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Phase 2a > GI > Flashcards

GI Flashcards

1
Q

Symptoms of GI disease?

A

Dyspepsia and indigestion

Discomfort of upper abdomen

Dysphagia

Vomiting

Abdo pain

Flatulence

Diarrhoea and constipation

Steaorrhoea

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2
Q

Types of endoscopies?

A

Osophagogatrodudenography (OGD)

Sigmoidography

Endoscopic retrograde cholangiopancreatography (ERCP)

Endoscopic ultrasound

Endoanal + Endorectal ultrasound

Balloon enteroscopy

Capsule Endoscopy

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3
Q

How can X rays be used for GI conditions?

A

Oesophageal perforations

Dilated loops of bowel

Calcification of the pancreas

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4
Q

Imaging that can be used to confirm malignancy?

A

CT or PET

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5
Q

What are contrast studies used for in GI disease?

A

using ingestible barium

Strictures and motility problems

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6
Q

Infective causes of mouth ulcers?

A

Coxsackie A

Herpes zoster or simplex virus type 1

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7
Q

Non-infective association of mouth ulcers?

A

Anaemia

IBD

Behcet’s (blood vessel inflammation)

Smoking or alcohol

Squamous cell carcinoma

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8
Q

What can cause oral white patches on the tongue?

A

Long term use of broad spec antibiotics

Inhaled steroids

DM or immunosuppressants

Smoking and alcohol

Lichen planus

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9
Q

Glossitis?

A

Red, smooth and sore tongue -

Decreased B12, Riboflavin, Folate or iron

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10
Q

Black and hairy tongue?

A

The proliferation of chemogenic microorganisms - build up of dead cells on the papillae of the tongue

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11
Q

Geographic tongue?

A

Harmless

Irregular red and white patches on the tongue

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12
Q

Gum bleeding?

A

Gingivitis - inflammatory condition of the gums caused by plaques

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13
Q

Vincent’s infection?

A

Acute ulcerative gingivitis which causes crater-like ulcers and spread laterally

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14
Q

Salivary gland disorders?

A

Xerostomia - dry mouth (sjorgrens syndrome, anxiety, tricyclics, dehydration)

Infection

Calculus forming on ducts of glands

Tumour of the parotid

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15
Q

Symptoms of oesophageal disorders?

A

Dysphagia

Odynophagia

Regurgitation

Heartburn

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16
Q

Short history of progressive dysphagia?

A

Due to mechanical stricture as the patient cant handle solids followed by liquids

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17
Q

Slow onset dysphagia for both solids and liquids?

A

Achalasia - motility disorder

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18
Q

Pathophysiology of GORD?

A

Reflux of gastric acid, bile, pepsin and duodenal content back into the oesophagus overcoming normal defences such as the LOS

(people with GORD are more predisposed to the LOS relaxing)

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19
Q

Risk factors of GORD?

A

Increased abdominal pressure (pregnancy)

Delayed gastric emptying

Decreased LOS pressure

Post-prandial

Nocturnal

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20
Q

Clinical features of GORD?

A

Heartburn

Sometimes regurgitation then cough or nocturnal asthma due to aspiration of gastric contents in the lungs

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21
Q

Investigations done to confirm GORD?

A

>55 + alarm symptoms - OGD - suspected malignancy as it can show inflammation

24 Hour intraluminal pH monitoring - use to confirm GORD before surgery if the patient no respond to PPI

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22
Q

Management of GORD?

A

Mild - lifestyle factors + antacids

Alginate containing antacids

Dopamine antagonist prokinetic agents

H2 receptor antagonist

PPI

Surgery - mechanical fundoplication

Linx reflux management system

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23
Q

MOA alginate containing antacids?

A

Forms a protective foam over gastric contents stopping them escaping the stomach

Mg containing - diarrhoea

Aluminium containing - constipation

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24
Q

MOA dopamine antagonist prokinetic agent?

