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Gastroenterology Flashcards

1
Q

What are the symptoms and signs suggestive of GI perforation?

A

Acute Abdomen pain worse on coughing/moving

Hx of alcohol/NSAIDs/ulcer/cancer/IBD

Tachcycardia +/- hypotension

Increased RR

Peritonism (abdo tender, guarding, rebound, rigidity)

Reduced/absent bowel sounds

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2
Q

What would your initial investigations be for someone presenting with peritonism?

A

Bedside- basic obs, ECG, urine dip + BhCG if female

Bloods- FBC, CRP, lactate, amylase, ABG (acidosis)

Imaging- Erect CXR (air under diaphragm), Abdomen XR if ? obstruction

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3
Q

What is the initial management of perforation?

A

Resuscitate with IV fluids

O2

IV access

Analgesia (IV morphine 5-10mg IV with cyclizine 50mg/8hr)

Cross match blood

IV abx

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4
Q

What are the causes of perforation?

A

Ulcer, appendicitis, IBD, diverticulitis, obstruction, GI cancer, gallbladder perforation

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5
Q

What are the main causes of bowel obstruction?

A

Small bowel- adhesions, hernia, IBD

Large bowel- malignancy, diverticulitis, volvulus, faeces

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6
Q

What are the symptoms and signs of bowel obstruction?

A

Vomiting, constipation (if no flatus = complete), colicky abdominal pain, bloating, anorexia

Small bowel= early vomiting, late constipation

Large bowel= early absolute constipation, late vomiting Tachycardia +/- hypotension

  • Increased RR
  • Abdo distension
  • Absent/tinkling bowel sounds
  • Peritonitis
  • Surgical scars/hernia
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7
Q

How would a strangulated bowel present?

A

Constant severe pain

Ill patient

Peritonitis

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8
Q

What is the management of strangulated bowel?

A

Urgent surgery

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9
Q

What is the management of a small bowel obstruction?

A

Drip and suck- IV fluids, NG tube, NBM

Surgery if deteriorate

K often lost and needs replacing

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10
Q

What is the management of a large bowel obstruction?

A

IV fluids, NBM, surgical r/v If caecum >10cm on AXR need urgent surgery

Otherwise investigate cause with CT/colonoscopy Then surgery

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11
Q

What is paralytic ileus? What are the investigations and management?

A

Loss of bowel motility as a response to inflammation e.g. surgery, pancreatitis

Can mimic intestinal obstruction

Usually less abdo pain

Imaging to exclude obstruction

Management: conservative with IVT, NBM, NG tube until resolves. May need electrolyte replacement e.g. Mg and K.

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12
Q

What are the possible complications of bowel obstruction?

A

Perforation, bowel infarction, strangulation, hypokalaemia, hypovolaemia

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13
Q

What are the causes of acute pancreatitis?

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion venom
  • Hypercalcaemia, hypertriglyceridaemia, hypothermia
  • ERCP
  • Drugs (azathioprine, bendroflumethiazide, furosemide, steroids, sodium valproate etc)
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14
Q

What are the risk factors for Barrett’s oesophagus?

A

GORD

Male

Smoking

Central obesity

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15
Q

Histology of Barrett’s oesophagus

A

lower oesophageal mucosa squamous epithelium replaced by columnar epithelium

Goblet cells

Brush border

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16
Q

What is the increased risk of oesophageal adenocarcinoma associated with Barrett’s?

A

50-100 fold

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17
Q

What is the management of Barrett’s oesophagus?

A

Endoscopic survelliance + biopsies

High dose PPI

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18
Q

Which biliary disease is associated with UC?

A

Primary sclerosing cholangitis

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19
Q

Features of PSC

A

Cholestasis- jaundice and pruritis

RUQ pain

Fatigue

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20
Q

Investigation to diagnose PSC

A

ERCP/MRCP

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21
Q

PSC is associated with an increased risk of…

A

Cholangiocarcinoma

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22
Q

Main autoAbs in PSC

A

ANCA

ANA

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23
Q

Beaded appearance of bile ducts suggests…

A

PSC

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24
Q

Features of Wilsons disease

A

Hepatitis

Cirrhosis

Speech, behavioural, psychiatric problems

Asterix, chorea, dementia

Kayser-Fleischer rings

Renal tubular acidosis

Haemolysis

Blue nails

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25
Q

Dx of Wilsons

A

Reduced serum caeruloplasmin

Reduced serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)

