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4th Year Surgery Block > Upper GI > Flashcards

Upper GI Flashcards

1
Q

What is acute cholangitis and what causes it?

A
  • Infection of the biliary tree
  • Infection is coming from the GI tract so may organisms = E. coli, Klebsiella, enterococcus
  • Any condition that impairs drainage of the biliary tree can cause infection
  • Most commonly due to stones in the common bile duct but could also be caused by a cancer or surgical injury
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2
Q

Presentation of acute cholangitis?

A
  • Charcot’s triad = fever, RUQ pain/ biliary colic and obstructive jaundice
  • May also complain of itching and pale stool with dark urine from the obstructive jaundice
  • Patient history may include gallstones, recent biliary tract instrumentation or previous cholangitis
  • Signs include pyrexia, rigors, jaundice and RUQ tenderness, confusion, hypotension and tachycardia may also be present
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3
Q

Differences in presentations of biliary colic, cholecystitis and cholangitis?

A

Biliary colic presents with RUQ but no fever
Acute cholecystitis presents with RUQ pain and fever but NO jaundice
Acute cholangitis presents with all 3 (because you are blocking bilirubin from being excreted if the biliary tree is blocked)

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4
Q

Investigations for acute cholangitis?

A
  • FBCs and LFTs
  • Blood cultures if concerns of sepsis
  • US of biliary tract will show bile duct dilation, may also see stones
  • Gold standard investigation is ERCP as is both diagnostic and therapeutic
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5
Q

Management for acute cholangitis?

A
  • Initially may need fluids and broad spectrum antibiotics (as may be septic) – amoxicillin, metronidazole, gentamicin
  • Definitive management is by ERCP
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6
Q

What is acute pancreatitis and causes?

A
  • Acute inflammation of the pancreas involving destruction by its own enzymes – autodigestion
  • Most common causes are gallstones blocking the ampulla of vater causing bile to reflux up the pancreatic duct and alcohol abuse (mechanism not as simple)
  • Other causes remembered by:

I: Idiopathic
G: Gallstones
E: Ethanol (alcohol)
T: Trauma
S: Steroids
M: Mumps
A: Autoimmune
S: Scorpion sting
H: Hypercalcemia, Hypertriglyceridemia
E: ERCP
D: drugs e.g. liraglitide for T2DM

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7
Q

Presentation of acute pancreatitis?

A
  • Patient usually has an acute onset of severe upper abdominal pain that usually begins in the epigastrium but may radiate to the back
  • Often accompanied by nausea and vomiting
  • Cullen’s sign (periumbilical bruising) and Grey Turner’s sign (flank bruising) are specific signs for necrotising pancreatitis
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8
Q

Investigations for acute pancreatitis?

A
  • Check serum amylase – this is raised in acute pancreatitis
  • FBCs, U and E, glucose and CRP
  • Check bilirubin (could suggest gallstones)
  • Hypocalcaemia is common
  • Plain erect AXR to exclude other causes
  • CT scan with contrast may be diagnostic
  • US can show swollen pancreas and also presence of gallstones
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9
Q

Management for acute pancreatitis?

A
  • Anyone with suspected acute pancreatitis needs admitted to hospital
  • Analgesia
  • IV fluids
  • Can eat if feel able to
  • Treat underlying cause e.g. remove gallstones
  • Only need surgery if infection and necrosis, in these cases also give antibiotics
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10
Q

Explain the different types of alcoholic liver disease?

A
  • Fatty liver occurs in most heavy drinkers even after one episode of heavy intake, fat accumulates in hepatocytes due to abnormalities in the intermediate metabolism of lipids and carbohydrates
  • Fatty liver is completely reversible on withdrawal of alcohol
  • If alcoholism continues the liver can become inflamed (alcoholic hepatitis) due to the fatty changes, this can be asymptomatic or symptomatic and signs of liver failure may be seen
  • Alcoholic hepatitis is potentially reversible on withdrawal
  • If inflammation continues cirrhosis will occur and this is irreversible
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11
Q

Presentation of alcoholic fatty liver and hepatitis?

A
  • The majority of patients with fatty liver will be asymptomatic although may report persistent fatigue, malaise or RUQ pain
  • Alcoholic hepatitis may present with loss of appetite, nausea and vomiting, RUQ tenderness, low grade fever, fatigue and weakness
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12
Q

Management of alcoholic fatty liver and alcoholic hepatitis?

A
  • Abstinence – fatty liver is reversible if stop drinking, hepatitis may be partially reversible and it will stop it progressing
  • Diet changes for those with hepatitis – avoiding salty foods reduces risk of fluid build up, may not be able to store as much glycogen so have to ensure adequate protein and energy in diet
  • Sometimes corticosteroids for hepatitis but this is controversial
  • May need a transplant with hepatitis if progresses to cirrhosis and liver failure
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13
Q

Describe briefly the structure of haemoglobin?

A

there are lots of haemoglobin molecules in one red blood cell
there are 2 beta globin chains and 2 alpha globin chains
each has haem group which is a porphyrin ring and iron

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14
Q

Define anaemia?

A
  • Reduced total red cell mass
  • Hb concentration is a marker for this
  • In men aged over 15 years — Hb below 130 g/L.
  • In non-pregnant women aged over 15 years — Hb below 120 g/L.
  • In children aged 12–14 years — Hb below 120 g/L
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15
Q

Causes of normocytic anaemia?

A
  • Causes include acute blood loss, anaemia of chronic disease, marrow infiltration/ fibrosis, endocrine disease and the haemolytic anaemias
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16
Q

Microcytic anaemia is due to ______

A
  • This is due to deficient Hb synthesis
  • The defects in Hb results in small cells because the cells keep dividing as they try to accumulate Hb because there isn’t an adequate one to trigger them to stop dividing
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17
Q

Causes of microcytic anaemia?

