Brainscape's Knowledge GenomeTM

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


See full index

med 2a > GI > Flashcards

GI Flashcards

1
Q

UC: Pathophysiology / what does it look like under a mc? / histology?

A
  1. Crypt abscess.
  2. Increase in plasma cells in the lamina propria.

Continuous inflammation affecting ONLY the mucosa.!!!!
Microscopic:
• Mucosal inflammation - inflammation DOES NOT GO DEEPER e.g. transmural

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

UC: management?

A

Anti-inflammatories

For mild/moderate UC:
Mesalazine.

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

UC: define?

Affects which part of bowel? (3 TYPES)

A

which affects ONLY the COLON
Relapsing and remitting inflammatory disorder of the COLONIC MUCOSA

  1. may affect just the rectum - proctitis (50%) - most common!!!
  2. rectum and left colon - left-sided colitis (30%) !!!
  3. entire colon (entire large bowel) UP TO the ILEOCAECAL VALVE - pancolitis/extensive colitis (20%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

UC: complications?

A
  1. Colon: blood loss and colorectal cancer.!!!!
  2. JOINTS - Arthritis., ANKYLOSING SPONDYLITIS!!
  3. EYES - Iritis and episcleritis.
  4. Fatty liver and PRIMARY SCLEROSING CHOLANGITIS!!!
  5. SKIN — Erythema nodosum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

UC: epidemiology?

PROTECTIVE FACTORS?

A

Higher incidence than Crohn’s per year

Affects males and females equally

Is 3 times more common in NON/EX SMOKERS - symptoms may relapse on stopping of smoking!!!
Is a PROTECTIVE FACTOR against UC

Appendicectomy = also PROTECTIVE FACTOR

Cause is UNKNOWN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

UC: symptoms?

A
  • Runs a course of remissions and exacerbations
  • Restricted pain usually in LOWER LEFT QUADRANT
  • Episodic or chronic diarrhoea with blood and mucus
  • Cramps
  • Bowel frequency linked to severity
  • In acute UC there may be fever, tachycardia and tender distended abdomen
  • In acute attack patients have bloody diarrhoea (passing 10-20 liquid stools per day), diarrhoea also occurs at night, with urgency and incontinence that is severely disabling
  • Extraintestinal signs; clubbing, aphthous oral ulcers, erythema nodusum (red round lumps below skin surface)and amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

UC: investigations?

Gold standard?

A

Blood tests:
• White cell count and platelets raised in moderate/severe attacks
• Iron deficiency anaemia
• ESR and CRP raised
• Liver biochemistry may be abnormal
• Hypoalbuminaemia is severe disease
• pANCA (Anti-neutrophilic cytoplasmic antibody) may be positive (in Crohn’s this is negative)

Stool samples; to exclude C.diff and Campylobacter etc. - Faecal calprotectin - indicates IBD but not specific

Colonoscopy with mucosal biopsy:
• GOLD STANDARD for diagnosis
• Allows for assessment of disease activity and extent
• Can see inflammatory infiltrate, goblet cell depletion, crypt abscesses and mucosal ulcers

Abdominal X-ray:
Useful when UC too severe for colonoscopy

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

CD: define

A

can affect ANY PART of the GI tract (mouth-anus)

A chronic inflammatory GI disease characterised by transmural (goes deep into mucosa) granulomatous inflammation affecting ANY part of the gut from mouth to anus (especially in TERMINAL ILEUM and PROXIMAL COLON)

Unlike in UC, there is unaffected bowel BETWEEN areas of active disease - these are SKIP LESIONS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CD: Pathophysiology / histology?

A

Patchy, granulomatous, transmural inflammation (can affect just the mucosa or go through the bowel wall - Inflammation EXTENDS through ALL LAYERS (transmural) of the bowel).

Macroscopic:
• NOT CONTINUOUS i.e. there are SKIP LESIONS/patchy areas where there is a gap between affected and unaffected mucosa

Granulomas present in 50-60% - these are non-caseating epithelioid cell aggregates with Langhans’s giant cells

Increase in chronic inflammatory cells and there is lymphoid
hyperplasia

• Less crypt abscesses’ than UC

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

CD: aetiology? And risk factors?

A

Cause is UNKNOWN but
May be caused by
BUT could be caused by a non-functioning mutation in NOD2!!!!!

  • Genetic association is stronger in CD than in UC:
    • Mutations on NOD2 (CARD 15) gene on chromosome 16 increases risk
  • Smoking
  • NSAIDs may exacerbate disease
  • Family history
  • Chronic stress and depression triggers flares
  • Good hygiene - those who live in poor hygiene families have a lower risk of developing CD
  • Appendicectomy may increase the risk of CD development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CD: symptoms?

A
  • Diarrhoea with urgency (need to go 5-6 times in 45 mins), bleeding and pain due to deification
  • Abdominal pain - can present as an emergency with acute right iliac fossa pain mimicking appendicitis SOMETIMES RIF PAIN!!!
  • Weight loss
  • Malaise
  • Lethargy
  • Anorexia
  • Abdominal tenderness/mass
  • Perianal abscess
  • Anal strictures
  • Extraintestinal signs; aphthous oral ulcerations, clubbing, skin, joint & eye problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CD: investigations?

A
  • Examination:
    • Tenderness of RIGHT ILIAC FOSSA
    • Anal examination
  • Bloods:
    • Anaemia is common due to malabsorption and thus deficiency of iron and folate
    • However, despite terminal ileal involvement, B12 anaemia is unusual
      • Raised ESR and CRP
      • Raised white cell count and platelets
      • Hypoalbuminaemia present in severe disease as part of an acute phase response to inflammation associated with a raised CRP
      • Liver biochemistry may be abnormal
      • NEGATIVE pANCA
  • Stool sample to exclude C.difficile and Campylobacter - Faecal calprotectin - indicates IBD but not specific
  • Colonoscopy:
    • Biopsy to confirm will see spot lesions and granulomatous transmural inflammation
  • Upper GI endoscopy:
    • Exclude oesophageal and gastroduodenal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CD: management?

A

Anti-inflammatories

  • Smoking cessation
  • Anaemia due to iron, B12 or folate should be treated with replacement

Mild attacks:
• Controlled-release corticosteroids e.g. BUDESONIDE -
]

Moderate to severe attacks:
• Glucocorticoids e.g. ORAL PREDNISOLONE - reduce dose every 2-4 weeks if symptoms resolve

Severe attacks:
IV HYDROCORTISONE

Maintain remission:
• AZATHIOPRINE - side effects; bone marrow suppression, acute
pancreatitis and allergic reactions
• METHOTREXATE if intolerant of azathioprine

Surgery:
• 80% require surgery at some point
• Avoided and only minimal resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

IBS: define

A

Denotes a mixed group of abdominal symptoms for which no organic cause ca be found

A FUNCTIONAL BOWEL DISORDER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IBS: epidemiology?

