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Systems revision > GI > Flashcards

GI Flashcards

1
Q

What is the aetiology and risk factors of oesophageal reflux

A

Problems with Lower oesophageal spinchter

-abnormal oesophageal anatomy
eg LOS relaxed, decreased resistance to acid

  • Hiatus hernia
  • sliding
  • paraesophageal

Risk Factors

  • Pregnancy
  • Obesity
  • smoking
  • alcohol excess
  • Drugs: lowering LOS pressure
  • alcohol
  • hypo-mobility
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2
Q

What is the pathology of oesophageal reflux

A

Reflux of gastric acid into oesophagus causing thickening of squamous epithelium cells, due to the healing process of fibrosis, as oesophagus lining cant tolerate the acid

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3
Q

What is the alarm features of oesphgeal reflux and the possible complications

A

Alarm Features:

  • Dysphagia
  • Vomiting
  • Weight loss

Ulcerations
(as epithelium not adapted)

Barrets oesophagus

Healing by fibrosis

  • Impaired motility
  • Oesophageal obstruction
  • Stricture formation
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4
Q

What is the symptoms of oesophageal reflux

A
  • Dyspepsia due to reflux of acid
  • Water brash - sudden flow of saliva
  • Cough
  • Sleep disturbance
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5
Q

What is the management of oesophageal reflux

A

Management

  • Lifestyle modification
  • PPI therapy eg omeprazole, lanzoprazole
  • Aliginates eg gaviscon
  • H2Ra (ranitidine)
  • Antacid (malox)

Surgery
-Laparoscopic Hiatus Hernia repair
(Fundoplication)

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6
Q

What is the pathology of barrels oesophagus

A

Type of metaplasia that has the transformation from squamous epithelium to glandular epithelium
(mucin secreting columnar epithelial cells)

Is a premalignant for oesophageal adenocarcinoma

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7
Q

What is the investigations fro Oesophageal reflux and barrels oesophagus

A

oesophageal pH studies manometry

Endoscopy+/-biopsy/ Ultrasound (used in alarm features)

CT +/-PET
-allows staging

CT contrast Barium swallow
-for dsyphagia

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8
Q

What is the treatment for barrels oesophagus with high grade dysplasia

A
  • Endoscopic Mucosal Resection (EMR)
  • Radio-Frequency Ablation (RFA)
  • Oesophagectomy (rarely due to high mortality)
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9
Q

What is the two types of oesophagus cancers and their aetiologies

A

Squamous (TOP)

  • Smoking
  • Alcohol
  • Dietary carcinogen

Adenocarcinoma (BOTTOM)

  • Barretts oesophagus
  • Obesity
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10
Q

What is the local and distant effects of oesophageal cancer

A 
Local Effects 
- Obstruction 
- Ulceration 
- Perforation 
(Food passes into thorax due to perforation causing a potential abscess)

Metasases occurs through:
Direct spread
Lymphatic spread
Blood Spread (liver)

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11
Q

What is the symptoms of oesophageal cacer

A

Symptoms caused by Local Effect

  • Dysphagia
  • Weight loss, anorexia
  • Odynophagia
  • Chest/heart burn
  • Cough
  • Anaemic (due to blood loss via ulceration)
  • Hematemesis (blood in vomit)
  • vocal cord paralysis
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12
Q

What is used for the diagnosis and staging of oesophageal cancer

A

DIAGNOSIS
Endoscopy and over 8 biopsies

oesophageal pH studies manometry

Barium swallow

STAGING

CT scan - distant metastases

Endoscopic US
- TNM staging

PET scan

Bone scan

Laparoscopy
-peritoneal spread

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13
Q

What is the treatment of oesophageal cancer

A

Osesophagectomy (remove oesophagus and use either stomach or colon as conduit) +chemotherapy (fit)

Chemo/radiotherapy (unfit)

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14
Q

What is the aetiology of peptic ulcer

A
  • Liver disease
  • Alcohol
  • Smoking
  • H.Pylor (due to acid production)
  • NSAIDS/aspirin (reduced mucus and HCO3)
  • Systemic stress ulcers
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15
Q

What is the symptoms and signs of peptic ulcer

What is the complications

A

Haematemesis

Melaena

Elevated Urea (h.p)

dyspepsia,

reflux,

epigastric pain, back pain

Complications: Bleeding, Perforation, stricture formation

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16
Q

Management of peptic ulcers

A

Proton pump inhibitors - omeprazole
Antacid
H2 receptors antagonists

Endoscopy with endotherapy
-Injection 
 (Adreanline constricts area)
-Thermal 
 (heat area to damage BV) 
- Mechanical (Clip) 
- Heamospray
 (mineral blend powder)

Angiography with embolization

Laparotomy

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17
Q

Aeitiology of gastritis

A

Autoimmune (atrophy and loss leads to inflammation)
Bacterial H.Pylori (increased acid production and inflammation)
Chemical: Drugs, alcohol, bile reflux (inflammation)

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18
Q

What is the aetiology of gastric cancer

A

Previous/current
H. Pylori infection (in body and antrum)

Diet

Genetic (most sporadic though)

Previous gastric resection

Biliary reflux

Smoking

Peptic ulcer

Pre malignant gastric pathology

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19
Q

What is the cell type of gastric cancer

what is the prognosis

A

Adenocarcinoma
- Develops through phase of intestinal metaplasia and dysplasia and is a malignant tumour carcinoma form in glandular epithelium