Increased 24hr urinary copper excretion

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26
Q

1st line treatment for Wilson s

A

Penicillamine

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27
Q

Inhertiuance of Wilsons disease

A

Autosomal recessive

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28
Q

Disease characterised by excess copper deposition

A

Wilson’s

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29
Q

H pylori is most associated with

A

Peptic ulcer disease

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30
Q

H pylori eradication

A

7 days of: PPI + amox + clarithromycin

or

PPI + metronidazole + clarithromycin

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31
Q

Definition of constipation

A

Infrequent stools

Difficulty passing stools

Sensation of incomplete emptying

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32
Q

Chronic constipation

A

Sx for at least 12 weeks in last 6 months

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33
Q

Functional constipation

A

Unknown cause

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34
Q

Secondary constipation

A

Due to drug/medical condition

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35
Q

Management of constipation (adults)

A

Manage underlying causes/drugs

Lifestyle- increase fibre, fluid intake, activity levels

If faecal loading/impaction manage this 1st

Laxatives (titrate to produce soft formed stool w/out straining at least 3x per week):

1) Bulk forming e.g. ispaghula
2) Osmotic e.g. macrogol (1st line)/lactulose/phosphate enema
3) Stimulant e.g. Senna, docusate, bisacodyl, sodium picosulfate

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36
Q

Management of opioid induced constipation

A

osmotic laxative + stimulant laxative

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37
Q

Features indicating constipation in children

A

Stool patterns:

  • Fewer than three complete stools per week (unless exclusively breastfed, when stools may be infrequent).
  • Hard, large stool.
  • ‘Rabbit droppings’ stool.
  • Overflow soiling in children older than 1 year of age (commonly very loose, smelly stools, which are passed without sensation or awareness)

Symptoms associated with defecation in a child at any age:

  • Distress or pain on passing stool.
  • Bleeding associated with hard stool.
  • Straining.

Symptoms associated with defecation in a child older than 1 year of age:

  • Poor appetite that improves with passage of large stool.
  • Waxing and waning of abdominal pain with passage of stool.
  • Evidence of ‘retentive posturing’ — typical posture is straight-legged, on tiptoes with an arched back.
  • Anal pain.

Past history of constipation.

Previous or current anal fissure.

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38
Q

Management of constipation in children

A
  • Offering reassurance that underlying causes of constipation have been excluded.
  • Advising that idiopathic constipation is treatable with laxatives, although they may need to be taken for several months.
  • Offering sources of information and support.
  • Treating faecal impaction with a recommended disimpaction regimen.
  • Starting maintenance laxative drug treatment if impaction is not present or has been successfully treated.
  • Advising on behavioural interventions such as scheduled toileting, use of a bowel habit diary, and reward systems.
  • Arranging regular follow-up to assess adherence and response to treatment.
  • Considering the need for specialist referral if symptoms do not respond to optimal treatment in primary care, or if there is faecal impaction and the child is very distressed.
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39
Q

1st line treatment for feacal impaction in children

A

Movicol 1st line

If not working after 2 weeks add stimulant laxative e.g. Senna

Once disimpacted start maintenance laxatives

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40
Q

Choice of laxatives in children

A

Osmotic laxatives - increase fluid in large bowel, softening stool and stimulating peristalsis

e.g. Movicol, lactulose

Stimulant laxatives - cause peristalsis by stimulating colonic and rectal nerves

e.g. Senna, Docusate, Bisacodyl, Sodium picosulfate

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41
Q

Most common risk factors for peptic ulcer disease

A

H.pylori infection

NSAIDs

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42
Q

Complications of peptic ulcer disease

A

Haemorrhage

Perforation

Gastric outlet obstruction

Gastric malignancy (increased risk in H.pylori positive gastric ulcer disease)

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43
Q

Management of peptic ulcer disease

A

Lifestyle measures:

  • Weight loss
  • Avoid triggers e.g. coffee, chocolate, tomatoes, fatty, spicy foods
  • Smaller meals
  • Eat meals 3-4 hours before bed
  • Stop smoking
  • Reduce alcohol

Manage stress/anxiety/depression

Medication review:

  • Stop NSAIDs
  • Consider reducing or stopping (if possible and appropriate) any other potential ulcer-inducing drugs, such as:

Aspirin, bisphosphonates, corticosteroids, potassium supplements, selective serotonin reuptake inhibitors (SSRIs), or recreational drugs such as crack cocaine.