A
  • Age of onset is under 40
  • More common in FEMALES than males
  • Common, in western world around 1 in 5 report symptoms consistent with IBS -
  • Symptoms are exacerbated by stress, food, gastroenteritis or menstruation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IBS: aetiology?/TRIGGERS

A
  • Depression, anxiety
  • Psychological stress and trauma •
  • GI infection
  • Sexual, physical or verbal abuse •
  • Eating disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IBS: 3 types?

A

IBS-C - with constipation
• IBS-D - with diarrhoea
• IBS-M - with constipation and diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

IBS: Pathophysiology?

A

Multi factorial pathophysiology

The following factors can all contribute to IBS:

  • Psychological morbidity / mood / stress e.g. trauma in early life.
  • Abnormal gut motility.
  • Genetics.
  • Altered gut signalling (visceral hypersensitivity).

Also altered gut microbiota
And post GI infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

IBS: symptoms?

A
  1. ABDOMINAL PAIN!
  2. Bloating.
  3. Change in bowel habit.
    (Top 3)!!!!
    ABC!!!!
  4. Pain is relieved on defecation. !!!!!
  5. Mucus.
  6. Fatigue.

Painful period
• Urinary frequency, urgency, nocturia and incomplete emptying of bladder
• Back pain

Symptoms are chronic (more than 6 months) and exacerbated by stress, menstruation or gastroenteritis (post-infection IBS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

IBS: DDx?

A
  1. Coeliac Disease
  2. Lactose intolerance.
  3. Bile acid malabsorption.
  4. IBD.
  5. Colorectal cancer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

IBS: investigations?

A
  1. Bloods - FBC (anaemia), U+E, LFT.
  2. CRP. —> inflammation
  3. Coeliac serology. —

Colonoscopy to rule out IBD or colorectal cancer

Faecal calprotectin - raised in IBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

IBS: management?
For mild IBS?
Moderate IBS>
Severe IBS?

A

MILD IBS
Education, reassurance, dietary modification e.g. FODMAP.

MODERATE IBS
Pharmacotherapy and 
• Psychological treatment
- Antispasmodics for pain.
- Laxatives for constipation. 
- Anti-motility agents for diarrhoea. 
- CBT and hypnotherapy.

SEVERE IBS:
MDT approach, referral to specialist pain treatment centres.
- Tri-cyclic anti-depressants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In someone with coeliac disease, what are they most likely to be deficient in - iron, folate, or B12?

A

Iron.

Coeliac disease mainly affects the duodenum and iron is absorbed in the duodenum. Folate is absorbed in the jejunum and B12 in the terminal ileum.

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

Coeliac Disease: pathophysiology????!!!

Name the break down product of gluten digestion that can trigger coeliac disease.

A

Duodenum is mainly affected by coeliac disease

T-cell mediated autoimmune disease of the small bowel in which PROLAMIN (alcohol-soluble proteins in wheat, barley, rye and oats) intolerance causes villous atrophy and malabsorption

Gliadin (product of gluten digestion) = immunogenic.
It can have direct toxic effects by up-regulating the innate immune system or HLADQ2 can present it to T helper cells in the lamina propria -> inflammation -> villi atrophy -> malabsorption.

Gliadin.

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

Coeliac Disease: symptoms?

Suspect in all if they have??

A

SUSPECT in ALL with DIARRHOEA, WEIGHT LOSS or ANAEMIA (especially if iron or B12 deficient)

  1. Diarrhoea.
  2. Weight loss.
  3. Irritable bowel.
  4. Iron deficiency anaemia.
  5. Mouth ulcers. !!!!!!!!!!!!
  6. Abnormal liver function.

Steatorrhoea - stinky/fatty stool!!!!!!!!!!!!!!!
Abdominal pain
N and V
- Osteomalacia - softening of bones due to impaired bone metabolism due to lack of phosphate, calcium and vitamin D leading to OSTEOPOROSIS (40-60% risk in untreated patients leading to fracture risk)
- Dermatitis hepetiformis - red raised patches, often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks!!!!!!!!!!!!!!!!!!!

1/3 are asymptomatic (silent disease) and only detected on routine blood tests (raised MCV)

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

Coeliac Dx: investigations?

Gold standard?

What 3 histological features are needed in order to make a diagnosis of coeliac disease?

A
  1. Serology - look for auto-antibodies - TTG and EMA.
    - Both are IgA antibodies
    - These correlate with the severity of mucosal damage and can thus be used fro dietary monitoring
  2. Gastroscopy - duodenal biopsies. - -gold standard!!
    Duodenal biopsy is the gold standard for diagnosis:
    • See villous atrophy, crypt hyperplasia and increased intraepithelial
    white cell count - seen histologically
    • All reverse on gluten free diet

FBC:
• Low Hb
• Low B12
• Low ferritin

  1. Raised intraepithelial lymphocytes.
  2. Crypt hyperplasia.
  3. Villous atrophy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Coeliac Dx: risk factors?

What disorders might be associated with coeliac disease?

A
  • IgA deficiency
  • Breast feeding
  • Age of introduction to gluten into diet
  • Rotavirus infection in infancy increases risk
    And below !!

Other autoimmune disorders: since having one will increase risk of others:
1. T1 diabetes.

  1. Thyroxoicosis.
  2. Hypothyroidism.
  3. Addison’s disease.
    Osteoporosis is also ckmnly seen in those w coeliac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Coeliac Dx: epidemiology?

A
  • Around 1% of population affected
  • Occurs at any age but peaks in infancy and 50-60yrs
  • Affects males and females equally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Coeliac Dx: management?>

A

Lifelong gluten free diet i.e. no prolamins - use serum antibody testing for monitoring:
• Eliminate wheat, barley and rye - results in days/weeks
• Poor compliance is main reason for recurrent issues
• Oats usually tolerated unless contaminated with flour during production • Meat, dairy product, fruits and vegetables are all gluten-free

Correction of vitamin and mineral deficiencies e.g. B12, folate, iron, calcium and vitamin D
DEXA scan to monitor osteoporotic risk

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

GORD: symptoms

A
  1. Heart burn.
  2. Acid reflux.
  3. Dysphagia.

