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Yr 3 - Core Conditions > Abdominal > Flashcards

Abdominal Flashcards

1
Q

Name some RED FLAG symptoms for abdominal conditions

A
  • Sudden onest abdominal pain
  • Jaundice (confusion, bruising, fever, painless jaundice)
  • Change in bowel habits
  • Dysphagia
  • Persistent vomiting
  • Haematemesis
  • Rectal bleeding: melaena/fresh blood
  • Cachexia
  • Anaemia (unexplained)
  • Age (?60 y/o)
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2
Q

What is GORD?

A

Gastro-oesophageal Reflux Disease → Stomach acid frequently flows back into the oesophagus

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3
Q

What is the cause of GORD?

A

Lower oesophageal sphincter relaxes abnormally or weakens which irritates the lining of the oesophagus.

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4
Q

How common is heartburn?

A

1 in 4 adults in UK

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5
Q

What are the risk factors for GORD?

A
  • Smoking
  • Fatty/fried foods
  • Obesity
  • Alcohol
  • Eating large meals or late at night
  • Medications e.g. aspirin
  • Caffeine
  • Hiatal hernia (bulging at top of stomach into diaphragm)
  • Pregnancy
  • Connective tissue disorders e.g. scleroderma
  • Delayed stomach emptying
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6
Q

What are potential complications of GORD?

A
  • Barrett’s oesophagus (pre-cancerous changes)
  • Oesophageal strictures (can lead to dysphagia)
  • Oesophageal ulcer
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7
Q

What are the symptoms of GORD?

A
  • Heartburn; usually after eating or at night
  • Chest pain
  • Difficulty swallowing
  • Regurgitation of food or sour liquid
  • Sensation of lump in throat
  • Night-time reflux; chronic cough, laryngitis, new or worsening asthma, disrupted sleep
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8
Q

What investigations can be done in GORD?

A
  • Upper endoscopy
  • Ambulatory acid (pH) probe test
  • Oesophageal manometry
  • X-ray of upper digestive system
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9
Q

What 3 drugs are primarily used in the pharmacological treatment of GORD?

A
  • Antacids e.g. Rennie → neutralise stomach acid but will not heal inflamed oesophagus
  • PPIs e.g. lansoprazole → block acid production AND heal oesophagus
  • H2 receptor blockers e.g. cimetidine → reduce acid production
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10
Q

What lifestyle changes can be made in patients with GORD?

A
  • Maintain healthy weight
  • Stop smoking
  • Elevate head of bed (more pillows are NOT effective)
  • Don’t lie down after meal
  • Chew slowly and thoroughly
  • Avoid food & drink triggers: alcohol, caffeine, fried foods, fatty foods, garlic, onion etc
  • Avoid tight fitting clothes
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11
Q

Key questions for GORD consultation

A
  • When did you begin experiencing symptoms? How severe are they?
  • Have your symptoms been continuous or occasional?
  • What, if anything, seems to improve or worsen your symptoms?
  • Do your symptoms wake you up at night?
  • Are your symptoms worse after meals or lying down?
  • Does food or sour material ever come up in the back of your throat?
  • Do you have difficulty swallowing food, or have you had to change your diet to avoid difficulty swallowing?
  • Have you gained or lost weight?
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12
Q

What is a peptic ulcer?

A

A breach in the epithelium of the gastric or duodenum mucosa which is confirmed on endoscopy

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13
Q

How common are peptic ulcers?

A
  • Lifetime prevalence in general population is 5-10%
  • Incidence of peptic ulcer disease peaks at age 45-64 y/o
  • Duodenal ulcers 2x more common in men but gastric ulcer incidence similar in men and women
  • Gastric ulcer incidence increases with age
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14
Q

What is the biggest risk factor for peptic ulcers?

A

Helicobacter pylori infection

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15
Q

Why does H. pylori infection cause peptic ulcers?

A

Bacteria infects stomach and weakens the protective mucous coating of the stomach and duodenum, allowing the acid to get through to the sensitive lining underneath

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16
Q

What are other causes of peptic ulcers?

A
  • Anti-inflammatory drugs (NSAIDs): interfere with the stomach’s ability to protect itself from gastric acids
  • Smoking
  • Alcohol consumption
  • Stress
  • Zollinger-Ellison syndrome (rare)
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17
Q

What are potential complications of peptic ulcers?

A
  • Haemorrhage → acute massive haemorrhage is life-threatening, can cause iron deficiency anaemia
  • Perforation → can cause peritonitis (life-threatening)
  • Gastric outlet obstruction → results from strictures and stenosis
  • Gastric malignancy → increased risk in H. pylori
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18
Q

Symptoms of peptic ulcer?

A
  • Upper abdominal pain (gnawing/burning)
  • Heart burn
  • Acid reflux
  • N&V
  • Feeling of fullness, bloating or belching
  • Intolerance to fatty foods
  • Weight loss
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19
Q

What are the RED FLAG symptoms for peptic ulcer?