A

Increase rate of peristalsis and gastric emptying

metoclopramide

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25
Q

H2 receptor antagonists?

A

(-tinide)

Decrease gastric acid

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26
Q

PPI?

A

Inhibits the H+/K+ ATP-ase and decreases acid secretion

Long term use associated with osteoporosis and C.diff

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27
Q

Mechanical fundoplication?

A

Wrapping the fundus of the stomach around the lower part of the oesophagus

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28
Q

Linx reflux management system?

A

Uses row of magnets to increase LOS closure pressure

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29
Q

Complications of GORD?

A

Peptic stricture

Barrets oesophagus - squamous epithelium to columnar epithelium so can be more like the stomach - increase risk of oesophageal cancer

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30
Q

NERD?

A

Non-endoscopic reflux disease - people who don’t respond to PPI

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31
Q

Achalasia?

A

Aperistalisis and impaired relaxation of the LOS - >50% of patient found to have an elevated LOS

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32
Q
A
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33
Q

Clinical features of achalasia?

A

Long history of dysphagia for solids and liquids

Difficulty swallowing, discomfort and regurgitation

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34
Q

Investigations done to confirm Achalasia?

A

CXR - dilated oesophagus

Barium swallow - birds beak and lack of peristalsis and dilation

CT + oesophagoscopy - exclude carcinoma

Manometry - shows aperistalsis and contracted LOS

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35
Q

Management of Achalaisa?

A

Nitrates or nifedipine

Endoscopic balloon dilatation

Surgical division of LOS

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36
Q

A complication of Achalasia?

A

A marginal risk of squamous carcinoma

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37
Q

What is systemic sclerosis?

A

Smooth muscle of oesophagus replaced by fibrous tissue which further decreases the LOS pressure (+ hypomotility) so increased reflux of gastric acid into the oesophagus

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38
Q

Diffuse oesophageal spasms?

A

simultaneous contractions in distal oesophagus

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39
Q

Nutcracker oesophagus?

A

High amplitude peristaltic waves

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40
Q

Hypersensitive LOS?

A

Increased contractive pressure of LOS

Dysphagia and chest pain

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41
Q

Difference between sliding and para-oesophageal hernia?

A

Sliding - GO junction slides through the O hiatus alongside the oesophagus and lies above the diaphragms

Para-oesophageal - fundus rolls up the hiatus alongside the oesophagus but the GO junction remains below the diaphragms

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42
Q

Benign oesophageal strictures?

A

Secondary to GORD

Ingestion of corrosives

After radiotherapy

Endoscopic treatment of varices

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43
Q

Iatrogenic perforation?

A

After endoscopic dilatation of O strictures or achalasia

Treat with an expanding covered oesophageal stent to seal the hole

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44
Q

Traumatic or spontaneous oesophageal rupture?

A

Occur after blunt chest trauma or forceful vomiting (Boerhaave)

Pain, fever, hypotension and crepitation (surgical emphysema)

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45
Q

Which part of the oesophagus is most likely for an adenocarcinoma to develop?

A

Lower 1/3 and cardia

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46
Q

Which part of the oesophagus would a squamous cell carcinoma most likely develop?

A

Middle and upper 1/3

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47
Q

Clinical features of oesophageal cancer?

A

Dysphagia

Weight loss

Chest pain from bolus food impaction

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48
Q

Investigations to diagnose oesophageal cancers?

A

OGD + tumour biopsy

Barium swallow - rule out motility disorders

CT - look for distant metastasis

EUS - depth of wall invasion and local lymph node involvement (stage)

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49
Q

Management of oesophageal cancer?

A

Surgical resection

Induce tumour necrosis (endoscopic metal stent across tumour, laser or alcohol injections)

Radio or chemotherapy

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50
Q

The role of stomach acid?

A

To kill food bourne infections

reservoir for food

secretion of intrinsic factor

Emulsification

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51
Q

Pathophysiology of H.pylori?

