis occur due to gall stones?

A

Stones could move and obstruct the pancreatic duct

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141
Q

What is cholangitis?

A

Inflammation of the bile duct system

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142
Q

What’s biliary atresia?

A

Babies born with the absence of the bile duct. Needs significant reconstruction

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143
Q

Primary sclerosing cholangitis is autoimmune, yes or no

A

Yes

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144
Q

How does primary sclerosing cholangitis present?

A

Jaundice
Some pain
(Blocked bile ducts remember)

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145
Q

How could a biliary-enteric fistula happen due to gallbladder?

A

Through inflammation, gallbladder perforated into the duodenum

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146
Q

Why would jaundice occur due to malignant tumours?

A

Intra or extra hepatic

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147
Q

What’s the only treatment option for cholangicarcinoma: intrahepatic

A

Surgery

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148
Q

Cholangio-carcinoma is classified how?

A

Based on where the duct is blocked eg right hepatic duct, cystic duct, common hepatic duct etc.

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149
Q

Presentation of pancreatic cancer

A

obstructive jaundice
Weight loss
Upper abdominal pain

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150
Q

What happens to bilirubin levels in pancreatic cancer?

A

Raises
Obvs cause of obstructive jaundice

151
Q

What’s the kausch-whipple surgery? (For pancreatic cancer)

A

Entails taking half/quarter of the stomach,
Head of the pancreas
Lower end of the bile duct
Duodenum

Then anastomosing all of them together

152
Q

The pacemaker to get the stomach to empty is located where

A

In the pylorus

153
Q

Obstructive jaundice- could that be treated with stenting?

A

Yes

Don’t rlly know why

154
Q

Definition of acute pancreatitis

A

An acute inflammatory process of the pancreas, with variable involvement of other organs

Can be mild- uneventful recovery
Or can be severe- organ failure or local complications

155
Q

Would a cute pancreatitis ever lead to pancreatic necrosis?

A

Yes

156
Q

What causes acute pancreatitis?

A

Alcohol
Gall stones
Post ERCP procedures

(Other reasons too eg scorpion venom but just learn alcohol and gall stones just now)

157
Q

How does alcohol cause acute pancreatitis?

A

Acetaldehyde -as an oxidation product
Also direct injury

158
Q

How would gall stones cause acute pancreatitis?

A

Obstructing pancreatic duct
Raised pancreatic ductal pressure

159
Q

Jaundice can occur in pancreatic cancer why?

A

1) obstruction of the bile duct (pancreas is located near the bile ducts, so tumour can prevent bile from flowing into the small intestine- SO IT GOES TO THE BLOODSTREAM INSTEAD. Bilirubin then accumulates in the blood
2) compression of the duodenum = pancreatic tumours. Same as before but at duodenum level, not bile duct level.
3) liver metastasis, cancer cells go to liver and impair liver’s ability to process bilirubin

160
Q

Difference in chronic and acute pancreatitis?

A

Chronic = irreversible deterioration in pancreatic function
Acute = rapid onset and normal function does return

161
Q

Why would a gallstone cause inflammation in the pancreas ie pancreatitis?

A

Blockage and ampulla of vater = reflux of bile and pancreatic juice

162
Q

Why does alcohol cause pancreatitis?

A

Alcohol is directly toxic to the pancreas

163
Q

Causes of pancreatitis with the mnemonic ‘I get smashed’

A

Idiopathic
Gall stones
Ethanol
Trauma
Steriods
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP procedures
Drugs

164
Q

What’s the most important investigation. For acute pancreatitis? And why not chronic?

A

Amylase
Can be raised 3 x upper limit in acute.
May not rise at all in chronic pancreatitis

165
Q

Which investigative thing shows level of inflammation? (Might be useful eg in acute pancreatitis!)

A

C-reactive protein (CRP) > level of inflammation

166
Q

What investigation for pancreatitis to check for gallstones?

A

Ultrasound

167
Q

Necrosis, abscesses and fluid collections could never be a complication of pancreatitis, why?