A
  • Haematemesis
  • Melaena
  • Sudden sharp pain in tummy that steadily gets worse
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20
Q

Investigations for peptic ulcer?

A
  • Endoscopy to confirm
  • H. pylori test → carob-13 urea breath test or stool antigen test (ensure patient has not taken PPI in past 2 weeks or antibiotics in past 4 weeks)
  • Barium swallow
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21
Q

What is the non-pharmacological management for peptic ulcers?

A
  • Weight loss
  • Avoid trigger foods & drinks
  • Stop smoking
  • Eat smaller meals and 3-4 hours before bed
  • Reduce alcohol
  • Assess for anxiety, stress & depression
  • Review/stop NSAIDs
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22
Q

What is the pharmacological management for peptic ulcers?

A
  • H. pylori treatment
  • PPIs
  • H2 blockers
  • Antacids
    *
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23
Q

What is the treatment for H. pylori?

A

Triple therapy: PPI & 2 antibiotics (amoxicillin and either clarithromycin/metronidazole

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24
Q

What define an acute GI bleed?

A

Bleeding from the oesophagus, stomach or duodenum

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25
Q

What is the prognosis of an acute GI bleed?

A

10% hospital mortality rate (poorer if older/comorbidities)

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26
Q

What are the risk factors for an acute GI bleed?

A
  • Chronic vomiting
  • Alcoholism
  • NSAIDs
  • GI surgery
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27
Q

What is the most common cause of an upper GI bleed?

A

Peptic ulcer

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28
Q

Name 3 other causes of an upper GI bleed

A
  • Mallory-Weiss tears
  • Oesophageal varices
  • Oesophagitis
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29
Q

What are Mallory-Weiss tears? Who are they seen in?

A

Tears in the lining of the oesophagus that can cause lots of bleeding

Most common in alcoholics

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30
Q

What are oesophageal varices? Who are they most common in?

A

Abnormal, enlarged veins in the oesophagus

Most common in people with serious liver disease

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31
Q

What is oesophagitis? What is the most common cause of it?

A

Inflammation of the oesophagus

Most commonly caused by GORD

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32
Q

What is the most common cause of a lower GI bleed?

A

Diverticular disease

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33
Q

What are other causes of a lower GI bleed?

A
  • IBD
  • Tumours
  • Colon polyps
  • Haemorrhoids
  • Anal fissures
  • Proctitis
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34
Q

What are haemorrhoids?

A

Swollen veins in the anus/lower rectum

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35
Q

What are anal fissures?

A

Small tears in lining of anus

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36
Q

What are the potential complications of a GI bleed?

A
  • Shock
  • Anaemia
  • Death
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37
Q

What do the symptoms of an acute GI bleed depend on?

A
  • Location of bleed (from mouth and anus)
  • Rate of bleeding
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38
Q

What are the symptoms of an acute GI bleed?

A
  • Haematemesis (bright red or dark brown, resemble coffee grounds in texture)
  • Melaena
  • Rectal bleeding
  • With occult bleeding: light-headedness, difficulty breathing, fainting, chest pain, abdominal pain
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39
Q

Location of bleed if coffee ground vomit is present?

A

Coffee ground vomitus is a sign of possible upper gastrointestinal bleeding as within organic heme molecules of red blood cells is the element iron, which oxidises following exposure to gastric acid. This reaction causes the vomitus to look like ground coffee.

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40
Q

What investigations are done in an acute GI bleed?

A
  • Investigation of choice guided by suspected location of bleeding based on clinical presentation
  • Endoscopy (1ary diagnostic tool)
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41
Q

What is the 1ary diagnostic tool for an acute GI bleed?

A

Endoscopy

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42
Q

What is the non-pharmacological treatment for an acute GI bleed?

A
  • Limit NSAIDs
  • Limit alcohol
  • Quit smoking
  • Treat GORD
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43
Q

What is the pharmacological treatment for an acute GI bleed?

A
  • Transfuse those with massive bleeding
  • Endoscopic treatment
  • PPIs
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44
Q

What is IBD?

A

Umbrella term for 2 main diseases causing inflammation of the GI tract; ulcerative colitis** & **Crohn’s disease. They both involve inflammation of the walls of the GI tract and are associated with periods of remission and exacerbation.

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45
Q

What are the risk factors for IBD?

A
  • Age → often diagnosed <30 y/o
  • Race or ethnicity → whites have highest risk
  • Family history
  • Cigarette smoking → most important controllable risk factor for developing Crohn’s BUT may help prevent UC
  • NSAIDs
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46
Q

What is the most important controllable risk factor for developing Crohn’s?