​​Test for H.pylori: carbon-13 urea breath test or stool antigen test (no PPI for 4 weeks, no abx for 2 weeks):

  • If positive and not associated with NSAIDs, prescribe eradication therapy
  • If positive and associated with NSAIDs, give full dose PPI for 2 months then eradication therapy
  • If negative prescrive full dose PPI 4-8 weeks
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44
Q

Symptoms of infective gastroenteritis

A
  • Rapid onset
  • Recent vomiting/diarrhoea
  • Feels unwell
  • Crampy abdominal pain
  • Flu-like symptoms
  • Pyrexia
  • Other household members/contacts affected
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45
Q

Causes of infectious diarrhoea

A
  • Viral infection- norovirus, sapovirus, rotavirus
  • Bacterial causes- Salmonella, Camylobacter, E.coli, Shigella, C.difficile.
  • ​Parasitic- Cryptosporidium, Giardia, Entamoeba histolytica, and Cyclospora.
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46
Q

Causes of bloody diarrhoea

A

Bacterial: Campylobacter jejuni, Salmonella, Escherichia coli O157:H7, Vibrio parahaemolyticus, Shigella, Yersinia, Aeromonas, Clostridium difficile.

Viruses: cytomegalovirus.

Parasites: Entamoeba histolytica, schistosomiasis.

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47
Q

Features of E.coli infection

A

Common amongst travellers
Watery stools
Abdominal cramps and nausea

48
Q

Giardiasis

A

Prolonged, non-bloody diarrhoea

49
Q

Cholera

A

Profuse, watery diarrhoea
Severe dehydration resulting in weight loss
Not common amongst travellers

50
Q

Shigella

A

Bloody diarrhoea

Vomiting and abdominal pain

51
Q

Staphylococcus aureus

A

Severe vomiting

Short incubation period

52
Q

Campylobacter

A

A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
May mimic appendicitis
Complications include Guillain-Barre syndrome

53
Q

Bacillus cereus

A

Two types of illness are seen

  • vomiting within 6 hours, stereotypically due to rice
  • diarrhoeal illness occurring after 6 hours
54
Q

Amoebiasis

A

Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks

55
Q

Incubation period for gastroenteritis…

  • 1-6 hrs:
  • 12-48 hrs:
  • 48-72 hrs:
  • > 7 days:
A

Incubation period:

  • 1-6 hrs: Staphylococcus aureus, Bacillus cereus*
  • 12-48 hrs: Salmonella, Escherichia coli
  • 48-72 hrs: Shigella, Campylobacter
  • > 7 days: Giardiasis, Amoebiasis
56
Q

Management of gastroenteritis

A

Fluid intake

Oral rehydration salts in children/adults with risk factors (>60yrs, frail, comorbidities)

Antidiarrhoeal drugs and anti-emetics are not usually necessary (anti-diarrhoeals may be used in adults for symptom control, loperamide is 1st line but do not use if blood/mucus, high fever, E.coli 0157 or Shigellosis. Can use metoclopramide if severe vomiting)

Treat cause

e.g. antibiotics for Entamoeba, Campylobacter (severe sx only), Giardia

57
Q

Notify pubic health if…

A

Suspected:

  • Cholera
  • Bloody diarrhoea due to gastroenteritis
  • Food poisoning
  • Haemolytic uraemic syndrome
58
Q

Treatment for amoebiasis (Entamoeba histolytica)

A

Metronidazole 400mg TDS 5-10d

Followed by diloxanide 500mg TDS 10d

59
Q

Treatment for E.coli 0157

A

Supportive

Avoid anti-motility drugs

Advise against NSAIDs

60
Q

Treatment of Giardiasis

A

Metronidazole

400mg TDS 5d or 500mg BD 7-10d or 2g OD 3d

61
Q

Treatment of Salmonella gastroenteritis

A

Antibiotics not recommended for healthy people

Consider abx if >50yrs, immunocompromised or cardiac valve disease/endovascular abnormalities: ciprofloxacin 500mg BD 1d

62
Q

Risk factors for haemorrhoids

A
  • Constipation.
  • Straining while trying to pass stools.
  • Ageing.
  • Heavy lifting.
  • Chronic cough.
  • Conditions that cause raised intra-abdominal pressure (such as pregnancy and childbirth).
63
Q

Secondary care treatments for haemmorrhoids

A

Non-surgical treatments include rubber band ligation, injection sclerotherapy, infrared coagulation/photocoagulation, and bipolar diathermy and direct-current electrotherapy.