A

Trick question. It is. Assess with CT

168
Q

What score assesses severity of pancreatitis?

A

Glasgow

169
Q

‘Pancreas’ mnemonic for Glasgow scale for testing how severe pancreatitis is?

A

Look at zeros to finals, can’t be bothered writing it out

170
Q

Patient with acute pancreatitis. Has hall stones. What do you do?

A

ERCP procedure
Or
Cholecystectomy

171
Q

When would you give antibiotics for pancreatitis?

A

If evidence of specific infection eg necrosis or abscess in the pancreas

172
Q

How many days to improve after acute pancreatitis?

A

3-7 days

173
Q

What’s the most common cause of chronic pancreatitis?

A

Alcohol

174
Q

What’s happened, very simply, in chronic pancreatitis?

A

Fibrosis and reduced function

175
Q

Pseudocysts and abscesses form in which one, acute or chronic pancreatitis

A

Chronic pancreatitis

176
Q

Loss of exocrine function in chronic pancreatitis means what

A

Lack of pancreatic enzymes secreted e.g. lipase

Also no insulin = diabetes

177
Q

Why is there steatorrhoea in chronic pancreatitis?

A

Because no pancreatic enzymes released- no lipase for digesting fat. So greasy stools.

178
Q

What’s creol used for in chronic pancreatitis?

A

Replace lipas- pancreas can’t produce enzymes anymore.

179
Q

How important is nutrition for acute pancreatitis patients?

A

Extremely

180
Q

How to deal with post pancreatitis fluid?

A

Endoscopic ultrasound guided drainage

181
Q

Why use a nasogastric tube in acute pancreatitis?

A

To prevent stimulating pancreatic secretions

182
Q

Why use a stent in pancreatitis?

A

1) inflammation of the pancreas can lead to narrowing or blockage of the pancreatic ducts, so use stent to relive obstruction (blockage can cause digestive enzymes and bile to accumulate in the pancreas, leading to further inflammation and pain)

Might keep stent there to prevent recurrence!

2) drainage of pseudocysts when in severe acute pancreatitis. (Fluid filled). Stents can create drainage path from pseudo cyst to the digestive

183
Q

Cough, shortness of breath, fever, and poor appetite - why would this ever be acute pancreatitis?

A

Due to ascites
In severe cases, fluid can put pressure on the diaphragm= sob

Also if fluid moves from ascites into the pleural space, can cause pleural effusion = breathing difficulties and a persistent cough

184
Q

We look at amylase for what disease?

A

Pancreatitis
This is because: pancreas could leak digestive enzymes, into surrounding tissue and blood stream

185
Q

What is a sphincterotomy?

A

Making a small cut in the papilla of vater to enlarge the opening of the bile duct and/or pancreatic duct- to either improve drainage or to remove stones in the ducts.

186
Q

Destruction if both exocrine and endocrine cells in chronic pancreatitis leads to what

A

Loss of function

187
Q

Most common cause of chronic pancreatitis?

A

Alcohol

Then after that cystic fibrosis, maybe some congenital anatomical abnormalities

188
Q

Why vitamin deficiency for chronic pancreatitis?

A

Exocrine deficiency

Enhanced dietary intervention important for this group

189
Q

Why is there pain in pancreatic cancer?

A

1) Pain from tumour growth/ inflammation pressing on tissues, nerves, and blood vessels. (Celiac plexus)
2) obstruction of bile duct = buildup of digestive enzymes or bile

190
Q

Digestion happens mainly in what part of the small intestine?

A

Suodenum

191
Q

Where in the small intestine does gastric acid secretion occur?

A

Duodenum
So that’s where bicarbonate secretion occurs, and also bicarbonate from pancreatic juice and also from the bile

192
Q

T or f, the jejunum is usually empty

A

True unless during a meal, chyme will be there, otherwise mostly empty

193
Q

Where in the small intestine does the most:
Nutrient absorption
Digestion
Occur?

