GI 4 Flashcards
(102 cards)
1
Q
How is ethanol metabolised?
A
Alcohol dehydrogenase changes it to acetaldehyde
Acetaldehyde dehydrogenase converts to acetate
2
Q
What does ethanol lead to in biochemical terms?
A
Prevention of g6p to glucose, hypoglycaemia
Excess lipids
Excess pyruvic acid leading to excess lactic acid and acidosis
Excess acetyl CoA leading to ketosis
3
Q
What diseases does alcohol lead to in the liver?
A
Steatosis (fatty liver)
Steatohepatitis (fatty liver with inflammation)
>Neutrophil infiltration
>Fibrosis and cirrhosis (build up of scar tissue)
>Gentically susceptible to – fat deposited scars liver
4
Q
What is the clinical picture with excessive alcohol?
A
Majority none until advanced liver disease
Signs of chronic liver disease –
> spider naevi, palmar erythema, gynecomastia, loss of axillary and pubic hair, ascites, encephalopathy
Jaundice
Muscle wasting
5
Q
What tests confirm alcoholic liver disease?
A
Aspartate Amino Transferase (AAT) > alanine Amino Transferase (ALT). Ratio >2
Raised Gamma Glutamyl Transferase (aso raised in other diseases)
Macrocytosis
Thrombocytopenia (low platelets)
6
Q
What can trigger hepatic encephalopathy?
A
Infection Drugs Constipation GI bleed Electrolyte disturbance (Try to exclude infection, hypoglycaemia and intracranial bleeds) (Overload of toxins)
7
Q
How do you treat hepatic encephalopathy?
A
Clear out bowel – lactulose (keeps bowel moving) or enemas Antibiotics Supportive – ITU, airway support Nasogastric tube for meds Clear toxins – NH3 decrease – wake up
8
Q
What is the clinical picture of spontaneous bacterial peritonitis?
A
Abdominal Pain
Fever, Rigors
Renal impairment
Signs of Sepsis, tachycardia, temperature
9
Q
How do you diagnose SBP?
A
Ascitic tap >Fluid protein and glucose levels >Cultures >White cell content Neutrophil count >0.25x109 /L Protien <25g/L Exclude surgical causes
10
Q
How do you treat SBP?
A
IV antibiotics
Ascitic fluid drainage
IV albumin infusion (20% ALBA)
11
Q
How does alcoholic hepatitis present?
A
Jaundice
Encephalopathy
Infection common
Decompensated hepatic function – low albumin and raised prothrombin time/ INR
12
Q
What is the prognosis of alcoholic hepatitis?
A
Dependent on abstinence or ongoing alcohol consumption
Any sign of decompensating liver disease – 70% mortality 5yrs
Present with encephalopathy – 64% 1yr mortality
13
Q
How do you diagnose alcoholic hepatitis?
A
Raised bilirubin
Raised GGT and AlkP
Alcohol histry
Exclude other causes
14
Q
How do you treat alcoholic hepatitis?
A
Supportive
Nutritional
Treat infection, encephalopathy + alcohol withdrawl
Protect against GI bleeds
Airway protection – ITU care
Some get better as liver regenerates
Steroids -only if grading severe (Glasgow alcoholic hepatits – only if less than 9)
15
Q
How many people with alcoholic hepatits are malnourished?
A
100% malnourished, 33% severely
– survival 15%, 70% if well nourished)
– high energy requirements
>Low thiamine leads to permanent brain damage
16
Q
What are the two types of fatty liver?
A
Steatosis (fatty liver, non alcoholic – NAFLD)
Steatohepatitis ( non alcoholic steatohepatits (NASH))
17
Q
What are the tisk factors of fatty liver?
A
Obesity Diabetes Hypercholesterolaemia Alcohol 25-40% of population (due to living longer + inc. incidence of diabetes)
18
Q
What is steatohepatitis?
A
Fat + inflammation in liver Histoligically similar to alcohol induced damage ¼ develop cirrhosis Often asymptomatic Raised alanine amino transferase Fatty liver on USS Liver biopsy Treatment – weight loss, exercise
19
Q
What are the symptoms of oesophageal disease?