5 year survival 20%

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20
Q

How and where does Gastric cancer metastases

A

Metastasis How

  • Direct
  • Lymphatic spread
  • Blood spread (liver)
  • Trancoelomic spread (spread within peritoneal cavity)

Metastases Where

  • Lymph nodes
  • Liver
  • Lungs
  • Peritoneum
  • Bone marrow
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21
Q

What is the signs and symptoms of Gastric cancer

A

GI bleeding
-Iron deficiency
- anaemia
Gastric outlet Obstruction

Usually symptomatic

  • dyspepsia
  • early satiety
  • nausea/vomiting
  • weight loss
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22
Q

What is the investigations and stagings of gastric cancer

A

Test for Heliobacter Pylori

Histological Diagnosis
-Endoscopy and biopsies

Staging of Gastric Cancer

  • CT Chest/ Abdomen
  • Asses patients fitness
  • Determine the histology

Imaging

  • Endoscopy
  • Contrast meal/barium enema
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23
Q

What is the treatment of gastric cancer

A

Surgery

  • Sub total gastrectomy - preserves some of the stomach
  • Total Gastrectomy and roux en reconstruction
  • Laparoscopic distal gastrorectomy
  • Open gastrorectomy

Chemotherapy

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24
Q

What is the alarm symptoms of dyspepsia (bad digestion pain) for an endoscopy

A
  • Anorexia
  • Loss of weight
  • Anaemia – iron deficiency
  • Recent onset >55 years or persistent despite treatment
  • Melaena/haematemesis (GI bleeding) or mass
  • Swallowing problems dysphagia

ALARMS

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25
Q

What is H.Pylori

A

A gram negative spiral shaped microaeriphilli that is flaggelated allowing movement,

Can only colonise in gastric type mucosa in stomach, but provoked an immune response in underlying mucosa

Creates an alkaline environment around itself by promoting own survival and neutralising acid
by releasing enzyme urease that breaks down urea into ammonia and bicarbonate

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26
Q

What does H.Pylori response depend upon

A

Response dependant on:

  • Genetic susceptibility
  • Environmental factors (smoking)
  • Site of colonisation
  • Expresses different proteins that evoke different responses
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27
Q

What is the tests for H.Pylori

A

Non Invasive:

Serology
test IgG against H. pylori

Urea Breath test
uses up urea for food source and creates product Bicarbonate that is CO2 in your breath that can be determined in test

Stool antigen test
need to be on PPI 2 weeks prior

Invasive:

Endoscopy 
- Histology, gastric biopsies stained for bacteria 
- Culture of gastric biopsies,
- Rapid slide urease test 
test for ammonia
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28
Q

What is the treatment for H.pylori

A

ERADICATION THERAPY
Triple therapy of Clarithromycin 500mg bd
Amoxycillin 1g bd or Metronidazole 400mg bd
(tetracycline if penicillin allergic)
PPI: e.g. omeprazole 20mg bd
For 7 days

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29
Q

What is the two main aetiologies of acute liver failure

A

Hepatitis

Bile duct obstruction

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30
Q

What is the pathology of acute liver failure

A

Fatty liver develops into liver fibrosis then causes liver cirrhosis

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31
Q

What is important signs of liver failure

A
  • Low albumin
  • Raised INR
  • Elevated LFTs

(abnormal LFTs with normal albumin levels means you arent in liver failure)

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32
Q

What are the liver function tests

A

ALP - shows obstruction of liver infiltration, gall bladder problems

AST/AAT- alcohol involvement

ALT - Inflammation of liver

(AAT/AST> ALT - means alcohol cause of liver damage)

GGT

Albumin (synthetic function of liver)

Prothombin (function, liver transplant)

Creatinine (kidney function)

Platetete count (spleen)

Bilirubin

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33
Q

Prioritisation of liver transplant is dependant on

A
  • Bilirubin
  • Creatinine
  • INR
  • Sodium
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34
Q

What is the drugs administrated post liver transplant

A

Anti fungal
Prophylactic antibiotics

Antirecession
steroids
azaithoprine

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35
Q

What is the main aetiologies of hepatitis, what is the pathology and outcomes

A

Hepatits Virus
Alcohol
Drugs
Auto-immune

Inflammation of the liver, liver cells become damaged causing death of individual liver cells

3 Possible Outcomes 
- Resolution
- Liver failure
- Progression to chronic hepatitis and cirrhosis
(usually after death of 75% of cells)
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36
Q

What is the symptoms and signs of alcohol hepatitis

A
  • Jaundice
  • Encephalopathy
  • Infection usually present
  • Decompensated hepatic function

Biomarkers

  • Raised GGT ALP
  • Raised Bilirubin
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37
Q

What is the treatment for Autoimmune and alcohol hepatitis

A

Treatment of Autoimmune Hepatitis
- Long term azathioprine and steroid

Treatment for Alcohol Hepatitis 
- Avoid alcohol, treat alcohol withdraw
- Liver transplant (if abstinence from alcohol fo 6 moths)
Treat: encephalopathy, Infection
Protect against GI bleed

Drug treatment if severe
- Oral prednisolone 40mg steroid

Nutrient treatment

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38
Q

What hepatitis Virus is most likely to cause cirrhosis

A 
Hep B 
Hep C (asymptomatic until cirrhosis)
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39
Q

