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MED-Y3 > GI > Flashcards

GI Flashcards

1
Q

What are the signs/symptoms of acute peritonitis ?

A
  • Generalised, severe abdominal pain
  • Guarding when palpated
  • Rigidity (persistent tightness)
  • Rebound tenderness
  • Cough will result in pain
  • Percussion tenderness.
  • Fever
  • Vomiting
  • Tachycardia
  • Hypotension
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2
Q

What is localised peritonitis ?

A

Localised peritonitis can be caused by an underlying organ inflammation like appendicitis or cholecystitis

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3
Q

What is generalised peritonitis ?

A

Can be caused by perforation of an organ releasing contents into the abdomen and hence causing inflammation.

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4
Q

What is spontaneous bacterial peritonitis ?

A

Associated with spontaneous infection of ascities in patients with liver disease. Treated with BSA and has a poor prognosis.

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5
Q

What is the first line of treatment of spontaneous bacterial peritonitis ?

A

Piperacillin/Tazobam.

Cefotaxamine can also be used

Levofloxacin and metronidazole can be used in penicillin allergy

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6
Q

How is peritonitis diagnosed ?

A

Clinical features and sample of fluid from the abdomen

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7
Q

What are the Common causative organisms in intra-abdominal infection ?

A
  • Anaerobes (clostridium and bacteroides)
  • E.coli
  • Klebsiella
  • Enterococcus
  • Streptococcus.
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8
Q

When are erect CXR indicated in suspected peritonitis?

A

When looking for signs of perforation like due to a perforated gastric ulcer and pneumoperitenum.

May also have Abdo x ray to look for bowel perforation.

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9
Q

How is peritonitis treated ?

A

Treatment of underlying cause

IV antibiotics

Morphine

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10
Q

What is acute cholangitis ?

A

Infection and inflammation of the bile ducts. Surgical emergency and has a high mortality due to sepsis and septicaemia.

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11
Q

What are the two main causes of acute cholangitis ?

A
  • Obstruction in the bile ducts stopping bile flow like gallstones in the common bile duct
  • Infection introduced during an ERCP procedure (x ray and endoscopy procedure)
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12
Q

What are the most common bacterial causes of acute cholangitis ?

A
  • Escherichia coli
  • Klebsiella species
  • Enterococcus species.
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13
Q

What are the components of Charcots triad (acute cholangitis)

A
  • Right upper quadrant pain
  • Fever
  • Jaundice (raised billirubin)
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14
Q

How is acute cholangitis managed initially ?

A
  • Emergency admission

Need management of sepsis and acute abdomen pain and prep for surgical admission

  • NBM
  • IV fluids
  • Blood cultures
  • IV antibiotics
  • Seniors
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15
Q

What are the best imaging modalities in imaging acute cholangitis ?

A
  • Abdominal USS scan
  • CT scan
  • MRCP (most important) this is viewing not diagnostic !!
  • Endoscopic USS

Patient will have deranged LFT and raised CRP

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16
Q

How is acute cholangitis managed internationally ?

A

ERCP can be used to remove stones that are blocking the bile duct. Procedures that can be done with an ERCP are ….

  • ERCP can be used to remove stones that are blocking the bile duct. Procedures that can be done with an ERCP are ….
  • Cholangio-pancreatography: retrograde injection of contrast into the duct through the sphincter of Oddi and x-ray images to visualise biliary system
  • Sphincterotomy: making a cut in the sphincter to dilate it and allow stone removal
  • Stone removal: a basket can be inserted and pulled through thecommon bile ductto remove stones
  • Balloon dilatation: a balloon can be inserted and inflated to treat strictures
  • Biliary stenting: a stent can be inserted to maintain a patent bile duct (for strictures or tumours)
  • Biopsy: a small biopsy can be taken to diagnose obstructing lesions
  • Treat underlying cause - like in gallstones may need a cholecystectomy.
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17
Q

What can be used in patients with acute cholangitis but ERCP not suitable/unsuccessful ?

A

In patients where ERCP is not suitable or where ERCP has failed, a percutaneous transhepatic cholangiogram involves insertion of a drain into the bile ducts and relieves immediate obstruction. A stent can be inserted to give longer lasting relief.

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18
Q

What is an ERCP ?

A

Endoscopic retrograde cholangiopancreatography. Combines USS and endoscopy to remove gallstones.

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19
Q

What is acute cholecystitis ?

A

Inflammation of the gallbladder, often caused by the blockage of the cystic duct preventing the gallbladder from draining.

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20
Q

What is one of the key complications of gallstones ?

A

Acute cholecystitis

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21
Q

Apart from gallstones, what are some of the other possible causes of acute cholecystitis ?