Belching

  • Food/Acid brash (food, acid or bile regurgitation)
  • Water brash (increased salivation)
  • Odynophagia (painful swallowing)

Extra-oesophageal:
• Nocturnal asthma
• Chronic cough
• Laryngitis (hoarseness and throat clearing) • Sinusitis

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

GORD: define and pathophysiology????!!

A

reflux of stomach contents (acid with/without bile) causes troublesome symptoms (defined as 2 or more heartburn episodes a week) and/or complications

Reflux of gastric contents is normal but when there is prolonged contact of gastric contents with the mucosa this results in clinical symptoms

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

GORD: management?

A
  1. PPI. 2ND LINE = H2 ANTAGONISTS EG RANITIDINE And other meds —- antacids, alginates,
  2. Lifestyle modification.
    Encourage weight loss
    • Smoking cessation
    • Small, regular meals
    • Avoid; hot drinks, alcohol, citrus fruits and eating less than 3 hours before be
  3. Anti-reflux surgery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

GORD: aetiology?

A
  1. Lower oesophageal sphincter hypotension •
  2. Hiatus hernia:
    - Sliding hiatus hernia (80%):
    • Where the gastro-oesophageal junction and part of the stomach ‘slides’ up into the chest via the hiatus so that it lies above the diaphragm
    • Acid reflux often happens as the lower oesophageal sphincter become less competent in many cases
    - Rolling or para-oesophageal hiatus (20%):
    • Where the gastro-oesophageal junction remains in the abdomen but part of the fundus of the stomach prolapses through the hiatus alongside the oesophagus
    • NOTE: as the gastro-oesophageal junction remains intact, reflux is UNCOMMON
  3. Loss of oesophageal peristaltic function •
  4. Abdominal obesity
  5. Gastric acid hypersecretion
  6. Slow gastric emptying
  7. Overeating •
  8. Smoking
  9. Alcohol
  10. Pregnancy - results in increased abdominal pressure
  11. Fat, chocolate, coffee or alcohol ingestion
  12. Drugs e.g. antimuscarinic, calcium channel blockers and nitrates • Systemic sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Barrett’s Oesophagus: define

A

when squamous cells undergo meta plastic changes and → become COLUMNAR CELLS

There is always a hiatus hernia present

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

Barrett’s Oesophagus: Complications?

And describe how Barrett’s leads to this?

A

Risk of progressing to oesophageal cancer - its premalignant for
adenocarcinoma!!!!! of the oesophagus

  1. GORD damages normal oesophageal squamous cells.

2. Glandular columnar epithelial cells replace squamous cells (metaplasia).

  1. Continuing reflux leads to dysplastic oesophageal glandular epithelium.
  2. Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Barrett’s Oesophagus: aetiology?

A
  1. GORD

2. Obesity

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

Mallory Weiss Tear: define?

A
  • DefinitionThis is a linear mucosal tear occurring at the oesophagogastric junction and produced by a sudden increase in intra-abdominal pressureIt often follows a bout of coughing or retching and is classically seen after
    alcoholic ‘dry heaves’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Mallory Weiss tear: management?

A
  • most bleeds are minor and heal in 24 hours
  • Haemorrhage may be large but tend to stop spontaneously
  • If surgery is required then it involves the oversewing of the tear but this is rarely needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Mallory Weiss tear: investigation and symptoms?

A

Endoscopy to confirm

  • Vomiting
  • Haematemesis after vomiting -
  • Retching
  • Postural hypotension
  • Dizziness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What can helicobacter pylori infection cause?

A

H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.

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

peptic ulcer: aetiology?

A
  1. Prolonged NSAID use -> decreased mucin production.
  2. H.pylori infection.
  3. Hyper-acidity.(Increased gastric acid secretion )

Smoking (minor)
Delayed gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Peptic ulcer: symptoms?

A

Often acute onset of symptoms:
1. Pain. Recurrent burning epigastric pain:

  1. Bleeding.
  2. Perforation.
  • • Pain of duodenal ulcers classically occurs at night (as well as during the
    day) and is worse when the patient is hungry
    • Pain in both gastric and duodenal ulcers can be relieved by antacids
    • Gastric ulcer = pain inc when eating and goes away 2-3 hrs later
    • Duodenal ulcer = pain decreases when eating and causes pains several hours after eating!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Peptic ulcer: Investigations?

A
  1. H.pylori test e.g. urease breath test and faecal antigen test.
  2. Gastroscopy.
  3. Barium meal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Peptic ulcer: Management?

Why are all gastric ulcers re-scoped 6-8 weeks after treatment?

A
  1. Stop NSAIDS.
  2. PPI’s e.g. omeprazole.
  3. H.pylori eradication.

All peptic ulcers are re-scoped to ensure they’ve healed. If they haven’t healed it could be a sign of malignancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Achalasia: define and symptoms?

A

is a rare disorder of the food pipe (oesophagus), which can make it difficult to swallow food and drink

  • Dysphagia for fluids and solids
  • Regurgitation of food particularly at night and aspiration pneumonia is a complication
  • Substernal cramps
  • Weight loss - but is usually minimal
  • Spontaneous chest pain occurs and is said to be due to oesophageal ‘spasm’; it may be misdiagnosed as cardiac pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Achalasia: investigations? CONFIRMS DX??

A
  • CXR:
    • Dilated oesophagus
    • May be fluid level behind/above the heart
  • Barium swallow:
    • Shows lack of peristalsis
    • Lower end shows a ‘birds beak’ due to failure of sphincter to relax
  • OESEOPHAGEAL Manometry:!!!!!!!
    • Confirms diagnosis
    • Shows aperistalsis of the oesophagus and failure of relaxation of the lower oesophageal sphincter
  • CT & Oesophagoscopy used to rule out carcinoma at the lower end of the oesophagus which can produce a similar x-ray appearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Acute mesenteric Ischaemia: define
and symptoms?

1st line investigation:

A
  • -symptomaticischemia* without irreversible tissue damage* caused by insufficient blood supply to the gastrointestinal tract.
    • divided into embolic, thrombotic, or venous
  • –affects small intestine

Classical clinical TRIAD:

  • Acute severe abdominal pain - tends to be constant, central or around the right iliac fossa
  • No abdominal signs on exam
  • Rapid hypovolaemia resulting in shock - pale skin, weak rapid pulse, reduce urine output, confusion
  • NOTE: the degree of illness is often far out of proportion with clinical signs
    !!!!!If you see ATRIAL FIBRILLATION (AF) with abdominal pain then think MESENTERIC ISCHAEMIA

investigatiosn:
CT!! (MRI) angiography:!!!!!! 1st LINE!!!
• Provides non-invasive alternative to simple arteriography

Laparotomy (surgical procedure → cut into abdominal wall → access to abdominal cavity):
• To make diagnosis
• May see necrotic bowel if not treated quickly

Bloods:
• Raised Hb due to plasma loss
• Raised white cell count
• Persistent METABOLIC ACIDOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ischaemic Colitis: define and aka?

pathophysiology and most commonly affected site?