What is the biomarkers of viral hepatitis

A

B
Antigens detected
- Hep B e (virus active- released from core)
- Hep Bs (virus is present-located on surface)
- Hep Bc/e (virus replicating-core open)
IgM <6months
IgG > 6 months

Abnormal LFTS

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40
Q

What is the treatment of Hep B

A 
Pegylated interferon 
(3 drug therapy of alpha 2a, alpha 2b and beta 1a, targeting intracellular signalling)

oral antiviral drugs

  • Entercavir
  • Lamiduvine
  • telbivudine
  • tenofovir
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41
Q

What is the treatment for Hep C

A

interferon free combination of direct acting antiviral drugs given for three months

  • ledipasvir,
  • simeprevir
  • sofosbuvir
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42
Q

What is the pathology of alcohol fatty liver disease

A

Excess alcohol in the liver disrupts metabolism of fatty acids in the liver, leaving excess fat in the liver called steatosis

Steatosis eventually causes steaohepatitis
as fat deposited in the liver triggers inflammation, and neutrophilial infiltration occurs
resulting in liver cell damage and death

This process of fibrosis occurs as scare tissue is deposited

This leads to `liver cirrhosis
= chronic liver disease

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43
Q

What is the investigations for fatty liver disease

A

AUDIT/FAST
- tests severity of alcohol usage

Imaging 
-Ultrasound 
(fibrocan determine how much fibrosis or fat)
-MRI Spectrum 
(see fat)
-CT

LFT: AST/ALT ratio
= AST>ALT (if alcohol fatty liver disease )

Liver Biopsy

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44
Q

What is the risk factors for Non alcoholic fatty liver disease

A

Metabolic Risk Factors

  • Diabetes mellitus
  • Obesity
  • Hyper-triglyceridemia
  • Hypertension

Other Risk Factors
- Age (high risk over 45yrs)
-Ethnicity (eg hispanics)
Genetic factors (PNPLA3 gene)

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45
Q

What is the management of fatty liver disease

A

Weight reduction

  • Diet and Exercise
  • Surgery

ALCOHOL
- Avoid alcohol and treat withdraw

NON ALCOHOL
Insulin sensitisers
e.g. Metformin, Pioglitazone

Glucagon-like peptide-1 (GLP-1) analogues
e.g. Liraglutide

Farnesoid X nuclear receptor ligand
e.g. Obeticholic acid, Vitamin E

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46
Q

What is the pathology of jaundice and what is three three types

A

Excess circulating bilirubin (exceed 34 µmol/L) due to altered metabolism and pathway

Pre hepatic
Hepatic
Post hepatic

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47
Q

What is the investigations for jaundice

A

LFT
- Bilirubin elevated

IMAGING
Ultrasound of abdomen

CT/MRI scan

Endoscopic retrograde
cholangiopancreatography (ERCP)

Magnetic resonance cholangiopancreatography (MRCP)

Percutaneous Transhepatic Cholangiogram

Endoscopic Ultrasound (EUS)

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48
Q

What is the main aetiology of pre hepatic jaundice

A

Increased Heamolysis (breakdown to heam in spleen, that is converted into bilirubin)

Impaired transport

= Increased in uncongugated billirubin before the liver

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49
Q

What is the specific signs of pre hepatic jaundice

A

Splenomegaly
pallor
Anemia

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50
Q

What is the main aetiology of hepatic jaundice

A

If Defective:

  • Uptake of bilirubin
  • Conjugation
  • Excretion

Intra hepatic duct obstruction
Cholestasis - accumulation of bile within the hepatocyte or bile canaliculi

= Increase in conjugated bilirubin in the liver

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51
Q

What i is the specific signs of hepatic jaundice

A

Ascites - accumulation of fluid in peritoneal cavity

Variceal bleed - dilated blood vessels

encephalopathy

Spider naevi,
Gynaecomastia (moobs)

Asterixis - flapping tremor

(associated with IV drug abusers)

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52
Q

What is the main aetiology of post hepatic jaundice (obstructive jaundice)

A

Defective transport of bilirubin by biliary duct

  • Cholelithiasis (gallstones)
  • Extra-Hepatic bile duct obstruction

=conjugated bilirubin after the liver

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53
Q

What is the specific signs of post hepatic jaundice

A

Abdominal pain

Pruritus

pale stools
(normal colour if before liver)

Steatorrhoea

High coloured urine (dark)

Palpable gallbladder

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54
Q

What are causes of intrahepatic and extra hepatic bile duct obstruction

A

INTRA
Autoimmune
- Primary biliary cholangitis
-Primary scerlosing colangiti

Tumpurs

  • Hepaticellular carcinoma
  • Tumours of interherpatic ducts
  • Metastatic
EXTRA 
-Cholelithiasisis 
-Bile duct tumours 
Benign strictures 
-External compression
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55
Q

How are bille duct obstruction examined and treated

A

endoscopic retrograde cholangiopancreatography

  • stenting of biliary duct obstruction
  • Stone retrieval
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56
Q

Primary Biliary cholangtitis

A

Autoimmune disease: Granulamtous infection involving bile ducts, leading to loss of intrahepatic ducts

Biomarkers:
Anti mitochondrial antibody postive
- IgM elevates
- Increased alkaline phosphate (ALP)