A
  • The most common cause is iron deficiency
  • All causes however can be remembered by TAILS (thalassaemia, anaemia of chronic disease, iron deficiency, lead poisoning and sideroblastic anaemia)
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18
Q

Macrocytic anaemia can be classed as ______

A

megaloblastic or non-megaloblastic

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19
Q

In megaloblastic macrocytic anaemia the problem is with _____
2 main causes are _________

A

nuclear maturation
folate or B12 deficiency

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20
Q

Non-megaloblastic macrocytic anaemia can be caused by ______

A

alcohol, liver disease, hypothyroidism or marrow failure

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21
Q

Symptoms and signs of anaemia?

A

SYMPTOMS:
- Can be asymptomatic
- Fatigue
- Headaches
- Fainting
- Breathlessness
- Anaemia can exacerbate cardiorespiratory problems in the elderly and cause angina, intermittent claudication and palpitations

SIGNS:
- Pallor (particularly of mucous membranes)
- Tachycardia
- Systolic flow murmur
- Cardiac failure

There may be specific features due to the underlying cause e.g. signs of haemolysis, signs of iron deficiency, signs of B12 or folate deficiency

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22
Q

Causes of iron deficiency anaemia?

A
  • It may be due to diet, malabsorption or chronic blood loss or a combination of all 3 (e.g. a poor intake plus small blood loss – neither on their own may cause deficiency but combined there is an issue)
  • The main causes of chronic blood loss include menorrhagia and GI bleeding (worry about a GI cancer), another potential cause is haematuria
  • There are higher iron demands in menstruating women, pregnancy and adolescents, so these groups are more likely to become iron deficient
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23
Q

Specific signs of iron deficiency?

A
  • Brittle nails, koilonychia (spoon nails), atrophy of the papillae of the tongue, angular stomatitis and brittle hair
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24
Q

Investigations for iron deficiency anaemia?

A
  • Serum ferritin level is the biochemical test which most reliably correlates with relative total body iron stores
  • In all people a serum ferritin level of less than 30 micrograms/L confirms the diagnosis of iron deficiency
  • However, ferritin levels are raised in infection and inflammation making it more difficult to interpret in these scenarios
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25
Q

Management of iron deficiency anaemia?

A
  • below about 70 probably going to need a transfusion
  • Cause of iron deficiency anaemia needs determined and treated
  • Iron replacement is also recommended and in adults they are given oral ferrous sulfate tablets
  • These tablets can cause some GI side effects such as nausea, diarrhoea or constipation
  • Sodium feredetate is a liquid solution used in children
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26
Q

explain why the cells are bigger in megaloblastic anaemia and why this causes anaemia?

A
  • A megaloblast is an abnormally large nucleated red cell precursor with an immature nucleus
  • Megaloblastic anaemias are characterised by a lack of red cells due to predominant defects in DNA synthesis and nuclear maturation in developing precursors in the bone marrow
  • The megaloblast cytoplasm still develops and they accumulate Hb, once Hb level in the cell is optimal the nucleus is extruded leaving a bigger than normal red cell i.e. a macrocyte
  • Compared to normal precursors megaloblasts have reduced division and increased apoptosis which is what causes the anaemia (because there are less of these bigger red cells due to the reduced division and increased apoptosis)
  • Note: important to understand that the large cell size is not due to an increase in the size of the developing cell but a failure of the cell to become smaller
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27
Q

B12 is present in ______
folate is present in __________

A
  • B12 is present in animal products e.g. meat, fish, milk, cheese and eggs
  • Folate is present in liver, leafy green veg and some fortified cereals
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28
Q

Absorption of B12?

A

intrinsic factor secreted by parietal cells allows it to be absorbed, it is absorbed in the ileum

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29
Q

Folate is absorbed in the

A

duodenum and jejenum

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30
Q

Body stores of folate and B12? Relevance?

A
  • Body stores of B12 are 2-4 years but folate only 4 months, so symptoms of B12 deficiency take longer to manifest
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31
Q

Causes of B12 deficiency?

A
  • Diet
  • Pernicious anaemia
  • Surgical resection of the small bowel
  • Gastrectomy
  • Pernicious anaemia is the most common cause of B12 deficiency in adults and it is an autoimmune condition causing destruction of gastric parietal cells resulting in intrinsic factor deficiency causing malabsorption of B12
  • Pernicious anaemia is associated with a family or personal history of other autoimmune diseases particularly hypothyroidism, vitiligo and Addisons
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32
Q

Causes of folate deficiency?

A
  • Diet – more common in alcoholics who may have a very poor diet
  • Malabsorption in coeliacs or Crohns
  • Excess utilisation e.g. haemolysis, exfoliating dermatitis, pregnancy, some malignancies
  • Certain drugs such as anti-epileptics can cause a folate deficiency
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33
Q

Clinical features of B12 and folate deficiency?

A
  • Patient may be mildly jaundiced
  • Glossitis – beefy red sore tongue
  • B12 neuropathy: posterior dorsal column abnormalities, peripheral neuropathy, psychiatric manifestations (these neurological disturbances may be irreversible)
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34
Q

Investigations of B12 and folate deficiency?

A
  • Can check for serum B12 or folate levels
  • With pernicious anaemia can check for anti-gastric parietal cell and anti-intrinsic factor
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35
Q

Treatment of B12 and folate deficiency?

A
  • B12 deficiency: IM B12 injections can be given, at first they are given several doses over a few weeks and then the patient is given doses every three months for the rest of their life
  • Folate deficiency can be corrected by giving 5mg folic acid daily, this should be taken for at least 4 months to replace body stores, any underlying cause should be treated and if it can’t then the person should continue on folic acid supplements
  • There isn’t any particular harm in starting B12 or folate before confirmation so if the person is very ill it is better to start the vitamins because the neurological symptoms can be irreversible
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36
Q

Grey turner and cullens sign?

A

cullens = periumbilical bruising
grey turner = flank bruising

necrotising pancreatitis

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37
Q

What is the most common cause of acute abdomen in the UK?