A
Retrosternal discomfort/burning
>May be associated with waterbrash, cough
Heartburn (dyspepsia)
Dysphagia /odynophagia (pain whilst swallowing, may accompany dysphagia)
20
Q
What can cause heartburn(dyspepsia)?
A
Reflux occurs physiologically (like after swallowing)
Certain drugs/foods (e.g alcohol, nicotine, dietary xanthines) reduce LOS pressure, resulting in increased heartburn
>Persistent reflux leads to gastroesophageal reflux disease (GORD) and leads to long-term complications
21
Q
What questions are pertinent in dysphagia history?
A
Type of food (solid vs liquid) Pattern? Progressive, intermittent Associated features (weight loss, regurgitation, cough) Location – oropharangeal, oesophageal?
22
Q
What are the causes of oesophageal dysphagia?
A
Benign stricture Malignant stricture Motility disorders (e.g. achalasia, presbyoesophagus) Oesinophillic oesophagitis Extrinsic compression (eg lung cancer)
23
Q
What investigations can be done into dysphagia?
A
Endoscopy (oesophago-gastro-duodenoscopy (OGD), Upper GI, (UGIE)) Contrast radiology (barium swallow – now reserved only if needed) Oesophageal pH and manometry
24
Q
What are the three most common motility disorders?
A
Hypermotility
Hypomotility
Achalasia
25
What are the features of hypermotility?
Corkscrew appearance on Ba swallow.
Idiopathic
Severe, episodes of chest pain +/- dysphagia
Manomerty – hypertonic contractions, uncoordinated
26
How do you treat hypermotility?
Treatment - smooth muscle relaxants
27
What is hypomotility?
Causes failure of LOS mechanism, leading to heartburn/reflux symptoms
Associated with connective tissue disease, diabetes and neuropathy
28
What is achalasia?
The functional loss of myenteric plexus ganglion cells in distal oesophagus and LOS
Mainly failure of LOS to relax, leading to functional distal obstruction of oes
Increases risk of oesophageal (squamous) carcinoma + lung disease/aspirational pneumonia
29
What are the symptoms of achalasia?
Symptoms – progressive dysphagia, weight loss, chest pain, regurgitation and chest infection
30
How do you treat achalasia?
Pharmacological - Nitrates, Calcium Channel blockers
Endoscopic - Botulinum Toxin, Pneumatic balloon dilation
Radiological - Pneumatic balloon dilation
Surgical - Myotomy
31
What is GORD?
Gastro-oesophageal reflux disease
Caused due to pathological acid/bile in lower oesophagus
7% adults experience symptoms, although many experience episodes with no symptoms
32
What are the symptoms of GORD?
heartburn,
cough,
water brash,
sleep disturbance
33
What are the risk factors of GORD?
```
Pregnancy,
obesity,
drugs lowering LOS pressure,
smoking,
alcoholism,
hypomotility,
male,
caucasion
```
34
What is the aetiology of GROD?
Without abnormal anatomy – increase in transient relaxations of LOS
Hypotensive LOS leads to delayed gastric emptying
>Thus delayed oesophageal emptying
Decrease oesophageal acid clearance, thus decrease in resitiance to acid/bile
Due to hiatus hernia – anatomical distortion of the OG junction (many have both)
35
What are the different types of hiatus hernia?
Sliding and paraoesophageal – both where fundus of stomach moves proximally through diaphragmatic hiatus
Sliding - stomach neck pushes up the oesophagus
Para-oesophageal – fundus moves parallel to oesophagus above diaphragm
36
What is the pathophysiology of GORD?
Mucosa exposed to acid pepsin + bile
Increased cell loss and regenerative activity (ie inflammation)
Healing by fibrosis + stricture formation
Erodes oesophagus
37
What are the complications of GORD?
Ulceration
Stricture
Glandular metaplasia (Barrett’s oesophagus)
Carcinoma
38
What is Barrett's oesophagus?
Intestinal metaplasia cause related to prolonged acid exposure in distal oes.
Change from squamous to mucin secreting columnar (gastric) in lower oes
Precursor to dysplasia/adenocarcinoma
Much more common in men than women
39
What is the treatment of barrett's oesophagus?
Once it gets to high grade dysplasia (risk goes from 0.3%/yr to 6%/yr)
Endoscopic mucosal resection (EMR)
Radio-frequency ablation (RFA)
Oesophagetomy (RARE! 10% mortality rate)
40
What is the treatment of GORD?
