Gastrointestinal H Yield Flashcards

1
Q

Pathophysiology GORD

Gastro-oesophageal reflux disease (GORD) may be defined as symptoms of oesophagitis secondary to refluxed gastric contents

A
  • Stomach acid flows through the lower oesophageal sphincter and into oesophagus, where it irritates the lining and causes symptoms.
  • Oesophagus = squamous epithelial lining Stomach = columnar epithelial lining
  • Squamous more sensitive to acid than columnar.

Triggers

  • Greasy and spicy foods
  • Coffee and tea
  • Alcohol
  • Non-steroidal anti-inflammatory drugs
  • Stress
  • Smoking
  • Obesity
  • Hiatus hernia
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2
Q

Presentation of GORD

A
  • Heartburn
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating
  • Nocturnal cough
  • Hoarse voice
  • Dyspepsia
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3
Q

Red Flags in patient’s presenting with GORD

two week wait referral for further investigation

A
  • Dysphagia (difficulty swallowing) at any age gets an immediate two week wait referral
  • Aged over 55 (this is generally the cut-off for urgent versus routine referrals)
  • Weight loss
  • Upper abdominal pain
  • Reflux
  • Treatment-resistant dyspepsia
  • Nausea and vomiting
  • Upper abdominal mass on palpation
  • Low haemoglobin (anaemia)
  • Raised platelet count
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4
Q

Different causes of Dysphagia

Detected using oesophago-gastro-duodenoscopy (OGD) (ENDOSCOPY)

A
  • Oesophageal Cancer
  • Oesophagitis - Inflammed Oesophagus
  • Oesophageal candidiasis - often caused by steroid inhalers or HIV +ve
  • Achalasia - oesophageal sphincter contraction (increased pressure) - food can’t pass to stomach
  • Pharyngeal pouch - Sac which can develop between the lower part of the pharynx + upper oesophagus
  • Systemic sclerosis - Oesphageal sphincter decreased pressure. - Dysmotility
  • Myasthenia Gravis
  • Globus hystericus - anxiety related?

Pharyngeal pouch: posteromedial herniation - often presents as dysphagia, regurgitation, aspiration, chronic cough & halitosis

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5
Q

GORD Investigations & Management

A
  • Investigate with Endoscopy if Red flags
  • Lifestyle Changes
  • Medication Review - NSAIDs

Short Term
- Antacids - Gaviscon

Long term
- Full dose PPI 1m - then reduce dose if better - Omeprazole
- If not resolving then Double dose PPI 1m
- Consider H2Receptor Anatagonists - Ranitidine

24-hr oesophageal pH monitoring (gold standard test for diagnosis)

Surgery for reflux is called laparoscopic fundoplication. This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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6
Q

What is Hiatus Hernia and its types

4 types

Management?

A

Herniation of the stomach up through the diaphragm
Type 1: Sliding - 95% - stomach slides up through the diaphragm, with the gastro-oesophageal junction passing up into the thorax.
Type 2: Rolling - Other part of stomach such as fundus ends up in thorax
Type 3: Sliding & Rolling
Type 4: Additional Organs enter thorax.

RF: Obesity, multiparity, other abdo pressures

Ix: Barium swallow is the most sensitive test.
Usually coinicidental find on OGD
Tx: Weight loss, PPI and in some rare cases surgery

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7
Q

What is H. Pylori & its investigations

Gram -ve bacteria which causes gastrointestinal problems.

A
  • Bacteria damages epithelial lining -> Gastritis + Ulcers (Increased risk of cancer)
  • Using Flagella to propel it self into gastric mucosa producing NH3- - protecting itself from Acid as NH3- alkalizes it.
  • Toxins (cagA toxin) and NH3- from HPylori damage gastric mucosa

Investigations:

  1. Urea Breath test - Mass Spec of breath after consuming isotope C-13 - avoid if abx treatment within 4wk or PPi treatment within 2wk
  2. Rapid Urease Tests - CLO - Biopsy test
  3. Serum antibody - Oft stays +ve even after eradication
  4. Gastric Culture - to see if there’s any Abx sensitivity
  5. Stool Antigen test
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8
Q

Management of H Pylori

A
  • 7 day treatment with

1.) PPI - Omeprazole
2.) Abx - Amoxicillin
3.) Abx - Clarithromycin or Metronidazole

If Allergic to Penicillin

1.) Omeprazole
2.) Clarithromycin
3.) Metronidazole

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9
Q

Zollinger–Ellison Syndrome

Definition, Features, Diagnosis, Management

A
  • Excessive levels of Gastrin 2ndry to Gastrin-secreting tumour - often found in first part of duodenum as well as pancreas
  • Gastrin produces excessive acid in this case
  • Association with MEN Type I syndrome (AD genetic condition)
  • Features: Dyspepsia, Diarrhoea, multiple gastroduodenal ulcers, malabsorption.
  • Diagnosis: Fasting Gastrin Level
  • Management: PPIs
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10
Q

What is Barret’s Oesophagus and its management

premalignant condition

A
  • The lower oesophageal epithelium changes from squamous to columnar epithelium by metaplasia
  • Risk factor for developing oesophageal adenocarcinoma
  • More common in Males (7:1), Obese and Smokers
  • Often seen by chance on OGD for dyspepsia

Treatment

  • High dose PPI
  • Endoscopic Monitioring with biopsy to see if it develops in to an Adenocarcinoma - 3-5y
  • Ablation can be used to destroy abnormal columnar epithelial cells, which are then replaced with normal squamous epithelial cells. Ablation has a role in treating low and high-grade dysplasia to reduce cancer risk.
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11
Q

Diagnosis IBS

IBS is a functional disorder - no identifiable cause

IBS occurs in up to 20% of the population. It affects women more than men and is more common in younger adults.