A

Smoking

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47
Q

Pneumonic for remembering Crohn’s → NESTS

A
  • No blood or mucus
  • Entire GI tract
  • Skip lesions
  • Terminal ileum most affected and Transmural (full thickness) inflammation
  • Smoking (risk factor)
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48
Q

Pneumonic for rememebering UC → CLOSEUP

A
  • Continuous inflammation
  • Limited to colon and rectum
  • Only superficial mucosa affected
  • Smoking is protective
  • Excrete blood and mucus
  • Use aminosalicylates
  • Primary sclerosing cholangitis
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49
Q

Is blood and mucus more common in Crohn’s or ulcerative colitis?

A

UC

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50
Q

What are skip lesions? Is it seen in Crohn’s or UC?

A

A skip lesion is a wound or inflammation that is clearly patchy, “skipping” areas that thereby are unharmed. It is a typical form of intestinal damage in Crohn’s disease.

Continuous inflammation is seen instead in UC.

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51
Q

Which area of the GI tract is most affected in Crohn’s?

A

Terminal ileum

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52
Q

Which type of IBD exhibits transmural inflammation and which exhibits inflammation of the superficial mucosa only?

A

Crohn’s → transmural

UC → superficial mucosa

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53
Q

Which type of IBD affects the entire GI tract?

A

Crohn’s

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54
Q

What area of the GI tract does UC affect?

A

Colon and rectum only

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55
Q

What type of medication can be used to treat IBD?

A

Aminosalicylates (5-ASAS)

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56
Q

What is primary sclerosing cholangitis?

A

A chronic disease in which the bile ducts inside and outside the liver become inflamed and scarred, and eventually narrowed or blocked

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57
Q

What type of IBD is primary sclerosing cholangitis associated with?

A

UC

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58
Q

What investigations can be carried out for IBD?

A
  • Labs: FBC, LFTs, TFTs, U&Es, CRP, vitamin D, folate, B12, ferritin, coeliac serology
  • Faecal calprotectin
  • Endoscopy with biopsy (diagnostic)
  • Imaging
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59
Q

What is the diagnostic tool for IBD?

A

Endoscopy with biopsy

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60
Q

What is faecal calprotectin? How useful is it in screening for IBD?

A

Released by intestines when inflamed

Is a useful screening test (>90% sensitive and specific to IBD in adults)

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61
Q

Pathophysiology behind UC?

A

Unknown but thought to be immune mediated caused by environmental triggers in genetically susceptible people

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62
Q

What are the potential complications of UC?

A
  • Negative psychosocial impact
  • Toxic megacolon
  • Bowel obstruction
  • Anaemia
  • Malnutrition
  • Growth failure
  • Colorectal cancer
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63
Q

Symptoms of UC?

A
  • Bloody diarrhoea >6 weeks
  • Rectal bleeding
  • Faecal urgency and/or incontinence
  • Nocturnal defecation
  • Tenesmus
  • Abdominal pain
  • Weight loss
  • Non-specific symptoms e.g. fatigue, anorexia, malaise, fever
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64
Q

What is tenesmus?

A

Tenesmus is the feeling that you need to pass stools, even though your bowels are already empty. It may involve straining, pain, and cramping.

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65
Q

What are the signs of UC?

A
  • Clubbing
  • Pallor
  • Abdominal distension
  • Tenderness
  • Mass
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66
Q

What medication is used in the management of UC?

A

5-ASAs (more effective in UC than Crohn’s)

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67
Q

What are the potential complications of Crohn’s?

A
  • Psychosocial impact
  • Abscesses
  • Strictures
  • Fistulas
  • Anaemia
  • Malnutrition
  • Faltering growth and delayed puberty
  • Cancer of small and large intestine
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68
Q

Symptoms of Crohn’s?

A
  • Persistent diarrhoea (including nocturnal diarrhoea) with possible blood or mucus in stool
  • Abdominal pain or discomfort
  • Weight loss
  • Faltering growth or delayed puberty (children)
  • Non-specific symptoms; fatigue, malaise, anorexia, fever
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69
Q

What are the signs of Crohn’s?

A
  • Finger clubbing
  • Abdominal tenderness or mass e.g. right lower quadrant
  • Perianal pain or tenderness
  • Signs of malnutrition or malabsorption;
  • Abnormalities of joints, eyes, liver and skin
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70
Q

What is the first line management for Crohn’s?

A

Steroids (e.g. oral prednisolone or IV hydrocortisone)

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71
Q

What is IBS?

A

A chronic, relapsing and often lifelong disorder of the lower GIT. It is a ‘functional’ disorder i.e. the symptoms are a result of the abnormal functioning of an otherwise normal bowel.

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72
Q

What is the cause of IBS?

A

Unknown

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73
Q

How common is IBS?

A

Common - prevalence 17% in UK

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74
Q

What are the 2 major risk factors for IBS?

A
  • Female gender
  • Younger age
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75
Q

What are common differentials for diarrhoea?