A

TPN or ICU admission, as gallbladder is not being stimulated by food regularly and emptying hence resulting in a build up of pressure.

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22
Q

How does acute cholecystitis present ?

A
  • RUQ pain that may radiate to the right shoulder.
  • Fever
  • Nausea
  • vomiting
  • Tachycardia/tachypnoea
  • RUQ tenderness
  • Murphys sign
  • Raised IFLM and WCC
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23
Q

What is murphys sign suggestive of ?

A

Acute cholecystitis

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24
Q

How is Murphys sign tested ?

A
  • Hand on RUQ and apply pressure
  • Ask the patient to take a deep breath in
  • Gallbladder will move downwards and come into contact with the hand on inspiration and this will result in pain and stoppage of inspiration

A positive sign is if this elicits pain

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25
Q

What imaging modalities are used in diagnosing acute cholecystitis ?

A
  • 1st step (abdominal USS)
  • 2nd MRCP if the stone is not detected on the bilary tree on USS but is suspected due to signs like raised bilirubin or bile duct dilation.
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26
Q

What are the signs of acute cholecystitis on abdominal USS ?

A
  • Gallbladder wall thickening
  • Stones or sludge in the bladder
  • Fluid around the gallbladder.
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27
Q

How is a patient with acute cholecystis managed initially ?

A

Patients firstly need emergency admission for investigations and management. Conservative ….

  • Conservative - NBM, IV fluids, Antibiotics, NG tube if needed for vomiting.
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28
Q

How are patients with acute cholecystitis managed ?

A

Cholecystectomy (removal of the gallbladder), usually performed during acute admission, within 72 hours of symptoms. Sometimes may be delayed to allow the acute inflammation to settle.

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29
Q

What are some of the possible complications of acute cholecystitis ?

A
  • Sepsis
  • Gallbladder empyema
  • Gangrenous gallbladder
  • Perforation.
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30
Q

What is gallbladder emphyema ?

A

Gallbladder empyema is infected tissue and pus collecting in the gallbladder.

Managed with IV antibiotics and cholecystectomy/cholecystostomy.

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31
Q

What is the definitive management of acute cholecystitis ?

A

according to NICE guidelines, a laproscopic cholecystectomy should be offered within one week. All patients with an acute flair of cholecystitis should have this

Untill then IV analgesia, antibiotics and fluids should be given to the patient.

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32
Q

What is the most common bacterial cause of acute cholecystitis ?

A

E.coli

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33
Q

What are the three most common causes of acute pancreatitis ?

A
  • Gallstones
  • Alcohol
  • Post ECRP
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34
Q

Why does alcohol cause pancreatitis ?

A

Alcohol is directly toxic to pancreatic cells and this results in inflammation.

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35
Q

Why do gallstones cause pancreatitis ?

A

Caused by gallstones getting trapped at the end of the bilary system and blocking the flow of bile and pancreatic juice into the duodenum.

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36
Q

What are some of the other causes of pancreatitis (apart from the key 3 ) _ I GET SMASHED.

A
  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion sting
  • Hyperlipidaemia
  • ERCP
  • Drugs ( diuretics like furosemide, thiazide and Asathioprine)
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37
Q

How does acute pancreatitis present ?

A
  • Acute onset of pain
  • Severe epigastric pain that radiates to the back.
  • Vomiting
  • Abdominal tenderness
  • Systemically unwell (low grade fever and tachycardia)
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38
Q

What marker will be raised a lot in acute pancreatitis ?

A

amylase 3x the upper limit and lipase.
CRP will also be rised

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39
Q

What scoring system is used to monitor the severity of acute pancreatitis and what are the three divisions ?

A

The modified Glasgow criteria
- 0 or 1– mild pancreatitis
- 2– moderate pancreatitis
- 3 or more– severe pancreatitis

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40
Q

What are the different divisions of the modified glasgow score (used in pancreatitis assessment)
?

A

Can be remembered by PANCREAS pneumonic

  • P–Pa0< 8 KPa
  • A–Age > 55
  • N–Neutrophils (WBC > 15)
  • C–Calcium < 2
  • R– uRea >16
  • E–Enzymes (LDH > 600 or AST/ALT >200)
  • A–Albumin < 32
  • S–Sugar (Glucose >10)
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41
Q

What should happen to all patients that are admitted with pancreatitis ?

A

Patients can become unwell rapidly. In patients who are moderate or severe, they should be considered for management on the high dependency unit or the ICU.

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42
Q

How is acute pancreatitis managed ?

A
  • Bedside symptomatic management - ABCDE, IV fluids, NBM, analgesia.
  • Invasive treatments - ERCP/cholecystectomy in patients who have gallstone pancreatitis.
  • Treatment of complications like endoscopic or percutanous drainage of large collections
  • ABx if evidence of infection like abscess or infected necrotic area.
  • Most patients will improve within a week.
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43
Q

What are some of the possible complications of acute pancreatitis ?