Symptoms:
Fatigue
Pruiritus
Jaundice

Treatment

  • ERCP stenting
  • Ursodeoxycholic acid

Complications:
Liver cirrhosis

57
Q

Primary scerlosing cholangtitis

A

Autoimmune disease: Chronic inflammation and fibrous obliteration of intra and extra hepatic bile duct
leading to the loss of hepatic bile ducts
(associated with IBD)

Biomarker: pANCA postive

Treatment:
Liver transplant
Billary stent

Complications:
Liver cirrhosis
Cholangiocarcnoma

58
Q

What is Cholelithaisis and its risk factors

A

The Formation of Gall stones
Composed of cholesterol and Pigment

Risk Factors

  • Obesity
  • Diabetes
  • age
  • genfer
  • OCP

PreCurso:
- Cholesterolosis, change in gallbladder wall due to excess cholestrol

59
Q

What is the pathology of choleithialss

A

Cholecystitis
= Disease of the Gall bladder resulting in inflammation (acute or chronic)

Choledocholithiasis
= The presence of 1 or more gallstones in the common bile duct (CBD)
- acute pancreatitis 
-Post hepatic jaundice 
-ascendong cholangitis

Gallstone Illeus
- small bowel obstruction due to gallstone at the lumen of small intestine

Mirizis syndrome
- Stones stuck on the neck of the gallbladder, compressing the bile duct

60
Q

What is the signs of cholelithiasis

A

Asymptomatic 10-30%

Flatulent

dyspepsia/indegestion

Biliary colic:
Nausea, vomiting, upper abdomen pain

Tenderness

61
Q

What is the main investigations for cholelithiasis

A

Ultrasound scan

Endoscopic ultrasound
-picks up small stones

IV cholangiography

Endoscopic retrograde
cholangiopancreatography (ERCP)

Magnetic resonance cholangiopancreatography (MRCP)

62
Q

What is the treatment for cholelithiasis

A

Dissolution
-Split up Gall stones

Lithotripsy
- Ultrasound waves to break up gall stones

Laparoscopic Cholecystectomy
(Gold standard)
Or
Open/Mini//Single port/NOTES

ERCP

Urosodeoxycholic acid

63
Q

What is the treatment for Choledocholithiasis

A

Laparoscopic trans-cystic CBD exploration

Laparascopic exploration of CBD

Open exploration of CBD

ERCP - Transhepatic stone retrieval

64
Q

What is the aetiology of chronic liver disease/hepatic cirrhosis

A

Alcohol

Non alcohol fatty liver disease

Drugs

Hepatitis B,C
(blood born)

Immune mediated liver disease

  • Auto-immune hepatits
  • Primary cholangitis

Metabolic disorders

  • Primary haemochromatosis (excess iron)
  • Wilsons disease (excess copper)

Obesity

cystic fibrosis

Cryptogenic

65
Q

What is the pathology of chronic liver to hepatic cirrhosis

A

End stage chronic liver disease persisting beyond 6 moths leading to hepatic cirrhosis

Chronic liver injury occurs causing infiltrating lymphocytes
this causes fibrosis as extracellular matrix proteins gather blocking the sinusoids of the liver therefore increasing resistance to blood flow so liver cant receive nutrients or oxygen from the blood

Cirrhosis occurs as a diffuse process involving whole liver as hepatocytes death is replaced by nodules of hepatocytes that are separated by the broad band of fibrous tissue
leading to loss of normal liver structure

66
Q

What is the signs of chronic liver disease

A

Spider naevi
(increased oestrogen in the blood)

palmar erythema,

gynaecomastia (moobs)

loss of axillary and pubic hair

ascites

  • shifting dullness
  • dullness in flanks

JVP elevation

Umbilical nodule

Abdominal veins

encephalopathy

Jaundice

Muscle wasting

67
Q

What is the complications of chronic liver disease

A

Altered liver function

Abnormal blood flow from the Liver causing portal hypertension

Variceal bleeding

Hepatic Encephalopathy

Jaundice

Ascites

Increased risk of hepatocellualr carcinoma

68
Q

What is the investigatiosn for chornic liver disease

A

IMAGING
Ultrasound of abdomen - See fat on liver

CT/MRI scan

Endoscopic retrograde
cholangiopancreatography (ERCP)

Magnetic resonance cholangiopancreatography (MRCP)

Percutaneous Transhepatic Cholangiogram

Endoscopic Ultrasound (EUS)

69
Q

What is the biomarkers for alcohol causing chronic liver disease

A

AAT/AST > ALT.
Raised GGT
Low platelets
(Thrombocytopenia)

Macrocytosis - enlarged red blood cells

70
Q

What is the Investigation and treatment of ascites - accumulation of fluid in the peritoneal cavity

A 
DIAGNOSIS 
Paracentesis (removal of ascitic fluid) and test for:
- Protein and albumin conc 
-Cell count and differentation 
-SAAG (serum ascites albumin gradient)

TREATMENT
Diuretics

Large volume paracentesis
TIPS (transjugular intrahepatic portosystemic shunt)

Aquaretics
(drug that promotes excretion of water without electrolyte loss)
Liver transplantation

71
Q

What is the three complications arising from portal hypertension

A

Varices Haemorrhage

  • Small blood vessels cant handle blood pressure and burst, mostly occurring at porto-systemic anastomoes
  • Skin,Caput medusa
  • Oesophageal varicose
  • rectal
  • posterior abdominal wall
  • stomal

