Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Conditions + definitions > GI 4 > Flashcards

GI 4 Flashcards

1
Q

How is ethanol metabolised?

A

Alcohol dehydrogenase changes it to acetaldehyde

Acetaldehyde dehydrogenase converts to acetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the clinical picture of spontaneous bacterial peritonitis?

A

Abdominal Pain
Fever, Rigors
Renal impairment
Signs of Sepsis, tachycardia, temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you treat SBP?

A

IV antibiotics
Ascitic fluid drainage
IV albumin infusion (20% ALBA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does alcoholic hepatitis present?

A

Jaundice
Encephalopathy
Infection common
Decompensated hepatic function – low albumin and raised prothrombin time/ INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you diagnose alcoholic hepatitis?

A

Raised bilirubin
Raised GGT and AlkP
Alcohol histry
Exclude other causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two types of fatty liver?

A

Steatosis (fatty liver, non alcoholic – NAFLD)

Steatohepatitis ( non alcoholic steatohepatits (NASH))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the three most common motility disorders?

A

Hypermotility
Hypomotility
Achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the features of hypermotility?

A

Corkscrew appearance on Ba swallow.
Idiopathic
Severe, episodes of chest pain +/- dysphagia
Manomerty – hypertonic contractions, uncoordinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do you treat hypermotility?

A

Treatment - smooth muscle relaxants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is hypomotility?

A

Causes failure of LOS mechanism, leading to heartburn/reflux symptoms
Associated with connective tissue disease, diabetes and neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is achalasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the symptoms of achalasia?

A

Symptoms – progressive dysphagia, weight loss, chest pain, regurgitation and chest infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do you treat achalasia?

A

Pharmacological - Nitrates, Calcium Channel blockers
Endoscopic - Botulinum Toxin, Pneumatic balloon dilation
Radiological - Pneumatic balloon dilation
Surgical - Myotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is GORD?

A

Gastro-oesophageal reflux disease
Caused due to pathological acid/bile in lower oesophagus
7% adults experience symptoms, although many experience episodes with no symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the symptoms of GORD?

A

heartburn,
cough,
water brash,
sleep disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the risk factors of GORD?

A 
Pregnancy, 
obesity, 
drugs lowering LOS pressure,  
smoking, 
alcoholism, 
hypomotility, 
male, 
caucasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the aetiology of GROD?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the different types of hiatus hernia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the pathophysiology of GORD?

A

Mucosa exposed to acid pepsin + bile
Increased cell loss and regenerative activity (ie inflammation)
Healing by fibrosis + stricture formation
Erodes oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the complications of GORD?

A

Ulceration
Stricture
Glandular metaplasia (Barrett’s oesophagus)
Carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is Barrett’s oesophagus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the treatment of barrett’s oesophagus?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the treatment of GORD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are te types of oesophageal cancer

Who gets it?

A

Squamous
+ Adenocarcinoma
Men more likely 3x than women

42
Q

What is the presentation of oesophgeal cancer?

A 
Progressive dysphagia
Anorexia/weight loss
Odenyophagia
Chest pain
Cough
Pneumonia (due to trachea-oesophageal fistula)
Vocal cord paralysis
Haematemesis
43
Q

What are the distinguishing features of squamous cell oesophageal carcinoma?

A

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
Q

Where are the two cancers found?

A

Squamous cell - Top and middle thirds

Adenocarcinoma - bottom (distal) third

45
Q

What are the distinguishing features of adenocarcinoma?

A

Occurs in distal oesophagus
Associated with Barrett’s oesophagus (through progression)
Predisposing factors – obesity, male sex, middle age, caucasion

46
Q

How do you investigate oesophageal cancer?

A

Diagnosis by endoscopy/biopsy

Staging – CT scan, endoscopic ultrasound, PET scan, Bone scan

47
Q

How do you treat oesophgeal cancer?

A

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
Q

What is the palative care of oesophgeal cancer?

A

Endoscopic stent, laser/APC, PEG

Chemo, Radiothearpy, Brachtherapy

49
Q

What are the risk factors of pancreatic cancer?