A

appendicitis

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38
Q

What is appendicitis? Is it common? In Who?

A
  • Inflammation of the appendix usually initiated by obstruction of the lumen
  • This is most commonly caused by a faecolith or lymphoid follicle growth (in children)
  • About 10% of population will get appendicitis
  • It is most common in ages between 10 and 20
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39
Q

Complications of appendicitis?

A
  • If the appendix ruptures then can get peritonitis
  • Sometimes the inflamed appendix becomes surrounded by omentum which adheres and localise the infection forming an appendix mass or abscess
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40
Q

Presentation of appendicitis?

A
  • Classically starts as dull periumbilical pain moving to a sharper pain in the RIF as the peritoneum becomes involves
  • Movement and coughing aggravate the pain
  • May have nausea, vomiting and anorexia
  • May be constipated
  • Temperature and pulse initially normally but may get low grade fever
  • On examination localised tenderness, guarding and rebound tendereness in RIF
  • Rosvigs sign: palpation of the left increases pain felt on the right
  • McBurneys point: this is 2/3 of the distance from the umbilicus to the R ASIS and is thought to be the point of maximum tenderness in appendicitis
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41
Q

Rosvigs sign?

A

palpation of the left increases pain felt on the right

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42
Q

McBurney’s point?

A

this is 2/3 of the distance from the umbilicus to the R ASIS and is thought to be the point of maximum tenderness in appendicitis

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43
Q

Investigations for appendicitis?

A
  • Must exclude other causes of acute abdomen – pregnancy test, urine dipstick, bloods (FBC, U and E, CRP)
  • Imaging is helpful and ultrasound, CT and MRI are most commonly used
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44
Q

Management of appendicitis?

A
  • ABCDE management and analgesia
  • Removal of the appendix is the gold standard treatment for uncomplicated appendicitis
  • Laparoscopic is preferred if possible (vs open)
  • In selected patients non-operative management with IV fluids and antibiotics can be safe and effective
  • All removed appendices are sent to pathology to check for pseudomyoma peritonei and adenocarcinoma of the caecum as well as carcinoid of the appendix, this also allows to confirm diagnosis as other source may need to be checked
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45
Q

Explain why gallstones form and the different types?

A
  • Gallstones are the principle cause of gallbladder disease and its consequences
  • Gallstones are formed in the gallbladder when there is an insufficient balance between the ratio of cholesterol to bile salts
  • Cholesterol stones are associated with excess cholesterol and pigment stones with excess bilirubin
  • Majority of gallstones are actually mixed
  • Risk factors for mixed and cholesterol stones include: diabetes, Caucasian, female, obesity, age > 40 yo, OCP
  • Pigment stones are associated with excess bilirubin so are usually due to haemolytic anaemia (as bilirubin is an end product of red blood cells)
  • The majority of gallstones are asymptomatic and remain so during a person’s lifetime
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46
Q

Define biliary colic?

A
  • This refers to pain associated with temporary obstruction of the cystic or common bile duct by a stone usually migrating from the gallbladder
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47
Q

Presentation of biliary colic?

A
  • Sudden onset of severe epigastric pain that may also be present in the RUQ often related to eating fatty foods
  • Nausea and vomiting may be associated with severe attacks
  • Attacks usually cease after a couple of hours or on administration of analgesics
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48
Q

Investigations for biliary colic?

A
  • Abdominal ultrasound and LFTs
  • If gallstones are not detected but suspicion of symptomatic gallstone disease remains high further tests in secondary care need to be arranged
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49
Q

Management of biliary colic?

A
  • Everyone can be considered for laparoscopic cholecystectomy
  • Should also offer appropriate pain relief, advise to lose weight if overweight
  • If unfit for surgery patients may be given ursodeoxycholic acid which helps stop the formation of stones
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50
Q

What is acute cholecystitis?

A
  • Inflammation of the gallbladder that occurs when a stone obstructs the emptying
  • Infection with E. coli and other gut organisms may occur as drainage is impeded
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51
Q

Presentation of acute cholecystitis?

A
  • Initial features are similar to biliary colic but usually progresses over a number of hours to severe RUQ pain due to involvement of parietal peritoneum
  • Pain is associated with tenderness, muscle guarding and rigidity
  • Positive Murphy’s sign: pain on taking a deep breath when the examiner’s fingers are on the approximate location of the gallbladder (this is because the diaphragm moves down when you breathe in and if you are palpating where the gallbladder is it can’t move down causing pain if it’s inflamed)
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52
Q

Investigations for acute cholecystitis?

A
  • Abdominal ultrasound is gold standard for differentiating between biliary colic and acute cholecystitis and US can also be used to check for presence of gallstones
  • FBCs and LFTs
  • MRCP may also be required
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53
Q

Management for acute cholecystitis?

A
  • Antibiotics, analgesia and fluid resuscitation
  • Once stable will need a cholecystectomy
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54
Q

What is chronic cholecystitis?

A
  • Gallbladder is damaged by repeated attacks of acute inflammation
  • The gallbladder is full of gallstones and the wall is thickened and fibrosed
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55
Q

Presentation of chronic cholecystitis?

A
  • May be a history of acute attacks
  • Vague symptoms of intolerance of fatty foods, RUQ pain
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56
Q

Investigations for chronic cholecystitis?

A
  • Abdominal US
  • ERCP or MRCP may be used to
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57
Q

Management of chronic cholecystitis?

A
  • Need cholecystectomy
  • Chronic cholecystitis increases risk of developing carcinoma of the gallbladder
  • Side note: carcinoma of the gallbladder is uncommon but almost always associated with gallstones
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58
Q

What is a hiatus hernia?

A
  • Hiatus hernia refers to herniation of the abdominal viscera through the oesophageal aperture of the diaphragm
  • The vast majority of hiatus hernias involve only the herniation of a part of the gastric cardia through the muscular hiatal aperture of the diaphragm
  • Rarely large defects allow other organs through e.g. spleen and pancreas
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59
Q

Types of hiatus hernia?