A

6 month history of
* Abdominal Pain
* Bloating and/or
* Change in Bowel habit (diarrhoea &/or constipation)

Other Symptoms
- Mucus
- incomplete evacuation

IBS C= Constipation IBS D = Diarrhoea sometimes both interchangeable

Red flags:
* rectal bleeding
* unexplained/unintentional weight loss
* family history of bowel or ovarian cancer
* onset after 60 years of age

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12
Q

Management of IBS

Pharma & Dietary

Suggested primary care investigations are:
* full blood count - Anaemia
* ESR/CRP
* coeliac disease screen (tissue transglutaminase antibodies)
* Faecal calprotectin for inflammatory bowel disease
* CA125 for ovarian cancer

A

First Line
Pain: antispasmodic agents ( mebeverine, alverine, hyoscine butylbromide)
Constipation: Bulk forming laxatives but avoid lactulose - can cause bloating
Diarrhoea: Loperamide

No response to conventional laxatives: Linaclotide

Second-line pharmacological treatment
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptake inhibitors

Third Line
Consider CBT if symptoms over 12m

Dietary
- Consider Low FODMAP foods with dietician
- 12wk trial of Probiotics
- Regular meals, avoid large gaps
- Regular excercise
- Regularly Drink Water
- Avoid Caffiene, fizzy drinks and Alcohol
- More fibre if predominantly constipated, (less with diarrhoea/bloating)
- Diarrhoea, avoid sorbitol
- Wind and bloating consider increasing intake of oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day).
- Limit Fresh Fruit x3 daily

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13
Q

Crohn’s Disease Features

Inflammatory Bowel Disease

A
  • Commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to anus.
  • Cause is unknown but there is a strong genetic susceptibility
  • Transmural Inflammation - so all layers to serosa inflamed
  • This is why patients with Crohn’s are prone to strictures, fistulas and adhesions
  • Present in 20s

Symptoms
- Weight loss lethargy
- Bloodless Diarrhoea (crohn’s colitis may cause bleed)
- Abdominal Pain (RLQ)
- Perianal Disease - Tags or ulcers.
- No mucus in faeces
- Smoking is a RF

Most patients: ileum affected,

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14
Q

Crohn’s Disease Investigations

A
  • Raised CRP
  • Faecal calprotectin 90% sensitive and specific for IBD. It is used as an initial test before moving on to endoscopy.
  • Endoscopy (investigation of choice) - Skip Leisions + deep ulcers
  • Histology: Goblet Cells, Granulomas, Inflammation in all layers
  • Small Bowel Enema (used for terminal ileum): Rose thorn ulcers, strictures: showing Kantor’s string sign, fistulae.
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15
Q

Crohn’s Disease Management

Stop Smoking

A

Inducing Remission
* Prednislone or IV hydrocortisone
* Enteral nutrition - if concerns with steroids affecting growth in kids
* 2nd line: mesalazine - but not as affective
* can add azathioptrine or mercaptopurine to help induce

Maintaining Remision
* Azathioprine or mercaptopurine is used first-line to maintain remission
* Methotrexate Second line

Surgery
* Resecting the terminal ileum - ileocaecal resection
* Treating strictures - stricturoplasty
* Treating (perianal) fistulas - MRI is the investigation of choice for suspected perianal fistulae - give metronidazole & if perianal abscess then drain
* Draining seton used for complicated fistulas

assess TPMT activity before offering azathioprine or mercaptopurine

CD Risk
- Small Bowel Cancer
- Colorectal Cancer
- Osteoporosis

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16
Q

What is Enteral nutrition and how does it induce remission?

A

Enteral nutrition involves a specially formulated liquid diet given orally or by NG feed that replaces the patient’s diet. This induces remission by:

  • Treating nutritional deficiencies
  • Improving the gut microbiome
  • Removing inflammatory foods
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17
Q

Ulcerative Colitis Features

A
  • Inflammation always starts at rectum (most common site)
  • Continous inflammation - not deep like CD - never beyond ileocaecal valve.
  • Limited to large colon + rectum
  • Smoking may be protective

Symptoms
* Bloody Diarrhoea
* short intervals between bouts
* Tenesmus - Urge to go toilet even when not required
* Abdominal Pain - LLQ

incidence: ages 15-25 years and in those aged 55-65 years.

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18
Q

Ulcerative Colitis Investigations

A
  • Raised CRP
  • Faecal calprotectin 90% sensitive and specific for IBD. It is used as an initial test before moving on to endoscopy.
  • Endoscopy + biopsy - avoided in severe colitis due to risk of perforation
  • Opt for flexible sigmoidoscopy: Red Mucosa, Bleeds eaily, submucosal inflammation only, widespread ulceration with preservation of adjacent mucosa (polyps), crypt abscesses & depletion of goblet cells
  • Barium Enema: Loss of Haustrations, Pseudopolyps, narrow and short colon
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19
Q

Classifying Severity of UC

Mild Moderate & Severe

A
  • mild: < 4 stools/day, only a small amount of blood
  • moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
  • severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
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20
Q

Ulcerative Colitis Management

Including Flare ups which can be caused by NSAIDs + Abx + stop smoking

Mild - Moderate
Severe
Remission

A

Mild - Moderate
- Proctitis - Rectal Mesalazine (aminosalicylate) - 2nd line Oral aminosalicylate.
- Proctosigmoiditis & left-sided ulcerative colitis - Rectal Mesalazine (aminosalicylate) - 2nd line + Oral aminosalicylate.
- Extensive Disease - Oral + Rectal aminosalicylate

Severe Colitis
- Treat in Hospital - IV steroids.intravenous ciclosporin may be used if steroid are contraindicated (consider surgery >72h)

Remission

  • Oral aminosalicylate - mesalazine

Flare up
- Increase dosage of aminosalicylate - use more intermittently
- Severe relapse then oral azathioprine or oral mercaptopurine

avoid methotrexate in UC

Ulcerative colitis typically only affects the large bowel and rectum. Therefore, removing the entire large bowel and rectum (panproctocolectomy) will remove the disease. The patient has either a permanent ileostomy or an ileo-anal anastomosis (J-pouch).