A
  • Necrosis of the pancreas
  • Infection in a necrotic area
  • Abscess formation
  • Acute peripancreatic fluid collections
  • Pseudocysts (collections of pancreatic juice) can develop 4 weeks after acute pancreatitis
  • Chronic pancreatitis
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44
Q

What would be the typical exam presentation of a patient with acute pancreatitis ?

A

Patient presenting tachycardic and hypotensive with severe epigastric pain radiating to the back. Associated vomiting. Raised amylase/lipase and CRP

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45
Q

What is the most common cause of chronic pancreatitis ?

A

Alcohol

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46
Q

What type of DM develops as a consequence of chronic pancreatitis ?

A

Type 3c

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47
Q

How do patients with chronic pancreatitis present ?

A

Patients usually have weight loss, loss of appetite, in advanced cases jaundice, symptoms of diabetes and ongoing nausea and vomiting.

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48
Q

What are some of the common complications of chronic pancreatitis ?

A
  • Chronic epigastric pain
  • Loss of exocrine funcion (reduced lipase)
  • Loss of endocrine function, lack of insulin leading to diabetes.
  • Damage and strictures to the duct system leading to obstruction
  • Formation of pseudo-cysts and abscesses.
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49
Q

why do patients with chronic pancreatitis get steorrhoea ?

A

Lack of lipase enzymes can lead to malabdorbtion of fat, greasy stool and deficiency in fat soluble vitamins.

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50
Q

What can be given to patients with chronic pancreatitis to replace pancreatic lipase ?

A

Creon

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51
Q

How is chronic pancreatitis managed ?

A
  • Abstinence from alcohol and smoking
  • Analgesia
  • Replacement pancreatic enzymes like creon (lipase). Lack of enzymes due to an obstruction can lead to malabsorbtion of fat, greasy stool (steatorrhoea) and deficiency in fat soluable vitamins
  • SC insulin if diabetic
  • ERCP with stenting to treat strictures and obstructions.
  • Surgery may be required to treat chronic pain, obstruction, psudocysts and abscesses.
  • Bilary decompression - Roux - en - Y cholecystectomy.
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52
Q

What is third spacing ?

A

loss of fluid from the GI tract into the intravascular space. The higher up the intestine the obstruction, the greater the fluid loss.

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53
Q

what type of bowel obstruction is most common ?

A

Small bowel

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54
Q

What are the three most common causes of bowel obstruction ?

A
  • Adhesions (small) - RF endo and surgery
  • Hernias (small)
  • Malignancy (lg)
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55
Q

Apart from the big three, what are the other common causes of bowel obstruction ?

A

Volvulus (lg), diverticular disease, strictures (young person with chrones) and intussusception in young children.

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56
Q

What is the initial imaging investigation in bowel obstruction ?

A

XRay abdo and chest.

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57
Q

What is a diagnostic investigation for bowel obstruction ?

A

Ct abdo and pelvis

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58
Q

What are adhesions ?

A

Scar tissue that bind the abdominal contents together. They can cause kinking or squeezing of the bowel, leading to obstruction in the small bowel typically

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59
Q

What are the main causes of adhesions ?

A
  • Abdominal or pelvic surgery
  • Peritonitis
  • Abdominal or pelvic infections
  • Endometriosis
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60
Q

What is a closed loop obstruction ?

A

Two points of obstruction along the bowel, meaning there is a middle section sandwiched between the two points of obstruction.

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61
Q

What are the main causes of close loop obstruction ?

A
  • Adhesions - compress two sections of bowel
  • Hernias
  • Volvulus
  • Competent ileocaecal valve (does not allow any movement back into the ileum from the caecum). When there is a lg bowel obstruction and this valve, a section of the bowel becomes isolated
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62
Q

What are the main causes of close loop obstruction ?

A
  • Adhesions - compress two sections of bowel
  • Hernias
  • Volvulus
  • Competent ileocaecal valve (does not allow any movement back into the ileum from the caecum). When there is a lg bowel obstruction and this valve, a section of the bowel becomes isolated
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63
Q

What is there an increased risk of in closed loop obstruction ?

A

Due to the nature of this obstruction, there is an increased risk of ischaemia and perforation.

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64
Q

How does bowel obstruction present ?

A
  • Vomiting (green bilious vomiting)
  • Abdominal distention
  • Diffuse abdominal pain
  • Rebound tenderness and rigid tenderness - Sign of peritonitis and indication for urgent surgical intervention as risk of perforation
  • Absolute constipation and lack of flatulence
  • Tinkling bowel sounds in early bowel obstruction.
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65
Q

What is rebound tenderness and rigid tenderness a sign of in bowel obstruction and what does it indicate ?