A

aka chronic colonic ischaemia
inflammation and injury of the large intestine result from inadequate blood supply.
Usually follows low flow in the inferior mesenteric artery (IMA) territory and ranges from mild ischaemia to gangrenous colitis

Sudden drop in blood flow -> insufficient perfusion -> poor oxygen/nutrient delivery to bowel -> compromised cellular metabolism -> ischaemia, inflammation, infarction, nerosis
Affects the large bowel
- Occlusion of branched of the superior mesenteric artery (SMA) or inferior mesenteric artery (IMA), often in the older age group
- The anatomy of the vascular supply to the colon results in a watershed area at the splenic flexure - which is thus the MOST COMMON SITE AFFECTED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

ischaemia colitis: symptoms?

A
  1. Sudden onset Left Iliac Fossa pain
  2. Signs of hypovolaemic shock
    - Sudden onset lower LOWER LEFT SIDE abdominal pain
    - Passage of bright red blood with/without diarrhoea
    - May be signs of shock (pale skin, weak rapid pulse, reduce urine output, confusion) and evidence of underlying cardiovascular disease

Decreased bowel sounds, guarding + rebound tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Ischaemic colitis: investigations and gold standard~?

A
  • Urgent CT scan to exclude perforation
  • Flexible sigmoidoscopy:
    • Biopsy shows epithelial cell apoptosis

!!!!!!!!- Colonoscopy and biopsy - GOLD STANDARD:
• Only done AFTER patient has fully recovered to exclude stricture
formation at the site of disease and confirm mucosal healing

  • Barium enema:
    • Thumb printing of submucosal swelling at splenic flexure

management = antibiotics and fluid resusucitaion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Appendicitis: define and pathophysiology?

A

painful swelling of theappendix
Theappendixis a small, thin pouch about 5 to 10cm (2 to 4 inches) long.

Occurs when the lumen of the appendix becomes obstructed by lymphoid hyperplasia, filarial worms or a FAECOLITH (most common) resulting in the
invasion of gut organisms into the appendix wall

  • This leads to oedema, ischaemia, necrosis and perforation as well as INFLAMMATION
  • If the appendix ruptures then infected and faecal matter will enter the peritoneum resulting in life threatening peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Appendicitis: aetiology?

A
  • Faecolith (stone made of faeces)
  • Lymphoid hyperplasia
  • Filarial worms
53
Q

Appendicitis: symptoms?

A

Should be considered for ALL RIGHT SIDED PAIN if appendix is present in patient (i.e. not already removed)

Pain in the umbilical region (periumbilical pain) that migrates → to the right iliac fossa, specifically McBurney’s point after a few hours

  • Anorexia is important
  • Nausea and vomiting and occasionally diarrhoea can occur
  • Constipation is usual
  • Examination of abdomen reveals tenderness in the right iliac fossa with guarding due to localised peritonitis
  • May be a tender mass in the right iliac fossa
  • Patient is pyrexic
54
Q

Appendicitis: investigations?

1st line and gold standard?

A

1st line - Blood tests:
• Raised white cell count !!!!with neutrophil leucocytosis
• Elevated CRP and ESR!!!!

  • Ultrasound:
    • Can detect inflamed appendix and can also indicate an appendix mass or other localised lesion
  • CT:!!!!!!
    • Highly sensitive and specific - GOLD STANDARD for diagnosis
    • Reduces risk of removal of a healthy appendix
  • Pregnancy test - to exclude
  • Urinalysis - to exclude UTI
55
Q

Appendicitis: management?

A

Gold standard: Appendicectomy

IV antibiotics IV
METRONIDAZOLE and IV CEFUROXIME & fluids

No food/water orally

56
Q

Appendicitis: complications?

A
  • Perforation:
    • Commoner if faecolith present and in young children as diagnosisis often delayed since harder
  • appendix mass:
    • When an inflamed appendix becomes covered in omentum (thus forming a mass) - ultrasound or CT can help diagnose
    • Treat with antibiotics and then surgery to remove appendix later to prevent further events
  • Appendix abscess:
    • Results if appendix mass fails to resolve but instead enlarges and the patient get more unwell
    • Treat by draining appendix
    • Antibiotics too can be used to treat
57
Q

Diverticulitis: epidemiology?

A

Older patients and those with low fibre diets.

Frequently found in the colon and occur in 50% of pts over the age of 50 yrs

58
Q

Diverticulitis: define and pp?

What part of the bowel is most likely to be affected by diverticulitis?

A

inflammation (sometimes infection) of one or more diverticula in large intestine

Out-pouching of bowel mucosa -> faeces can get trapped here and obstruct the diverticula -> abscess and inflammation -> diverticulitis.
in a low fibre diet = BC fibres helps gut motility SO = LESS FIBRE = LESS GUT MOTILITY = colon must push harder to move things alonG SO pressure increases
→ MEANS pouches of mucosa being extruded/thrust or forced out -through the muscular wall through weakened areas near blood vessels leading to diverticula formation

The descending colon.

59
Q

Acute diverticulitis: define and pp?

A

A sudden attack of swelling in the diverticula. Can be due to surgical causes.

  • Acute diverticulitis is when:
    • Occurs when faeces obstruct the neck of the diverticulum, causing stagnation and allowing bacteria to multiply and produce inflammation→ lead to bowel perforation (peridiverticulitis), abscess formation, fistulae into adjacent organs, haemorrhage and generalised acute peritonitis and possibly death
60
Q

Acute diverticulitis: signs and symptoms?

A

Asymptomatic in 95% of cases and is usually detected incidentally on colonoscopy or barium enema examination

  • In symptomatic cases:
  • Intermittent left iliac fossa pain
  • Erratic bowel habit - constipation
  • In severe cases:
  • Severe pain and constipation due to luminal narrowing
  • fever
  • tachycardia
    Abdominal examination:
    • Tenderness, guarding and
    rigidity on the LEFT SIDE of
    abdomen
    • A palpable tender mass is
    sometimes felt in the left iliac fossa
61
Q

diverticulitis: investigations?