A
  • IBS
  • IBD
  • Coeliac
  • Laxative misuse
  • Hyperthyroidism
  • Antibiotic associated
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76
Q

What are common differentials for abdominal pain?

A
  • IBS
  • Appendicitis (children)
  • Diverticular disease
  • GORD
  • Peptic ulcer disease
  • Chronic pancreatitis
  • Gallstones
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77
Q

What are the RED FLAGS in IBS presentation?

A
  • Rectal bleeding
  • Change in bowel habit in older adults
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78
Q

What symptoms should make you consider IBS?

A

Consider in a person who has had any of the following for >6 months:

  • Abdominal pain/discomfort:
    • Relieved on opening bowels, or
    • Associated with a change in bowel habit
  • AND 2 of;
    • Abnormal stool passage
    • Bloating
    • Worse symptoms after eating
    • PR mucus
  • Improved by opening bowels
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79
Q

How is abdominal pain affected by opening bowels in IBS?

A

Typically improved by opening bowels

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80
Q

What investigations should be done to investigate IBS?

A

NOTE IBS is a diagnosis of exclusion as there is no specific investigation to confirm a diagnosis. Investigations can be done to exclude other pathology:

  • Normal FBC
  • Normal inflammatory markers (ESR, CRP)
  • Negative faecal calprotectin (to exclude IBD)
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer not suspected/excluded if suspected
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81
Q

What lifestyle advice can be offered to patients with IBD?

A
  • Support, reassurance and information
  • Adequate fluid intake
  • Eat small, regular meals with a healthy balanced diet
  • Low FODMAP diet
  • Regular physical activity
  • Over the counter probiotics
  • Limit caffeine and alcohol
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82
Q

What first line medication is used to treat IBS symptoms (diarrhoea, constipation and cramps)?

A
  • Diarrhoea → Loperamide
  • Constipation → Laxatives (avoid lactulose as can cause bloating)
  • Cramps → Antispasmodics e.g. hyoscine butylbromide (Buscopan)
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83
Q

What defines infective gastroenteritis?

A

An illness of <14 days duration characterised by the presence of diarrhoea (3 or more loose stools per day or bloody stools).

It is typically a self-limiting illness.

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84
Q

Define acute diarrhoea

A

3 or more episodes of liquid or semi-liquid stool in a 24-hour period, lasting for <14 days (stool takes the shape of the sample pot)

85
Q

Transmission routes of infective gastroenteritis?

A
  • Faeco-oral route
  • Foodborne
  • Environmental
  • Airborne
86
Q

Is viral or bacterial infective gastroenteriritis more common?

A

Viral

87
Q

What is the most common cause of viral gastroenteritis?

A

Norovirus

88
Q

Name the 3 most common causes of viral gastroenteritis

A
  1. Norovirus
  2. Rotavirus
  3. Adenovirus
89
Q

Why has there been a significant decrease in rotavirus cases?

A

Due to vaccine

90
Q

What are the 4 most common causes of bacterial gastroenteritis?

A
  1. Campylobacter (campylobacteriosis)
  2. E. coli
  3. Salmonella
  4. Shigella
91
Q

What is campylobacter often referred to as?

A

Traveller’s diarrhoea

92
Q

Who is Shigella often seen in?

A

MSM

93
Q

What are the 2 most common causes of parasitic gastroenteritis?

A
  1. Cryptosporididium
  2. Giardia
94
Q

What are the risk factors for infective gastroenteritis?

A
  • Increasing age >60 y/o
  • <5 y/o
  • Eating raw or undercooked foods
  • Farmers or workers in meat industry
95
Q

What are the potential complications of infective gastroenteritis?

A
  • Dehydration
  • Electrolyte imbalance
  • AKI
  • Sepsis
  • Haemolytic uraemic syndrome
  • IBS
96
Q

Important areas to cover in patient history for infective gastroenteritis:

A
  • Onset, frequency and duration of symptoms
  • Risk factors for complications; pregnancy, immunosuppression, symptoms >7 days
  • Recent foreign travel?
  • Fluid/food intake
  • Urinary output
  • Recent exposure to other affected cases/outbreaks
  • Recent drug treatment
  • Recent hospital admission
97
Q

What must be ruled out in all females presenting with abdominal pain?

A

Ectopic pregnancy → DO A PREGNANCY TEST

98
Q

Symptoms of gastroenteritis?

A
  • Diarrhoea
  • N&V
  • Abdominal pain
  • Fever
  • General malaise
99
Q

What investigations should be done in severe cases of gastroenteritis?

A
  • Examine for clinical features of dehydration/shock
  • Abdominal examination
  • Stool culture/sensitivity testing if indicated
100
Q

What is the management for gastroenteritis?