A
  • Peritonitis (perforation)
  • Immediate surgical intervention
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66
Q

How do you distinguish between small and large bowel on abdominal x ray ?

A
  • Valvulae conniventes - small bowel and form lines that extend the full width of the bowel.
  • Haustra - Lg bowel, do not extend the whole length of the bowel.
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67
Q

What will be present in CXR, AXR in bowel obstruction ?

A

Dilated bowel
Pneumoperitoneum in perforation

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68
Q

How is bowel obstruction managed before surgical intervention ?

A

NG tube with free drainage to allow stomach contents to freely drain
Drip and suck

  • ABCDE
  • Patients may develop - Sepsis, bowel perforation, bowel ischaemia and hypovolaemic shock.
  • NBM
  • IV fluids
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69
Q

What will be present on investigation (bloods and imaging) in bowel obstruction ?

A
  • Metabolic alkalosis
  • Bowel ischaemia - raised lactate
  • Electrolyte imbalance
  • Pneumoperiteneium.
  • Dilated bowel loops
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70
Q

How are patients managed surgically in bowel obstruction ?

A
  • Exploratory surgeryin patients with an unclear underlying cause
  • Adhesiolysisto treat adhesions
  • Hernia repair
  • Emergency resectionof the obstructing tumour

Stents can also be inserted in patients with obstruction due to tumour.

CAN BE MANAGED CONSERVATIVE

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71
Q

What is hereditary haemochomatosis ?

A

Disorder of iron metabolism, where excessive iron accumulates in the body and is deposited (liver, heart, joints, pituitary, pancreas and skin).

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72
Q

Where is the gene mutation in hereditary haemochromatosis ?

A

HFE gene

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73
Q

What are some of the possible complications of hereditary haemochromatosis ?

A
  • Liver fibrosis
  • Liver cirrhosis
  • Hepatocellular carcinoma
  • Myocardial siderosis
  • Cardiomyopathy (improves in response to venesection)
  • DM
  • Skin hyperpigmentation ( improves in response to venesection)
  • Arthropathy.
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74
Q

What are the clinical features of hereditary haemochromatosis ?

A
  • Bronze skin
  • Type 2 DM
  • Fatigue
  • Joint pain
  • Testicular atrophy (due to liver cirrhosis)
  • Hepatomegaly.
  • Liver cirrhosis
  • Adrenal insufficiency
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75
Q

What is the characteristic skin change in hereditary haemochromatosis ?

A

Bronze skin

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76
Q

What tests can be used to aid diagnosis in hereditary haemochromatosis ?

A

-Raised serum ferritin
- Raised transferrin saturation
-Deranged LFTs

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77
Q

What investigation (GENE) gives a definitive diagnosis of hereditary haemochromatosis ?

A

HFE gene defects

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78
Q

How is hereditary haemochromatosis managed ?

A

Primary therapy - Phlebotomy/venesection. Stimulates erythropoiesis and mobilises iron from parenchymal cells and other storage sites.

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79
Q

How is hereditary haemochromatosis managed ?

A

Primary therapy - Phlebotomy/venesection. Stimulates erythropoiesis and mobilises iron from parenchymal cells and other storage sites.

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80
Q

How can hereditary haemochromatosis managed with medication ?

A

Desferrioxamine - iron chelating agent

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81
Q

Why should vitamin C be avoided in hereditary haemochromatosis ?

A

It increases the body rate of absorbtion of iron

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82
Q

A 45 year old male presents with a two week history of jaundice and feeling generally unwell. He was diagnosed with type II diabetes mellitus at the age of 34, and also experiences frequent joint pain. His bloods show deranged liver function tests.

What is the most appropriate treatment for his condition?

A

He most likely has hereditary haemochromatosis and should be treated with venesection or desferrioxamine.

83
Q

A 40 year old gentleman presents to Accident & Emergency with a sudden onset of severe abdominal pain which started 7 days ago. He has had several episodes of vomiting and has passed bloody diarrhoea. He has a history of ulcerative colitis (UC) and is currently on sulfasalazine for it.

On examination, the patient looks unwell. He has a distended abdomen which is tympanic to percussion. Heart rate 125 bpm, respiratory rate 22, blood pressure 95/70 mmHg and temperature 38.6. An abdominal x-ray (AXR) was taken and is shown below:

A

Toxic megacolon

Complication of UC and occurs due to increased release of NO from inflammed colonic wall.

Tympanic percussion and thumbprinting.

84
Q

What is a typical history for a patient with ulcerative colitis ?