A

Most cases are a sliding hiatus hernia where the gastro-oesophageal junction slides up into the thoracic cavity (this is 85-95% of cases)

Para-oesophageal (rolling) hiatus hernia- the junction remains in place but a part of the stomach herniates into the chest next to the oesophagus (5-15% of cases), many are mixed with a sliding component also

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60
Q

Presentation of hiatus hernia?

A
  • Clinical significance of a sliding hiatus hernia is increased risk of GORD
  • [the concern of para-oesophageal hernias is the potential for obstruction, volvulus or ischaemia]
  • Many individuals with sliding hiatus hernia will be totally asymptomatic, others may present with:
  • Retrosternal burning sensation ‘heartburn’ especially on bending or lying
  • Gastro-oesophageal reflux
  • Difficulty in swallowing
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61
Q

Diagnosis of hiatus hernia?

A
  • Hiatus hernias are often intermittent so investigations can be unreliable
  • CXR – may be seen
  • Barium study
  • Endoscopy
  • Oesophageal manometry when considering surgery

Often found as an incidental finding when you have a CXR for something else

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62
Q

Management of hiatus hernia?

A
  • Treatment is not needed in the absence of symptoms except in para-oesophageal hiatus hernia where the potential risks are greater and surgery may even be considered in absence of symptoms
  • Lifestyle factors are similar to those with GORD: avoid tight clothing and things that increase abdominal pressure, weight loss, elevate head of bed when sleeping, avoidance of foods that trigger symptoms (fatty foods, spicy foods, caffeine, citrus juices)
  • PPIs can help relieve symptoms
  • Asymptomatic sliding hernias do not need surgery but surgery is considered in those with very bad symptoms or complications of the condition and also in para-oesophageal hernias as these have greater risk of complications
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63
Q

Explain what cirrhosis is?

A
  • Cirrhosis is the end stage of many liver diseases and is defined as a diffuse process characterised by fibrosis and conversion of the liver architecture into abnormal nodules
  • The common mechanism is hepatic stellate cells found in the space of Disse are activated and transformed into myofibroblasts under the influence of cytokines, these activated cells synthesise collagen leading to fibrosis
  • Cirrhosis may be compensated where there are few or no symptoms or decompensated where the patient is very unwell
64
Q

Presentation of cirrhosis?

A

Symptoms
* May be asymptomatic
* Non-specific symptoms of malaise, fatigue, anorexia, weight loss, muscle wasting and abdominal pain
* Should suspect cirrhosis in people with risk factors and these symptoms e.g. known alcohol misuse, hepatits B or C infection, NAFLD etc.

On examination
* Hepatosplenomegaly (the spleen is enlarged because fluid backs up as can’t get through liver)
* Jaundice – increase in unconjugated bilirubin as liver is failing and cannot conjugate it
* Abnormal bruising – clotting factors are produced in liver and failing liver produces less
* Variceal bleeding
* Encephalopathy – asterixis
* Ascites
* Spider naevi and palmar erythema – caused by excess oestrogen as liver usually metabolises this
* Clubbing
* Gynaecomastia – abnormal metabolism of hormones e.g. oestrogen and relatives

65
Q

Explain the different types of jaundice and if bilirubin is conjugated or unconjugated?

A
  • Pre-hepatic jaundice is due to increased RBC destruction e.g. haemolytic anaemia so the bilirubin is therefore unconjugated as it has not reached the liver yet
  • Hepatocellular jaundice is due to liver cell damage e.g. in hepatitis so the liver cannot conjugate bilirubin so there is therefore a rise in unconjugated bilirubin
  • Post hepatic obstructive jaundice e.g. a stone blocking the common bile duct- this is due to failure to excrete the bilirubin and it is therefore conjugated
66
Q

Investigations for cirrhosis?

A
  • LFTs – AST, ALT, ALP, unconjugated bilirubin, and GGT are all likely to be raised
  • Hypoalbuminemia in advanced cirrhosis
  • Coagulation screen may show abnormalities
  • If don’t know cause then need to look for hepatitis, markers of alcohol abuse, autoantibodies etc.
  • US, CT or MRI may be used to detect complications of cirrhosis
  • Transient elastography can be used to quantify liver fibrosis, liver biopsy should be used for people who this is not appropriate for
67
Q

List some complications of cirrhosis?

A

portal hypertension
varices
ascites
encephalopathy
hepatorenal syndrome
hepatopulmonary syndrome
hepatocellular carcinoma

68
Q

Explain portal hypertension and varices as a complication of cirrhosis?

A
  • Normal portal pressure is 5-8 mmHg
  • Pressure rises due to areas of fibrosis compressing blood vessels
  • As pressure rises the areas of portal systemic anastomoses become engorged, dilated or varicosed and are at risk of rupture
  • Three main sites are the rectum, the umbilicus (caput medusae sign) and the oesophagus
  • Oesophageal varices are most at risk of rupture as are quite superficial, when oesophageal varices rupture there is usually catastrophic haemorrhage, massive haemoptysis, this is a medical emergency
69
Q

Management of ruptured oesophageal varices?

A

terlipressin and IV antibiotics then urgent endoscopy

70
Q

Explain ascites as a complication of cirrhosis? Management?

A
  • Fluid accumulates in the peritoneal cavity due to sodium and water retention, portal hypertension and hypoalbuminaemia
  • Abdominal swelling occurs and the presence of fluid can be demonstrated by shifting dullness to percussion
  • Treatment involves sodium restriction, spironolactone
  • If large ascites may need paracentesis to drain the fluid
  • TIPS procedure for refractory ascites
71
Q

Explain encephalopathy as a complication of cirrhosis? Maangement?