A

Nutrient absorption occurs mainly in the jejunum
Digestion mainly occurs in the duodenum

194
Q

Main function of ileum

A

Absorption of sodium chloride and water

195
Q

In the villus are mini capillaries that absorb fats, what are these called

A

Lacteals

So days don’t go directly to the blood capillaries, they go to the lacteals

196
Q

Goblet cells in the small intestine secrete mucus. Where are these located

A

On surface of villi

197
Q

Purpose of crypts between villi of the intestine

A

Secrete water
And contain stem cells to be used in regeneration of intestinal, epithelial cells

198
Q

Dead epithelial cells in small intestine can be used as what

A

A source of nutrients because made of proteins

199
Q

Why does chemo have lots of gastrointestinal side effects?

A

Because we have rapidly dividing cells in the epithelial of the GIT,

200
Q

Brunners glands (purple) are where in the small intestine

A

Submucosa

201
Q

What type of cell in the oesophagus?

A

Stratified squamous non-keratinised epithelium

202
Q

What do the cells look like histologically in the liver?

A

Almost exclusively epithelium
Cuboidal hepatocytes with sinusoids in between

203
Q

Epithelium in the intestines is:

A

Simple columnar epithelial cells

204
Q

Villus is made of epithelial cells, and in between some of the cells on the surface are what type of cell

A

Mucus secreting goblet cells

205
Q

How is water secreted in intestine from the epithelial cells lining the crypts of lieberkuhn?

A

H20 is secreted passively/ osmotic ally as a consequence of active secretion of chloride into intestinal lumen

There are sodium potassium ATPase pumps, sodium out, potassium in and therefore chloride out

206
Q

How does secretion of water in intestines promote the mixing of nutrients with digestive enzymes?

A

Action of enzymes higher than if in liquid state vs solid state

207
Q

Water in intestines is secreted by crypts and absorbed by **?

A

Villi
Paracellularly through tight junctions between the cells

208
Q

By what channel does chloride move out into lumen of intestines?

A

A transmembrane channel known as CFTR- cystic fibrosis transmembrane conductance regulator

209
Q

Why is the cystic fibrosis transmembrane conductance regulator called that?
(Channel critical in moving the chloride outside the crypt epithelial and therefore moving water indirectly).

A

Because if there are genetic changes/defect, then cystic fibrosis

210
Q

What problem occurs in cystic fibrosis?

A

Problem of chloride outside the crypt epithelial and this affects the secretion of water

211
Q

What enzyme activates the cystic fibrosis transmembrane conductance regulator?

A

Adenylate cyclase

212
Q

What does adenylate cyclase do?

A

It will convert ATP to cyclic amp, which will activate protein kinase A, which will phosphorylated the channels and make it active

213
Q

What are the two different types of movement in the small intestine?

A

Segmentation and peristalsis

214
Q

Segmentation movement in the small intestines is most common when?

A

During meals

215
Q

How does segmentation movement work?

A

Contraction, then relaxation. To move chyme up and down- provides mixing of contents with digestive enzymes, and brings chyme into contact with absorbing surface

216
Q

Segmentation contractions is initiated by what?

A

Depolarisation of the pacemaker cells in the longitudinal muscle layer

217
Q

What’s the intestinal basic electrical rhythm that helps initiate segmentation contractions? (Pacemaker cells in longitudinal muscle layer).

A

BER produces oscillations in membrane potential that reach threshold therefore contraction

218
Q

BER decreases in what directions of the intestine?

A

BER decreases as move down intestine towards rectum

219
Q

Innervation that increases contraction in segmentation?

A

Parasympathetic (vagus)

220
Q

What decreases contraction of the segmentation?

A

Sympathetic nervous system

221
Q

When does peristalsis occur?

A

Following the absorption of nutrients

222
Q

Why does peristalsis occur?

A

After nutrients absorbed, peristalsis will try and get rid of unabsorbed/ non absorbed nutrients e.g. cellulose

223
Q

Difference between segmentation and absorption?