A

Diverticular disease:
• In the absence of clinical signs of acute diverticulitis (i.e. excluding this) then COLONOSCOPY is best option

  • *Blood tests:**
  • Polymorphonuclear leucocytosis - increased levels of the white blood cell polymorphonuclear leukocytes
  • ESR and CRP raised
  • *CT colonography:**
  • BEST for diagnosis
  • Will show colonic wall thickening and diverticula
  • Also pericolic collections and abscesses
  • Finding above are DIAGNOSTIC for acute diverticulitis and differ from those of malignant disease
  • *Abdominal X-ray:**
  • May identify obstruction or free air (indicative of perforation)
  • *Barium enema:**
  • Can clarify diagnosis in patients with abdominal pain and altered bowel habit
62
Q

Management of diverticular disease vs diverticulitis?

A
  • Diverticular disease:
    • In uncomplicated symptomatic disease recommend a well-balanced HIGH FIBRE DIET**

with smooth muscle relaxants i.e. antispasmodics e.g. MEBEVERINE!!!!

  • Acute diverticulitis:
    • Mild attacks can be treated with oral antibiotics e.g. CIPROFLOXACIN and METRONIDAZOLE
  • Those with signs of systemic upset (fevers, tachycardia) and significant abdominal pain require bowel rest, IV fluids and IV antibiotics
  • Surgical resection is occasionally required
63
Q

Diverticular disease: complications? (IO and how?)

A

intestinal obstruction - Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.

  • Perforation:
    • Usually occurs in association with acute diverticulitis
    • Can lead to paracolic or pelvic abscess or generalised peritonitis
    • Surgery may be required
  • Fistula formation into:
    • The bladder resulting in dysuria (pain when urinating) or
      pneumaturia (gas or air in urine resulting in bubbles)
    • The vagina resulting in discharge
64
Q

SBO vs LBO: aetiology

A

SBO:
1. Majority is caused by previous surgery (60%) adhesions
2. Hernia:
Abnormal protrusion of an organ or tissue out of the body cavity in which it normally lies
3. Malignancy
4. Crohn’s disease is also a significant cause (25%)

and intusseception
(gallstone in ileum and diaphragm disease)

LBO:

  1. 90% due to colorectal malignancy/adenocarcinoma in US/Europe (60%) most common
  2. In African countries the cause is more likely to be volvulus ——→ twisting of bowel
  3. diverticular disease
65
Q

Psuedo-obstruction of bowel: aetiology?

A
  1. myopathy - problem w muscle = NO peristatlic contractionneuropathy - problem w nerves = NO innervation to the smooth muscle = THUS ABNORMAL movement → obstruction
  2. Hirschsprung’s disease = a congenital disease = MISSING NERVES at DISTAL end of colon!! - THUS ABNORMAL peristalsis = bowel obstruction
66
Q

sbo: signs and symptoms?

A

SIGNS:
– Pain - initially colicky (starts and stops abruptly) then diffuse, - CENTRAL - pain is higher in the abdomen than in LBO

– vomiting - EARLIER in SBO compared to LBO - BC MORE PROXIMAL = will vomit bilious/undigested food

– Vital signs e.g. increased HR, hypotension, raised temperature. - hypotension —> shock

  1. Tenderness and swelling.
  2. Resonance.
  3. Bowel sounds.

SYMPTOMS:
– toxins in circulation –> sepsis

– perforation —> peritonitis

– Constipation with NO passage of wind occurs LATE in SBO

67
Q

sbo: investigations?

gold standard?

A
  1. Take a good history - ask about previous surgery (adhesions)!
  2. FBC, U+E, lactate.
  3. X-ray.
  4. CT, ultrasound, MRI.

Examination of hernia orifices and rectum

CT:
• Gold standard to localise lesion accurately!!!!

68
Q

sbo: manageemtm?

A
  1. Fluid resuscitation.
  2. Bowel decompression. - DRIP AND SUCK = INTIAL SUPPORTIVE MANAGEMENT

‘Drip and suck’ management: Any 3 from Make the patient nil-by-mouth (NBM), Insert a nasogastric tube to decompress the bowel (‘suck’), Start IV fluids and correct any electrolyte disturbances (‘drip’).
Urinary catheter and fluid balance, Analgesia as required, suitable anti-emetics

  • Aggressive fluid resuscitation - Start IV fluids and correct any electrolyte disturbances (‘drip’).
  1. Analgesia and anti-emetics.
  2. Antibiotics.
  3. Surgery e.g. laparotomy, bypass segment, resection.
69
Q

lbo: symtpoms and signs?

A
  1. Tenesmus.
  2. Constipation. EARLY FINDING
  3. Abdominal discomfort. – Abdominal pain that is more constant - LONGER LASTING SPASMS than in SBO
  4. Bloating.
  5. Vomiting. - Late vomiting which is more faecal like - suggestive of LBO -
  6. Weight loss.

Abdominal distension

70
Q

LBO: investigations?

A
  1. Digital rectal examination.
    • Empty rectum
    • Hard stools
    • Blood
  2. Sigmoidoscopy.
  3. Abdo X-ray.
  4. CT scan.
  5. FBC essential - see low Hb sign of chronic occult blood loss
71
Q

LBO: management?

A
  1. Fast the patient.
  2. Supplement O2.
  3. IV fluids to replace losses and correct electrolyte imbalance.
  4. Urinary catheterisation to monitor urine output.
  • Aggressive fluid resuscitation
  • Bowel decompression
  • Analgesia and antiemetic
  • Antibiotics
  • Surgery - to remove obstruction done by laparotomy (open surgery)
    • Obstruction due to malignancy required colorectal stents followed by
    elective surgery
72
Q
  • 3 complications for untreated intestinal obstrcutions
A
  1. Ischaemia.2. Necrosis.3. Perforation.
73
Q

Acute diarrhoea: aetiology?

A

Infectious Diarrhoea;
- - bacterial infections: E.coli, Campylobacter,

  • viral infections: Rotavirus, Norovirus,
  • parasites: entamoeba histolytica, Giardia lamblia,

Non-infectious diarrhoea
- medications: antacids containing magnesium; antiarrhythmics (quinidine)

74
Q

Traveller’s diarrhoea: diagnpstic criteria

A

> 3 unformed stools per day and at least one of:
- Abdominal pain.

  • Cramps.
  • Nausea.
  • Vomiting.

It occurs within 3 days of arrival in a new country.

75
Q

Traveller’s diarrhoea: aetiology?