A
  • In cirrhosis the blood bypasses the liver via collaterals and the toxic metabolites pass directly to the brain, ammonia is the main toxin responsible for encephalopathy
  • Patients may have disorder of personality, mood and intellect, they may have slurred speech, vomiting or nausea
  • Signs include fetor hepaticus (sweet smelling breath), liver flap, constructional apraxia (can’t copy a drawing) and decreased mental function
  • Need to treat the underlying cause of cirrhosis to treat the encephalopathy
  • can give lactulose to encourage bowel excretion of ammonia and rifaximin to modify gut flora to produce less ammonia
72
Q

What is hepatorenal and hepatopulmonary syndrome?

A

Hepatorenal Syndrome
* This is basically renal failure caused by cirrhosis
* Mechanism is not fully understood but cirrhosis decreases renal blood flow

Hepatopulmonary Syndrome
* Lung Failure caused by cirrhosis
* Mechanism not fully understood but liver failure causes vessels in lungs to dilate and increase in number

73
Q

Hepatocellular carcinoma and cirrhosis?

A
  • Most important risk factor for developing hepatocellular carcinoma is cirrhosis of any cause
  • Cirrhotic patients must be screened regularly for HCC
74
Q

Management of cirrhosis?

A
  • Aim is to delay progression and prevent/ treat any complications
  • Need to treat the underlying cause of cirrhosis
  • If alcohol is the cause they need to stop drinking
  • Zinc deficiency is common and may need zinc supplements
  • Regular exercise to prevent muscle wasting
  • Prophylactic antibiotics in some patients
  • Vaccinations for hep A, influenza and pneumococci
  • Careful prescribing of drugs metabolised by the liver
  • Liver transplantation is the ultimate treatment of cirrhosis
75
Q

What is GORD?

A
  • Most people have a degree of reflux but if acidic stomach contacts stay in contact with oesophagus for longer than normal, people may complain of symptoms of GORD
  • GORD is caused by combination of incompetent LOS, poor oesophageal clearance and visceral sensitivity (someone may be very sensitive to reflux and complain of severe symptoms but actually very little oesophagitis present)
76
Q

Risk factors for GORD?

A
  • Increased intra-abdominal pressure e.g. obesity or pregnancy
  • High fat diet
  • Caffeine
  • Alcohol
  • Smoking (nicotine relaxes sphincter)
  • Certain drugs can cause reflux such as antihistamines, steroid, CCBs, benzodiazepines and antidepressants
  • Some medical conditions increase risk: hiatal hernia (part of stomach has squeezed up into diaphragm), scleroderma, Zollinger-ellison syndrome (gastrin secreting tumours cause your stomach to secrete too much acid))
77
Q

List some drugs that can cause GORD?

A

antihistamines, steroid, CCBs, benzodiazepines and antidepressants,

78
Q

List some medical conditions that increase risk of GORD?

A

hiatal hernia (part of stomach has squeezed up into diaphragm), scleroderma, Zollinger-ellison syndrome (gastrin secreting tumours cause your stomach to secrete too much acid))

79
Q

Presentation of GORD?

A
  • Main symptom is heartburn (burning pain behind sternum), may also complain of regurgitation and odynophagia (due to oesophagitis)
  • If there is severe oesophagitis there can be scarring of the oesophagus which causes oesophageal stenosis and then patient may complain of dysphagia
  • If reflux is severe, it can cause chronic coughing and hoarseness
80
Q

Diagnosis of GORD?

A
  • Clinical diagnosis can be made without investigation but if red flag symptoms or uncertainty can do endoscopy
  • 24hr pH monitoring can be helpful to confirm diagnosis if not responding to treatment
  • Therapeutic trial – try PPIs – if they work it’s GORD
81
Q

Management of GORD?

A
  • PPIs (omeprazole) are best drug treatment as they both eliminate symptoms and heal oesophagitis
  • Take for 8 weeks, see if symptoms come back or if settles, if symptoms come back can start taking again
  • Patients should also be encouraged to make lifestyle changes e.g., lose weight and diet changes
  • Antacids and H2 antagonists can provide symptomatic relief
  • Those who are young and suitable can have surgery to help with GORD (Nissen fundoplication – wrap part of the gastric fundus around the LOS)
82
Q

What is Barrett oesophagus? Why is it bad?

A
  • Barretts is a complication of GORD where there is intestinal metaplasia- change from the normal squamous epithelium to columnar epithelium
  • Barretts increases risk of adenocarcinoma
83
Q

Management of barretts oesophagus?

A
  • Barretts increases risk of adenocarcinoma so those with it on endoscopy need lifelong PPI treatment and regular surveillance (made on case by case basis how much surveillance etc)
  • If Barretts appears dysplastic on endoscopic surveillance then may ablate it
84
Q

Reynolds pentad =

A

charcots triad plus hypotension and confusion

85
Q

Explain what coeliac disease is and what happens to the bowel?

A
  • Condition in which there is inflammation of the mucosa of the small bowel (mainly duodenum) that improves when gluten is removed from the diet and relapses when gluten is reintroduced
  • Life long condition, not an allergy, it is T cell mediated, it is not antibody mediated
  • In the small bowel when consuming gluten there is inflammation resulting in villous atrophy, the villi become flat and surface area is lost meaning there is impaired absorption of nutrients
86
Q

Who gets coeliacs disease?

A
  • Genetically predisposed people, triggered by exposure to gluten
  • Coeliac disease can develop at any age, cause is not fully understand but HLA-DQ2 and HLA-DQ8 are thought to be associated, does tend to run in families
  • Also more common in people with other autoimmune diseases e.g. type 1 diabetes, Addisons, autoimmune hepatitis, pernicious anaemia etc.
87
Q

List some foods with and without gluten?

A

What foods have gluten in them?
* Gluten is in wheat, rye and barley
* Bread
* Cake
* Pies
* Cereal
* Pasta noodles

What foods are gluten free?
* Rice
* Potato
* Polenta
* Quinoa

88
Q

Presentation of coeliac disease?