Mainly empirical (no investigation in absence of alarm features)
Lifestyle measures
Pharmacological – alginates (gaviscon) H2RA (ranitidine), proton pump inhibitor (omeprazole, lansoprazole)
Following investigation – anti-reflux surgery
41
What are te types of oesophageal cancer
| Who gets it?
Squamous
+ Adenocarcinoma
Men more likely 3x than women
42
What is the presentation of oesophgeal cancer?
```
Progressive dysphagia
Anorexia/weight loss
Odenyophagia
Chest pain
Cough
Pneumonia (due to trachea-oesophageal fistula)
Vocal cord paralysis
Haematemesis
```
43
What are the distinguishing features of squamous cell oesophageal carcinoma?
Often large, exophytic, occluding tumours
Occur in proximal and middle thirds of oesophagus
Preceeded by dysplasia
Tobacco and alcohol significant risk factors
Associated with Achalasia, Caustic strictures, Plummer-Vinson Syndrome
44
Where are the two cancers found?
Squamous cell - Top and middle thirds
| Adenocarcinoma - bottom (distal) third
45
What are the distinguishing features of adenocarcinoma?
Occurs in distal oesophagus
Associated with Barrett’s oesophagus (through progression)
Predisposing factors – obesity, male sex, middle age, caucasion
46
How do you investigate oesophageal cancer?
Diagnosis by endoscopy/biopsy
| Staging – CT scan, endoscopic ultrasound, PET scan, Bone scan
47
How do you treat oesophgeal cancer?
Only potential cure is surgical oesophagectomy +/- adjunctive or neoadjunctive chemo (before/after) –
>limited to localised disease, no co-morbid disease, below 70
> mortality @10%
Combined chemo + radiotherapy now offer some prospeect of long term survival with advanced inoperable diseases
Palliatation of symptoms
48
What is the palative care of oesophgeal cancer?
Endoscopic stent, laser/APC, PEG
| Chemo, Radiothearpy, Brachtherapy
49
What are the risk factors of pancreatic cancer?
Smoking
Chronic pancreatitis
Hereditary
Male
50
What are the pathological types of pancreatic cancer?
```
75% duct cell mucinous adenocarcinoma
Also can be:
Carcinosarcoma
Acinar cell
Cystadenocarcinoma (better prognosis)
```
51
How does pancreatic carcinoma present?
```
Obstructive jaundice!
Diabetes
Abdominal pain/back pain
Anorexia
Vomiting
Weight loss
Recurrent bouts of pancreatitis
Tender subcutaneous fat nodules
Thrombophlebitis
Ascities, portal hypertension
```
52
What are the physical signs in pancreatic carcinoma?
```
Hepatomegaly
Jaundice
Abdominal mass/tenderness
Ascities, splenomegaly
Supraclavicular lymphadenopathy (all above indicate unresectable)
Palpable gallbladder
```
53
How do you investigate pancreatic carcinoma?
Clinical suspicion -> abdominal US +/- CT +/- EUS
If jauncide +/- mass do an ERCP +/- stent (then biopsy)
If mass without jaundice then
EUS/Percutaneos needle biopsy
If carcinoma – CT/EUS/Laparoscopy/laparotomy
Decide if operable/inoperable
54
How do you manage pancreatic cancer?
Palliation of jaundice of jaundice – stent, palliative surgery – cholechoduodenostomy
Pain control
Surgery if you can (<10%)
55
What are the types of surgery available for pancreatic cancer?
Kausch wipple
PPPD
Palliative bypass vs ERCP or PTC stent for obstructive jaundice
Palliative bypass vs duodenual stent for duodenal obstruction
56
What is Kausch wipple surgery?
– bottom part of stomach removed, pancreatic duct removed. Stomach attached to jejunum. Pancreas attached to duodenum
>Very radical, now replaced with PPPD (pyloric preserving)
57
What is PPPD?
Gall bladder + duodenum + head of pancreas removed
| Jejunum mobilised attatched to pyloric sphinter + tail of pancreas + bile duct
58
What is acute pancreatitis?
Acute inflammation of the pancreas, resulting in upper abdominal pain and may be associated with multi-organ failure in several cases (when severe)
59
What is the aetiology of acute pancreatitis?