Enlarged spleen
Increases pressure in splenic vein, enlarging the spleen, putting it in danger or injury and decreasing its functional capacity

Fector Hepticas
portosystemic shunting allows thiols to pass directly into the lungs

72
Q

What is a specific sign of Splenomegally

A

Low platelet count

- due to over reactive spleen

73
Q

What is the treatment for varies

A
  • Blood transfusion as required
  • Emergency endoscopy with band ligation to stop bleeding
  • Telipressin (vasoactive drug used in management of low blood pressure)
  • Sengstaken-blakemore tube (insested through nose or mouth to help with oesopheal varcose heamorrhage)
74
Q

What is the hepatocellular carcinoma and its aetiology

A

Malignant tumour of hepatocytes
Tumour marker: AFP

Aetiology:

  • hepatic cirrhosis
  • chronic hepatitis B, C
75
Q

What is the symptoms of hepatocellular carcinoma

A
  • Liver disease
  • Abdominal mass
  • Abdominal pain
  • weight loss
  • bleeding from tumour
76
Q

What is the Investigations for hepatocellular carcinoma

A

Imaging

  • Ultrasound
  • CT scan
  • MRI

Liver biopsy

Paracentesis (high SAAG)

77
Q

What is the treatment for hepatocellular carcinoma

A
  • Hepatic resection
  • Liver transplantation

-Chemotherapy
(local -Transcatheter arterial chemo-embolization or systemic)

  • Locally ablative
    (alcohol injection or radio-frequency ablation)
  • Sorafenib (Tyrosinase kinase inhibitor)
  • Hormonal therapy: Tamoxifen
78
Q

Ampullary tumours

A

Rare malignant tumour occuring at the ampulla of water

Adenoma or adenocarcnoma

Increased risk with Fap inherited gene

Treatment: Endoscopic/transduodenal excision, panctreatico-duodenectomy

79
Q

What is the aetiology of acute pancreatitis

A

Alcohol Abuse

Gall Stones

Trauma: Blunt/postoperative/post
ERCP

Drugs (Steroids, azathioprine, diuretics)

Viruses

Pancreatic carcinoma

Metabolic changes:
Increased Calcium
Increased Triglycerides
Decreased Temperature

Autoimmune

Idiopathic

Anatomical abnormalites
-pancrease divisum

80
Q

What is the pathophysiology of pancreatitis

A

Primary insult happens to the pancreas
Affecting the exocrine portion
Causing the release of activated pancreatic enzymes, this then causes autodigestion to occur

Resulting in:
Pro-inflammatory cytokines
Reactive oxygen species
Oedema
Fat necrosis
Haemorrhage

Overall causing acute inflammation of the pancreas

81
Q

What is the symptoms of acute pancreatitis

A

Abdominal/epigastric pain occurring with no warning

Vomiting

Significant bruising

Pyrexia

Jaundice

Tachycardia

Olguria (small amount of urine - due to renal failure)

Hypoxia - extreme case

82
Q

What is the signs of acute pancreatic

A

Biomarker: Elevated serum amylase levels

Increased
Ca2+

Decreased Glucose

Acute renal failure

83
Q

What is the Investigations for acute pancreatic

A

Imaging:

ERCP 
Endoscopic ultrasound
Abdominal X ray
Abdominal Ultrasound
CT scan (contrast enhanced)
-Shows complications
CT guided fine needle aspiration

Blood Tests:

serum amylase/lipase 
FBC, 
U&amp;Es, 
LFTs, 
Ca2+, 
glucose, 
arterial blood gases, 
lipids, coagulation screen
84
Q

What is the complications fo acute pancreatitis

A

Pancreatic necrosis
Abscess
pseuedocyte
Effusions

85
Q

What is the treatment and managment fo acute pancreatitis

A 
General Management:
Analgesia (pethidine, indomethacin)
Intravenous fluids
Blood transfusion
Monitor urine output (catheter)
Naso-gastric tube
Oxygen
May require: 
insulin 
calcium supplements 
Nutrition

Treatment of Pancreatic Necrosis

  • Antibiotics
  • Surgery
86
Q

The severity of acue pancreatitis is determined

A

have a score >3 of the following:

Glucose > 10 mmol/L
Serum [Ca2+] < 2.00 mmol
WCC > 15000/mm3

Albumin< 32 g//L
LDH > 700 IU/L
Urea > 16 mmol/L
AST/ALT > 200 IU/L
Arterial pO2 < 60mmHg

GLASGOW SCHOOL WARRIORS ARE LETHAL UNDER ATTACK ALWAYS

87
Q

What is the aeitiology of chronic pancreatitis

A

Alcohol

Cystic Fibrosis: CFTR

Duct Obstruction

  • Gall stones
  • Inflammation
  • Protein Plugs

Abnormal Spinchter of oddi Function

  • Spasms, Increasing intra-pancreatic pressure
  • Relaxation, resulting in reflux of duodenal contents
Congenital anatomical abnormalities: 
- annular pancreas 
(duodenum surrounded by ring of pancreatic tissue)  
- Pancrease divsum
(failure of pancreatic duct to fuse)

Genetic polymorphism, abnormal trypsin activation PRSS1 – cationic trypsinogen,
SPINK1 – pancreatic secretory trypsin inhibitor,