A

Tenesmus
Bloody diarrhoea
LIF pain

85
Q

If a patient presents with UC that has not responded to oral ASA (like sulfalazine) what is the most appropriate next stage of treatment ?

A

Oral pred

86
Q

What extra intestinal manifestations are more common in UC rather than crohns ?

A
  • Toxic megacolon
  • PSC
87
Q

What extra intestinal manifestations are more common in crohns rather than UC ?

A

Gallstones
Renal stones
Apcanthous ulcers

88
Q

How is a toxic megacolon managed and what is an indication for surgery ?

A

Iv steroids (hydrocortisone) and IV fluids.

Failure to respond within 48-72 hours

89
Q

What histological findings are consistent with UC ?

A

Surface inflammation with loss of goblet cells and crypt abscesses

90
Q

What histological findings are consistent with chrones ?

A

Transmural inflammation with non ceasating granulomas

91
Q

What symptoms are more typical of UC ?

A

Diarrhoea with blood/mucus, tenesmus and LIF pain

as well as systemic features like weight loss.

92
Q

What will be present on examination in a patient with UC ?

A

PR - Bleeding
Pain
Clubbing
Distention/tenderness of the abdomen

93
Q

What extraintestinal manifestation is more common in UC and how would it present ?

A

PSC

Pruritis/jaundice/deranged LFT

Diagnosed with MRCP

94
Q

What are some of the extra intestinal manifestations of IBD ?

A
  • Derm manifestations - Erythema nodosum, pyroderma gangrenosum.
  • Ocular manifestations - Anterior uveitis, episcleritis, conjunctivitis
  • MSK manifestations - Clubbing, non deforming asymmetrical arthritis, sacroilitis
  • Hepatobilary - PSG (more common in UC)
  • AA amyloidosis
95
Q

What marker will be raised in IBD ?

A

Faecal calprotectin.

96
Q

What will be present histologically in UC ?

A

Continuous erythematous inflammation with loss of goblet cells, crypt abscesses and inflammatory cells.

97
Q

What type of inflammation is present in UC ?

A

Continuous

98
Q

In an acute flair of UC, why is colonoscopy and barium enema CI ?

A

Due to risk of toxic megacolon/perforation

99
Q

What criteria is used to measure UC flair severity ?

A

Truelove and witt criteria

100
Q

What is used in UC to induce remission ?

A

ASA like (zine suffix) and if not within a month, consider oral prednisolone.

101
Q

What is used in UC to maintain remisssion ?

A

Oral ASA - zine suffix
or
Azathiopurine

102
Q

What treatment is used in an acute flair of uc ?

A

IV corticosteroids like prednisolone

103
Q

When is surgery review needed in an acute flair of UC ?

A

If not improved after 72 hours of IV steroids

If not then IV ciclosporin is needed

104
Q

What are some of the short term complications of UC ?

A
  • Toxic megacolon (severe form of colitis)
  • Massive lower GI haemorrhage#- PSC ( inflammation and fibrosis of the extra and intrahepatic bilary tree)
  • Inflammatory pseudo-polyps
105
Q

What are some of the long term complications of UC ?

A

Colorectal cancer (bilary tract carcinoma)

Cholangiocarcinoma

Colonic strictures that can cause large bowel obstruction

106
Q

What complication of UC can cause large bowel obstruction ?

A

Strictures

107
Q

What is a significant risk factor for the development of IBD ?

A

FHX

108
Q

What symptoms are more specific to chrones rather than UC ?

A

Less likley to be blood/mucus
Crampy abdo pain, diarrhoea, weight loss ect

109
Q

What signs are seen on crohns ?

A
  • Cahectic and pale
  • May be clubbing
  • Apthanous ulcers in the mouth
  • May be abdominal/right lower quadrant tenderness and RIF pain
  • PR
  • May be peri anal fistulae or peri anal abscess
110
Q

What extra intestinal sign is more common in crohns rather than UC ?

A

Gallstones

111
Q

What will an upper GI series show in crohns ?

A

Show string sign of Kantour. String like appearance of contrast filled narrowed terminal ileum and is suggestive of chrones.

112
Q

What type of inflammation is present in crohns ?

A

Intermittent inlammation (skip lesions)

113
Q

What is present on histology in crohns ?

A
  • Cobblestone mucosa
  • Intermittent inflammation/skip lesions
  • Non ceasating granulomas.
114
Q

What medications are used to induce remission in crohns ?

A

Monotherapy with glucocorticoids (like hydrocortisone)
Azathioprine if two of more remissions in a 12 month period

115
Q

What is used to maintain remission in crohns ?

A

Azathioprine
Methotrexate in CI or not responsive

116
Q

In what IBD is surgery curative ?