A

An estimated 80% to 90% of cases are caused by the ingestion of bacterially contaminated food or water. Common bacterial culprits include

  1. Enterotoxigenic e.coli (ETEC).
  2. Campylobacter.
  3. Norovirus.
  4. Shigella
  5. . Salmonella

Viral aetiology:

  1. rotavirus in children,
  2. norovirus (typically affecting people on cruise ships), a
  3. and many enteroviral infections.

Parasitic origin:

  1. Giardia
  2. Entamoeba
76
Q

define diarrhoea and acute and chronic and traveller’s

A

The abnormal passage of loose or liquid stool more than 3 times daily

  • Acute Diarrhoea
    • Acute diarrhoea is defined as that lasting less than 2 weeks
  • Chronic Diarrhoea
    • Chronic diarrhoea is defined as lasting more than 2 weeks
77
Q
  • List 5 important questions a GP should ask when taking a history to establish a cause of diarrhoea.
A
  1. Blood or mucus in the stools.
    1. Family history of bowel problems?
    2. Abdominal pain
    3. Recent foreign travel history.
    4. Bloating.
    5. Weight loss.
78
Q

acute diarrhoea: clinical manifestations in inflammatory vs non-inflammatory diarrhoea?

A

inflammatory = mucoid and bloody stool, tenesmus, fever, and severe crampy abdominal pain.

non-inflammatory = watery, large-volume, frequent stool (>10 to 20 per day) (no tenesmus, blood in the stool, fever, or faecal leukocytes)

79
Q

diarrhoea: investigations?

A
  1. FBC.
  2. ESR/CRP.

Stool culture.

Faecal calprotectin.

Faecal occult blood!!

Flexible sigmoidoscopy with colonic biopsy is performed if symptoms persist and no diagnosis has been made

80
Q

acute diarrhoea: management?

A

Treatment is symptomatic to maintain hydration with anti-diarrhoeal agents (LOPERAMIDE HYDROCHLORIDE) for short-term relief

and antibiotics for specific indications

81
Q

chornic diarrhoea; aetiology?

A
  • Colonic causes include:
    • Inflammatory bowel disease (ulcerative colitis, Crohn’s colitis)
  • Small bowel causes include:
    • Coeliac disease
    • Crohn’s disease
  • Pancreatic insufficiency causes include:
    • Chronic pancreatitis
  • Functional:
  • IBS
  • Endocrine causes include:
    • Hyperthyroidism
    • Diabetes
  • Systemic causes include:
    • Drug effects
    • Alcohol
  • Finally, miscellaneous causes include:
    • Surgical resections (short gut syndrome) or bypass
82
Q

Gastritis: define and aetiology?

A

Gastritis is inflammation that is associated with mucosal injury

  1. Not enough blood - mucosal ischaemia.
  2. H.pylori.!!!!!!!!!
  3. Aspirin, NSAIDS. eg naproxen
  4. Increased acid - stress.
  5. Bile reflux - direct irritant.
  6. Alcohol.
  7. autoimmune gastritis!!!
  8. Viruses e.g. cytomegalovirus and herpes simplex
    9/ Specific causes e.g. Crohn’s (more common in children than adults)
83
Q

Gastritis: management?

A
  • **Remove causative agents such as alcohol
  • Reduce stress
  • H2 antagonists e.g. RANITIDINE or CIMETIDINE - to reduce acid release
  • PPIs e.g. LANSOPRAZOLE or OMEPRAZOLE - to reduce acid release
  • Antacids

BUT IF H PYLORI:
- triple therapy
- PPI for acid suppression such as LANSOPRAZOLE or
OMEPRAZOLE
- Plus TWO of:
• METRONIDAZOLE, CLARITHROMYCIN (has high resistance),
AMOXICILLIN, TETRACYCLINE, BISMUTH
• Note: amoxicillin and tetracycline have low resistance
• Quinolones such as CIPROFLOXACIN, FUROZOLIDONE AND
RIFABUTIN are used when standard regimens have failed as
‘rescue therapy’

84
Q

GASTRITIS: INVESTIGATIONS?

A
  • Endoscopy - will be able to see gastritis
  • Biopsy
  • H.pylori urea breath test
  • H.pylori stool antigen test
85
Q

gastritis: symptoms?

A
  • Nausea or recurrent upset stomach
  • Abdominal bloating
  • Epigastric pain
  • Vomiting
  • Indigestion
  • Haematemesis
86
Q

H. pylori: consequences?

A
  • Inflammation e.g. antral gastritis
  • Gastric cancer
    • BC Normal gastric mucosa → H.pylori infection → ACUTE GASTRITIS →
      Chronic active gastritis → Atrophic gastritis → Intestinal metaplasia →
      DYSPLASIA → ADVANCED GASTRIC CANCER
  • Peptic ulcers

BC H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation.

87
Q

Describe h.pylori.

A

A gram negative bacilli with a flagellum.

BC H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation.

88
Q

H pylori: management?

A

Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromyocin and amoxicillin.

1 PPI = PPI for acid suppression such as LANSOPRAZOLE or
OMEPRAZOLE (to prevent yhpersecretion of HCl)

2 AB =
Plus TWO of:
• METRONIDAZOLE, CLARITHROMYCIN (has high resistance),
AMOXICILLIN, TETRACYCLINE, BISMUTH
• Note: amoxicillin and tetracycline have low resistanc

89
Q

H. pylori: investigations?

A
  • Faecal antigen testing/Stool antigen test:
    • Immunoassay using monoclonal antibodies for detection of
      H.pylori
    • Monitors the efficacy of eradication therapy
    • Patients should be off PPIs for 2 weeks before
  • C-Urea breath test:
    • Quick and reliable test for H.pylori
    • Measures CO2 in breath after the ingestion of C-Urea
    • Used to monitor infection after eradication
    • Highly sensitive and specific
    • No antibiotics or proton-pump inhibitors (PPIs) before test
  • INVASIVE H.pylori testing - ENDOSCOPY:
    • Histology - direct visualisation of H.pylori, reduced if on PPIs
  • Biopsy urease test:
    • H.pylori produces urease
    • Which splits urea to release ammonia which in turn will raise pH of
      the solution and causes a rapid colour change of yellow to red
    • No PPIs or antibiotics since will give false negatives
90
Q

oesophageal carcinoma: symptoms?

A
  1. Dysphagia. - Progressive dysphagia:
    • Initially there is difficulty in swallowing solids but dysphagia for liquids
      follows within weeks
    • If there is dysphagia to solids AND liquids from the start this indicates
      BENIGN DISEASE
  2. Odynophagia (painful swallowing)
People often present very late.
3. Vomiting.
4. Weight loss.
5. Anaemia.
6. GI bleed.
7. Reflux.
Lymphadenopathy
  • Signs from upper third of oesophagus:
    • Hoarseness and cough
91
Q

Oesophageal carcinoma: aetiology/more rf?