Surgical treatments include haemorrhoidectomy, stapled haemorrhoidectomy, and haemorrhoidal artery ligation.

64
Q

Affects of poisoning

A

Impaired respiration

Respiratory depression

Hypotension

Hypertension (amphetamines, phencyclidine, cocaine)

Cardiac conduction defects/arrythmias (TCAs, anti-psychotics, some anti-histamines)

Hypothermia (esp. OD of barbiturates/phenothiazines)

Hyperthermia (CNS stimulants)

Convulsions

Methaemoglobinaemia

65
Q

Repeated doses of activated charcoal are used for elimination of which drugs?

A
  • Carbamazepine
  • Dapsone
  • Phenobarbital
  • Quinine
  • Theophylline
66
Q

Features of acute alcohol intoxication

A

Ataxia

Nystagmus

Dysarthria

Drowsiness

Coma

Hypotension

Acidosis

Aspiration of vomit

67
Q

Management of acute alcohol intoxication

A

Conservative management

Maintain airway

Reduce risk of aspiration

Measure blood glucose and give glucose if needed

68
Q

Features of salicylate poisoning

A

Hyperventilation causing respiratory alkalosis

Tinnitus

Deafness

Vasodilation

Sweating

Coma (uncommon)

Acid-base disturbances- metabolic acidosis

69
Q

Management of salicylate poisoning

A

Measure plama salicylate, pH and electrolytes

Activated charcoal if within 1hr on ingesting >125mg/kg aspirin

Replace fluid losses

IV sodium bicarbonate (after correcting K+)

Haemodialysis if severe (plasma-salicylate [>700mg/L] or severe metabolic acidosis)

70
Q

Features of opioid poisoning

A

Coma

Respiratory depression

Pinpoint pupils

Hypotension

Hypothermia

Hyporeflexia

71
Q

King’s College Hospital criteria for liver transplantation (paracetamol liver failure)

A

King’s College Hospital criteria for liver transplantation (paracetamol liver failure)

Arterial pH < 7.3, 24 hours after ingestion

or all of the following:

  • prothrombin time > 100 seconds
  • creatinine > 300 µmol/l
  • grade III or IV encephalopathy
72
Q

Management of benzodiazepine overdose

A

Flumazenil
The majority of overdoses are managed with supportive care only due to the risk of seizures with flumazenil. It is generally only used with severe or iatrogenic overdoses.

73
Q

Management of TCA overdose

A
  • IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity
  • arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias
  • dialysis is ineffective in removing tricyclics
74
Q

Features of TCA overdose

A

Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.

Features of severe poisoning include:

  • arrhythmias
  • seizures
  • metabolic acidosis
  • coma

ECG changes include:

  • sinus tachycardia
  • widening of QRS
  • prolongation of QT interval

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

75
Q

Beta blocker overdose- management

A

Management

  • if bradycardic then atropine
  • in resistant cases glucagon may be used
76
Q

Cause of oesophagitis

A

Acid reflux into oesophagus

77
Q

Symptoms of oesophagitis

A

Heartburn

Acidic taste

Belching

Dysphagia

Uncommon: Hoarseness Persistent cough Asthma type symptoms

78
Q

Complications of oesophagitis

A

Stricture

Barrett’s oesophagus

Oesophageal cancer (risk slightly increased)

79
Q

Treatment of oesophagitis

A

Omeprazole/lansoprazole

Ranitidine

80
Q

GORD definition

A

chronic condition reflux of gastric contents into oesophagus

81
Q

Symptoms of GORD

A

Heartburn

Acid regurgitation

82
Q

Risk factors for GORD

A

Obesity

Smoking

Alcohol

Coffee

Stress

Pregnancy

Drugs- Ca channel blockers, anticholinergics, theophylline, benzos, nitrates (all decrease lower oesophageal sphincter pressure)

83
Q

Management of GORD

A

Lifestyle advice

Sleep with head of bead raised

Medication review

Full dose PPI for 4 weeks for proven GORD or 8 weeks if severe oesophagitis

84
Q

Complications of GORD

A

Barrett’s oesophagus (10-15%)

Oesophageal Ca (1-10% of those above)