A
  • Diarrhoea
  • Steatorrhoea (increase in fat secretion in stools due to malabsorption of fat – stools are looser and paler)
  • Abdominal pain
  • Weight loss
  • In children may present with failure to thrive
  • Skin manifestation: dermatitis herpetiformis which is an itchy blistering rash which usually arises on the elbows and extensor surfaces (IgA mediated)
89
Q

Investigations for coeliac disease?

A
  • Duodenal biopsy would show villus atrophy and crypt hyperplasia
  • Biopsy was previously considered gold standard for diagnosis but seem to be moving to serological testing as accuracy is increasing
  • Main serological test is tissue transglutaminase IgA, only issue with this test is that person still has to be eating gluten for it to be accurate
90
Q

Management of coeliac disease?

A
  • Only effective treatment is long term adherence to gluten free diet
  • Selection of gluten free products can be prescribed on the NHS
91
Q

Complications of coeliac disease?

A
  • Increased risk of T cell lymphomas and small bowel carcinomas
  • Risk of these is reduced if patient adheres to a gluten free diet
92
Q

What is the most common cancer of the stomach? What are other types?

A
  • Gastric carcinoma (adenocarcinoma) is the most common cancer of the stomach
  • Other types include lymphomas, carcinoid tumours and GISTs
93
Q

Describe the 2 types of gastric carcinoma?

A
  • Gastric adenocarcinomas can be intestinal or diffuse
  • Intestinal (well-differentiated) gastric carcinomas tend to arise as lesions on the lesser curvature and are usually well differentiated
  • Diffuse (poorly differentiated) gastric carcinomas arise in any region of the stomach and tend to be less obvious as lesions, they can cause linitus plastica which is when there is a thick hard stomach as cancer is affecting the whole stomach, histologically see signet ring cells (cells where nucleus has been pushed right to edge in a C shape like signet rings, this is because the cell cytoplasms are full of mucin)
94
Q

Linitus plastica?

A

diffuse gastric carcinoma
thick hard stomach as cancer is affecting all of it

95
Q

Most common site of metastases for gastric cancer?

A

the liver

96
Q

signet ring cells?

A

gastric carcinoma
cells where nucleus has been pushed right to edge in a C shape like signet rings, this is because the cell cytoplasms are full of mucin

97
Q

Risk factors for gastric cancer?

A
  • Smoking, alcohol and family history of gastric cancer are risk factors
  • H. pylori infection is a risk factor for intestinal gastric cancer
98
Q

Presentation of gastric cancer?

A
  • Gastric carcinomas tend to present late
  • Epigastric pain
  • Nausea and vomiting
  • Haematemesis, coffee ground vomit or melaena (black coloured stool) (both dark vomit and dark stools is because the stomach has started digesting the blood)
  • weight loss
  • Dysphagia if the tumour is near the gastro-oesophageal junction
99
Q

Investigations for gastric cancer?

A
  • Endoscopy is done to obtain a biopsy allowing diagnosis
100
Q

Management of gastric cancer?

A
  • Main treatment is surgery, this may be combined with chemotherapy
  • Due to late presentation may only be able to provide palliative treatment
101
Q

Hepatitis A:

Spread
Acute or chronic
Risk of cancer
vaccine
Other info

A

face-oral
almost always acute
no risk of cancer
vaccine available
generally unwell with nausea and anorexia, then become jaundiced before recovery

102
Q

Hepatitis B:

Spread
Acute or chronic
Risk of cancer
vaccine
Other info

A

parenteral
often severe
can be acute or chronic, chronic disease more likely to occur if infected in childhood
risk of cancer
vaccine available
need follow up for chronic disease and carrier status

103
Q

Hepatitis C:
Spread
acute or chronic
risk of cancer
vaccine
other info

A

parenteral
usually mild
almost always chronic
risk of cancer
no vaccine available

104
Q

Hepatitis D:
Spread
acute or chronic
risk of cancer
vaccine
other info

A

parenteral
needs hep B to cause infection, if hep b then hep D then get superinfection and 95% are chronic, v severe, if infected with b and d at same time slightly less severe
risk of cancer
protected if had hep b vaccine

105
Q

Hepatitis E:
Spread
acute or chronic
risk of cancer
vaccine
other info

A

face-oral
acute
no risk of cancer
no vaccine
often mild disease but if get in pregnancy can be severe

106
Q

Diagnosis of viral hepatitis?

A
  • Many episodes of viral hepatitis are subclinical and go undetected
  • Mild symptoms include nausea, fever and anorexia
  • Severe attacks can be fatal with jaundice and liver failure
  • Will have elevated AST, ALT, bilirubin increase (both conjugated and unconjugated) and potential presence of atypical lymphocytes as well as increased urobilinogen in the urine
107
Q

Management of viral hepatitis?

A
  • If anyone with hepatitis A is severely unwell, admit to hospital, if not can give supportive treatment with pain relief, anti-emetic etc
  • Those with hepatitis B and C need referred to secondary care, get supportive treatment and antivirals e.g. peginterferon, entecavir or tenofovir
  • Important to monitor those who have had a chronic infection for hepatocellular carcinoma
108
Q

HBsAg?

A

acute or chronic infection

109
Q

Anti-HBs?

A

immunity through exposure or vaccination

110
Q

Anti-HBc?

A

previous or current infection

111
Q

HBeAg?

A

active disease

112
Q

HBVDNA?

A

measure of replication/ active disease

113
Q

IgM antibodies?

A

active disease

114
Q

IgG antibodies?

A

recovery or vaccination

115
Q

Person with immunity from vaccination?

A

will be positive for Anti-HBs but negative for everything else

116
Q

Person with immunity from infection?

A

will be positive for Anti-HBs and Anti-HBc but negative for everything else

117
Q

A person with active disease?

A

will be positive for HBsAg, Anti-HBc, HbeAG, high HBVDNA but negative for Anti-HBs

118
Q

A person with chronic disease?

A

will be positive for HBsAG and Anti-HBc but negative for everything else

119
Q

Pathology for pancreatic cancer?