A
  1. GORD -> Barrett’s.
  2. Smoking.
  3. Alcohol.
    Obesity - since increased reflux
92
Q

Oesophageal carcinoma: investigations?

A
  1. Barium swallow.
  2. Endoscopy. — Oesophagoscopy with biopsy: (OGD w biopsy)
    • To confirm diagnosis with histological proof of carcinoma
  3. CT scan/MRI/PET for tumour staging - note: PET is more sensitive in
    detecting metastases
93
Q

Oesophageal carcinoma: management?

inc treat,etm of dysphagia

A
  1. Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
  2. Medically unfit and metastases = palliative care. Stents can help with dysphagia.

Treatment of dysphagia:
• Endoscopic insertion of expanding metal stent across tumour to
ensure oesophageal patency
• Laser and alcohol injections to cause tumour necrosis and increase
lumen size

94
Q

Oesophageal carcinoma: location of SCC vs adenocarcinomas?

A

Squamous cell carcinoma occurs in the middle third (40% of all
oesophageal cancer) and in the upper third (15%) of the
oesophagus

Adenocarcinomas occur in the lower third of the oesophagus and at
the cardia and represent around 45% of tumours

95
Q

Benign Oesophageal carcinomas: epidemiology?

management?

A

Account for 1% of all oesophageal tumours
LEIOMYOMAS are most common
scc»> adenocarcinomas

  • Endoscopic removal
  • Surgical removal of larger tumours
96
Q

colorectal cancer - pp?

A
  1. Normal epithelium.
  2. Adenoma.
  3. Colorectal adenocarcinoma.
  4. Metastatic colorectal adenocarcinoma.

Spreads by direct infiltration through the bowel wall then spread to
lymphatic and blood vessels and metastasis to LIVER and LUNG

97
Q

Give 3 reasons why bowel cancer survival has increased over recent years.

A
  1. Introduction of the bowel cancer screening programme.
  2. Colonoscopic techniques.
  3. Improvements in treatment options.
98
Q

Colorectal cnacer: rf?

how would hnpcc cause cancer?

A
  1. Low fibre diet.
  2. Diet high in red meat.
  3. Alcohol.
  4. Smoking.
  5. A PMH of adenoma or ulcerative colitis.
  6. A family history of colorectal cancer; FAP or HNPCC.

in HNPCC
There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.

99
Q

Colorectal cancer:

Rectal cancer - signs and symptoms?

A
  1. PR bleeding.
  2. Mucus.
  3. Thin stools.
  4. Tenesmus.
100
Q

Colorectal cancer:

Left sided / sigmoid cancer - signs and symptoms?

A
  1. Change of bowel habit e.g. diarrhoea, constipation.

2. PR bleeding.

101
Q

Colorectal cancer:

right sided cancer - signs and symptoms?

A
  1. Anaemia.
  2. Mass.
  3. Diarrhoea that doesn’t settle.
102
Q

emergency presentation of a left sided colon cancer.

emergency presentation of a right sided colon cancer.

A

The LHS of the colon is narrow and so the patient is likely to present with signs of obstruction e.g. constipation; colicky abdominal pain; abdominal distension; vomiting.

The RHS of the colon is wide and so the patient is likely to present with signs of perforation.

103
Q

Colorectal cancer: investigations?

A

Colonoscopy = gold standard!
It permits biopsy and removal of small polyps.

  • Tumour markers are good for monitoring progress.
  • Faecal occult blood is used in screening but not diagnosis.

Double contrast barium enema:
• 2nd line alternative to colonoscopy
• Doesn’t require sedation

104
Q

Small bowel cancer: rare or common?

investigations?

management?

A

Small intestine is relatively resistant to the development of neoplasia
Quite a rare place for cancer to develop - 1% of all malignancies

  • Ultrasound
  • Endoscopic biopsy to histologically confirm diagnosis
  • CT scan:
    • May show small bowel wall thinking and lymph node involvement -
    seen in lymphoma
  • Surgical resection
  • Radiotherapy
105
Q

gastric cancer: aetiology?

A mutation in what gene can cause familial diffuse gastric cancer?

A
  1. Smoked foods.
  2. Pickles.
  3. H.pylori infection.
  4. Pernicious anaemia.
  • Smoking
  • Helicobacter pylori infection:
    • H.pylori infection causes chronic gastritis which eventually leads to atrophic gastritis and pre-malignant intestinal metaplasia
  • Dietary factors:
    • High salt and nitrates increase risk
    • Non-starchy vegetables, fruit, garlic and low salt
      DECREASE RISK
  • Loss of p53 (tumour suppressor gene) and APC genes
  • First degree relative with gastric cancer - CDH1 gene
  • Pernicious anaemia increases risk due to accompany atrophic gastritis

CDH1 - 80% chance of gastric cancer.
Prophylactic gastrectomy is done in these patients.

106
Q

gastric cancer: signs and symptomd?

A
  1. Weight loss.
  2. Anaemia.
  3. Vomiting blood.
  4. Melaena.
  5. Dyspepsia.
107
Q

gastric cancer: investigations?

What is the advantage of doing a laparoscopy in someone with gastric cancer?

A
  1. Endoscopy.
  2. CT.
  3. Laparoscopy.

–
- Gastroscopy and biopsy to histologically confirm adenocarcinoma:
• Positive biopsies can be obtained in almost all cases of obvious
carcinoma, but a negative biopsy does not rule out diagnosis
• Thus 8-10 biopsies are taken
- Endoscopic ultrasound to evaluate the depth of invasion
- CT/MRI for staging
- PET scan to identify metastases

It can detect metastatic disease that may not be detected on ultrasound/endoscopy.

108
Q

gastric cancer management

What is the treatment for proximal gastric cancers that have no spread?

What is the treatment for distal gastric cancers that have no spread?

A
  • Nutritional support
  • Surgery and combination chemotherapy; EPIRUBICIN + CISPLATIN + 5-
    FLUOROURACIL known as ECF chemo (given around same time as surgery)
    and post-op radiotherapy

3 cycles of chemo and then a full gastrectomy. Lymph node removal too.

3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.

109
Q

oesophago-gastroduodenoscopy (OGD): indications?

A
  1. Dyspepsia.
  2. Dysphagia.
  3. Anaemia.
  4. Suspected coeliac disease.
110
Q

Dyspepsia: criteria?

A

> 1 of the following:
- Postprandial fullness.