A
  • Most patients with acute gastroenteritis have no adverse complications from acute gastroenteritis and derive no benefit from antibiotic therapy → NO ANTIBIOTIC TREATMENT RECOMMENDED
    • Rehydration, infection control precautions, alert to PHE
  • Don’t return to work/school until 48 hours after symptoms have cleared
  • Who to treat with antibiotics:
    • Pregnant women
    • Immunosuppression patients
    • Symptoms lasting over a week
101
Q

Who should be treated with antibiotics in the case of gastroenteritis?

A
  • Pregnant women
  • Immunosuppressed patients
  • Symptoms lasting >1 week
102
Q

What is acute pancreatitis\?

A

Acute inflammation of the pancreas (mild/moderately severe/severe/recurrent acute pancreatitis).

Classification:

  • Mild: most common, no organ dysfunction/complications, resolves normally within a week
  • Moderate: initially some evidence of organ failure which improves within 48 hours
  • Severe: persistent organ dysfunction for >48 hours, together with local or systemic
103
Q

How common is acute pancreatitis in the UK?

A

56 per 100,000 annually in UK

104
Q

What is the mortality rate of pancreatitis?

A
  • Damage from acute pancreatitis is often reversible
  • Mild in most people (<1%) but patients can deteriorate quickly
  • High mortality rate (15%) in those with severe pancreatitis
105
Q

What is the pathophysiology of acute pancreatitis?

A

Inflammation is typically caused by hypersecretion or backflow (due to obstruction of exocrine digestive enzymes) which results in autodigestion of the pancreas.

106
Q

Pancreatic damage can be classified into what 2 major categories?

A
  1. Interstitial oedematous pancreatitis (more common, better prognosis)
  2. Necrotising pancreatitis (less common, more severe)
107
Q

Which category of pancreatic damage is more common?

A

Interstitial oedematous pancreatitis

108
Q

Potential complications of acute pancreatitis?

A
  • Necrotising pancreatitis
  • Infected pancreatic necrosis
  • Pancreatic abscess
  • Acute respiratory distress syndrome (ARDS)
  • Chronic pancreatitis
  • Pancreatic insufficiency
109
Q

What are the 2 most common causes of acute pancreatitis?

A
  • Gallstones
  • Alcohol
110
Q

Other (rarer) causes of acute pancreatitis?

A
  • Trauma
  • Steroids
  • Mumps
  • Malignancy
  • Autoimmune
  • Scorpion sting
  • Hypertriglyceridemia
  • Hypercalcaemia
  • ERCP (endoscopic retrograde cholangiopancreatography)
  • Drugs: azathioprine, thiazides, septrin, tetracyclines
111
Q

What are the risk factors for acute pancreatitis?

A
  • Male gender
  • Increasing age
  • Obesity
  • Smoking
112
Q

2 out of 3 criteria must be met for a diagnosis of acute pancreatitis to be made. What are these criteria?

A
  1. Abdominal pain PLUS a history suggestive of acute pancreatitis
  2. Serum amylase/lipase of over 3x the upper limit of normal
  3. Imaging findings characteristic of acute pancreatitis
113
Q

What 2 important differentials must be ruled out in all cases of epigastric pain (e.g. in acute pancreatitis)? How would you rule them out?

A
  • Myocardial infarction (MI may masquerade as epigastric pain) → perform ECG
  • Ectopic pregnancy (epigastric pain) → check beta-hCG levels
114
Q

What are the 3 main symptoms of acute pancreatitis?

A
  • Epigastric pain: typically, severe, sudden onset and may radiate to back
  • Nausea & vomiting
  • Decreased appetite
115
Q

What signs may be present in acute pancreatitis and why?

A
  • Epigastric tenderness
  • Abdominal distension → due to local reactive ileus or retroperitoneal fluid
  • Reduced bowel sounds (if an ileus has developed)
  • Evidence of a systemic inflammatory response (indicates severe pancreatitis)
    • Fever, hypotension, tachycardia, tachypnoea
    • If febrile and hypotensive on admission, the [patient is more likely to develop organ failure
    • Tachycardia (less helpful sign as adrenergic response can be driven by pain and stress)
  • Cullen’s sign (peri-umbilical) → late sign of haemorrhagic pancreatitis
  • Grey-Turner’s sign (flanks) → late sign of haemorrhagic pancreatitis
116
Q

What bedside investigations should be performed in acute pancreatitis?

A
  • ECG → rule out MI
  • Urinalysis
117
Q

What lab tests should be performed in acute pancreatitis?

A
  • FBC → anaemia (may increase CVS strain), raised WCC
  • CRP
  • U&Es → fluid depletion common in pancreatitis
  • LFTs → may be deranged in obstructive causes of pancreatitis
  • Lipase → very specific; >3x upper limit of normal is highly suggestive of pancreatitis
  • Serum amylase → less specific than amylase; >3x upper limit of normal is suggestive of pancreatitis
  • VBG
  • ABG
  • beta-hCG → rule out ectopic pregnancy
118
Q

What is the most specific lab test for acute pancreatitis?