A

Smoking
Chronic pancreatitis
Hereditary
Male

50
Q

What are the pathological types of pancreatic cancer?

A 
75% duct cell mucinous adenocarcinoma
Also can be:
Carcinosarcoma
Acinar cell
Cystadenocarcinoma (better prognosis)
51
Q

How does pancreatic carcinoma present?

A 
Obstructive jaundice!
Diabetes
Abdominal pain/back pain
Anorexia
Vomiting
Weight loss
Recurrent bouts of pancreatitis
Tender subcutaneous fat nodules
Thrombophlebitis
Ascities, portal hypertension
52
Q

What are the physical signs in pancreatic carcinoma?

A 
Hepatomegaly
Jaundice
Abdominal mass/tenderness
Ascities, splenomegaly
Supraclavicular lymphadenopathy (all above indicate unresectable)
Palpable gallbladder
53
Q

How do you investigate pancreatic carcinoma?

A

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
Q

How do you manage pancreatic cancer?

A

Palliation of jaundice of jaundice – stent, palliative surgery – cholechoduodenostomy
Pain control
Surgery if you can (<10%)

55
Q

What are the types of surgery available for pancreatic cancer?

A

Kausch wipple
PPPD
Palliative bypass vs ERCP or PTC stent for obstructive jaundice
Palliative bypass vs duodenual stent for duodenal obstruction

56
Q

What is Kausch wipple surgery?

A

– 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
Q

What is PPPD?

A

Gall bladder + duodenum + head of pancreas removed

Jejunum mobilised attatched to pyloric sphinter + tail of pancreas + bile duct

58
Q

What is acute pancreatitis?

A

Acute inflammation of the pancreas, resulting in upper abdominal pain and may be associated with multi-organ failure in several cases (when severe)

59
Q

What is the aetiology of acute pancreatitis?

A

Alcohol abuse
Gall stones
Trauma – blunt, postop etc
Misc - Drugs, viruses, pancreatic carcinoma, metabolic (calcium, triglycerides inc, dec temp), auto immune

60
Q

What are the local complications of acute pancreatitis?

A

Acute fluid collections
Pseudocyst
Pancreatic abscess
Pancreatic necrosis

61
Q

What is the pathophysiology of acute pancreatitis?

A

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
Q

What is the pathogensis of acute pancreatitis?

A

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
Q

How does acute pancreatitis present?

A 
Abdominal pain
Nausea/vomiting
Collapse
Pyrexia
Dehydration
Abdominal tenderness
Circulatory failure
64
Q

How do you investigate acute pancreatitis?

A 
Bloods
Abdominal + chest Xrays
Abdominal US
CT (contrast)
Check severity – Glasgow criteria >=3 = severe
65
Q

How do you manage acute pancreatitis?

A

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
Q

What are the complications of acute pancreatitis?

A

Pancreatic necrosis
Gallstones
Abscess
Pseudocyst

67
Q

How do you manage pancreatic necrosis?

A

CT guided aspiration – then antibiotics +/- surgery

Necrostectomy – laparotomy or minimally invasive

68
Q

How do you manage a pancreatic abscess?

A

Antibiotics + drainage

69
Q

How do you manage pseudocyst of pancreas?

A

endoscopic drainage or surgery if persistent pain/complications
Treat otherwise Can lead to haemorrhage. Portal hypertension and PD stricture
What is a pseudocyst?

70
Q

What is chronic pancreatitis and who is likely to get it?

A

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
Q

What is the aetiology of chronic pancreatitis?

A

Tumours (adenocarcinoma, IPMT)
Alcohol
CF
Main pancreactic duct obstruction

72
Q

What is the pathogenesis of chronic pancreatitis?

A 
Duct obstruction (calculi, inflammation, protein plugs)
Abnormal sphinter of oddi function (spasm (inc pressuer)/relaxation (reflux)
73
Q

What is the pathology of chronic pancreatitis?

A

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
Q

How does chronic pancreatitis present?

A

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
Q

How do you investigate chronic pancreatitis?