A

Crohns

117
Q

What are some of the rectal manifestations of crohns ?

A

Peri - anal fistulae
Per anal abscess

118
Q

How are peri-anal fistulae managed ?

A

Drainage seton for high fistulae and fistulotomy in low fistulae (submucosal)

119
Q

How are peri anal abscess managed ?

A

IV antibiotics like ceftiaxone and metronidazole. Typically patients require exam under anaesthetic and inscision/drainage.

120
Q

What is the treatment for H pylori negative endoscopy confirmed peptic ulcer disease ?

A

4-8 weeks full PPI dose

121
Q

What is the common presentation of cholangiocarcinoma ?

A
  • Jaundice
  • weight loss
  • Clay coloured stools
  • Colicky RUQ pain
  • RUQ mass
122
Q

What is the common history of primary scleorisng cholangitis ?

A

a 40-year-old man with a history of ulcerative colitis presents with fatigue, jaundice and pruritus and right upper quadrant pain

123
Q

What does a narrow pulse pressure and slow rising pulse indicate ?

A

Aortic stenosis

124
Q

How is hyperkalaemia managed ?

A

Loop diruretics like furosemide

125
Q

How is ascities managed ?

A

Spirinolactone and reducing sodium intake

126
Q

A recent traveller presents with watery diarrhoea with stomach cramps and diarrhoea, what is the most likely cause of the infection ?

A

Enterotoxinogenic E.coli

127
Q

What is a common disease pattern in UC ?

A

Proctitis (inflammation of the rectum)

128
Q

Why should metocloparamide be avoided in bowel obstruction ?

A

It has prokinetic properties and hence can stimulate peristalsis and precipitate perforation.

129
Q

What is a common GI symptom of metformin ?

A

Abdominal upset and dirrhoea

130
Q

What is cholera gastroenteritis treated with ?

A

Tetracycline

131
Q

What ABx is salmonella and shigella treated with ?

A

Ciprofloxacin

132
Q

What Abx is camplylobacter gastroenteritis treated with ?

A

macrolide like erythromycin

133
Q

What is liver cirrhosis ( compensated and decompensated ) ?

A

Diffuse fibrosis and structural abnormality of the liver characteristic of chronic liver disease.

Compensated is where sufficient liver function remains to keep the patient systemically well.

134
Q

What are some of the signs and symptoms of compensated liver cirrhosis ?

A
  • Fatigue and anergia
  • Anorexia/cahexia
  • Nausea/abdominal pain
  • Spider naevi
  • Gynaecomastia
135
Q

What are some of the features of decompensated liver cirrhosis ?

A
  • Ascites and oedema
  • Jaundice
  • Pruritus
  • Palmar erythema
  • Gynaecomastia and testicular atrophy
  • Easy bruising
  • Along with the features of compensated cirrhosis.
136
Q

What are some of the common causes of liver cirrhosis ?

A

Most common causes include alcohol, hepatitis B and C and NAFLD.

Less common causes include PSC, primary bilary cirrhosis, autoimmune hepatitis and sarcoid.

Genetic causes like haemochromatosis, wilsons disease and Alpha 1 antitrypsin deficiency.

137
Q

What drugs can cause liver cirrhosis ?

A
  • Methotrexate
  • Amiodarone
  • Isoniazid
138
Q

What scoring system is used to determine the severity of liver cirrhosis ?

A

Child Pugh score

Child-Pugh A (<7 points), B (7-9 points) or C (>9 points).

139
Q

What investigations are used in investigating liver cirrhosis ?

A
  • Liver biopsy
  • NAFLD - advanced liver fibrosis score
  • Transient elastography/acoustic radiation
140
Q

What are some of the possible complications of liver cirrhosis ?

A
  • Ascities as a result of portal hypertension and hypoalbuminaemia. Gives rise to other problems like spontaneous bacterial peritonitis.
  • Spontaneous bacterial peritonitis. Should be suspected in patients which deteriorate suddenly with no other obvious cause. Ascitic tap> 250 neutrophils.
  • Liver failure
  • Hepatocellular carcinoma - Especially patients with cirrhosis and hepatitis B and C
  • Lower oesophageal varicies and haemorrhage.
  • Renal failure
141
Q

What does a high SAAG gradient (more than 11) in ascities indicate ?

A

Portal hypertension - cirrhosis

142
Q

What does an ascitic tap of more than 250 indicate ?

A

Spontaneous bacterial peritonitis

143
Q

What is a sequestration crisis in SCA ?

A

Sickle cells cause the spleen to become grossly enlarged due to sicking in organs. This causes organomegaly and pain.

144
Q

What liver condition are patients with haemochromatosis at a higher risk of ?