A

Serum lipase

119
Q

What imaging can be done in acute pancreatitis?

A
  • Erect CXR
  • Abdominal US
  • CT abdomen and pelvis (CT-AP)
120
Q

Why would you perform an erect CXR in patients with potential acute pancreatitis?

A

look for free gas under diaphragm (pneumoperitoneum) in patients who present with epigastric tenderness

121
Q

What is the immediate management for acute pancreatitis?

A
  • IV fluid resuscitation
  • Correction of electrolyte disturbances
  • Analgesia: IV paracetamol and opioids
  • Antiemetics
  • Nil by mouth: until initial pain improves
  • Control of blood glucose
122
Q

Would you use routine antibiotics in the treatment of acute pancreatitis?

A

No - routine antibiotic use does NOT provide any benefits

123
Q

Long-term management of acute pancreatitis?

A
  • Limit alcohol & manage withdrawal (benzodiazepines, thiamine & folate & B12 replacement)
  • Management of gallstones: ERCP, cholecystectomy
124
Q

What is chronic pancreatitis?

A

Chronic, irreversible, inflammation and/or fibrosis of the pancreas

125
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol (70-80%)

126
Q

What are the risk factors for chronic pancreatitis?

A
  • Alcohol abuse
  • Smoking
  • Hypertriglyceridaemia
  • Hypercalcaemia
  • Autoimmune
  • Obstructive causes
  • Genetic causes
  • Drugs: azathioprine, thiazides, septrin, tetracyclines
127
Q

Damage to what structure in the pancreas leads to endocrine insufficiency?

A

Islets of Langerhans

127
Q

Damage to what structure in the pancreas leads to endocrine insufficiency?

A

Islets of Langerhans

128
Q

Damage to what structure in the pancreas leads to exocrine insufficiency?

A

Acinar cells

129
Q

What hormone is produced by the alpha cells of the islets of Langerhans?

A

Glucagon

130
Q

How can chronic pancreatitis lead to insulin deficiency?

A

Due to damage to beta cells of islets of Langerhans

131
Q

What are 2 complications of insulin deficiency in chronic pancreatitis?

A
  1. Non-diabetic hyperglycaemia
  2. Pancreatogenic diabetes
132
Q

What is non-diabetic hyperglycaemia?

A

Non-diabetic hyperglycaemia (pre-diabetes, impaired glucose regulation) refers to raised blood glucose levels, but not in the diabetic range. People with non-diabetic hyperglycaemia are at increased risk of developing Type 2 diabetes. They are also at increased risk of other cardiovascular conditions.

133
Q

What is pancreatogenic diabetes?

A

Pancreatogenic diabetes is a form of secondary diabetes, specifically that associated with disease of the exocrine pancreas.

134
Q

What do the pancreatic acinar cells produce?

A

Pancreatic acinar cells produce, store and secrete enzymes necessary for the digestion and absorption of food in the small intestine.

135
Q

How can chronic pancreatitis lead to maldigestion and malabsorption?

A

damage to acinar cells leads to decreased secretion of digestive enzymes

136
Q

Other potential complications of chronic pancreatitis?

A
  • Chronic pain
  • Osteoporosis, osteopenia, fracture risk
  • Pancreatic cancer
137
Q

What type & location of pain may be present in chronic pancreatitis? Does it radiate anywhere? Alleviating/exacerbating factors?

A

Severe epigastric pain (may radiate to back or localise to right or left upper quadrants). Can be chronic or recurrent.

  • Often precipitated by eating
  • Sitting upright and leaning forward may relieve it
138
Q

Symptoms of chronic pancreatitis?

A
  • Severe epigastric pain (chronic or recurrent)
  • N&V
  • Symptoms of exocrine insufficiency → malabsorption, steatorrhoea, diarrhoea, abdominal cramps, bloating, excessive flatus, weight loss, malnutrition
  • Symptoms of endocrine insufficiency → diabetes
139
Q

What are symptoms of exocrine insufficiency?

A

malabsorption, steatorrhoea, diarrhoea, abdominal cramps, bloating, excessive flatus, weight loss, malnutrition

140
Q

Signs of chronic pancreatitis?

A
  • Anorexia
  • Signs of chronic liver disease
  • Jaundice
  • Epigastric tenderness
  • Abdominal distension
  • Cullen’s sign
  • Grey-Turner’s sign
141
Q

What is elastase? What is it produced by?

A

Elastase in an enzyme (serine protease) produced by the acinar cells of the pancreas.

142
Q

Why is elastase still present in stool?

A

It is resistant to degradation in the intestine.

143
Q

What is the faecal elastase test used to investigate?

A

This test measures the amount of elastase in your stool. Its measurement in faeces is used to assess pancreatic exocrine sufficiency due to its simplicity, but it lacks sensitivity for mild to moderate pancreatic insufficiency.