A 
AXR
US/EUS
CT scan
Blood tests (serum amylase up, albumin down, lfts up)
Pancreatic function tests
76
Q

How do you manage chronic pancreatitis?

A 
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
Q

What interventional procedures are there for pancreatic duct stenosis/obstruction?

A

Endoscopic PD sphincetortomy, dilation and lithotripsy

78
Q

What are the types of gastric cancer? What do they depend on?

A

The location of tumour –
sub total, gastrectomy
total gastrectomy + roux en Y reconstruction

79
Q

What is a subtotal gastrectomy?

A

Cut at pyloric sphincter, and try to preserve top part of stomach (the more preserved better survival)

80
Q

What is a total gastrectomy + roux en Y reconstruction?

A

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
Q

What are the side effects of a hiatus repair>?

A

Dysphagia
Difficulty to belch + vomit
Gas bloating/excessive flatulence
Diarrhoea

82
Q

What are the options with bariatric surgery?

A

Restrictive (decrease size of stomach)
Malabsorptive (resect some of small bowel)
Combination of the two
Combination of patients and surgeons choice

83
Q

What are the advantages of gastric bands?

A

Relatively minor + reversible+adjustable

Low complication rate – mortality 0.1%

84
Q

What are the disadvantages of gastric bands?

A

Dis – requires implanted medical device
Easier to cheat
Risk of prolapse/slippage
15% need further revisional surgery

85
Q

What are the advantages of laprascopic gastric bypass?

A

Quick + dramatic weight loss

Pedigree, no dumping syndrome

86
Q

What are the disadvantages of laprascopic gastric bypass?

A

Disadvantages – more invasive,
malabsorptive component requires life long supplements
More complex if revision is needed
Mortality – 0.5%

87
Q

What are the advantages of sleeve gastrectomy?

A

Adv – good medium term outcome
No dumping syndrome
No foreign body
No bowel manipulation

88
Q

What are the disadvantages of sleeve gastrectomy?

A

Disadvantages – more invasive
Long staple line
Short pedigree
Mortality – 0.4%

89
Q

What is a gastric band surgery?

A

band put in that can be pumped full of saline to restrict size of sphincter

90
Q

What is a gastric bypass?

A

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
Q

What is a sleeve gastrectomy?

A

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
Q

What are the complications of bariatric surgery?

A 
Anastomotic leak
DVT/PE
Infection
Malnutrition/vitamin/mineral deficiencies
Hair loss
Excessive skin
93
Q

What is steatorrhoea?

A

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
Q

What can cause malabsorption?

A 
Coeliac/crohns
Infections
Whiples disease
Amyloid
Diabetes, obstruction
Chronic pancreatitis
CF
95
Q

What are the signs of whipples disease?

A 
Weight loss
Malabsorption
Abdominal pain
PAS material in villi
Skin, brain joints and cardiac effects
Mostly effects middle aged men
96
Q

What are the signs of malabsorption?

A

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
Q

What is dermatitis herpetiformis?

A

Cutaneous manifestation of coeliac disease
Blistering of skin on scalp, shoulders, elbows and knees
Intensely itchy
Due to IgA deposit in skin

98
Q

What is the pathology of coeliac disease?

A

Produces inflammatory response to the gliadin fraction of gluten
Results in partial or subtotal villous atropy
Increased intra epithelial lymphocytes

99
Q

How do you diagnose coeliac disease?

A

Diagnose with distal duodenal biopsy
Serology – anti-endomysial IgA
Anti-tissue transglutaminase

100
Q

How do you treat coeliac disease?

A

Withdraw gluten – for life

Must refer to registered dietician

101
Q

What conditions are associated with coeliac disease?

A 
Dermatitis herpetiformis
IDDM
Autoimmune thyroid disease
Automimmune hepatitis
Primary biliary cirrhosis
Autoimmune gastritis
Sjorgren syndrome
IgA deficiency
Down’s syndrome
102
Q

What are the complications of coeliac disease?

A 
Refractory coeliac disease
Small bowel lymphoma
Oesophageal carcinoma
Colon cancer
Small bowel adenocarcinoma

Conditions + definitions (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions