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Year 2 - Semester 1 > Gastro - week 3 > Flashcards

Gastro - week 3 Flashcards

1
Q

what happens when swallowing is initiated

A

Upper oesophageal sphincter relaxes
Primary peristaltic wave triggered

Lower oesophageal sphincter relaxes as soon as swallowing is initiated

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2
Q

what kind of muscle does the oesophagus have

A

striated muscle

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3
Q

what are some signs of oesophageal disease

A 
•	Common
o	Dysphagia
o	Odynophagia
o	Heartburn 
o	Acid regurgitation
o	Waterbrash

•	Less common
o	Chest pain
o	Food regurgitation
o	Food bolus obstruction
o	Globus (sensation that there is something at the 
        back of the throat)
o	Cough
o	Dysphonia
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4
Q

what are the symptoms of oesophageal cancer

A

Very few symptoms for oesophageal cancer until late state where patients have dysphagia for solids and then liquids at which point the tumour is quite advanced

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5
Q

describe dysphagia

A

• Alarm symptom for immediate evaluation

•	Classified as either
o	Oropharyngeal
	Neuromuscular 
	Skeletal muscular disorders
	Mechanical obstruction
	Miscellaneous 
•	Decreased saliva
•	Alzheimers	
•	depression
o	Oesophageal  (when the patient can swallow food into the oesophagus but then becomes stuck)
	Mechanical obstruction
	Motility disorders
	Miscellaneous
•	Diabetes
•	Alcoholism
•	GORD
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6
Q

what are clinical signs of oesophageal disease

A
  • Dental erosion in GORD
  • Weight loss
  • Anaemia
  • Lymphadenopathy
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7
Q

describe GORD

A 
Reflux with transient lower oesohageal relaxations
o	More common
o	Daytime reflux
o	Small or no hiatus hernia (when the top of the stomach slides through the diaphragm)
o	Often no oesophagitis
•	Reflux with low lower oesophageal sphincter pressures
o	Less common (20%)
o	Nocturnal reflux
o	Often large HH
o	More severe oesophagitis
o	Barrett’s
•	Typical symptoms
o	Heartburn
o	Acid regurgitation
o	Water brash
o	Often meal related
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8
Q

what are the investigations for oesophageal disease

A 
•	Endoscopy
•	Barium swallow
•	Oesophageal function tests (manometry, pH and impedence monitoring)
•	If suspicion of cancer
o	Urgent upper GI endoscopy
o	CT
o	CT-PET
o	Endoscopic ultrasound
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9
Q

describe barrett’s oesophagus

A
  • Specialised intestinal metaplasia in the lower oesophagus
  • Commonest in obese men >50
  • Often asymptomatic
  • Premalignant
  • Surveillance for patients and ablation to remove abnormal tissue if low grade dysplasia is found
  • Treat GORD with long term with PPI
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10
Q

what are some complications of GORD

A
  • Oesophagitis
  • Peptic stricture
  • Barrett’s oesophagus
  • Adenocarcinoma
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11
Q

what is the treatment for GORD

A 
•	Lifestyle changes
o	Smoking
o	Alcohol
o	Diet
o	Weight reduction
•	Mechanical
o	Posture, clothing, elevate bed-head
•	Antacids
•	Acid suppression – PPI
•	Surgery
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12
Q

describe achalasia

A

• Failure of LOS relaxation
• Absence of peristalsis
• 1/100,000 incidence
• Degenerative lesion of oesophageal innervation
• Typically present in younger people with
dysphagia equal for liquids and solids
o Also often weight loss and chest pain
• Endoscopic appearances usually normal
• Can progress to oesophageal dilatation and respiratory complication (infection)
• Treatment
o Dilating and disrupting the LOS with endoscopic
dilatation
o botox is very effective but not long lasting
o surgical myotomy
o POEM – incision in the wall of the oesophagus to
cut the oesophageal sphincter

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13
Q

describe eosinophilic oesophagitis

A

• Commonly presents with food bolus obstruction, dysphagia
• Younger age, M>F, 50/100,000 incidence
• History of atopy (asthama, hayfever)
• Endoscopy – furrows, rings, strictures, exudates which are lumpy areas in the oesophagus
• Biopsy for diagnosis - >15 eosinophils / high power field - 3 from lower, 3 from mid
• Treatment
o Diet – elimination of egg, wheat, milk, nuts, soya, fish
o Drugs – PPI, topical steroids (main treatment)
o Dilatation for strictures

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14
Q

describe an oesophageal stricture

A

• Narrowing of gullet

• Benign
o GORD – 10%
o Barrett’s
o Extrinsic compression - masses in mediastinum or
lung
o Post-radiotherapy
o Anastomotic following surgery/oesophagectomy
o Rings and webs – often associated with acid reflux
o Accidental or suicidal ingestion of corrosives

• Malignant
o Oesophageal cancer

• Treatment
o PPI
o Dilatation of the narrowed oesophagus

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15
Q

describe oesophageal cancer

A 
•	Adenocarcinoma
o	Lower third 
o	Younger
o	Reflux – barrett’s 
o	Obesity
o	More common
o	Increasing

•	Squamous cell
o	Mid, upper oesophagus
o	Older
o	Smoking
o	Alcohol
o	Less common
o	Declining

• Palliation aims for malignant strictures
o To relieve symptoms without necessarily altering the course of the disease by dilating the oesophagus to help the patient swallow and improve quality of life

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16
Q

what are some tips for diagnosing elderly patients

A

o Neurological – particularly if intermittent or long standing

o Oesophageal cancer - if new, progressive, with
regurgitation and weight loss
 Presents with progressive dysphagia for
solids and then liquids

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17
Q

what are some tips for diagnosing patients who arent elderly

A

o Dysmotility
 Achalasia
 Or secondary to acid reflux
 Dysphagia equal for liquids and solids

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18
Q

what is the likely dianosis for a young patient with food bolus obstruction

A

o Eosinophilic oesophagitis
• If hoarse voice think ENT causes
• If regurgitation of food from previous days think
pharyngeal pouch

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19
Q

describe the helicobacter breath test

A

• Drink C13 urea which would be split be helicobacter into ammonia and C13 CO2 which could be detected in the breath

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20
Q

what is the treatment for helicobacter

A 
•	First line (90% efficacy)
o	Lansoprazole
o	Clarithromycin 
o	Metronidazole
o	All for one week
•	Second line
o	Lansoprazole
o	Clarithromycin
o	Amoxycillin
o	For one week
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21
Q

what is the qFIT test for

A

quantitative faecal immunochemical test

screening for colorectal cancer
• Detects hidden or “occult” blood in stool
• Uses antibodies for human haemoglobin

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22
Q

describe colonic polyps

A
  • Not all colonic polyps progress to adenocarcinoma
  • Adenomas have the highest progression potential to adenocarcinoma
  • Hyperplastic polyps don’t have malignant potential
  • A special type of hyperplastic polyp called serrated polyp has some malignant potential
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23
Q

describe the APC protein

A

The APC protein (tumour suppressor) is encoded by the APC gene, a negative regulator that controls beta-catenin concentrations and interacts with E-cadherin which are involved in cell adhesion. Deletion of this gene predisposes to cancer

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24
Q

what are alarm features of colorectal cancer

A
  • Weight loss
  • Rectal bleeding
  • Anaemia, thrombocytosis
  • Persistent diarrhoea
  • Frequent nocturnal symptoms
  • New onset over 50 years
  • FHx bowel cancer
  • PMHx IBD
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25
what are risk factors for colorectal cancer
* Diet high in red meats and processed meats * Cooking meats at very high temperatures * Diet low in fibre * Obesity * Physical inactivity * Smoking * Alcohol excess * FHx of colorectal polyps or cancer * History of IBD * Older age
26
where are most colorectal cancers
Around 2/3rd of colorectal cancers in rectum, sigmoid and descending colon (i.e. left side)
27
causes of mucosal injury
``` • GI tract secretions o Acid and pepsin in stomach o Biliary and pancreatic secretions • Ischaemia • Drugs o NSAIDs, antibiotic, steroids o Chemotherapy • Immunological o Coeliac disease • Infections • Radiation • Trauma • Idiopathic ```
28
manifestations of mucosal injury
* Inflammation * Apoptosis or necrosis * Erosion and ulceration * Hypoplasia and atrophy * Hyperplasia * Metaplasia * Dysplasia +/- neoplasia
29
what is the sydney system of classifying gastritis
``` • Acute gastritis o Acute erosive/ haemorrhagic gastritis  Ingestion of irritants o Acute H. pylori infection  Usually no symptoms ``` ``` • Chronic gastritis o Non-atrophic  Chronic H. pylori o Atrophic  Autoimmune gastritis  Chronic H. pylori ``` ``` • Chronic gastritis (special forms) o Chemical  Bile reflux, NSAIDs o Radiation gastritis o Lymphocytic o Non-infectious granulomatous gastritis  Crohn’s disease or sarcoidosis o Eosinophilic gastritis  Food sensitivities o Other infectious agents ```
30
possible aetiologies of IBD
• Infection? • Loss of tolerance to commensal bacteria? • Familial/genetic component o Having a family member with IBD is greatest risk factor • Environmental factors o Food antigens o Smoking (may be protective vs UC)
31
what is important to remember UC and crohn's?
Need to take biopsies from multiple sites Crohn’s can affect any part of the GI tract 70% of crohn’s cases have granulomas Malabsorption, strictures and fistulas only in crohn’s
32
what are some mimics of IBD
``` • Infective colitis • Ischaemic colitis o Most common in splenic flexure and descending bowel. • Diverticular disease o Most common in sigmoid colon • Drug induced colitis • Radiation colitis • Neoplasia ```
33
describe microscopic colitis
watery diarrhoea in older patients – normal endoscopy Increase in chronic inflammation cells in lamina propria – lymphocytic or collagenous Cause often not identified Lymphocytic colitis can be associated with coeliac disease Drugs implicated in some cases Can be treated with steroids
34
what is malabsorption
defective mucosal uptake and transport of adequately digested nutrients. Selective or global
35
what is maldigestion
impaired breakdown of nutrients, luminal phase e.g. pancreatic insufficiency
36
what is malassimilation
encompasses both malabsorption and maldigestion
37
what can cause malabsorption in the luminal phase
• Nutrient hydrolysis o Enzyme deficiency: pancreatic insufficiency o Enzyme deactivation: ZE syndrome o Inadequacy of mixing: rapid transit, surgical resection • Fat solubilization o Decreased bile salts: cholestasis o Bile salt deconjugation: bacterial overgrowth o Bile salt loss: ileal disease or resection • Lumenal availability o Bacterial consumption of nutrients (bacterial overgrowth: B12 deficiency o Decreased intrinsic factor (pernicious anaemia) : B12 deficiency
38
what can cause malabsorption in the mucosal phase
• Brush border hydrolysis: lactase deficiency (post gastroenteritis, radiation, alcohol) ``` • Epithelial transport o Reduced absorptive surface – resection o Damaged absorptive surface – coeliac disease, tropical sprue, crohn’s disease, ischaemia o Infections – giardia, SIBO o Infiltration – lymphoma, amyloid ```
39
what can cause malabsorption in the post-mucosal phase
• Post-absoptive processing | o Lymphatic obstruction
40
clinical symptoms of malabsorption
* Diarrhoea and weight loss despite adequate intake * Bloating, distention, cramps, borborygmi * Lethargy and malaise * Symptoms often mild, non-specific * Malabsorption can be global, or specific nutrients * Malabsorption syndrome (steatorrhoea, distention, weight loss, oedema) is a rare presentation
41
clues in history for malabsorption
* Weight loss * Diarrhoea, steatorrhoea * Abdominal distention/gas * Intestinal “angina” after eating * Metabolic bone disease * GI surgery * Pancreatitis * Cystic fibrosis * Alcohol * FHx coeliac
42
evidence of malabsorption
• Skin o Angular cheilitis (corners of mouth cracking) , glossitis (tongue inflammation) o Dermatitis herpetiformis o Oedema (rare) • Neurologic (B12) o Peripheral neuropathy o Ataxia (posterior column) o Psychosis, dementia
43
lab clues for malabsorption
* Microcytosis: iron deficiency (common in coeliac, otherwise suspect GI blood loss) * Macrocytosis: B12, folate deficiency but also common in coeliac, alcohol * Elevated ALP +/- low Ca * Hypoalbuminaemia * Evidence of multiple nutritional deficiencies
44
diagnostic testing for the 3 most common conditions
o Tissue transglutaminase (TTG) – coeliac disease o Faecal elastase – pancreatic insufficiency o Glucose H2 breath test – SIBO • Then if clinically suspected move on to more targeted testing
45
what types of investigation might you do if the 3 common causes of malabsorption are negative
* Microbiology of stool (giardia) * Faecal calprotectin (crohn’s) * 7alpha-cholestenone or SeHCAT test (bile acid malabsorption) * Lactose H2 breath test * Small intestine biopsy (many things like definitive coeliac diagnosis) * Small bowel imaging (stricture in crohn’s) * CT/CT angiogram
46
what are the effects of coeliac's
o Mucosal inflammation o Villous atrophy o Crypt hyperplasia
47
what triggers coeliac's
• Occurs upon exposure to gluten in the diet | o Triggers gliaden-reactive t lymphocytes
48
describe the genetic predisposition to coeliac's
o About ¼ of people have the genes for it but not known why some people get it and some don’t o Prevalence up to 1/100 o Many subclinical or asymptomatic o Iceberg of coeliac disease where a small number are diagnosed, many more are asymptomatic and even more have the potential to get it
49
what is the clinical picture of coeliac's
``` o Diarrhoea o Anaemia o Dyspepsia o Abd pain/ bloating o Weight loss o Mouth ulcers o Fatigue o Neuropsychiatric symptoms ```
50
what are investigative clues of coeliac's
``` o Anaemia (microcytic/macrocytic) o Iron/folate deficiency o Macrocytosis without anaemia o Hyposplenic blood film o Low calcium, elevated Alkaline phosphatase o Raised transaminases o Hypoalbuminaemia (severe cases) ```
51
what diseases are caused by coeliac's
```  Osteoporosis  Infertility  Dermatitis herpetiformis  Lymphocytic colitis  Ulcerative jejunitis  Lymphoma of the small intestine ```
52
what diseases are associated with (not caused by) coeliac's
``` o Type 1 diabetes o Downs syndrome o Thyroid disease o Autoimmune liver disease o Sjogrens syndrome o Cerebellar ataxia ```
53
how do you diagnose coeliac's
o Anti-tissue transglutaminase antibody (IgA)  Sensitivity and specificity >95% o Small intestinal biopsy
54
describe pancreatic insufficiency
* Produces 1.5L/day of bicarbonate and enzyme rich fluid * Enzymes for fat, protein and Carb digestion * Lipolytic activity declines first – fat absorption mainly affected * Overt clinical consequences unlikely unless >90% of function lost * Steatorrhoea, weight loss, vitamin deficiency (A, D, E, K)
55
what are the causes of pancreatic insufficiency
``` o Chronic pancreatitis  Alcohol • 80% present with pain  Duct obstruction • Tumours, stones  Cystic fibrosis  Systemic disease e.g. SLE  Autoimmune (IgG4) pancreatitis ``` o Pancreatic cancer o Cystic fibrosis  Autosomal recessive  Impairment of bicarbonate and chloride secretion – thick sticky mucous  85% effected, starts early o Haemochromatosis o Pancreatic resection o Gastric resection
56
how do you diagnose pancreatic insufficiency
``` o Risk factors o Symptoms o Imaging o Tests for function  Direct – secretin stimulation tests  Indirect – faecal elastase, pancreolauryl ```
57
how do you treat pancreatic insufficiency
o Enzyme replacement o Taken with meals and snacks o Gastric acid suppression o Vitamin supplements
58
what is the distribution of bacteria in the bowel like usually
* Normally 105 to 109 bacteria/ml present in distal small bowel * Colon has up to 1012/ml * Mostly gram negative aerobic in ileum, gram positive anaerobic in colon * In bacterial overgrowth this balance is lost
59
what other diseases is SIBO a feature of
Liver disease, IBS, obesity, CF, coeliac disease
60
what are the causes of SIBO
``` o Stasis  Strictures • Crohn’s • TB  Hypomotility • Old age • Opiate analgesics • Diabetes • Systemic sclerosis ``` o Blind loops  Gastric bypass for obesity etc
61
what are the concequences of SIBO
``` o Vit B12 malabsorption o Bile acid deconjugation o Intraluminal protein utilization o Brush border damage o Ulceration of mucosa o Bowel dysmotility ```
62
how do you diagnose SIBO
o Culture of jejunal fluid but this is cumbersome and not routine o Glucose/hydrogen breath test more practical – not that accurate  Human metabolism doesn’t produce hydrogen but bacteria do
63
how do you treat SIBO
o 2 weeks of antibiotics (tetracycline, ciprofloxacin, rifaximin) o Repeat treatment often needed
64
describe bile salt malabsorption
• Bile acids specifically absorbed in the distal ileum • Disease or resection of distal part of small intestine leads to malabsorption • Bile salts can irritate colonic mucosa • Leads to secretory diarrhoea • Also impaired in post-cholecystectomy, rapid transit and other malabsorptive states • Primary BAM may reflect over production rather than malabsorption • Types o Type 1 – ileal disease or resection (maybe due to crohn’s) o Type 2 – idiopathic o Type 3 -associated with post-cholecystectomy, rapid transit, coeliac, SIBO, chronic pancreatitis.
65
how do you treat bile salt malabsorption
o Cholestyramine and colesevelam  Bind to bile acids and stop them irritating the bowel
66
describe giardia
``` • Non-invasive • Malabsorption due to many factors o Brush border damage o Reduction in absorptive surface o Bile acid utilization o Induction of hypermotility o Enterotoxin • Metronidazole is very effective ```
67
describe whipples disease
* Uncommon disease of older men * Presents with diarrhoea, arthritis, cough, headache, muscle weakness * Antibiotic therapy from months to years

Year 2 - Semester 1 (13 decks)

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