Hypercalcaemia/hyperlipidaemia

Diet

88
Q

What is the pathology of chronic pancreatitis

A

Continuous inflammation of pancreas causing glandular atrophy & replacement by fibrous tissue
Ducts become dilated, tortous & strictured
Thicken secretions may calcify

= loss of function and irreversible

89
Q

What is the signs and symptoms of chronic pancreatitis

A

Exocrine insufficiency

  • Protein malabsorption
  • Fat malabsorption
  • Steatorhoea

Endocrine insufficiency
-diabetes

Abdominal pain

Increased serum amylase in acute exasperations

90
Q

What is the investigations for chronic pancreatitis

A

Sweat Test: CFTR

Imaging 
Abdominal Xray 
Ultrasound 
Endoscopic Ultrasound 
CT scan
-shows complicatiosn
ERCP 
MRCP
Blood test 
Increased: 
LFT 
Prothrombin time/INR 
glucose
Decreased: Albumin, ca2+, Mg2+. vitamin B2

Pancreatic Exocrine Function Tests

  • Lundh
  • Pancreolauryl (trypsin response to stimuli)
  • faecal/serum enzymes
  • diagnostic enzyme replacement
91
Q

What can be seen on a blood test of chronic pancreatic

A

Increased:
LFT
Prothrombin time/INR
glucose

Decreased: 
Albumin, 
Ca2+
Mg2+ 
Vitamin B2
92
Q

What is the management of chronic pancreatits

A

Avoid alcohol

Opiate analgesia (dihydrocodeine, pethidine)

Celiac plexus blocks (injections of pain medication to relieve abdominal pain)

Endoscopic treatment of pancreatic duct stones and strictures

Exocrine Insufficiency Management
Low Fat diet
Pancreatic enzyme supplements

Endocrine Insufficiency management
Insulin

Surgery

  • Drainage
  • Resection
93
Q

What is the aetiology of pancreatic cancer

A 
cigarette smoking
chronic pancreatitis
Diabetes Melitus (less than 2 yrs duration)
Hereditary pancreatitis 
Inherited predisposition
94
Q

What is the pathological cell types of pancreatic cancer

A
  • 75% duct cell mutinous adenocarcinoma
  • carcinosarcoma
  • cystadenocarcinoma
  • Acinar cell
95
Q

What is the signs of pancreatic cancer

A

Tender subcutaneous fat nodules

Thrombophlebitis migrans (vessels inflammation due to blood clot)

Hepatomegaly

Portal hypertension

Jaundice

Abdominal mass/tenderness

ascites

splenomegally

supravicular lymphadenopathy

palpable gallbladder

96
Q

What is the symptoms of pancreas cancer

A

Slow progression of Upper abdominal pain

Weight loss

anorexia

fatigue

diarrhoea/steatorrhoea

Nausea/vomiting
—————
Upper Abdominal Pain - If carcinoma located in body and tail

Painless obstructive Jaundice - if carcinoma located in head

97
Q

What is the investigations for pancreatic cancer

A 
*USS 
ERCP 
CT 
MR, 
MRCP 
Laparoscopy + Lap USS 
Peritoneal cytology 
EUS + FNA/ Bx 
Percutaneous needle biopsy 
PET
98
Q

What is the management of pancreatic cancer

A 
Palliation of Jaundice
- ERCP+ Stent 
-Palliative bypass 
cholechoduodenostomy 
(communication between bile duct and duodenum)

Pain control

  • Opiates
  • Coeliac Plexus Block
  • Radiotherapy

Chemotherapy

Palliative drainage
-Palliative bypass
ERCP
Stenting

Open/laparoscopic bypass

99
Q

What is the main treatment for pancreatic cancer

A

Pancreatoduodenectomy

whipples procedure

100
Q

What is the alarm symptoms of bowel function symptoms

A

Short symptomatic history

unintentional weight loss

Nocturnal symptoms

Family history of bowel/ovarian cancer

Anemia
rectal bleeding

Recent antibiotic use

Males (report less)

Abdominal Mass

101
Q

What is the aetiology of colorectal cancer

A

Sporadic

Familial risk

Previous adenomas/Colorectal cancer

Inheritable conditions:
FAP - Familial adeomatous polyposis
HNPCC - hereditary non-polyposis colorectal cancer
Peutz-jeghers

underlying inflammatory bowel condition

  • Extent of IBD
  • Duration of IBD
102
Q

What is the pathology and oncogenes of colorectal cancer

A

Arise from existing colorectal polyps (tubular/ villous/tubulovillous) that are benign adenomas that have epithelial origin, and become invasive adenocarcinomas

Oncogenes:
Kras
C-mv

103
Q

The high risk of colorectal polyps becoming adenocarcinoma lesions is dependant on

A
  • size of polys
  • number of polys
  • degree dysplasia
  • villous architecture
104
Q

What is the two types of rectal cancer

A

Anal squamous cell carcinoma

Rectal adenocarcinoma

105
Q

What are the symptoms of colorectal cancer

A

Palpable rectal
Loer abdominal/right sided abdominal mass

Rectal bleeding 
(itching, lumbs and discharge around anus)