An ileostomy is where the end portion of the small bowel (ileum) is brought onto the skin with a spout that drains stools directly into a tightly fitting stoma bag.

A J-pouch is where the ileum (small bowel) is folded back on itself and fashioned into a larger pouch, which is attached to the anus and functions like a rectum, collecting stools before the person opens their bowels.

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21
Q

Associated Symptoms with IBD

Crohns & Ulcerative Colitis

A
  • Arthritis: inflammatory
  • Erythema Nodusum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
  • Episcleritis (more common in Crohns)
  • Uveitis (more common in UC)
  • Osteoporosis
  • Pyoderma gangrenosum - rapidly enlarging, painful skin ulcers
  • Clubbing
  • Primary sclerosing cholangitis (common in UC)
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22
Q

Coeliac Disease Features

autoimmune condition triggered by eating gluten

A
  • It is strongly associated with HLA-DQ2 & HLA-DQ8
  • Intermittent diarrhoea w/cramping
  • fatigue
  • smelly, floating faeces
  • Wt loss, Anaemia

Complications

  • Folate B9 Deficiency
  • Osteoporosis, Osteomalacia,
  • Hyposplenism
  • Subfertility

Coeliac disease is associated with iron, folate and vitamin B12 deficiency

Repeated exposure leads to villous atrophy which in turn causes malabsorption.

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23
Q

Coeliac Disease Investigations

A
  • Stop Gluten free diet for 6m
  • TTG IgA Raised - First choice in NICE
  • Endomyseal IgA Raised

Gold Standard

  • Dudodenal or Jejunal Biopsy
  • Villous Atrophy
  • Crypt Hyperplasia
  • More Lymphocytes
  • Lamina propria infiltration

Coeliac disease increases the risk of developing enteropathy-associated T cell lymphoma

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24
Q

Coeliac Disease Management

A
  • Gluten Free Diet: Wheat (Bread, Pasta, Pastry), Barley Beer, Rye, Oats
  • Due to functional hyposplenism
    Vaccination against Pneumococcal infection given and booster every 5 years

Some notable foods which are gluten-free include:
* rice
* potatoes
* corn (maize)

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25
Q

Appendicitis

most common in young people aged 10-20 years.

lymphoid hyperplasia or a faecolith → obstruction of appendiceal lumen → gut organisms invading the appendix wall → oedema, ischaemia +/- perforation

A
  • Abdominal pain from umbilicus to RLQ (RIF) - peritoneal inflammation.
  • Singular episode of Vomit
  • Pyrexic
  • anorexia is common
  • Rebound tenderness on examination
  • Rovsing’s: palpate LIF = pain in RIF

Diagnosis

  • neutrophil-predominant leucocytosis seen
  • Urinalysis to excl. pregnancy & uti etc.
  • USS if not diagnosed clinically

Management

  • Laprascopic Appendicectomy
  • Prophylactic IV Abx given.
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26
Q

Peptic Ulcer

Duodenal & Gastric

Peptic ulcers involve ulceration of the mucosa of the stomach (gastric ulcer) or the proximal duodenum (duodenal ulcer). Duodenal ulcers are more common.

A

Symptoms

  • Epigastric Pain
  • N&V
  • Dyspepsia
  • Haematamesis (vomit blood)
  • Coffee Ground Vomit
  • Malena (Dark Stools)
  • Low Hb

Gastic Vs Duodenal

  • Gastric = pain w/eating (overall lose wt due to fear of eating.
  • Duodenal = Initial improvement w/eating (no wt loss seen)

Diagnosis

  • Endoscopy
  • Check CLO for HPylori
  • Biopsy to excl. malignancy

Management

  • Stop NSAID
  • Treat Hpylori
  • PPI

Complications

  • Bleeding - gastroduodenal artery, haematamesis with hypotension treat with endoscopic intervention.
  • Perforation of Peptic Ulcer - seen on X ray w/free air under diaphragm, present with acute abdo pain +/- Syncope

Mucosa secretes bicarbonate into this mucus coating to neutralise the stomach acid.

Factors that disrupt the mucus barrier or increase stomach acid risk mucosal ulcerations

RF: NSAIDs, HPylori, Stress, Alcohol, Smoking, Caffeiene, SSRIs

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27
Q

Small Bowel Obstruction

A
  • Adhesions from prev. surgery common cause.
  • Hernias another cause

Features

  • Billous (green) vomitting
  • Central abdo pain
  • constipation with no flatulence
  • Abdo distension
  • tinkling bowel soundfs

Ix

  • X ray - first line, Distended smll bowel loops with fluid level
  • CT - definitive diagnosis

Management

  • NBM
  • IV fluids
  • NG tube with free drainage

Some pts settle with conservative management but otherwise require surgery

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28
Q

Large Bowel Obstruction

A
  • Main cause is tumour, othersL volvulus, diverticular disease

Features

  • Abdo pain & distension
  • N&V
  • Peritonism
  • No Flatus or stool

Ix

  • Xray: free intra-peritoneal gas = perforation
  • CT definitive

Management

  • NBM
  • IV fluids
  • NG with free drainage
  • Surgery if perforation suspected
  • 75% require surgery
  • IV Abx given if surgery

Stents may be inserted into the bowel (during a colonoscopy) in patients with obstruction due to a tumour. Stents hold the tumour out of the way, creating space for the bowel contents to move through.