Alcohol abuse
Gall stones
Trauma – blunt, postop etc
Misc - Drugs, viruses, pancreatic carcinoma, metabolic (calcium, triglycerides inc, dec temp), auto immune
60
What are the local complications of acute pancreatitis?
Acute fluid collections
Pseudocyst
Pancreatic abscess
Pancreatic necrosis
61
What is the pathophysiology of acute pancreatitis?
Alcohol – direct injury leads to increased sensitivity to stimulation – oxidation products buildup and leads to metabolism of these, leading to build-up of fatty acid and ethyl esters
Gallstones – increases pancreatic ductal pressure
ERCP same as above
62
What is the pathogensis of acute pancreatitis?
In general – primary insult leads to release of activated pancreatic enzymes which lead to autodigestion which can lead to either
Pro-inflammatory cytokines and reactive oxygen species
Or oedema, fat necrosis and haemorrhage
63
How does acute pancreatitis present?
```
Abdominal pain
Nausea/vomiting
Collapse
Pyrexia
Dehydration
Abdominal tenderness
Circulatory failure
```
64
How do you investigate acute pancreatitis?
```
Bloods
Abdominal + chest Xrays
Abdominal US
CT (contrast)
Check severity – Glasgow criteria >=3 = severe
```
65
How do you manage acute pancreatitis?
Underlying factors – abstence of alcohol, cholelithaiasis – ERCP + ES, cholecystectomy, stop drugs
>Infection? --> Antibiotics
>Manage gallstones and investigate non-gallstone pancreatitis
>ERCP in gallstone pancreatitis
Collect fluids early – in pseudcyst and PD fistula
Analgesia
Oxygen + acute management
Nutrition
66
What are the complications of acute pancreatitis?
Pancreatic necrosis
Gallstones
Abscess
Pseudocyst
67
How do you manage pancreatic necrosis?
CT guided aspiration – then antibiotics +/- surgery
| Necrostectomy – laparotomy or minimally invasive
68
How do you manage a pancreatic abscess?
Antibiotics + drainage
69
How do you manage pseudocyst of pancreas?
endoscopic drainage or surgery if persistent pain/complications
Treat otherwise Can lead to haemorrhage. Portal hypertension and PD stricture
What is a pseudocyst?
70
What is chronic pancreatitis and who is likely to get it?
Continuing inflammatory disease of pancreas characterised by irreversible morphology leading to chronic pain and/or permanent loss of function
Men > women
Correlation to alcohol
71
What is the aetiology of chronic pancreatitis?
Tumours (adenocarcinoma, IPMT)
Alcohol
CF
Main pancreactic duct obstruction
72
What is the pathogenesis of chronic pancreatitis?
```
Duct obstruction (calculi, inflammation, protein plugs)
Abnormal sphinter of oddi function (spasm (inc pressuer)/relaxation (reflux)
```
73
What is the pathology of chronic pancreatitis?
Glandular atropy and replacement by fibrous tissue
Ducts become dilated, tortous and strictured
Inspissated secretions may calcify
Exposed nerves due to loss of perineural cells
Splenic, superior mesenteric nd portal veins may thrombose -> portal hypertension
74
How does chronic pancreatitis present?
Early asymptomatic
Abdominal pain – linked to binges, become more frequent
Endocrine insufficiency --> diabetes in 30%
Weight loss
Exocrine insuffiency --> fat malabsorption (steatorrhoea), protein malabsorption and decrease in fat soluble vitamins
Jaundice
Upper GI haemorrhage
75
How do you investigate chronic pancreatitis?
```
AXR
US/EUS
CT scan
Blood tests (serum amylase up, albumin down, lfts up)
Pancreatic function tests
```
76
How do you manage chronic pancreatitis?
```
Avoid alcohol
Pancreatic enzyme supplements
Pain manage
low fat, low protein
Endoscopic treatment
Surgery only after full evaluation
Celiac plexus block
Insulin if diabetic
```
77
What interventional procedures are there for pancreatic duct stenosis/obstruction?
Endoscopic PD sphincetortomy, dilation and lithotripsy
78
What are the types of gastric cancer? What do they depend on?