Oesophageal ulcers

Anaemia

Stricture

Aspiration pneumonia

85
Q

Dose of omeprazole

A

20mg OD

86
Q

Dose of lansoprazole

A

30mg OD

87
Q

Dose of ranitidine

A

150mg BD

88
Q

Definition of dyspepsia

A

UGI sx present for >4 weeks

  • Upper abdo pain/discomfort
  • Heartburn
  • Acid reflux
  • Nausea
  • Vomiting
89
Q

Common causes of dyspepsia

A
  • GORD
  • Peptic ulcer disease
  • Functional dyspepsia (non-ulcer dyspepsia)
90
Q

Management of dyspepsia

A
  • Lifestyle modification- weight loss, smoking cessation, reducing alcohol, smaller meals, avoid triggers (coffee, chocolate, tomatoes, fatty, spicy foods)
  • Manage anxiety/depression/stress
  • Medication review
  • If sx persist, full dose PPI for 4 weeks OR H.pylori testing (carbon-13 breath test)- if persist, try alternative strategy
91
Q

Drugs which exacerbate dyspepsia

A
  • NSAIDs
  • alpha and beta blockers
  • Aspirin
  • Anti-cholinergics
  • Benzos
  • Bisphosphonates
  • Steroids
  • Nitrates
  • Theophyllines
  • TCAs
92
Q

Assessing dyspepsia

A
  • Alarm symptoms- weight loss, recurrent vomiting, dysphagia, evidence of GI bleed
  • Frequency, duration and pattern of symptoms
  • Family hx of UGI malignancy
  • Lifestyle factors
  • Assess for stress/anxiety/depression
  • Review medication
  • Check weight and BMI
  • Check for signs of anaemia
  • Check for abdominal masses/tenderness
  • Check FBC for anaemia/raised platelets
93
Q

2WW criteria for oesophageal Ca

A

Anyone with dysphagia

>55 with weight loss + upper abdominal pain/reflux/dyspepsia

94
Q

Symptoms of gastritis/erosive gastritis

A

Epigastric discomfort

Gnawing/burning pain

Nausea, vomiting, loss of appetite, belching, and bloating.

Erosive gastritis= pain, bleeding or a stomach ulcer

95
Q

Investigations for gastritis

A

H pylori test

Stool test

Endoscopy

96
Q

Causes of gastritis

A

H. pylori

Excessive use of cocaine or alcohol

Regularly taking aspirin, ibuprofen or other NSAIDs

Stress

Autoimmune

97
Q

Treatment of gastritis

A

Lifestyle modification- smaller meals, avoid spicy/acidic/fried foods, reduce alcohol, manage stress

Antacids

PPIs

H2 receptor antagonists

98
Q

Complications of gastritis

A

Stomach ulcer

Stomach polyps

Stomach tumours

99
Q

What is a Mallory-Weiss tear?

A

Haematemsis, usually after prolonged or forceful retching, coughing, straining or hiccupping

100
Q

Management of a Mallory-Weiss tear

A

Resuscitation- maintain airway, O2, 2 wide bore cannulae, send bloods, IVT/blood

Most patients stop bleeding spontaneously

Some require endoscopic intervention

101
Q

2WW criteria for oesophageal/gastric Ca

A

Dysphagia at any age

Age 55+ with weight loss and any one of:

  • upper abdo pain
  • reflux
  • dyspepsia
102
Q

Treatment of oesophageal Ca

A

Localised oesophageal adenocarcinoma- surgical resection with neoadjuvant chemoradiotherapy, or chemotherapy( before, or before and after surgery)

Resectable non-metastatic SCC- radical chemoradiotherapy or chemoradiotherapy then surgical resection

Non-metastatic Ca but unsuitable for surgery- chemoradiotherapy, chemotherapy, local tumour treatment (stenting) or supportive care.

Advanced Ca- palliative combination chemotherapy (5-fluorouracil or capecitabine + cisplatin1 or oxaliplatin)

103
Q

Treatment of oesophageal stricture

A

Benign stricture- Endoscopic dilatation with baloon/bougie

Malignant stricture- Surgical excision (oescophagectomy) or stenting

104
Q

Pathophysiology of oesophageal varices and their causes

A

Variceal haemorrhage occurs from dilated veins (varices) at the junction between the portal and systemic venous systems.

Occur due to portal hypertension - most common causes are alcoholic and viral liver cirrhosis.