A

Segmentation = digestion and absorption

Peristalsis = moving chyme towards large intestine

224
Q

Migrating motility complex is what

A

Term to describe pattern of peristaltic activity travelling down from small intestine, starting from gastric antrum and ending at terminal ileum (large intestine)

225
Q

When does migrating motility complex stop? (Peristalsis)

A

Arrival of food in stomach = segmentation

226
Q

How does MMC limit bacterial colonisation of small intestine?

A

Keep moving chyme to large intestine where it’s okay to have undigested food- if bacteria colonises small we don’t get nutrients

227
Q

Which hormone is involved in initiation of MMC?

A

Motilin

228
Q

In segmentation, there is both relaxation and contraction in lots of different areas. Whereas in peristalsis, what’s the case?

A

Only contraction in one area, and mainly relaxation elsewhere

229
Q

When bolus of chyme reaches intestinal smooth muscle, does the oral side contract or relax? (Vice versa to the anal side)

A

Muscle on oral side of bolus contracts

230
Q

In gastric emptying, does segmentation activity in the ileum increase or decrease?

A

Increase

231
Q

Gastric emptying: segmentation activity in the ileum increases, leading to the opening of what sphincter

A

The ileocaecal valve

The sphincter between the ileum and the colon

The sphincter then reflex contracts to prevent backflux into the small intestine

232
Q
A
233
Q

Another name for the appendix?

A

Vermiform

234
Q

True or false, the appendix has no lymph nodes?

A

It has many
False

235
Q

What do I mean when I say that the longitudinal muscle of the large intestine is incomplete? (Vs circular muscle layer)

A

Three bands across the large intestine known as teniae coil

236
Q

Why is there a puckered appearance in the colon when it contracts?

A

Because of the teniae coli

237
Q

What is the mucosa of the large intestine comprised of?

A

It is comprised of simple columnar epithelium

238
Q

Are there Villi
in the large intestine?

A

No

239
Q

Are there crypts in the large intestine?

A

Yes! There are! Like small intestine, with epithelium stem cells at the bottom

240
Q

Why are there lots of goblet cells in the intestine?

A

They form a good layer of mucus to help lubricate the large intestine to help with the movement of faeces

(Or faeces will damage)

241
Q

What’s after the rectum

A

Anal canal

242
Q

The muscularis externa of the rectum: is this thicker or thinner compared to other regions of the alimentary canal?

A

Thicker
(To hold in faeces, and then push out)

243
Q

The muscularis externa layer of the anal canal forms what

A

Internal anal sphincter

244
Q

The internal anal sphincter is involuntary, and is controlled by what nervous system?

A

Autonomic

Obviously not somatic cuz that’s conscious stuff

245
Q

The external anal sphincter of the anus (there are two) is what type of muscle?

A

Skeletal muscle

246
Q

Whilst the rectum is simple columnar epithelium, what is the anal canal?

A

Stratified squamous

247
Q

What is located in the Baso-lateral membrane of the small intestine, that creates an electrochemical gradient for sodium?

A

Sodium potassium ATPase pump

248
Q

The bacteria in the colon/ large intestine helps in forming what vitamin?

A

Vitamin K, which is an important blood clotting factor, helps to prevent haemorrhage

249
Q

What are the symptoms associated with constipation?

A

Headache
Nausea
Loss of appetite
Abdominal distension

The symptoms come from the distension of the rectum

250
Q

What are the causes for diarrhoea?

A

1) pathogenic bacteria living in our colon
2) protozoans
3) viruses
4) toxins
5) stress

251
Q

What channel is involved in the secretion of water from crypt cells?

A

Sodium potassium chloride channel

252
Q

Chloride is transported outside the cell via what transporter?

A

CFTR

253
Q

How might bacteria cause diarrhoea?

A

Affects the CFTR channel, causing more chloride into the cell and therefore more water

254
Q

Example of bacteria causing diarrhoea?

A

Vibrio cholerae
> cholera

255
Q

How does the bacteria actually increase chloride eg cholera?

A

Entero-toxins they release work by elevating things such as cyclic AMP

256
Q

How many litres of water secreted into colon a day with cholera Vs not?