Persistent changes in bowel habit

weight loss

RIGHT SIDED

  • anemia
  • vague pain
  • weakness
  • obstruction

LEFT SIDED

  • Bleeding
  • altered bowel habit
  • obstruction
106
Q

What is the investigations for colorectal cancer

A

*Colonoscopy
+/- Biopsy

Contrast imaging - Barium enema

CT-Colonography

CT abdo/pelvis

MRI Guided colonoscopy

Staging 
CT 
MRI
PET scan 
Rectal endoscopic ultrasound
107
Q

What is used in screening for colorectal cancer

A 
Faecal occult blood test (FOBT) 
Faecal immunochemical test (FIT) 
Flexible Sigmoidoscopy 
Colonoscopy 
CT Colonography
108
Q

What is the treatment for colorectal cancer

A

Surgery:
laprascopy vs lapartomy
(+/- faecal divericulum colostomy/illeostomy)

Endoscopic/Local Resection

  • Polyps
  • Duke A classification

Colonoscopy + Polypectomy
- removes polyps

Chemotherapy (5FU-Florouracil)

  • after surgery
  • palliative care
  • Duke B + C
109
Q

What is the specific treatment for Rectal SCC

A

Radiotherapy

110
Q

What is the staging of colorectal cancer

A

A – Tumour confined to mucosa
B – Tumour extended through mucosa to muscle layer
C – Involvement of lymph nodes
D - Distant metastatic spread

111
Q

What is the extra manifestations of IBD

A

Eyes
-Inflammation/conjunctivitis

Joints
-Inflammation/arthritis

Renal Calculi

Liver and Biliary tree

  • fatty change
  • pericholangitis
  • scerlosing cholangitis
  • Gall stones

Skin

  • pyoderma gangrenosum
  • erythema nosdum
  • vasculitis
112
Q

What is IBDs

A

Strong exaggerated immune response against normal flora due to a defects in the epithelial barrier function allowing microbes access to muscle lymphoid tissue

  • Lyphocytic colitis
  • Collagenous colites
  • Microscopic colitis
  • ulcerative colitis
113
Q

What is the investigations for IBDS

A 
Endoscopy 
colonoscopy 
Contrast imaging - barium enema 
CT -colonscopy 
MRI
114
Q

What is the steps in medical management of IBDS

A
  1. 5-ASA/aminosalicylates or sulfasalazine(prodrug)
  2. Steroids:
    Predisolone /Budenoside (40mg then taper)

3.Immunosuppressants
Azathioprone (steroid sparing, lots of side effects eg hepatotoxicity)
Methotrexate (steroids
Ciclosporin

  1. Biologics (IV infusion 8 weekly, SC 2 weekly)
    - Infliximab

5.Surgery (total colectomy and rectal preservation)

Elemental feeding

Antibiotics (metronidazole)

115
Q

What additional procedures occur after colorectomy

A

pouch procedure
Protectomy

Ileostomy

116
Q

What is the aeitiology of crohns and ulcerative colitis

A 
Environmental triggers:
-Bacteria
-Diet
-Vaccination 
Social 
-Ethnicity

Genetic susceptibility

HLA - UC
NOD2- Crohns

117
Q

What is the pathology of ulcerative colitis

A

Continuous inflammation starting from the rectum and only affecting the colon
with various distribution and severity of symptoms

Results in Pseudopolyps and Ulceration

Minimal or no inflammation on serosal surface

appendix can be involved

118
Q

What is the pathology of crohns

A

Mouth to anus patchy disease due to skipped lesions of inflammation, resulting in strictures and fibulas

  • Granular serosa / dull grey 

    Wrapping mesenteric fat; Mesentry- thickened, oedematous and fibrotic 

    Wall thick, oedematous (accumulation of fluid) 

    Narrowing of lumen 

    Patchy lesions 

    Ulceration “cobbestone”
119
Q

What is the histology of ulcerative colitis

A

Limited mainly to mucosa and submucosa 

Mucosa – inflammation 

Cryptitis, Crypt abscesses, Architectural dissarray of crypts 

Mucosal atrophy 

Ulceration into submucosa- pseudopolyps 

Submucosal fibrosis 

NO granulomas

120
Q

What is the histology of crohns

A

Cryptitis and crypt abscesses

Architectural distortion

Atrophy –crypt destruction
Ulceration-deep

Transmural inflammation
(Chain of pearls)

Non-caseating granulomas

Fibrosis

Lymphangiectasia

Hypertrophy of mural nerves

Paneth cell metaplasia

121
Q

What is the biomarkers of IBD

A 
High ESR 
High platelet count 
High WBC 
Low Hb 
Low Albumin

Stool Marker
- Calcoprotein

122
Q

What is the non specific signs in crohns

A
  • Clubbing

- Mouth ulcers

123
Q

What is the symptoms of Ulcerative colitis, and what occurs in a severe attack

A

Bloody diarrhoea
abdominal pain
weight loss

Severe Attack:
>6 stools a day with blood
Fever
Tachycardia
Raised CRP
Anemia
Low Albumin
Leucocytosis
124
Q

What is the symptoms of Crohns

A

Variety Of Symptoms as Depend on Region Involved

Diarrhoea 
abdominal pain 
Weight loss 
Malaise 
Lethargy 
Anorexia 
Malabsorption: 
Anemia 
Vitamin deficiency
125
Q

How do you diagnose IBS (functional disorder)

A

Recurrent abdominal pain/discomfort for over 3 days a months in the past 3 months
associated with two or more symptoms
- improvement with defecation
- onset associated with change in stool frequent
- onset associated with change in stool form

126
Q

What is the symptoms and signs of IBS

A

Symptoms dont occur at night

Constipation (IBS-C)
Contractions may be reduced

Diarrhoea (IBS-D)
Muscular contractions may be stronger and more frequent than normal