A

Urease producing G-ve bacteria that is found in the antrum of the body of the stomach. It lowers the pH of the stomach

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52
Q

Conditions associated with H.pylori?

A

Chronic gastritis, Peptic ulcers, Gastric cancer or gastric B cell lymphoma

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53
Q

Non-invasive diagnostic techniques for H.pylori?

A

Serology (serum antibodies)

Urea breath test

Stool sample (antigens)

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54
Q

Management of H.pylori?

A

Triple PPI therapy

Omeprazole, metronidazole and clarithromycin

or

Omeprazole, amoxicillin and clarithromycin

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55
Q

What is a peptic ulcer?

A

Ulcer/ sores that develop in the stomach wall due to a weakness in the mucosal layer of the stomach lining

DU>GU

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56
Q

Causes of peptic ulcers?

A

H.Pylori

NSAIDS

Aspirin

(decrease prostaglandins by inhibiting cylco-oxygenase 1 decreasing the protection of the upper GI tract)

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57
Q

Clinical features of peptic ulcers?

A

Burning epigastric pain

Nausea, heartburn or flatulence

DU pain - when hungry or at night

Rare - painless haemorrhaging

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58
Q

PU: When would you use a non-invasive test for PU?

A

<55 + ulcer type symptoms

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59
Q

Other investigations to confirm peptic ulcer?

A

Routine endoscopy followed by biopsy

Barium meal - if there is suspected outflow obstruction

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60
Q

Management of peptic ulcer?

A

H.pylori +ve - triple therapy

H.Pylori -ve - PPI and stop causative medication

PPI prophylaxis

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61
Q

Complications of peptic ulcers?

A

Perforation

Gastric outlet obstruction (projectile vomit - mostly cancer)

Haemorrhage

(IV FLUIDS AND ANTIBIOTICS TO BE GIVEN)

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62
Q

Causes of gastritis?

A

H.pylori

Autoimmune (pernicious anaemia)

Virus

Duodenogastric reflux

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63
Q

Difference between acute and chronic gastritis?

A

Acute - neutrophil infiltration

Chronic - lymphocytes, macrophages, plasma cells and mononuclear cells

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64
Q

What kind of cancers are usually gastric cancers?

A

adenocarcinomas of the antrum

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65
Q

Clinical features of gastric cancer?

A

Nausea, anorexia and weight lost

Peptic ulcer pain

if near pylorus: Dysphagia + vomiting

Palpable epigastric mass

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66
Q

Investigations of gastric cancer?

A

Gastroscopy + biopsy - identify

CT, EUS and laproscopy - stage

67
Q

Signs of acute upper GI bleed?

A

Haematemesis - cough up blood

Melaena - dark tarry poop

if in shock and lots or rectal blood - badddddd

68
Q

Most common cause of upper GI bleed?

A

PU

Made worse by anticoagulants

(other varices, NSAIDs, alcohol, mallory-weis (tears of the mucosal membrane of the OE junction))

69
Q

Scoring system used to identify those at risk of recurrent or life-threatening upper GI haemorrhage or those low risk enough to be discharged?

A

Rockall Score - age, shock?, endoscopic stigmata and diagnosis

70
Q

What can cause a massive lower GI bleed?

A

Diverticular disease or ischaemic colitis

71
Q
A
72
Q

What can cause a minor lower GI bleed?

A

Haemorrhoids

Anal fissure

73
Q

What is a proctoscopy used for?

A

Anarectal disease

74
Q

What do chronic GI bleed present with?

A

Iron deficiency anaemia

75
Q

Causes of chronic GI bleeding?

A

Angiodysplasia (abnormal or enlarged blood vessels of the GI)

Cancer

Colitis

Polyps

Diverticular disease

76
Q

Investigations to confirm chronic GI bleeding?

A

OGD + endoscopy

Distal duodenal biopsy

Angiography

77
Q

Management of chronic GI bleed?

A

Treat the cause of bleeding

oral iron given to treat anaemia

78
Q

what are some presenting symptoms of small bowel disease?

A

Steatorrhoea

Diarrhoea

Abdo pain and discomfort

Anorexia

Malabsorption - deficiencies

79
Q

common investigations used to identify small bowel disease?

A

coeliac serology

small barium follow

MRI

Endoscopy

80
Q

Coeliac?

A

Villous atrophy and crypt hyperplasia due to inflammatory cause by gluten and gluten-sensitive T cells

81
Q

What component of gluten causes coeliac and dermatitis hepatiformis?

A

Gliadin

82
Q

Pathophysiology of coeliac?

A

In the jejunum

Gliadin is resistant to the proteases in the small intestine

The DQ code of inflammatory T cells recognise gluten and cause an inappropriate inflammatory response

Gliadin passes through the damaged epithelium and is deaminated by tissue transglutaminase - increases immunogenicity

83
Q

Which HLA are associated with coeliac?

A

HLA DQ 2.5

HLA DQ 8

HLA DQ 2.2

84
Q

Clinical features of coeliac?

A

Abdo pain

Malaise

Tiredness

Deficiency

associated with other autoimmune conditions

85
Q

Investigations done to confirm coeliac?

A

IgA tissue transglutaminase

IgA endomysial antibodies

Distal duodenal biopsy (histological features)

Blood count (deficiency and anaemia)

Bone densitometry

Small bowel radiology

86
Q

Management of coeliac?

A

Gluten free diet + correct vitamin deficiencies

Pneumococcal vaccination

87
Q

Complications of coeliac?

A

Dermatitis hepatiformis - skin manifestation of coeliac that itches and you get fluid-filled blisters (IgA at dermoepidermal junction)

Whipple’s disease - rare bacterial infection that affects joins and digestive system

Intestinal resection - malabsorption and short bowel syndrome

Bacterial overgrowth - stasis in upper small bowel normally sterile causes bacteria to grow and they can deconjugate bile salts and use up B12

Tropical sprue - abnormal flattening of the villi and inflammation fo the lining of the small intestine

88
Q

How can intestinal resection caused by coeliac lead to oxalate stones?

A

Malabsorption of B12 and bile sals causes diarrhoea’s so you lose water and electrolytes and you get increased oxalate - renal oxalate stones

89
Q

How to identify if a patient has bacterial overgrowth as a complication of coeliac?

A

Measure hydrogen after oral lactulose which is produced by colonic bacteria

90
Q

Conditions that can cause protein loss enteropathy?

A

Coeliac

Crohns

Thicken and enlargement of gastric folds (menetrier disease)

INCREASED PROTEIN LOSS DUE TO ABNORMAL MUCOSA

91
Q

Meckel’s diverticulum?

A

True diverticula of the small intestines that can contain gastric mucosa - secrete acid = ulcer

RULE OF 2 - 2 years old, 2ft from ileocecal valve and 2% of the population

LOWER GI BLEEDING, PERFORATION, INFLAMMATION, OBSTRUCTION

92
Q

where do carcinoid tumours of the small intestine originate form?

A

Enterochromaffin cells that produce serotonin

93
Q

Carcinoid syndrome?

A

Where they have liver metastasis and drain into the hepatic vein and therefore systemic circulation

symptoms: flushing, wheezing, diarrhoea, abdo pain, heart failure

94
Q

Investigations used to confirm carcinoid tumours?

A

liver ultrasound

Increased 5 - hydroxy-in-dole-actic acid

95
Q

Management of carcinoid tumours of the small intestine?

A

Serotonin antagonist

Somatostatin analogue (octreotide)

Surgical resection

96
Q

Host immune response in IBD?

A

Effector T cell > Regulatory T cell

Pro-inflammatory cytokines - IL12, INF-GAMMA, IL5, IL17

causes:

release of mast cells, neutrophils, eosinophils

Macrophages - TNF alpha, IL1 AND IL6

97
Q

Macroscopic differences between UC and CD?