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29
Q

Pseudo Obstuction

AKA Post-Operative Ileus

Pseudo-obstruction is a term used to describe a functional obstruction of the large bowel, where patients present with intestinal obstruction, but no mechanical cause is found. This is less common than ileus affecting the small bowel.

A
  • Also reffered to paralytic ileus is a common complication post surgery.
  • often associated with too much handling of bowels leading to injury
  • Reduced Peristalsis

Features

  • Abdo pain and distension
  • Billous Vomitting
  • unable to faltus or eat

Deranged electrolytes can contribute to the development of postoperative ileus, so it is important to check potassium, magnesium and phosphate.

Management

  • NBM
  • NG tube
  • IV fluids
  • parenteral nutrition
30
Q

Oesophageal Cancer

A
  • Adenocarcinoma of Oesophageal likely to occur in patients with history of GORD or Barret’s Oesophagus. In lower 1/3
  • Squamous cell occurs in smokking, alcohol, achalasia in upper 2/3 of oesophagus

Features

  • Dysphagia - difficult to swallow
  • Anorexia + Wt loss
  • Vomitting
  • Odynophagia - painful to swallow

Diagnosis

  • Upper GI Endoscopy w/biopsy
  • Endoscopic USS for locoregional staging

Management

  • T1N0M) - Surgical Ressection
  • Risk of anastomotic leak
  • Chemotherapy adjuvant alongside surgery
31
Q

Gastric Cancer

2% of cancer diagnosis

A
  • Cancer in older males usually
  • RF: HPylori, Atrophic gastritis, Salt, Smoking, Blood Group A

Features

  • Vague epigastric pain with N&V
  • wt loss
  • Dysphagia
  • Lymphatic spread: L Supraclavicular lymph node (Virchows) + periumbilical nodule (sister mary Joseph)

Ix

  • oesophago-gastro-duodenoscopy with biopsy
  • Signet ring cells (the more they are the worse the prognosis)

Management

  • Surgical w/chemo adjuvant

Staging done using CT

32
Q

Colo-Rectal Cancer

third most common type of cancer in the UK

three types of colon cancer
* sporadic (95%)
* hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
* familial adenomatous polyposis (FAP, <1%)

HNPCC (Lynch syndrome), an autosomal dominant condition, is the most common form of inherited colon cancer.

A

Screening

  • FIT used
  • Every 2y for ppl 60-74y
  • detects blood in stool sample
  • Recommended FIT: abdo mass, change in bowel habits, IDA, rectal bleeding. 60y w/Anaemia

Features

  • Constipation, Diarrohoea,
  • Rectal Bleeding; bright or melena
  • Abdo Pain
  • Weight loss
  • Anaemia - weakness, fatigue, SOB
  • Bowel Obstruction]

Management

All patients with new diagnosis should have:
* carcinoembryonic antigen (CEA)
* CT of the chest, abdomen and pelvis
* Evaluate Colon with colonoscopy or CT colonography
* Surgery is required but depends where site is.

Caecal, ascending or proximal transverse colon: Right Hemicolectomy

Distal, Transverse, Descending colon: Left Hemicolectomy

33
Q

Diverticular Disease

common surgical problem

The presence of diverticula is called diverticulosis and if these cause symptoms then it is referred to as diverticular disease If the diverticula is infected then it is diverticulitis

A
  • herniation of colonic mucosa through the muscular wall of the colon.

Features

  • PR Bleed
  • Abdo pain
  • Altered bowel habit Constipation or Diarrhoea

Complications

  • Diverticulitis
  • Haemorrhage
  • Fistulas

Diagnosis

  • Colonoscopy
  • CT cologram
  • Barium enema
    Use diagnostic tools in acutely unwell pt for signs of peritonitis or abscess formation etc.

Treatment

  • Increase Dietary Fibre
  • Abx for diverticulitis

Abscess Severity Classification- Hinchey

I Para-colonic abscess
II Pelvic abscess
III Purulent peritonitis
IV Faecal peritonitis

  • Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually a stoma. This group have a very high risk of post operative complications and usually require HDU admission. Less severe perforations may be managed by laparoscopic washout and drain insertion.
34
Q

Diverticulitis

The presence of diverticula is called diverticulosis and if these cause symptoms then it is referred to as diverticular disease If the diverticula is infected then it is diverticulitis

A
  • infection of a diverticulum

Features

  • Severe LLQ Pain with tender mass due to abscess
  • N&V
  • Constipation & Diarrhoea
  • Urinary Frequency
  • PR bleed
  • Colovesicall fistula
  • Colovaginal Fistula
  • Pyrexia
  • Guarding

Ix

  • Raised WCC, CRP
  • CT best mode
  • avoid colonoscopy due to risk of perforation

Management

  • Oral Abx
  • co-amoxiclav or cefalexin
  • no resolve within 72h, hospital IV Abx
  • Lack of improvement with treatment in seemingly uncomplicated diverticulitis may suggest the presence of an abscess.