Other causes:

  • Prehepatic; protal vein thrombosis/obstruction, fistula
  • Intrahepatic; acute hepatitis, schistosomiasis
  • Posthepatic; Budd-Chiari, compression (e.g. from tumour), constrictive pericarditis
105
Q

Management of variceal bleed

A

Risk assessment- Blatchford score

Resuscitation- assess airway, wide bore access x2, O2 if needed, fluids (crystalloid and colloid rapid infusion), transfuse blood ASAP, correct anaemia/coagulopathy

Terlipressin until haemostasis achieved or 5 days completed

Urgent endoscopy- band ligation, consider TIPS if bleeding not controlled

Baloon tube tamponade (Sengstaken-Blakemore tube) can be used as temporary treatment for uncontrolled haemorrhage

Antibiotic prophylaxis

Should have beta-blockers +/- nitrates and endoscopic screening and treatment long term

106
Q

Major risk factors for gastric cancer

A

Increasing age

Male

H.pylori

Low vegetable/fruit consumption

Smoking

Familial risk

107
Q

Management of gastric cancer

A

Nutritional support and symptom control

Surgery is treatment of choice with lymphadenectomy if curable

Perioperative combination chemo (5-fluoracil + epirubicin/cisplatin)

Palliative- chemotherapy, traztuzumab, stenting, gastrectomy if obstructing

108
Q

What are diverticula?

A

Diverticula are sac-like protrusions of mucosa through the muscular wall of the colon, which occur in the sigmoid colon in about 85% of people over the age of 80.

109
Q

Diverticulosis vs diverticulitis vs diverticular disease

A

Diverticulosis = diverticula present, no symptoms

Diverticular disease is a condition where diverticula cause symptoms, such as intermittent lower abdominal pain, without inflammation and infection.

Diverticulitis is a condition where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, change in bowel habit, and occasionally rectal bleeding.

110
Q

Management of diverticular disease

A

High fibre diet and adequate fluid

Weight loss, quit smoking

Bulk forming laxatives

Simple analgesia

111
Q

Symptoms of diverticular disease

A
  • Intermittent abdominal pain in the left lower quadrant. Pain may be triggered by eating and may be relieved by the passage of stool or flatus.
  • Constipation, diarrhoea, or occasional large rectal bleeds.
  • Bloating and the passage of mucus rectally.
  • Tenderness in the left lower quadrant on abdominal examination.
112
Q

Symptoms suggestive of diverticulitis

A
  • Constant abdominal pain, usually severe and starting in the hypogastrium before localizing in the left lower quadrant, with fever.

Note: in a minority of people and in people of Asian origin, pain may be localized in the right lower quadrant.

  • Change in bowel habit, and possible significant rectal bleeding.
  • Possible nausea, vomiting, dysuria, and urinary frequency.
  • A previous history of diverticulosis or diverticulitis.
  • Tenderness in the left lower quadrant, palpable abdominal mass or distention on abdominal examination.
113
Q

Management of diverticulitis

A

If mild and uncomplicated- oral co-amox 1 week (if infection suspected) or analgesia, clear fluids, reintroduce solid food gradually as symptoms improve

If more severe/complicated- admit, IV antibiotics/fluids/analgesia, surgery if complicated

114
Q

Symptoms/signs of appendicits

A

The classic symptoms are:

  • Abdominal pain — this is the primary presenting complaint, and it is typically described as a peri-umbilical or epigastric pain that worsens during the first 24 hours (becoming constant and sharp) and migrates to the right iliac fossa (RIF). The pain is typically worsened by movement.
  • Anorexia — almost always present.
  • Nausea.
  • Constipation.
  • Vomiting (profuse vomiting may indicate development of peritonitis).

On examination, there may be:

  • Tenderness on percussion, guarding, and rebound tenderness at the RIF — these are the most reliable clinical findings.
  • Facial flushing, dry tongue, halitosis, low-grade fever (not more than 38°C), and/or tachycardia.
115
Q

Investigations for ? appendicitis

A

Pregnancy test- rule out ectopic

Urine dip- exclude UTI (may be abnomral in 50% with appendicitis due to inflammation adjacent to bladder/UT)

Bloods- FBC (neutrophil predominant lecuocytosis in 80-90%), CRP

Imaging- US if dx doubtful, CT (more sensitive and specific)- enlarged appendix, wall thickening, fat stranding, wall enhancement.

116
Q
A

PA (12 decks)

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