A

Hepatocellular carcinoma - should be screened

145
Q

What LFTs indicate a cholestatic picture over a hepatocellular picture ?

A

Less than 10 fold increase in ALT but more than 3 fold increase in ALP. Also a rise in gamma GT

146
Q

What LFTs pain a hepatocellular issue over a cholestatic ?

A

More than 10 fold increase in ALT but less than 3 fold increase in ALP.

147
Q

What is coeliac disease ?

A

Autoimmune condition caused by sensitivity to gluten. Repeated exposure leads to villus atrophy and hence malabsorbtion.

148
Q

What are some of the associated conditions with coeliac disease ?

A

Dermatitis herpatiformis, D1DM, autoimmune hepatitis, autoimmune thyroid hepatitis

149
Q

What are the antibody associations with coeliac disease ?

A

HlA-DQ2 (95 percent of patients) and HLA-DQ8 (80 percent)

150
Q

What are the signs and symptoms of coeliac disease ?

A
  • Chronic or intermittent diarrhoea
  • Failure to thrive or faltering growth in children.
  • Persistent or unexplained symp like nausea and vomiting
  • Prolonged fatigue
  • Recurrent abdominal pain, cramping or distention
  • Sudden or unexplained weight loss
  • Unexplained iron deficiency anaemia
  • Iron deficiency anaemia, folate (more common) and vitamin B12 deficieny.
151
Q

What are the first line investigation for coeliac disease ?

A

TTG and IgA are first choice investigations

152
Q

What is the gold standard for diagnosis in coeliac disease and what will it show ?

A

Endoscopic intestinal biopsy typically in the jejunum.
Villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes and lamina propria infiltration with lymphocytes.

153
Q

How is coeliac disease managed ?

A

Gluten free diet

154
Q

What should all patients with coeliac be offered ?

A

Patients often have a degree of functional hyposplenism and hence all patients are offered the pneumococcal vaccine (everyone is vaccinated and has a booster every 5 years)

155
Q

What does raised transaminases with obesity indicate ?

A

NAFLD

156
Q

What is the investigation of choice for pancreatic cancer ?

A

High resolution CT

157
Q

What do you advise patients with coeliac before going for a biopsy ?

A

Continue with gluten free diet

158
Q

What are the signs of autonomic dysreflexia ?

A

severe hypertension and flushing/sweating above the level of injury

159
Q

When is lipase more useful than amylase in pancreatitis ?

A

If the patient presents later on (more than 24 hours)

160
Q

What are the associations of H.pylori ?

A
  • 95 percent of duodenal ulcers
  • 75 percent of gastric ulcers
  • Gastric cancer
  • B cell lymphoma or the MALT tissue
  • Atrophic gastritis
161
Q

What does a 10x fold increase in ALT (less than 3 ALP) indicate ?

A

Hepatocellular injury

162
Q

What does a less than 10x fold increase ALT and a more than 3x fold increase in ALP indicate ?

A

Cholestatic picture

163
Q

When is GGT used ?

A

In context of ALP. Rise in both =cholestatic picture

164
Q

What can an isolated rise in ALT indicate ?

A

-Bony metastasis or fracture
- Primary bone tumour
- Vitamin D deficiency

165
Q

What are the GI associations with H.pylori ?

A

H.pylori (gram negative bacteria) associated with peptic ulcer disease. It is present in

  • 95 percent of duodenal ulcers
  • 75 percent of gastric ulcers
  • Gastric cancer
  • B cell lymphoma or the MALT tissue
  • Atrophic gastritis
166
Q

What is the management of H.pylori infection ?

A

Management - PPI/Amox/Clarithromycin or metronidazole (if penicillin allergic both of these !!!)

167
Q

What is Zollinger Ellison syndrome ?

A

development of several ulcerations in the stomach and the duodenum due to uncontrolled release of gastrin from a gastrinoma. Usually presents in the pancreas but can also occur in the duodenum.

168
Q

What is Zollinger Ellison syndrome typically associated with ?

A

MEN-1

169
Q

What are the screening and diagnostic tests for Zollinger Ellison syndrome ?

A

Screening test - raised gastrin levels.

Diagnosis - Secretin stimulation test (secretin causes a very large increase in gastrin release)

170
Q

What is the treatment of Zollinger Ellison syndrome ?

A

Treatment - if no metastasis = resection of the tumor.

171
Q

What is bilary colic ?

A

Gallstones passing through the bilary tree

172
Q

What are some of the risk factors for gallstones/bilary colic ?

A

Fat, female, fertility and forty as well as DM, crones, rapid weight loss like OCCP and fib-rates.

173
Q

What are some of the features of bilary colic ?