A
  • Most pancreatic cancers are in the exocrine portion and are adenocarcinomas
  • Majority of tumours are found in the head of the pancreas
  • The tumours arise from the duct epithelium
120
Q

Risk factors for pancreatic cancer?

A
  • Chronic pancreatitis
  • Alcohol
  • Smoking
  • Diet high in fat and carbohydrate
  • More common in males over 65
121
Q

Presentation of pancreatic cancer?

A
  • Classically pancreatic cancer presents late on as painless jaundice when the tumour obstructs the common bile duct (can also be itchy with the jaundice though)
  • However, may present with weight loss, anorexia and vague abdominal pain (pain often radiates to the back and may be relieved by leaning forwards)
  • May also have pale stools and dark urine if bile duct obstructed
122
Q

Investigations for pancreatic cancer?

A
  • Ultrasound is often done first to allow visualisation of the bile ducts and the head of the pancreas however a negative result does not exclude cancer
  • CT and biopsy can then be done
123
Q

Management of pancreatic cancer?

A
  • Unfortunately, pancreatic cancer has a very bad prognosis and is often picked up too late and treated palliatively
  • If operable Whipple’s procedure is done for tumours of the head and neck- the head of the pancreas is removed, the duodenum, lower part of stomach, gall bladder and common bile duct (this is because of the shared blood supply everything needs removed)
  • Total pancreatectomy or distal pancreatectomy can also be done depending on size and location of the tumour
124
Q

Pathology of oesophageal cancer?

A
  • Carcinoma of the oesophagus can occur as a squamous cell carcinoma or as an adenocarcinoma
  • Squamous cell carcinomas tend to affect the upper 2/3 and are associated with smoking and alcohol
  • Adenocarcinoma tends to affect the lower 1/3 of the oesophagus and is associated mainly with Barrett’s oesophagus and GORD
125
Q

Presentation of oesophageal cancer?

A
  • Usually these cancers are initially asymptomatic, then present with progressive dysphagia to solids first, then liquids
  • Other signs are weight loss and loss of appetite, anorexia and lymphadenopathy
126
Q

Investigations for oesophageal cancer?

A
  • Patients with suspected oesophageal cancer should be offered an endoscopic biopsy
  • Barium swallow may be done
  • PET can be useful to see metastases etc.
127
Q

Management for oesophageal cancer?

A
  • Unfortunately, many patients present really late and palliative care is the only option (usually involves inserting a stent to relieve the dysphagia)
  • Surgery is the best option but can only be done if there is no invasion of the oesophageal wall
  • Some patients can be given preoperative chemoradiation therapy to make the surgery easier
128
Q

What is a peptic ulcer?

A
  • Peptic ulcer is a break in the mucosa of the stomach or duodenum
  • Gastric ulcers tend to occur on the lesser curvature of the stomach and duodenal ulcers tend to occur in the duodenal cap
129
Q

Who gets peptic ulcers?

A
  • Majority are caused by H. pylori infection
  • H pylori is a gram negative bacillus, spread by faeco-oral route, infection usually occurs in infancy, majority of those infected have no pathology, small number develop peptic ulcers, an even smaller number go on to develop gastric cancer
  • NSAID induced peptic ulcers occur due to long term NSAID use as NSAIDs increase stomach acid secretion and inhibit prostaglandins which usually stimulate mucus production
130
Q

Presentation of peptic ulcers?

A
  • Patients usually present with burning epigastric pain that may get worse at night or when the patient is hungry
  • Classically gastric ulcers are worse when eating but those with duodenal ulcers experience less pain when eating
131
Q

Investigations for peptic ulcers?

A
  • Peptic ulcers need confirmed by biopsy
  • Patients then need tested for H. pylori using carbon-13 urea breath test or stool antigen test (test is not accurate if patient has been on antibiotics or PPIs)
132
Q

Management of peptic ulcers?

A
  • Everyone should get general advice e.g. avoid alcohol, caffeine and smoking
  • If positive for H. pylori and on NSAIDs, start off by stopping NSAIDs and going on a PPI for 2 months then give H. pylori eradication therapy
  • If not on PPI go straight onto H. pylori eradication therapy
  • Antibiotic therapy for H. pylori involves amoxicillin with either clarithromycin or metronidazole
133
Q

Complications of peptic ulcers?

A
  • GI bleed if ulcer erodes through an artery
  • Perforation if ulcer erodes whole way through causing peritonitis and sepsis
  • Gastric outlet obstruction if chronic and there is oedema or scarring
134
Q

Management of a peptic ulcer bleed?

A
  • If bleeding peptic ulcer usually do dual therapy with endoscopic injection of adrenaline to cause vasoconstriction and heater probe therapy, IV omeprazole reduces risk of re-bleeding, if can’t get bleeding under control may need open surgery
135
Q

Describe the relationship between H. pylori and peptic ulcers

A

not everyone with h pylori will have ulcers, most will not, only a small amount get ulcers and even smaller amount develop cancer

136
Q

loop is _____ end is _____

A

loop ileostomy or colostomy is reversible, end is not

137
Q

What is haemochromatosis? Primary vs secondary?

A

iron overload

Primary Haemochromatosis
* Long term excess iron absorption with parenchymal rather than macrophage iron loading
* The commonest form is due to mutations in HFE gene which causes a decreased synthesis of hepcidin resulting in increased iron absorption

Secondary Haemochromatosis
* Sources of secondary iron overload include repeated red cell transfusions and excessive iron absorption related to over-active erythropoiesis
* This can occur in thalassaemia, sideroblastic anaemia, red cell aplasia and myelodysplasia

138
Q

Presentation of haemochromatosis?

A
  • Iron deposition in the liver causes fibrosis and cirrhosis
  • Deposition in the heart can cause cardiomyopathies and arrhythmias and in the skin there can be bronzing, the pancreas can be damaged leading to malabsorption (damage of exocrine portion) and diabetes (damage of endocrine portion)
  • Classic presentation is the “bronzed diabetic” although it’s usually picked up much earlier than this now
  • Although primary haemochromatosis is present from birth people tend not to present until later on in life, men at about 40 and women at about 60 (as they’ve been able to lose iron through menstruation previously)
139
Q

Investigations for haemochromatosis?