A

UC: Rectus and sigmoid colon - left-sided and transverse

rectum and extends proximally

continuous colonic involvement

Red mucosa that bleeds easily

Ulcers and pseudopolyps

CD: any part of the GI tract

ileocaecal and perianal - can affect small bowel

skip lesions

Deep ulcers and fissures - cobblestone appearance

98
Q

Microscopic differences between UC and CD?

A

UC: mucosal inflammation

no granulomata

goblet cell depleation

crypt abscess

CD: transmural inflammation

Granulomatous formation

99
Q

Differences in clinical features between UC and CD?

A

UC: Diarrhoea with blood and mucus

CD: SB - Abdo pain

TI - mimics appendicitis

COLON - diarrhoea, bleeding and pain at poo

PERIANAL - anal tags, fissure, fistulae or abscess formation

100
Q

Extragastrointestinal manifestations of IBD?

A

Eyes - conjunctivitis

Joins - Ankylosing spondylitis, small joint arthritis, inflammatory back pain

Skin - Erytherma nodosum, pyoderma gangrenosum (necrotising ulceration of ksin of lower leg)

Hepatobiliary - gall stones, PSC, Hepatitis

Renal - oxalate stones

Venous thrombosis

101
Q

Investigations done to confirm IBD?

A

Aim is to identify IBD - Severity and if it is UC or CD

BLOODS -Anaemia due to malabsorption (CD - platelet, ESR, C reactive protein and decreased albumin)

RADIOLOGY AND IMAGING -

Rigid or flexible sigmoidoscopy

Colonoscopy

Small bowel imaging

Plain Abdo X ray - toxic megacolon and loss of colon folds or gas

STOOL - faecal calprotein - migration of neurophils in mucosa

102
Q

Management of IBD?

A

Oral 5 ASA - aminosalicylic acid (mild) - interfere with arachidonic acid meaning enzymes needed to produce leukotrienes and prostaglandins don’t work - decrease leukocytes and production of cytokines

STEROIDS - prednisolone, hydrocortisone of budesonide

LIQUID ENTERAL NUTRITION

AZATHIOPRINE -bone marrow suppression

METRONIDAZOLE - antibiotic

METHOTREXATE - immunosuppressant

ANTI-TNF ANTIBODIES - for patients resistant to everything

103
Q

What needs to be measured when prescribing azathioprine?

A

Thioprine methyltransferase because this is needed to metabolise and active azathioprine so if there is no activity from the enzyme - greater risk of pancytopenia

104
Q

Surgical management of IBD?

A

Colectomy with ileoanal anastomosis - terminal ileum is used to form a reservoir so the patient can be continent a few times a day however this can become inflamed

Panprotocolectomy with ileostomy - whole colon and rectum removed and ileum attached to abdo wall as a stoma

105
Q

Complications of IBD?

A

Toxic megacolon + perforation

Stricture formation

Abscess formation

fistulae and fissures

colon cancer

106
Q

Microscopic colitis?

A

Colonic mucosa looks normal on colonscopy but histological examination shows:

lamina propia inflammation

Increased intraepithelial lymphocytes

Subepithelial collagen layer

107
Q

Symptoms and management of microscopic colitis?

A

Symptoms - watery diarrhoea induced by coeliac or NSAIDS

Loperamide - not to be given to people with bloody diarrhoea’s

Budesonide

108
Q

IBS?

A

Irritable bowel syndrome is a mixture of abdominal symptoms with no known organic or identifiable cause

problems with intestinal motility, enhanced visceral perception or microbial dysbiosis

109
Q

Epidemiology of IBS?

A

10 - 20% <40 years old

2:1 F:M

110
Q

Diagnostic criteria for IBS?

A

Abdo pain + 2 or more of the following:

Pain relief at defecation

Pain associated with change in stool consistency

Pain associated with change in frequency of defecation (Constipation or diarrhoea)

111
Q

Other symptoms of IBS?