RF: Age, no fibre, Obese, Sedentary lifestyle

Complications of diverticulitis include:
abscess formation
peritonitis
obstruction
perforation

35
Q

Diverticulosis

IMPORTANT BELOW

The presence of diverticula is called diverticulosis and if these cause symptoms then it is referred to as diverticular disease If the diverticula is infected then it is diverticulitis

A
  • characterised by multiple outpouchings of the bowel wall, most commonly in the sigmoid colon.
  • elderly or low fibre diet
36
Q

Ischaemic colitis

A
  • acute but transient compromise in the blood flow to the large bowel.
  • may lead to inflammation, ulceration and haemorrhage.
  • It is more likely to occur in ‘watershed’ areas such as the splenic flexure
  • ‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage
37
Q

Acute mesenteric ischaemia

Pts often have AF

A
  • Embolism in artery which supplies the small bowel, e.g. superior mesenteric artery.
  • Severe, sudden onset bowel pain
  • Immediate laparatomy especially if peritonitis or sepsis seen
  • Poor Prognosis
  • Serum Lactate raised - first line investigation
38
Q

Volvulus

A
  • Torsion of colon - compromised blood flow + closed loop obstruction.
  • Sigmoid (80%) + Caecal (20%)
  • Sigmoid: elderly, schornic constipation, chagas, parkinsons
  • Caecal: all ages, pregnancy, adhesions

Features

  • constipation
  • abdo bloating
  • abdo pain
  • N&V

Ix

  • Coffee bean sign on X ray (sigmoid)

Management

  • Rigid Sigmoidoscopy with rectal tube
39
Q

Oesophageal Varices

Significant complications of portal hypertension is oesophageal varices.

Patient will have signs of these conditions, such as ascites, jaundice and caput medusae.

A
  • large volume of fresh blood.
  • Swallowed blood may cause melena.

Management of ruptured varicies

  • terlipressin + Prophylactic Abx before endoscopy
  • endoscopic variceal band ligation is superior to endoscopic sclerotherapy. NICE recommend band ligation
  • Sengstaken-Blakemore tube if uncontrolled haemorrhage
  • Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
    connects the hepatic vein to the portal vein (exacerbation of hepatic encephalopathy is a common complication)

Prophylaxis of bleeds

  • Propranolol
  • EVL (band ligation)
  • PPi
40
Q

Mallory Weis Tear

(a tear of the oesophageal mucosa)

A
  • moderate volume of bright red blood following a bout of repeated vomiting.
  • Common in alcoholics
  • Malena rare.
  • Usually ceases spontaneously.

Mallory-Weiss tears tend to occur after heavy retching or vomiting, which may be caused by binge drinking, gastroenteritis or hyperemesis gravidarum (in early pregnancy).

41
Q

Glasgow-Blatchford Bleeding Score

the Rockall score is used after endoscopy

A

The Glasgow-Blatchford score is used at the initial presentation in suspected upper GI bleed. It estimates the risk of the patient having an upper GI bleed. A score above 0 indicates a high risk for an upper GI bleed. The NICE guidelines (updated 2016) suggest considering early discharge in patients with a score of 0.

  • the Rockall score is used after endoscopy - assessing risk of rebleed
42
Q

Achalasia

dysphagia of BOTH liquids and solids

A
  • Degenerative loss of ganglia from Auerbach’s plexus
  • Stiffens the oesophageal sphincter (contracted) which doesnt relax when food enterss
  • It also causes failure of oesophageal peristalsis.

Features

  • Heartburn
  • Dysphagia of food and liquid
  • regurgitation of food - aspiration pneumonia

Ix

  • Oesophageal manometry - loss of tone in sphincter.
  • Barium Swallow: birds beak
  • Xray - wide Mediastinum

Treatment

  • Pneumatic Dilation
  • surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
  • Botulinum toxin injection for high risk patients
43
Q

3 types

Systemic sclerosis

CREST

characterised by hardened, sclerotic skin and other connective tissues. It is four times more common in females.

A

Limited cutaneous systemic sclerosis
* a subtype of limited systemic sclerosis is CREST syndrome: Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
* associated with anti-centromere antibodies

Diffuse cutaneous systemic sclerosis

  • scleroderma affects trunk and proximal limbs predominately
  • anti scl-70 antibodies
  • Most common cause of death is now respiratory involvement, which is seen in around 80%: interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH)

Scleroderma (without internal organ involvement)

  • tightening and fibrosis of skin
  • may be manifest as plaques (morphoea) or linear
    *
44
Q

Anorectal Abscess

most common: perianal

A

E.coli, staph aureus
Positions: Perianal, Ischiorectal, Pelvirectal, Intersphincteric

Treatment

  • Treatment is usually surgical, with incision and drainage being first line, usually under local anaesthetic. The wound can then either be packed or left open, in which case it will heal in around 3-4 weeks;
  • Antibiotics can be of use, but are only usually employed if there is systemic upset secondary to the abscess, as they do not seem to help with healing of the wound after drainage.
45
Q

Anal Fissure

tears of the squamous lining of the distal anal canal. If present for less than 6 weeks they are defined as acute, and chronic if present for more than 6 weeks.

A
  • painful, bright red, rectal bleeding
  • if fissures occur at other than the anal then consider things liuke crohns

Management

Acute: High fibre, bulk forming laxative, Lube, analgesia
Chronic: topical glyceryl trinitrate (GTN) is first-line treatment
not effective after 8 weeks then onsidered for surgery (sphincterotomy) or botulinum toxin

* RF: constipation, IBD, STI

46
Q

Pilonidal disease

A
  • Sinuses + Cysts form near natal cleft of buttocks
  • result of hair debris in intergluteal pores
  • Acute inflammation leads to abscess, purulent discharge
  • Manage conservatively in patients with no symptoms - focus on local hygeine
  • if symptoms then incision and drain - wound closure by secondary intention
  • if chronic/recurrent then surgical options including excision of the pits and obliteration of the underlying cavity
47
Q

Haemorrhoids

Haemorrhoidal tissue is part of the normal anatomy which contributes to anal continence.