144
Q

How is faecal elastase affected in pancreatic exocrine failure?

A

Reduced

145
Q

Potential investigations for chronic pancreatitis:

  • BMI
  • LFTs
  • HbA1c
  • Abdominal US
  • Faecal elastase

Explain the purpose for each

A
  • BMI → malabsorption
  • LFTs → may be abnormal if coexistent liver disease or compression of intra-pancreatic bile duct
  • Serum HbA1c → diabetes mellitus or non-diabetic hyperglycaemia (endocrine insufficiency)
  • Faecal elastase → exocrine insufficiency
  • Abdominal US → gallstones, chronic pancreatitis signs e.g. pancreatic calcifications
146
Q

Lifestyle modifications for chronic pancreatitis?

A

Alcohol !

Smoking too

147
Q

Management of chronic pancreatitis?

A
  • Pain management:
    • Paracetamol or NSAIDs
    • Weak opioids
  • Management of malabsorption and/or malnutrition:
    • Pancreatic enzyme replacement therapy
    • Monitor BMI
148
Q

What is a cholelithiasis?

A

A gallstone

149
Q

What is cholecystolithiasis?

A

Gallstones in the bladder

150
Q

What is choledocholithiasis?

A

Gallstones in the common bile duct

151
Q

What is cholecystitis/

A

Inflammation of the gallbladder

152
Q

How common are gallstones?

A

Gallstone disease is a common condition, affecting around 10-14% in Western populations.

153
Q

What is bile formed from?

A

Bile is formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism)

154
Q

Where is bile stored? Where is it released into?

A

Stored in the gallbladder

Released into the duodenum

155
Q

What do gallstones form as a result of?

A

Gallstones form as a result of supersaturation of the bile (i.e. a problem relating to the chemical composition of bile).

156
Q

What are the 3 types of gallstones?

A
  1. Cholesterol stones
  2. Pigment stones
  3. Mixed stones
157
Q

What is the most common type of gallstone?

A

Cholesterol stones (90%)

158
Q

What are cholesterol stones composed of? Risk factors?

A

Composed purely of cholesterol from excess cholesterol production → poor diet, obesity

159
Q

What are pigment stones composed of? Risk factors?

A

Composed purely of bile pigments from excess bile pigments production → haemolytic anaemia

160
Q

What is haemolytic anaemia?

A

Haemolytic anemia is a disorder in which red blood cells are destroyed faster than they can be made.

161
Q

Why can haemolytic anaemia lead to pigment stones?

A

Haemolytic anaemia causes breakdown of RBCs which leads to excess bile pigments (e.g. bilirubin) in the blood (also can cause jaundice)

162
Q

What are mixed gallstones composed of?

A

Both cholesterol and bile pigments

163
Q

What are the risk factors for gallstones?

A
  • Obesity
  • Female gender
  • Increasing age
  • Diabetes mellitus
  • Diet – higher in triglycerides and refined carbs and lower in fibre
  • Genetic and ethnic factors
  • Medication e.g. somatostatin analogues
  • Non-alcoholic fatty liver disease
  • Prolonged fasting/weight loss
  • HRT & COCP
  • Malabsorption (Crohn’s disease, previous ileal resection)
164
Q

Are gallstones more prevalent in men or women?

A

Women

165
Q

What type of diet can be a risk factor for gallstones?

A

Higher in triglycerides and refined carbs and lower in fibre

166
Q

What medications can lead to gallstones?

A

Somatostatin analogues

167
Q

Why can HRT & COCP lead to gallstones?

A

Oestrogen causes more cholesterol to be secreted into bile

168
Q

What % of individuals with gallstones will develop complications/symptoms?

A
  • Most individuals with gallstones remain asymptomatic
  • 1-4% of individuals will develop symptoms/complications 2ary to their gallstones
169
Q

What are the 2 most common complications/symptoms of gallstones?

A
  1. Biliary colic (most common)
  2. Acute cholecystitis
170
Q

What is biliary colic? Location? Cause?

A

WHAT → A steady or intermittent ache in the upper abdomen, usually under the right side of the rib cage (RUQ) but may radiate to epigastrium and/or back

WHY → Gallbladder neck becomes impacted by a gallstone; no inflammatory response but the contraction of the gallbladder against the occluded neck causes pain

171
Q

How long does biliary colic last?

A

typically lasts for >30 minutes but <8 hours

172
Q

Does biliary colic cause an inflammatory response?

A

No i.e. no fever or abdominal tenderness

173
Q

Biliary colic pain can be precipitated by eating what type of foods? Why?

A

Fatty foods

Fatty acids stimulate duodenum endocrine cells to release CCK which stimulates the contraction of the gallbladder (causes biliary colic pain).

174
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder

175
Q

How does acute cholecystitis present?