A

Urgency

Incompetnant

Bloating

Mucous PR

112
Q

What can exacerbate IBS?

A

Stress

Menstruation

Gastritis

113
Q

Management of IBS?

A

Lifestyle and diet change

Constipation - Laxatives (lactulose - bloating), PRUCALOPRIDE, LUBIPROSTONE, LINACLOTIDE

Diarrhoea - Loperamide after loose stool

Bloating - mebeverine or hyoscine butyl bromide + low FODMAP- antispasmodics

Psychological - CBT or SSRI

114
Q

Appendicitis?

A

Inflammation of the appendix due to gut bacteria and leukocytes invading the wall of the appendix following obstruction

(most common surgical emergency of the abdomen)

115
Q

What 3 things can cause an obstruction of the appendix?

A

Faecolith

Pinworm infections

Lymphoid hyperplasia - increase in size during adolescence and increase more during viral infections and they can get so big the occlude the appendix

116
Q

Pathophysiology of appendicitis?

A

Lumen of the appendix is always filled with mucous and fluid to keep pathogens entering blood and to keep it moist but even when obstruction enters it continues to secrete + bacteria multiply

Increase pressure on the appendix wall puts pressure on the nerves which lead to RLQ pain

Puss formation and increased WCC

Increased pressure ow pressing on blood vessels and ischaemia occurs - cells die - bacteria are now able to invade the wall

Wall becomes weaker and thinner and then ruptures - bacteria now escape into peritoneum = peritonitis

Pus and fluid now surround the appendix and abscess form (periappendeal or subphrenic)

117
Q

Investigations done to confirm appendicitis?

A

CT

Increased CRP

Increased WCC

118
Q

Signs and symptoms of appendicitis?

A

Tachycardia

Fever

Pain during PR

Constipation

RLQ pain

Rebound sign - PRIF> PLIF when pressing on LIF

Psoas sign - Pain on extension of thigh

Cope’s sign - Pain on flexion and rotation of thigh

119
Q

Management of appendicitis?

A

Appendectomy

Drain the fluid around the appendix

Antibiotics - Tazobactam or piperacillin

120
Q

Complication of appendicitis?

A

Perforation

Appendix abscess

Appendix mass - inflamed appendix becomes covered with omentum

121
Q

Signs and symptoms of bowel obstruction?

A

Nausea

Vomiting

Cramping

Obstipation

Distended abdo

Fever

Tachycardia

Tinkling or absent abdo sounds

122
Q

5 causes of mechanical obstruction?

A

Adhesion - 2 parts connected by a fibrous band (most common)

Tumour - colorectal cancer

Intussusception - Bowel invaginates on itself

Herniation - protrusion of a part of bowel through the wall that is meant to contain it - can become ischaemic

Volvulus - twisting of intestines around its self at a single point

123
Q

3 causes of pseudo-obstruction?

A

Myopathy - no peristaltic contractions of the GI

Neuropathy - No innervation of smooth muscle so no peristaltic movements

Hirschprung disease - nerves missing at the distal end of the colon resulting in no/ abnormal peristalsis

124
Q

Investigations of bowel obstructions?

A

AXR

CT

125
Q

Complications of bowel obstruction?

A

Bowel ischaemia - due to venous compression - ischaemia and necrosis

Perforation

Sepsis - due to perforation as bowel cells die and rupture occurs - release of gut bacteria into circulation

Hypovolaemiac shock - venous compression means more fluid in the abdomen meaning loss of electrolytes and water or fluid loss through wanting to vomit

126
Q

Management of bowel obstruction?