A
  • Found at 3, 7 and 11 o’clock

Features

  • Painless PR bleed
  • Pruritus
  • Pain when thrombosed

Types & Grades

  • External: Below dentate line
  • Internal: above dentate line

Grade 1: Do not prolapse
Grade II: Prolapse on defecation but reduce spontaneously
Grade III: Can be manually Reduced
Grade IV: Cannot be Reduced

Management
* Fibre and Fluid intake
* topical local anaesthetics and steroids
* Rubber band ligation
* surgery for larger ones
* New: doppler guided haemorrhoidal artery ligation

Acutely Thrombosed

  • Significant pain
  • purple oedemaus tender perianal mass
  • Surgery within 72h if not they will resolve in 10days using stool softners and ice packs
48
Q

Hernia

Inguinal, Femoral, Incisional, Epigastric, Umbilical

A

Inguinal

  • Inguinal hernias account for 75% of abdominal wall hernias; superior and medial to pubic tubercle, discomfort and ache
  • unilateral inguinal hernias are generally repaired with an open approach
  • bilateral and recurrent inguinal hernias are generally repaired laparoscopically

Femoral

  • A lump within the groin, that is usually mildly painful;
  • Surgical repair is a necessity, given the risk of strangulation
  • Hernia support belts/trusses should not be used for femoral hernias, again due to the risk of strangulation;

Symptoms of strangulated hernias include:
* Pain
* Fever
* Increase in the size of a hernia or erythema of the overlying skin
* Peritonitic features such as guarding and localised tenderness
* Bowel obstruction e.g. distension, nausea, vomiting
* Bowel ischemia e.g. bloody stools

49
Q

Diarrhoea

A

World Health Organisation definitions
* Diarrhoea: > 3 loose or watery stool per day
* Acute diarrhoea < 14 days
* Chronic diarrhoea > 14 days

50
Q

Hepatitis

A to E

A

Hepatitis A

  • self-limiting disease, RNA Picornavirus
  • Faeco-oral spread
  • flu like illness, no real chronic progression
  • jaundice, hepatomegaly
  • Vaccine available, booster 12m
  • Vaccine for IVDUs, Gays, Lab workers, sewage workers

Hepatitis B

  • DNA Hepandavirus
  • Exposure to infected blood, bodily fluids, vertical transmission
  • Fever, Jaundice, Elevated liver transaminases
  • Ground glass hepatocytes on light microscopy
  • Develop into Chronic Hep B: Cirrhosis, HCC, cryoglobulinemia (vasculitis), polyarteritis nodosa, liver failure
  • Management: pegylated interferon-alpha, best response seen in F, U50s non ASIAN HIV -ve
  • Interpreting Serology: acute disease: Raised HBsAg (1m-6m), if present for more than 6m = its become chronic disease (infective), AntiHBs implies exposure or immunisation
  • previous immunisation: anti-HBs positive, all others negative
  • previous hepatitis B (> 6 months ago), not a carrier: anti-HBc positive, HBsAg negative
  • previous hepatitis B, now a carrier: anti-HBc positive, HBsAg positive

Vaccine

  • Babies: 3 dose 2m, 3m, 4m
  • Risk groups, sex workers, IVDU, HCPs
  • HBsAg via AlOH- adjuvant, yeast cells, using DNA
  • Anti HB >100mIU/ml = adequate response

Hepatitis C

  • Risk: IVDU, HIV
  • RNA Flavivirus. 6-9wk incubation
  • Spread sexually, needle stick & vertically (mother to foetus) no affect to breast feeding
  • No Vaccine
  • Jaundice, Fatigue, Arthralgia (30% symptoms visible)
  • HCV RNA is the investigation of choice
  • 15-45% clear virus but others develop chronic hepatitis C
  • Chron Hep C: Cirrhosis, HCC, cryoglobulinemia, Sjogren’s, arthralgia
  • Treatment: daclatasvir + sofosbuvir

Hepatitis D

  • Single stranded RNA virus
  • Requires HepB to complete replication and transmission
  • Transmitted like Hep B
  • Coinfection: HepB + HepD
  • Superinfection: Hep B surface antigen + Hep D
  • Superinfection can lead to chronic hepatitis and cirrhosis
  • Treated with Interferon
  • Prevention: Hep B vaccine

Hepatitis E

  • RNA Hepevirus
  • Faecal-oral route
  • C & SE Asia, N & W Africa
  • Similar to Hep A but could be fatal in pregnancy
  • No vaccine.
51
Q

Autoimmune Hepatitis

Type 1 and Type 2

Autoimmune hepatitis is a rare cause of chronic hepatitis (inflammation in the liver). It appears to occur due to a combination of genetic and environmental factors.

A
  • Type 1 typically affects women in their late forties or fifties.
  • Type 2 usually affects children or young people, more commonly girls
  • Raised immunoglobulin G (IgG) levels
  • Type 1: Raised ANA, anti-acin, antiSLA
  • Type 2: anti-LKM1, anti-LC1
  • Treatment is with high-dose steroids (e.g., prednisolone). Other immunosuppressants are also used, particularly azathioprine.
52
Q

Chronic Mesenteric Ischaemia

A

Aka abdominal angina

  • post prandial abdominal pain
  • weight loss
  • Abdominal Bruits
53
Q

Acute Liver Failure

hepatocellular dysfunction leading to a variety of systemic complications.

A

Causes
* paracetamol overdose
* alcohol
* viral hepatitis (usually A or B)
* acute fatty liver of pregnancy

Features
* jaundice
* coagulopathy: raised prothrombin time
* hypoalbuminaemia
* hepatic encephalopathy
* renal failure is common (‘hepatorenal syndrome’)

54
Q

Hepatocellular Carcinoma

HCC

RF
Liver cirrhosis, for example secondary to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis.