The location of tumour –
sub total, gastrectomy
total gastrectomy + roux en Y reconstruction
79
What is a subtotal gastrectomy?
Cut at pyloric sphincter, and try to preserve top part of stomach (the more preserved better survival)
80
What is a total gastrectomy + roux en Y reconstruction?
Cut at pyloric and cardiac sphincters – total resection of stomach
Cut in small intestine, mobilise tube to end of oesophagus.
Seal pyloric sphincter, and attach open end of duodenum into small intestine to preserve function
81
What are the side effects of a hiatus repair>?
Dysphagia
Difficulty to belch + vomit
Gas bloating/excessive flatulence
Diarrhoea
82
What are the options with bariatric surgery?
Restrictive (decrease size of stomach)
Malabsorptive (resect some of small bowel)
Combination of the two
Combination of patients and surgeons choice
83
What are the advantages of gastric bands?
Relatively minor + reversible+adjustable
| Low complication rate – mortality 0.1%
84
What are the disadvantages of gastric bands?
Dis – requires implanted medical device
Easier to cheat
Risk of prolapse/slippage
15% need further revisional surgery
85
What are the advantages of laprascopic gastric bypass?
Quick + dramatic weight loss
| Pedigree, no dumping syndrome
86
What are the disadvantages of laprascopic gastric bypass?
Disadvantages – more invasive,
malabsorptive component requires life long supplements
More complex if revision is needed
Mortality – 0.5%
87
What are the advantages of sleeve gastrectomy?
Adv – good medium term outcome
No dumping syndrome
No foreign body
No bowel manipulation
88
What are the disadvantages of sleeve gastrectomy?
Disadvantages – more invasive
Long staple line
Short pedigree
Mortality – 0.4%
89
What is a gastric band surgery?
band put in that can be pumped full of saline to restrict size of sphincter
90
What is a gastric bypass?
Y-shaped section of the small intestine is then attached to the pouch to allow food to bypass the lower stomach, the duodenum and the first portion of the jejunum
91
What is a sleeve gastrectomy?
A partial gastrectomy that results in removal of most of the stomach, with the remainder resembling a "banana" or "half moon."
What are the complications of bariatric surgeries?
92
What are the complications of bariatric surgery?
```
Anastomotic leak
DVT/PE
Infection
Malnutrition/vitamin/mineral deficiencies
Hair loss
Excessive skin
```
93
What is steatorrhoea?
Fat malabsorption resulting in high fat content in stool
Stool is less dense and so floats
Very pale and foul smelling
Can have weight loss and low/falling BMI
94
What can cause malabsorption?
```
Coeliac/crohns
Infections
Whiples disease
Amyloid
Diabetes, obstruction
Chronic pancreatitis
CF
```
95
What are the signs of whipples disease?
```
Weight loss
Malabsorption
Abdominal pain
PAS material in villi
Skin, brain joints and cardiac effects
Mostly effects middle aged men
```
96
What are the signs of malabsorption?
Calcium, magnesium + vi D – tetany, osteomalcacia
Vit A – night blindness
Vit K – raised PTR
Vit B – (thiamine – memory, dementia. Niacin – dermatitis, unexplained heart failure)
Vit C – scurvy
97
What is dermatitis herpetiformis?
Cutaneous manifestation of coeliac disease
Blistering of skin on scalp, shoulders, elbows and knees
Intensely itchy
Due to IgA deposit in skin
98
What is the pathology of coeliac disease?
Produces inflammatory response to the gliadin fraction of gluten
Results in partial or subtotal villous atropy
Increased intra epithelial lymphocytes
99
How do you diagnose coeliac disease?
Diagnose with distal duodenal biopsy
Serology – anti-endomysial IgA
Anti-tissue transglutaminase
100
How do you treat coeliac disease?
Withdraw gluten – for life
| Must refer to registered dietician
101
What conditions are associated with coeliac disease?
```
Dermatitis herpetiformis
IDDM
Autoimmune thyroid disease
Automimmune hepatitis
Primary biliary cirrhosis
Autoimmune gastritis
Sjorgren syndrome
IgA deficiency
Down’s syndrome
```
102
What are the complications of coeliac disease?
```
Refractory coeliac disease
Small bowel lymphoma
Oesophageal carcinoma
Colon cancer
Small bowel adenocarcinoma
```