A
  • Transferrin % saturation is high
  • Total iron binding capacity is reduced (because you are running out of stuff for iron to bind to)
  • Increased ferritin levels (ferritin helps store iron)
  • Genetic testing for hereditary haemochromatosis
  • Used to need liver biopsy with prussian blue staining but genetic tests are more accurate now so this is generally not necessary
140
Q

Management for haemochromatosis?

A
  • Primary: repeated venesection (basically remove the iron rich blood every week or two)
  • Secondary: you cannot do venesection because they are already anaemic, need to give iron chelating drugs e.g. desferrioxamine
141
Q

What is peritonitis?

A
  • Inflammation of serosal membrane lining abdominal cavity
  • Can be localized – inflammation limited to area e.g. adjacent to inflamed appendix or generalized e.g. after rupture of a viscus
142
Q

Causes of peritonitis?

A
  • Spontaneous bacterial peritonitis – more common in people with ascites/ cirrhosis
  • Leakage of GI contents from perforated viscera
  • Foreign material
  • Endometriosis
  • Peritoneal dialysis
143
Q

Signs and symptoms of peritonitis?

A
  • Fever, chills, tachycardia
  • Ascites, abdominal distension, rigidity and jaundice
  • Anorexia, nausea, vomiting, diarrhoea
  • In early stages there is dull poorly localised abdominal pain
  • In late stages severe localised abdominal pain – acute abdomen
144
Q

Investigations for peritonitis?

A
  • AXR – subhepatic/ subdiaphragmatic free air, abscesses in cases of perforated viscus
  • FBCs, U and Es, LFTs, blood cultures
  • Urinalysis
  • CRP
  • Paracentesis if ascites present looking at neutrophil count and serum ascites albumin gradient
145
Q

Management of peritonitis?

A
  • IV antibiotics
  • Surgery – percutaneous drainage of any abscesses, open surgery or laparoscopy
146
Q

Describe the function of the spleen?

A
  • The spleen is responsible for filtering the blood, phagocytosing debris and generating an immune response
  • The spleen consists of red pulp and white pulp
  • Red pulp consists of sinuses lined by endothelial macrophages and cords (spaces)
  • White pulp has a similar structure to that of lymphoid follicles
  • Blood enters via the splenic artery and is delivered to red and white pulp
  • During the flow the blood is skimmed with leucocytes and plasma preferentially passing to the white pulp
  • Some red cells pass rapidly through into the venous system while others are held up in the red pulp (older damaged RBCs)
147
Q

Causes of hyposplenism?

A
  • Physiological loss of function – e.g. damage associated with sickle cell anaemia, essential thrombocythaemia and ulcerative colitis or by a cancer
  • Splenectomy
148
Q

What are reasons patients may get a splenectomy?

A
  • Trauma: 25% injuries are iatrogenic (ie accidental in surgery)
  • Spontaneous rupture: this usually occurs in patients with massive splenomegaly e.g. in infectious mononucleosis and is precipitated by minor trauma
  • Hypersplenism: needs to be removed surgically because patient has hereditary spherocytosis or elliptocytosis causing pancytopenia
  • Neoplasia: spleen needs removed if there is lymphoma or leukaemia invasion
  • Needs removed when other viscera getting removed due to shared blood supply or artery lies on the organ e.g. distal pancreatectomy
  • Other: splenic cysts, abscesses etc.
149
Q

Complications of hyposplenism?

A
  • Increased risk of severe infection particularly those caused by encapsulated bacteria
  • Much higher risk of falciparum malaria
150
Q

Management of hyposplenism?

A
  • Advice – avoid malaria endemic areas, be aware of higher infection risk
  • Immunisations: annual flu, pneumococcal vaccine, menigitits ACWY and B, HiB
  • Prophylactic antibiotics
151
Q

Malnutrition is _______ it can occur __________
could be due to ________
examples ______________
can be assessed __________

A
  • Nutrient deficiency state of protein, energy or micronutrients e.g. vitamins and mineral
  • Malnutrition can occur as a consequence of ill health or be a cause of ill health
  • Could be due to inadequate intake or malabsorption
  • Kwashiokor: there is adequate energy but not enough protein, develop oedema and hepatomegaly
  • Marasmus: there is inadequate protein and energy intake, severe muscle wasting develops
  • Common micronutrient deficiencies include iron, iodine, vitamin A and zinc
  • Malnutrition in adults can be assessed using BMI (although note this will not work if oedema present which will mask weight loss)
152
Q

Malabsorption is _________
causes include ____________

A
  • Failure to fully absorb nutrients from GI tract
  • Causes malnutrition
  • Potential causes: coeliacs, cows milk protein allergy, lactose and other intolerances, short bowel syndrome, infection, pancreatic insufficiency, SIBO, crohns, systemic diseases
153
Q

What is mesenteric adenitis?

A
  • When the mesenteric lymph nodes become inflamed, generally occurs after a viral infection
  • Common cause of abdominal pain in children under 16, much less common in adults
154
Q

Presentation of mesenteric adenitis?

A
  • Symptoms often start following a sore throat or symptoms of a cold
  • Abdominal pain – either in umbilical or RIF region
  • Fever and generally feeling unwell
  • Nausea
  • Diarrhoea
  • Can be difficult as the symptoms can mimic appendicitis
155
Q

Investigations for mesenteric adenitis?

A
  • Bloods
  • Urinalysis
  • US or CT
  • Generally trying to rule out other causes
  • If can’t rule out appendicitis may end up having surgery
156
Q

Management of mesenteric adenitis?

A
  • Supportive – analgesia
  • Symptoms usually improve in a few days and most clear up completely in 2 weeks

4th Year Surgery Block (11 decks)

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