A
  • Worldwide: HepB cause of HCC
  • Europe: HepC cause of HCC
  • Late presentation
  • RUQ Pain, Jaundice, ascites, hepatomegaly, pruritus, splenomegaly
  • raised AFP
  • Screen for USS and AFP in high risk groups

Management

  • early disease: surgical resection
  • liver transplantation
  • radiofrequency ablation
  • transarterial chemoembolisation
  • sorafenib: a multikinase inhibitor

AFP: Alpha Feto protein

55
Q

Alcoholic Liver Disease

  • alcoholic fatty liver disease
  • alcoholic hepatitis
  • cirrhosis
A
  • Raised GGT
  • AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis
  • glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
  • Maddrey’s discriminant function (DF): prothrombin time and bilirubin concentration. Used to determine steroid use or not
56
Q

Acute

Pancreatitis

I GET SMASHED

Severity: Mild, Moderately Severe, Severe

A
  • The vast majority of cases in the UK are caused by gallstones and alcohol.
  • Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis

Features

  • Epigastric pain that may radiate through to the back
  • Low grade Pyrexia
  • Umbilical discolouration - Cullen’s
  • Flank Discolouration - Grey-Turner’s

Ix

  • Raised Serum Amylase (x3)
  • Serum Lipase - better than amylase in late presentations
  • Early USS if clincal diagnosis not made using serum amylase

Management

  • Fluid resus
  • Analgesia
  • Enteral nutrition should be offered to anyone with moderately severe or severe acute pancreatitis within 72h of presentation
  • Avoil NBM unless vomitting
  • Do not offer prophylactic antimicrobials

Complications

  • Peripancreatic fluid collections
  • Pseudocysts - observation
  • Pancreatic necrosis
  • Pancreatic abscess
  • Haemorrhage
  • ARDS

I GET SMASHED
Idiopathic Gallstones Ethanol Trauma Steroids Autoimmune Scorpion Hypercalcemia ERCP Drugs

factors indicating severe pancreatitis include:
* age > 55 years
* hypocalcaemia
* hyperglycaemia
* hypoxia
* neutrophilia
* elevated LDH and AST

57
Q

Chronic Pancreatitis

Around 80% of cases are due to alcohol excess with up to 20% of cases being unexplained, such as haemachromotosis, tumour, structural abnormalities including pancreas divisum and annular pancreas

A

Features

  • Pain following 15-30min post-prandial
  • steatorrhoea
  • DM

Ix

  • CT is more sensitive at detecting pancreatic calcification.
  • Imaging not clear = faecal elastase

Management

  • pancreatic enzyme supplements
  • analegsia
58
Q

Biliary colic

Cholelithiasis

Biliary colic is caused by gallstones passing through the biliary tree

A

RF: Fat, Female, Fourty (40y), Fertile (pregnant) , Crohns, DM

Pathophysiology

  • occur due to ↑ cholesterol, ↓ bile salts and biliary stasis
  • Pain: gallbladder contracting against a stone lodged in the cystic duct

Features

  • Post Prandial Colicky pain in RUQ radiating to back
  • N&V
  • No pyrexia or LFT derrgangment

Management

  • elective laparoscopic cholecystectomy

Around 15% of patients are found to have gallstones in the common bile duct (choledocholithiasis)

59
Q

Acute Cholecystitis

Acute cholecystitis describes inflammation of the gallbladder.

A
  • Normally caused secondary to Gallbladder

Features

  • Right upper quadrant pain
  • May radiate to the right shoulder
  • Fever and signs of systemic upset
  • Murphy’s Sign +ve
  • LFT normal apart from Mrizzi Syndrome

Ix & Management

  • USS
  • HIDA scan if USS unclear
  • IV Abx
  • early laparoscopic cholecystectomy, within 1 week of diagnosis

Mirizzi syndrome - a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct, features of jaundice

60
Q

Ascending Cholangitis

Ascending cholangitis is a bacterial infection of the biliary tree.

A
  • The most common predisposing factor is gallstones.
  • Linked to E.Coli

Features

  • Charcot’s Triad: Jaundice, Fever, RUQ pain
  • Reynolds’ pentad: Jaundice, Fever, RUQ pain, Hypotension & Confusion
  • Raised CRP

Ix & Management

  • ultrasound is generally used first-line in suspected cases to look for bile duct dilation and bile duct stones
  • IV Abx
  • ERCP - after 48h
61
Q

Primary sclerosing cholangitis

A
  • biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts.
  • Associated with UC

Features

  • cholestasis: jaundice, pruritus
  • raised bilirubin + ALP
  • right upper quadrant pain
  • fatigue

Ix

  • ERCP: Beaded appearance
  • pANCA +ve

Can lead to cholangiocarcinoma

62
Q

AutoImmune

Primary Biliary Cholangitis

previously referred to as primary biliary cirrhosis

chronic liver disorder typically seen in middle-aged females (female:male ratio of 9:1)

A

Features

  • atigue, pruritus
  • cholestatic jaundice
  • xanthelasmas, xanthomata

Ix

  • Interlobular bile ducts become damaged by a chronic inflammatory process
    causing progressive cholestasis which may eventually progress to cirrhosis.
  • anti-mitochondrial antibodies (AMA) M2 subtype are present
  • Raised IgM
  • MRCP

Management: first-line: ursodeoxycholic acid - slows disease progression
pruritus: cholestyramine