A

25 litres

Vs

1.5 litres

257
Q

Why do we give sodium/glucose solution in diarrhoea eg cholera?

A

For rehydration.
Bacteria hasn’t affected the SGLT1 translorter so glucose and sodium can still be absorbed, and this will help in the absorption of water

258
Q

Diarrhoea washes out the toxins. Why is it bad then?

A

Dehydration and loss of vitamins

259
Q

Where is the secretory mucosal type in the GI tract?

A

Seen only in stomach.

It’s the crypts that secrete water in the colon

260
Q

What score is related to AF patients for risk of bleeding?

A

HAS BLED

261
Q

What are the three types of gastritis (ABC)

A

Autoimmune
Bacterial
Chemical injury

262
Q

How does autoimmune gastritis work?

A

Autoantibodies to parietal cells and intrinsic factor.
Atrophy of gastric epithelium
Loss of specialised gastric epithelial cells (decreased acid secretion, loss of intrinsic factor)

263
Q

Pathology of bacterial gastritis?

A

Bacteria found in gastric mucus and produces an acute and chronic inflammatory response therefore increased acid production

264
Q

Gastritis definition

A

Inflammation of the stomach lining.

265
Q

Acid reflux causes inflammation of what

A

The oesophagus

266
Q

Which drugs may cause chemical gastritis?

A

NSAIDs
Non- steroidal anti-inflammatory drugs

267
Q

Peptic ulceration is an imbalance between what?

A

Acid secretion and mucosal barrier

268
Q

What parts of the GI tract do peptic ulcers affect?

A

Oesophagus, stomach, duodenum

269
Q

Acute Vs chronic bleeding from peptic ulcer leads to what?

A

Acute = haemorrhage
Chronic = anaemia

270
Q

Perforation of a peptic ulcer can lead to what

A

Peritonitis

271
Q

Healing by fibrosis of a peptic ulceration could lead to what?

A

Obstruction

272
Q

Gastric cancer is associated with previous infection of what

A

H pylori

273
Q

What is the dual blood supply of the liver from?

A

Hepatic artery
Portal vein

274
Q

Primary sclerosing cholangitis is associated with what disease?

A

Inflammatory bowel disease

275
Q

What’s cholecystitis?

A

Inflammation of the gall bladder

276
Q

3 types of cell in the small bowel?

A

Goblet cells
Columnar absorptive cells
Endocrine cells

277
Q

The small bowel has columnar absorptive cells. What about the large bowel?

A

Also columnar absorptive

278
Q

The large and small bowel peristalsis is mediated by both intrinsic (mesenteric plexus) and extrinsic (autonomic innervation) neural control. What are the two myenteric plexuses?

A

Meissners plexus within the submucosa
Auerbach plexus between the circular and longitude muscle of the muscularis propria

279
Q

2 main strands of inflammatory bowel disease?

A

Crohn’s disease
Ulcerative colitis

280
Q

What is IBD

A

Recurrent episodes of inflammation in the gastrointestinal tract - ulcerative colitis and Crohn’s disease.
Associated with exacerbation and remission

281
Q

Presenting features of IBD?

A

Diarrhoea
Abdominal pain
Rectal bleeding
Fatigue
Weight loss

282
Q

What are the differentiating features of crohns? (IBD). This can be remembered with the ‘crows’ NESTS mnemonic.

A

No blood or mucus
Entire GI tract is affected- mouth to anus
‘Skip lesions’ on endoscopy
T - terminal ileum most affected and full Thickness
Smoking is a risk factor (don’t set the nest on fire)

283
Q

Crypts abscesses are more seen in what type of IBD?

A

Ulcerative colitis
Not crohns

284
Q

What are ‘skip lesions’ of crohns?

A

The fact that inflammation isn’t continuous Vs it is in ulcerative colitis

285
Q

Why can fistula form in crohns?

A

Due to the trans mural nature of the inflammation

286
Q

Inflammation of ulcerative colitis?