A
  • Constant pain and tenderness in the RUQ or epigastrium
  • Signs of inflammation (as does cause inflammatory response) e.g. fever or lethargy
176
Q

What are the symptoms of gallstones?

A
  • Biliary colic
  • Acute cholecystitis
  • Obstructive jaundice
  • Cholangitis
  • Gallstone pancreatitis
177
Q

How does obstructive jaundice affect;

a) skin
b) urine
c) stools

A

AKA post-hepatic jaundice

a) yellow
b) dark urine (conjugated bilirubin excreted in urine)
c) pale stools (lack of bilirubin entering gut)

178
Q

What is Charcot’s triad?

A

Fever (often with rigors)

Jaundice

UQ abdominal pain

179
Q

What would Charcot’s triad indicate?

A

Cholangitis (inflammation of the bile duct system)

180
Q

What is gallstone pancreatitis?

A

Gallstone pancreatitis occurs when a gallstone blocks your pancreatic duct causing inflammation and pain in your pancreas.

181
Q

Symptoms of gallstone pancreatitis?

A

constant epigastric pain radiating to back and profuse vomiting

182
Q

What does a positive murphy’s sign indicate?

A

Acute cholecystitis (i.e. inflamed gallbladder)

183
Q

Describe eliciting Murphy’s sign

A

Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive

184
Q

What may guarding during palpation of the gallbladder indicate?

A

Gallbladder perforation

185
Q

Where would tenderness typically present with symptomatic gallstones?

A

RUQ tenderness

186
Q

What 2 main investigations are performed in the context of gallstones?

A
  1. Abdominal US
  2. Blood tests
187
Q

Give some features you may see on an abdominal US in the context of gallstones?

A
  • Presence of gallstones
  • Gallbladder wall thickness (inflammation)
  • Bile duct dilatation (stone in distal bile ducts)
188
Q

Does the absence of gallstones on an US exclude their existence?

A

No

189
Q

Describe potential blood tests results in gallstones:

  • FBC
  • CRP
  • LFTs
A
  • FBC - raised WCC (inflammatory response)
  • CRP - raised
  • LFTs - may be abnormal with gallstones in the common bile duct
190
Q

What test should always be done in women presenting with any abdominal pain?

A

Pregnancy test (risk of ectopic pregnancy)

191
Q

Why should amylase (or lipase) also be tested in the context of gallstones?

A

To assess for pancreatitis

192
Q

Treatment for gallstones in asymptomatic patients?

A

No treatment

193
Q

Lifestyle advice for gallstones?

A

diet, weight loss, exercise

194
Q

What is required in the context of acute cholecystitis?

A

IV antibiotics (and emergency admission for those who are systematically unwell)

195
Q

Which cells primarily produce stomach acid?

A

Parietal cells

196
Q

Which drug targets the parietal cells of the stomach in order to reduce stomach acid?

A

H2 antagonists e.g. ranitidine

197
Q

What is absorbed in the terminal ileum?

A

B12

198
Q

How can hyperparathyroidism cause pancreatitis?

A

Hyperparathyroidism causes hypercalcaemia that leads to activation of trypsinogen to trypsin, resulting in autodigestion of the pancreas and subsequent pancreatitis.

199
Q

What well known medications cause acute pancreatitis?

A
  • thiazide diuretics
  • azathioprine
  • tetracyclines
  • sodium valproate
  • furosemide
  • oestrogens
  • corticosteroids
  • sulphonamides
200
Q

Link between CCK and gallstones?

A

Anything that reduces CCK signalling (e.g. somatostatin analogues) to gallbladder smooth muscle results in reduced gallbladder emptying and promotes gallstone formation.

201
Q

Mechanism of somatostatin analogues?

A

Somatostatin inhibits the release of pancreatic hormones, including insulin, glucagon and gastrin, and pancreatic enzymes that aid in digestion.

In your GI tract, somatostatin reduces gastric secretion, which is stimulated by eating.

202
Q

how can somatostatin analogues lead to gallstones?

A

Somatostatin analogues cause increased formation of cholesterol-rich crystals in the bile and inhibition of post-prandial gallbladder motility and impaired relaxation of the sphincter of Oddi, particularly through inhibitory effects on CCK release.

203
Q

What is CCK?

A

Cholecystokinin is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein.

204
Q

What is CCK responsible for stimulating the digestion of?

A

Fat and protein

205
Q

Where is CCK synthesised and secreted?

A

CCK is synthesised and secreted by enteroendocrine cells in the duodenum.

206
Q

Where are CCK cells concentrated?

A

CCK cells are concentrated in the proximal small intestine, and hormone is secreted into the blood upon the ingestion of food.

207
Q

Function of CCK?

A

The physiological actions of CCK include stimulation of pancreatic secretion and gallbladder contraction, regulation of gastric emptying, and induction of satiety.

Yr 3 - Core Conditions (33 decks)

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