  • Early satiation.
  • Epigastric pain/burning.
111
Q

Dyspepsia: aetiology?

A

Dyspeptic symptoms are caused by disorders of the GI tract - the most common of
which is functional dyspepsia that affects around 75% with no known cause
• Other causes are PEPTIC ULCERS

  1. Excess acid.
  2. Prolonged NSAIDS.
  3. Large volume meals.
  4. Obesity.
  5. Smoking/alcohol.
  6. Pregnancy.
112
Q

Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.

A
  1. Unexplained weight loss.
  2. Anaemia.
  3. Dysphagia.
  4. Upper abdominal mass.
  5. Persistent vomiting.
113
Q

Dyspepsia: investigations?

A
  1. Endoscopy.
  2. Gastroscopy.
  3. Barium swallow.
  4. Capsule endoscopy.
114
Q

Dyspepsia: management?

What kind of lifestyle advice might you give to someone with dyspepsia?

A
  • Reassurance and lifestyle advice
  • meds review
  • Dietary review
  • Antidepressants e.g. selective serotonin reuptake inhibitors e.g.
    CITALOPRAM (low doses are use to reduce the sensitivity of the gullet)
  • Look for Helicobacter pylori using faecal antigen testing or breath test (less
    common now)
  1. Full dose PPI for 1 month.
    - Endoscopy to find clear picture of whats going on
  2. Lose weight.
  3. Stop smoking.
  4. Cut down alcohol.
  5. Dietary modification.
115
Q

E. Coli can cause which diseases?

ETEC =

  • EIEC
  • EHEC
  • EPEC
  • EAEC
  • DAEC
A
  • spontaneous bacterial peritonitis
  • diarrhoeal infection

(Enterotoxigenic e.coli (ETEC)) → causes traveller’s diarrhoea

EIEC = Enteroinvasive e.coli.

Enterohaemorrhagic e.coli (EHEC) aka e.coli 0157 → can cause bloody diarrhoea and has a shiga like toxin AND dysentery

Enteropathogenic e.coli (EPEC) = large volumes of watery diarrhoea

EAEC = Enteroaggregative e.coli.

DAEC = Diffusely adherent e.coli.

116
Q

c.dIFF: define and pp?

A

gram-POSITIVE spore forming bacteria THUS HIGHLY INFECTIOUS

Up to 5% have C.diff as part of normal flora

Can give rise to PSEUDOMEMBRANOUS COLITIS when C.diff
replaces the moral gut flora (when normal gut flora die due to
antibiotic use for example) - resulting in dangerous diarrhoea

117
Q

C.diff - which ab?

A

Antibiotic rule of Cs:
• In general, antibiotics beginning with C can give rise to antibiotic
induced Clostridium difficile diarrhoea:

  • Clindamycin
  • Ciprofloxacin (Quinolones)
  • Co-amoxiclav (Penicillins)
  • Cephalosporins
118
Q

C. diff - management?

A
  • Treatment:
  • METRONIDAZOLE
  • ORAL VANCOMYCIN
  • RIFAMPICIN/RIFAXIMIN
  • Stool transplant
  • Stop C antibiotic
119
Q

haemorrhoids: define and aetiology?

A

Disrupted and dilated anal cushions (masses of spongy VASCULAR (veins
and arteries) tissue due to swollen veins around the anus

  • Constipation with prolonged straining is a key factor
  • Diarrhoea
  • Effects of gravity due to posture
  • Congestion from a pelvic tumour, pregnancy, portal hypertension
  • Anal intercourse
120
Q

haemorrhoids: symptoms?

A
  • Bright red rectal bleeding (since blood from capillaries) that often coats
    stools, seen on tissue or drips into toilet
  • Mucus discharge and pruritus ani (itchy bottom)
  • Severe anaemia may occur
  • Weight loss and change in bowel habit should prompt thoughts of pathology
121
Q

haemorrhoids: investigations?

A
  • Abdominal examination to rule out other disease
  • PR (per rectum) exam:
    • Prolapsing piles are obvious
    • Internal haemorrhoids are not palpable
  • Proctoscopy (rectal scope) to see internal haemorrhoids
  • Sigmoidoscopy to see rectal pathology higher up
122
Q

haemorrhoids: management?

A 
- 1st degree:
• **Increase fluid and fibre
• Topical analgesic and stool softener**
- 2nd & 3rd degree or 1st degree if treatment fail:
    - **Rubber band ligation:**
    Cheap, produces an ulcer to anchor the mucosa (side effects are
    bleeding, infection and pain

- **• Infra-red coagulation:**

    Locally coagulates vessels and tethers mucosa to subcutaneous
    tissue
  • 4th degree - SURGERY:
    • Excisional haemorrhoidectomy - excision of piles
    • Stapled haemorrhoidopexy

FOR Prolapsed or thrombosed piles:
• Treated with analgesia, ice packs and stool softeners
• Pain usually resolved in 2-3 weeks

123
Q

anal fistula: define and symptoms?

A

An abnormal connection between the epithelised surface of the
anal canal and skin - essentially a track communicates between
the skin and anal canal/rectum

  • Pain
  • Discharge (bloody or mucus)
  • Pruritus ani (itchy bottom)
  • Systemic abscess if it becomes infected
124
Q

anal fistula: management?

A
  • Surgical - Fistulotomy and excision

- Drain abscess with antibiotics if infected

125
Q

anal fissure: define and aetiology?

A

Painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line
resulting in pain on defecation

  • HARD FAECES
  • Spasm may constrict the inferior rectal artery resulting in ischaemia
    which makes healing difficult and perpetuates the problem
  • Rare causes:
    • Syphilis
    • Herpes
    • Trauma
    • Crohn’s
    • Anal cancer
126
Q

anal fissure: management?

A
  • Increase dietary fibre and fluids to make stools softer
  • LIDOCAINE OINTMENT + GTN OINTMENT or topical DILTIAZEM
  • BOTULINUM TOXIN (botox) INJECTION (2nd line)
  • Surgery if medication fails
127
Q

perianal abscess: define and symptoms?

and management?

A

abscess adjacent to the anus

  • Painful swellings
  • Tender
  • Surgical excision
  • Drainage with antibiotics
  • Discharge
128
Q

Pilonidal sinus / abscess: define and management?

A

Hair follicles get stuck under the skin in the natal cleft (butt crack) resulting in
irritation and inflammation leading to small tracts which can become infected
(abscess)

  • Surgery:
    • Excision of the sinus tract and primary closure and pus drainage
    • Pre-op antibiotics
  • Hygiene and hair removal advice (near sinus)

med 2a (13 decks)

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