A

Mucosal involvement only

287
Q

Which IBD disease is Granulomatous?

A

Crohns
So the histological appearance of crohns is non-caseating Granulomatous inflammation

288
Q

Site of ulcerative colitis?

A

Large bowel

289
Q

Why would nail clubbing occur in crohns?

A

Secondary to malabsorption

290
Q

What hepatobiliady complication could occur in Crohn’s disease?

A

Primary sclerosing cholangitis, hall stone disease

291
Q

Gold standard investigation for IBD?

A

Colonoscopy to show evidence of inflammation, and biopsies can confirm diagnosis

292
Q

What imaging for IBD?

A

MRI small bowel imaging
Or
Urgent CT imaging to check for bowel obstruction or bowel perforation

293
Q

Patients in an acute flare of Crohn’s disease will require what as first line

A

Cortico steroid therapy

294
Q

What is patients with a remission in Crohn’s disease, fail first line therapy of corticosteroids?

A

Immunosuppressive agents like mesalazine or azathioprine

295
Q

Why would surgical management of Crohn’s disease be necessary?

A

For those with severe complications such as strictures or perforation

Eg resection (NB these are high risk patients to operate on).

296
Q

Two reasons crohns patients might have osteoporosis?

A

Secondary to:
Malabsorption
Long term steroid use

297
Q

Why are crohns patients at increased risk of fall stones?

A

Due to reduced reabsorption of bile salts at the terminal ileum

298
Q

Is smoking a risk factor for which IBD disease?

A

Crohns

299
Q

Sever exacerbations of crohns May result in what?

A

Life threatening severe systemic upset, bowel perforation or even mortality.

300
Q

Ulcerative colitis is the least common form of inflammatory bowel disease, true or false?

A

False
Most common

301
Q

Is the pathophysiology of ulcerative colitis understood?

A

Nahhhhhh

302
Q

What are three histological changes that occur with ulcerative colitis?

A

Non Granulomatous inflammation of mucosa and sub-mucosa
Crypt abscesses
Goblet cell hyperplasia

303
Q

How do pseudopolyps occur in ulcerative colitis?

A

Repeated cycles of ulceration and healing = raised areas of inflamed tissue termed pseudopolyps

304
Q

How to diagnose IBD?

A

Take history
Radio graphic examination

In most UC patients, they are ‘perinuclear antineutrophilic cytoplasmic antibody’

305
Q

Would the appendix ever be involved in IBD?

A

Yes
For ulcerative colitis , can also be localised to the rectum

306
Q

Are there any Granulomas in ulcerative colitis?

A

Yes

307
Q

How might ulcerative colitis lead to cancer?

A

Dysplasia of epithelium

308
Q

What happens to the mesentery in crohns?

A

Thickened and fibrotic

309
Q

How is anaemia secondary to ulcerative colitis?

A

Ulceration
Breakdown of surface
Haemorrhage and bleeding
Become anaemic

310
Q

What’s toxic megacolon? (Complication of ulcerative colitis)

A

Inflammation deep enough for perforations, =organisms can move beyond mucosa, into the sub mucosa, then you get an infective condition = toxic megacolon where colon expands very rapidly. And can be fatal

311
Q

Is there a gender bias in IBD?

A

Only in crohns- towards females

312
Q

What happens to the serosa in Crohn’s disease?

A

Becomes a granular dull grey

313
Q

What’s ischaemic enteritis?

A

Where blood supply to the bowel is impinged, and is insufficient, so the bowel dies off

314
Q

What happens when there is acute occlusion if one of the three major blood vessels eg coeliac s and I mesenteric arteries?

A

Infarction of segments of bowel

315
Q

5 things that happen in chronic ischaemia?

A

Mucosal inflammation
Ulceration
Sub-mucosal inflammation
Fibrosis
Stricture

316
Q

Why might vasodilation happen in chronic ischaemia?

A

Blood vessels dilate to try and provide more blood into the area

317
Q

Why inflammation in ischaemia (occlusion of blood vessels)

A

Inflammatory cells can move in and start to repair the damage

318
Q

Why stricture in chronic ischaemia?