63
Q

Cholangiocarcinoma

A
  • Bile duct cancer
  • Main RF: Primary sclerosing cholangitis
  • persistent biliary colic symptoms
  • anorexia, jaundice and weight loss
  • Courvoisier sign: a palpable mass in the RUQ
  • Sister Mary Joseph nodes periumbilical lymphadenopathy
  • Virchow node: left supraclavicular adenopathy
  • raised CA 19-9 levels
64
Q

Haemachromotosis

autosomal recessive

A
  • Disorder of iron absorption and metabolism resulting in iron accumulation
  • Mutations in the HFE gene on both copies of chromosome 6
  • Common in Europeans

Features

  • Erectile Dysfunction
  • Bronze skin
  • Fatigue
  • Arthralgia - In hands
  • Diabetes
  • Caridomyopathy

Screening

  • General Population: transferrin saturation is considered the most useful marker
  • Family members: genetic testing for HFE mutation

Investigations

  • Raised Ferritin & Iron
  • Low TIBC
  • transferrin saturation > 55% in men or > 50% in women

Management

  • venesection is the first-line treatment
    (transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l)
  • desferrioxamine may be used second-line
65
Q

Wilson’s Disease

autosomal recessive

A
  • Excessive copper deposition in the tissues
  • Defect in the ATP7B gene located on chromosome 13.
  • Age 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease

Features

  • Hepatitis, Cirrhosis
  • Basal Ganglia degeneration: most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
  • Psychiatric issues
  • Asterixis, chorea, dementia, parkinsonism
  • Kayser-Fleischer rings - around eyes
  • Blue nails

Investigation

  • slit lamp examination for Kayser-Fleischer rings
  • reduced serum caeruloplasmin
  • reduced total serum copper
  • Urinary copper

Management

  • penicillamine(chelates copper) has been the traditional first-line treatment
  • trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
66
Q

Alpha 1 antitrypsin deficiency

A
  • Emphysema in young non smoker
  • Liver cirrohosis -> HCC

Management

  • supportive: bronchodilators, physiotherapy
  • intravenous alpha1-antitrypsin protein concentrates
  • surgery: lung volume reduction surgery, lung transplantation
67
Q

Ascites

Ascites is the abnormal accumulation of fluid in the abdomen.

A

SAAG > 11

Liver disorders are the most common cause
* cirrhosis/alcoholic liver disease
* acute liver failure
* liver metastases
* RHF
* Cardiac failure
* Bud chiari
* Portal HTN

SAAG <11

  • Hypoalbuminaemia
  • nephrotic syndrome
  • severe malnutrition (e.g. Kwashiorkor)
  • peritoneal carcinomatosis
  • Pancreatitis
  • Biliary Ascites

Management

  • reducing dietary sodium
  • fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
  • aldosterone antagonists: e.g. spironolactone
  • Drainage in tense ascities (large-volume paracentesis)
  • prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. (ciprofloxacin)
  • TIPS
68
Q

Peritonitis

Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.

A
  • ascites
  • abdominal pain
  • fever

Ix

  • Paracentesis: Neutrophil >250
  • Cultures: E.coli

Managment

  • IV cefotaxime

Antibiotic prophylaxis should be given to patients with ascites if:
* patients who have had an episode of SBP
* patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
* NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’

69
Q

Pancreatic Cancer

often diagnosed late as it tends to present in a non-specific way.

A
  • Mostly Adenocarcinomas
  • Present at head of pancreas
  • RF: age, smoking, diabetes, chronic pancreatitis, hereditary non-polyposis colorectal carcinoma, multiple endocrine neoplasia, BRCA2 gene, KRAS gene mutation

Features

  • Painless Jaundice, pale stools, dark urine, and pruritus
  • hepatomegaly: due to metastases, gallbladder palpable
  • anorexia, wt loss
  • steatorrhoea
  • DM
  • migratory thrombophlebitis (Trousseau sign) is more common than with other cancers

Ix

  • High Res CT; GOLD standard
  • Double Duct sign
  • USS 60% specific

Management

  • 20% Surgery
  • Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas.
  • Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
  • adjuvant chemotherapy is usually given following surgery
70
Q

Non Alcoholic Fatty Liver Disease

NAFLD

  • steatosis - fat in the liver
  • steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH), see below
  • progressive disease may cause fibrosis and liver cirrhosis
A
  • Obesity and T2DM risk factors
  • Insulin resistance major player

Features

  • usually asymptomatic
  • hepatomegaly
  • ALT is typically greater than AST - opposite to alcoholic liver disease
  • increased echogenicity on ultrasound
  • enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis

Management

  • Lifestyle changes lose weight
71
Q

Cirrhosis

Causes:
* alcohol
* non-alcoholic fatty liver disease (NAFLD)
* viral hepatitis (B and C)

A

Ix

  • transient elastography and acoustic radiation force impulse imaging - Fibroscan
  • upper endoscopy to check for varices in patient’s with a new diagnosis of cirrhosis
  • USS every 6m of Liver to check for HCC
72
Q

Portal Hypertension

A

Portal hypertension refers to abnormally high blood pressure within the portal venous system, which carries blood from the digestive organs to the liver.

Causes: Cirrhosis (most common), liver fibrosis, portal vein thrombosis, schistosomiasis, and other liver diseases.

Complications: Esophageal varices, gastric varices, splenomegaly, ascites, hepatic encephalopathy, and portosystemic shunts.

Manifestations: Ascites, variceal bleeding (hematemesis or melena), splenomegaly, jaundice, and signs of liver failure.

Treatment: Depends on the underlying cause but may include medications (e.g., beta-blockers), endoscopic procedures (e.g., band ligation, sclerotherapy), transjugular intrahepatic portosystemic shunt (TIPS), or liver transplantation.