A
  • Colicky RUQ pain worse after eating fatty foods that may radiate to the right shoulder/intra-scapular region.
  • Nausea and vomiting are common
  • No fever - LFT/IFLM are all normal.
174
Q

What is the investigation of choice in bilary colic ?

A

USS

175
Q

What is the management of bilary colic ?

A

Elective laparoscopic cholecystectomy

176
Q

What is hepatocellular carcinoma ?

A

Primary tumour of the liver. Can present late with symptoms like jaundice, weight loss, pruritus and fevers. Also with signs of cirrhosis.

177
Q

What is serum AFP (and what is it a marker of ?)?

A

Tumor marker - raised in 60 percent of pateints with hepatocellular carcinoma but can also be raised in patients with chronic cirrhosis.

178
Q

What are the risk factors for Hepatocellular carcinoma ?

A
  • Chronic viral hepatitis (B/C)
  • Cirrhosis
  • NAFLD
  • Primary bilary cirrhosis
  • Inherited metabolic diseases
  • Alcohol misuse
  • Obesity
  • T2DM
179
Q

How is Hepatocellular carcinoma managed ?

A

Hepatic resection, liver transplantation and radio-frequency ablation.

180
Q

What is Gilberts syndrome ?

A

Autosomal recessive condition that is characteristic by decreased activity of the enzyme that conjugates bilirubin.

181
Q

What is present on examination in patients with Gilbert’s syndrome ?

A

Patients may experience intermittent mild jaundice in reaction to stress, fasting, infection or excerise

Mild increase in un-conjugated bilirubin.

182
Q

What does a positive p-ANCA indicate ?

A

autoimmune vasculitis

183
Q

Why is a CXR indicated in patients starting biologics ?

A

To look for signs of TB as they can cause TB re-activation

184
Q

Liver failure following MI ?

A

Ischaemic hepatitis

185
Q

What is used in the remission of mild to moderate ulcerative colitis ?

A

1- Topical/oral ASA
2-Consider steroids if not working

186
Q

What is used in the remission of severe ulcerative colitis ?

A

1)IV corticosteroids
2) IV ciclosporin
3) Surgery (if toxic mega colon or fails to improve with high dose steroids)

187
Q

Patients with UC are at a high risk of developing cholangiocarcinoma, what tumour marker can be used to identify this ?

A

CA-19-9

188
Q

What will be present on colonoscopy in UC ?

A

Continuous serous inflammation with loss of goblet cells and crypt abscesses.
Continuous erythematous mucosa and the rectum is always affected.

189
Q

What is used to maintain remission in UC ?

A

1) proctitis- topical or oral ASA
2) left sided - oral ASA, axithopurine then biologics.

190
Q

What is used to induce remission in crones ?

A

1) steroids
2)Azithioprine/mercaptopurine if patients have 2 ore more flares in a 12 month period (assess TMPT)
3) methotrexate

191
Q

What is used to maintain remission in crohns ?

A

1) Azithioprine/mercaptopurine
2) methotrexate

192
Q

What are the symptoms of short bowel syndrome ?

A

Post bowel resection
Diarrhoea/abdo pain and malabsorbtion.

193
Q

What is the treatment of a high fistula ?

A

Drainage seaton

194
Q

What is the treatment of a low fistula ?

A

Fistulotomy.

195
Q

What bone condition is coeliac disease associated with ?

A

OA - Patients need DEXA scans to monitor disease.

196
Q

What is the gold standard of diagnosis in coeliac disease ?

A

OGD with duodenal biopsy/jejunal biopsy.

197
Q

What does gallstones and pruritis mean in terms of gallbladder pathology ?

A

Obstructive cause of jaundice

198
Q

What is primary bilary cholangitis ?

A

Autoimmune condition that causes scarring and inflammation of the bile ducts, eventually leading to liver cirrhosis.

199
Q

What are the clinical features of primary bilary cholangitis ?

A

Extreme fatigue
Itching
Dry skin and eyes
Jaundice

200
Q

What are patients with primary bilary cholangitis at a higher risk of developing ?

A

Hepatocellular carcinoma

201
Q

What antibodies will be positive in primary bilary cholangitis ?

A

Positive anti mitrochondrial antibodies

202
Q

What are the positive investigation findings in primary bilary cholangitis ?

A
  • Abnormal LFTs
  • Positive anti-mitrochondrial antibodies
  • Liver biopsy will show inflammation and scarring
203
Q

What medications commonly cause constipation ?

A

-opiates and NSAIDS
-TCA and antihistamines
-Iron supplements
- urinary incontinence - oxybutynine/mirabegron ect.

204
Q

GI side effect of co-amoxiclav ?

A

Cholestatic jaundice (raised ALP/GGT and bilirubin)

MED-Y3 (24 decks)

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