A

Fibrosis comes to heal- that leads to structure formation

319
Q

What’s radiation colitis?

A

Well people get abdominal radiation for things like prostate cancer, other cancers etc
Radiation may impair normal normal proliferative activity

Symptoms mimic IBD

320
Q

How is acute appendicitis a classic IBD condition?

A

It can be caused by acute inflammation in the mucosa of the appendix

321
Q

What is the appendix suspended by?

A

The mesoappendix

322
Q

What is the point of the appendix?

A

Reservoir for intestinal flora

323
Q

Typical cause of appendicitis?

A

Obstruction of opening of the appendix
Usually result of hardened stool
Or
Lymphoid hyperplasia

324
Q

Explain migration of pain in appendicitis first stage then second stage

A

First stage: initial inflammation stimulates visceral afferent pain fibres which correspond to T10 dermatome, producing umbilical pain

Second stage: as appendix becomes more inflamed, it irritates parietal peritoneum which activates somatic nerve fibres, to produce localised pain, felt in the right iliac fossa
(McBurney’s point)

325
Q

Why do we vomit with appendicitis?

A

Non specific immune response from immune system

326
Q

The destruction of the appendix can increase Intraluminal pressure which can result in what?

A

Ischaemia of the mucosa, because the blood can’t get in because the pressure here is higher than outside the appendix, so it becomes inflamed and then perforates

327
Q

How does GI tract dysplasia often present?

A

Formation of a polyp (adenomatous)

328
Q

T or f, there is reduced mucin with dysplasia

A

True

329
Q

Most adenocarcinoma’s of the large bowel arise from what

A

They develop from epithelial cells lining the colon or rectum, as an adenocarcinoma. They develop via a progression of normal mucosa to colonic adenoma as polyps, to become invasive

330
Q

T or F, Inflammatlry bowel disease is a risk factor for what

A

colorectal cancer

331
Q

Which is worse, right sided or left sided colorectal cancer?

A

Right sided colon cancers are more aggressive

332
Q

Why are right sided colon cancers got a worse prognosis?

A

Right sided colon cancers often grow larger before noticeable symptoms, so more likely to be diagnosed at a more advanced stage.

333
Q

Is left or right sided colorectal adenocarcinoma related to altered bowel habit?

A

Left.
Now the stool on the left has become firmer (water at this point has mainly been absorbed) and therefore narrowing of the lumen due to lesion = altered bowel habit.

334
Q

When does the oesophagus begin?

A

At the cricoid cartilage about C6

335
Q

When does the esophagus end?

A

Like T11-T12, where it enters the stomach

336
Q

Peristalsis of the oesophagus is mediated by what nerve

A

Vagus nerve

337
Q

At lower oesophageal sphincter, a mucosal rosette is formed by the acute angle of what

A

His

338
Q

Persistent reflux and heartburn can lead to what?

A

GORD
Gastro-oesophageal reflux disease
Which in turn can lead to long term complications

339
Q

Possible causes of dysphagia?

A

Benign stricture
Malignant structure (oes cancer)
Extrinsic compression eg from lung cancer
Eosinophilic oesophagitis

340
Q

Hypermotility of the eosophagus example is diffuse oesophageal spasm. What appearance has this got on a barium swallow?

A

“Corkscrew” appearance.

341
Q

What does achalasia result from?

A

Loss of relaxation from the sphincter, secondary to loss of myenteric plexus ganglion cells

It’s a swallowing dusirdee

342
Q

What plexus innervates the lower oesophageal sphincter?

A

The myenteric plexus (between circular/longitudinal muscles of muscularis propria)

343
Q

Why is achalasia, a swallowing disorder, associated with chest infection?

A

Stasis of oesophageal food contents

344
Q

Treatments of achalasia?

A

Nitrates and calcium channel blockers

345
Q

GORD pathophysiology?