Both diarrhoea and constipation (IBS-M)

Variability

Urgency

Abdominal pain - due to bowel distension

Abdominal bloating

Belching, wind and flatus

Mucous in stools

127
Q

What is the investigations for IBS to make sure its not a different diagnosis

A 
Thyroid function 
Coeliac serology 
Calcoprotein 
Colonscopy 
Rectal examination and FOB
128
Q

What is the management of IBS

A

Diet review

FODMAP diet 
(fermentable oglio, Di and Mono-saccharides and plyols)

Avoid -Tea/Coffee/Alcohol/Sweetner

Exclude - Lactose, gluten

Drug therapy

Pain: 
Antispasmodics 
Linaclotide 
Antidepressants 
TCA, 
SSRIs

Bloating:
Probiotics
Linaclotide
(avoid bulking)

Constipation:
-Laxatives 
(bulking agents/softeners/stimulants/ osmotics)
- Linaclotide
-Avoid FODMAP

Diarrhoea:

  • Anti motility agents
  • FODMAP
  • avoid SSRIs

Psychological intervention

129
Q

What is the aetiology of coeliac disease

A

A small intestine disease caused by a sensitivity to giladin (component of gluten found in wheat, rye, barley)

Produces an inflammatory response via tissue transglutaminase that results in Partial or subtotal villous atrophy
and Increased intra-epithelial lymphocytes

130
Q

What is the symptoms and signs of small intestine coeliac disease

A

Weight loss, Increased appetites
Diarrhoea, steatorrhoea
Bloating
Fatigue

Clubbing
Dermatitis hepatiforms

Low or falling BMI

Deficiencies:
Iron 
Vitamin B 12 
Vitamin A,C,D,K 
Vitamin B complex 
- Thiamine 
- Niacin 
Ca2+ 
Mg2+ 
Non Specific signs 
Clubbing 
Scleroderma 
Mouth Ulcers 
Dermatitis herpetiformis
131
Q

What is the investigatiosn for small intestinal disease

A

Endoscopy + biopsy

Barium swallow

CT scan

MRI enteroscopy

Capsule/ballon enteroscopy

White cell scan

Bacterial Overgrowth

  • H2 Breath test
  • Culture a duodenal or jejunal aspirate
132
Q

What is the special tests for coeliac disease

A

Distal duodenal biopsy
- look for villous atrophy

Serology -
- IgA tests  (more reliable than IgG)
Anti endomysial IgA 
- Anti Tissue transglutaminase 
- Anti Gliadin 
(help in children but no diagnostic in adults)

HLA status
-present in normal and coelics

133
Q

What is the treatment for Coeliac disease

A 
Withdraw gluten 
(avoid wheat, + lifelong diet)
MUST refer to state registered dietitian
134
Q

What is the treatment of small bowel overgrowth

A 
Rotating antibiotics: 
Metronidazole 
Tetracycline 
Amoxycillin 
Each for 2 weeks

With Vitamin and nutritional supplements

135
Q

Whipples disease

A

Occurs in middle aged men due to causative organism tropheryma whipelli

Skin Drain, joints and cardaic effects
Weight loss, malabsorption, abdominal pain

Investigation: Distal duodenum biopsy-PAS material in Villi

136
Q

Heamrroids

A

Aetiology: Straining, constipation, low fibre diet

Pathology: Enlarged vascular cushion located internal and external

Complication: painful if thromboses, bleeding anemia

Symptoms: Extreme itching, painful, swollen anus
fecal leakge, painful bowel movements, melanea

Treatment:Pain relief
Fibre supplements
Rubber band ligation
Stapled anoplexy (also for rectal prolapse)

Elective surgical intervention

137
Q

Anal fissures:

A

Aetiology: Constipation, persistent diarrhoea, IBD, childbirth

Symptoms: Sharp pain weh Passion stool then long burn pain after, melanea

Management 
Should resolve independently
Pain relief
Hydration 
Fibre 
May be given laxatives by GP
Medical Treatment 
(aim to relax internal anal spinchter)
- Topical nitric oxide 
- Glycerine trinate pasta 
- Diltiazem Calcium blocker

Surgical Treatment
Internal lateral spinchtereotomy

138
Q

Perianal abscess

A

Aeitology: Infected fissure, STI, blocked anal gland, infection of small anal glands

Complication: fistulas

Symptoms: Painful red, warm tender boil swelling near anus with pus
Constant throbbing pain
Constipation or pain on passing

Treatment: Surgical incision, drainage (post drainage relief) antibiotics

139
Q

Anal fistula

A

Aetiology: develops after Abscess (channels from drainage), IBD, Diverticulitis

Pathology: Narrow channel with internal opening in anal canal and external opening in skin near anus

Symptoms:Skin irritation around anus,Constant throbbing pain 
Worse pain when: 
- Seated 
- Moving 
- Bowel movement 
- Coughing

Smelly discharge from anus
Melaena, Pus in stool
Bowel Incontinence

Treatment:
Fistulotomy
- cutting along the whole length of the fistula to open it up so it heals as a flat scar
(dont do when fistula pass through spinchter muscle)

Seton sutures
- drain and heal fissure

Or Fill fistula:

  • Advancement flap procedure
  • Bioprosthetic plug
  • Firbin glue

Systems revision (3 decks)

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