A

Mucosa exposed to acid-pepsin and bile
Increased cell loss and regenerative activity (inflammation)

346
Q

Complications of GORD?

A

Ulceration
Stricture
Barrett’s (glandular metaplasia)
Carcinoma

347
Q

What occurs in Barrett’s oesophagus histology

A

Change from squamous to mucin secreting columnar (ie gastric type)

348
Q

How do you usually treat Barrett’s?

A

Endoscopic mucosal resection

349
Q

Treatment of GORD?

A

Lifestyle eg obesity, smoking, diet etc

Proton pump inhibitor eg omeprazole, lansoprazole

350
Q

Biggest symptom of oesophageal cancer?

A

Progressive Dysphagia
Anorexia
Weight loss

351
Q

What percentage of the worlds population is infected with helicobacter pylori?

A

50% of the world’s population

352
Q

What clinical condition typically occurs in patients on long term or high doses of NSAIDs and aspirin?

A

Peptic ulcer disease
As prostaglandins are suppressed, making stomach more vulnerable to irritation and damage from stomach acid

353
Q

Acute mesenteric ischaemia refers to what condition

A

Where there is a sudden decrease in blood supply to the bowel, resulting in bowel ischaemia and eventual necrosis.

354
Q

Which are the fat soluble vitamins?

A

A, D, E and K

355
Q

If patients are gonna be on NSAIDs and aspirin for more than a few days, what other drugs are they prescribed?

A

PPI such as omeprazole to provide gastroprotection

356
Q

How would you expect chronic pancreatitis to affect glucose levels?

A

Hyperglycaemia

357
Q

Why hyperglycaemia in chronic pancreatitis?

A

Impact of pancreas function.
Patients can develop diabetes secondary to chronic pancreatitis, as insulin producing pancreatic cells can be damaged

358
Q

Opioids are commonly used for pain relief, or for suppression of diarrhoea. What is a common side effect

A

Constipation

359
Q

How does malabsorption occur in coeliac disease?

A

As a consequence of autoimmune destruction of villi

360
Q

How does coeliac disease present?

A

Diarrhoea, steatorrhea, weight loss, vitamin deficiency

361
Q

In iron deficiency, liver increases production of what?

A

Production of transferrin in order to increase iron uptake, and maintain iron homeostasis

362
Q

Ferritin is an iron store. So does it increase or decrease with iron deficiency?

A

Levels increase when there is a high amount of iron in the blood- and decreases with iron deficiency!

363
Q

A low ferritin is a marker of what

A

Iron deficiency
So it’s a commonly used test

364
Q

What is choledocolithiasis?

A

Gall stones in the bile duct

365
Q

What does primary biliary cholangitis affect?

A

The bile ducts within the liver

366
Q

How does cholestasis occur due to primary bilary cholangitis?

A

As bile ducts become damaged, they are less able to transport bile, so cholestasis and therefore accumulation of bile acids in the liver and blood stream

367
Q

Hall stones in the bile duct: does this present as painful or painless obstructive jaundice?

A

Painful

368
Q

Ascending cholangitis might be a result of what obstructing the bile duct

A

Gall stones in the bile duct

Cholangitis is an inflammation of the bile duct

369
Q

Bilary Cholangitis is caused by a combination of what two issues?

A

Biliary outflow obstruction and biliary infection. Because bile is within the gallbladder for too long, and bile sits and thickens, providing an ideal growth medium for bacteria.

370
Q

Why might biliary cholangitis lead to biliary sepsis?

A

Pressure due to obstruction increases. And this increases risk of bacterial translocation into the bloodstream- resulting in biliary sepsis

371
Q

Definitive diagnosis of Crohn’s disease?

A

Endoscopy findings, showing mucosal inflammation, cobblestone appearance with ulcers, skip lesions

372
Q

What can be a side effect of use of proton pump inhibitors such as omeprazole?

A

Increased risk of c. Diff infection

373
Q

Which autoantibodies are characteristic for primary biliary cholangitis?

A

Anti mitochondrial antibodies

YEAR 2 GI (7 decks)

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