A

NGT and IV fluids to rehydrate and correct electrolyte balance

Analgesia

CT

Surgery

Neostigmine - promotes colonic motility by increasing acetylcholine as it is a reversible acetylcholinesterase inhibitor

127
Q

Define:

Diverticulum

Diverticula

Divertculosis

Diverticular disease

Diverticulitis

A

OUTPOUCHING OF COLONIC MUCOSA AND UNDERLYING CONNECTIVE TISSUE THROUGH THE COLON WALL AT WEAK POINT OF THE WALL WHERE BLOOD VESSELS PENETRATE ALL THE LAYERS

Diverticulum - 1 outpouching

Diverticula - multiple outpouchings

Diverticulosis - multiple outpouching but no symptoms

Diverticular disease - multiple outpouching and symptoms

Diverticulitis - inflammation of the diverticula

128
Q

What is the difference in diverticula distribution between western patients and Asian patients?

A

Western - Sigmoid colon

Asian - Ascending, H. flexure and part of transverse

129
Q

Pathophysiology of diverticulitis?

A

IMA branches penetrate all the layers of the GI wall causing them to be weaker

insufficient dietary fibre increases intracolonic pressure and the mucosa forms an outpouching at these weak points in the wall

Diverticulitis - microflora or faeces get lodged in the neck of the diverticulum - ischaemia - necrosis and inflammation

130
Q

Risk factors for diverticulitis?

A

Age

M > F

Low fibre diet

NSAIDS

Corticosteroids

Exercise

131
Q

Signs and symptoms of diverticulitis/ diverticular disease?

A
  1. 95% asymptomatic + pain in LIF
  2. Constipation along with IBD
  3. Bleeding diverticulum - large volume of blood at defecation due to rupture of the blood vessels
  4. Diverticulitis - nausea, fever, tachycardia - acute LIF pain and loose stool
132
Q

Investigations use to confirm diverticular disease?

A

Colonoscopy

Barium enema

FBC, CRP, ESR

CT - identify complications

133
Q

Management of diverticular disease?

A

Increase fibre and water

ACUTE:

IV antibiotics - cephalosporin or metronidazole

Analgesia

fluid

Resection - SEGMENTAL COLECTOMY

134
Q

When is it recommended to do segmental colectomy on a patient who has diverticular disease?

A

Perforate

Undrainable abscess

Inflammation not responding to medical treatment

Fistulae formation

135
Q

Complications of diverticular disease?

A

Abscess

Diverticulitis

Perforation - peritonitis

Fistulae formation between colon and bladder or colon and vagina

Intestinal obstruction

136
Q

3 types of bowel ischaemia?

A

Acute mesenteric ischaemia

Chronic mesenteric ischaemia

Chronic colonic ischaemia

137
Q

Acute mesenteric ischaemia?

A

SMA + small bowel

Thrombosis, embolism or mesenteric vein thrombosis

Trauma, vasculitis, radiotherapy, strangulation

SEVERE ABDO PAIN OUT OF PROPORTION TO PHYSICAL EXAM FINDINGS

SYMPTOMS TRIAD:

Acute abdo pain, Rapid hypovolaemia, Minimal abdo signs on exam

138
Q

Investigations done to confirm acute mesenteric ischaemia?

A

AXR - gasless abdomen

ANGIOGRAPH

BLOODS - Increase Hb due to loss of plasma, WCC, amylase and metabolic acidosis (lactate)

LAPAROTOMY - nasty necrotic bowel

139
Q

Management of bowel ischaemia?

A

Fluid and antibiotics (tazobactam)

LMWH (long term anticoagulation)

Thrombolysis

Removal of dead bowel

Revasularisaition followed by 2nd laparotomy

140
Q

Complications of acute mesenteric ischaemia?

A

septic peritonitis and systemic inflammation

141
Q

Chronic mesenteric ischaemia?

A

Intestinal angina

SYMPTOM TRIAD: Decreased weight, upper abdo bruit, severe postprandial abdo pain

INVESTIGATIONS - CT/ MR angiography

MANAGEMENT - Revascularisation - Percutaneous transmural angiography or stent

142
Q

Chronic colonic ischaemia (ischaemic colitis)?

A

Low flow in IMA territory and this can range from mild ischaemia to gangrenous colitis

Symptoms - Lower left-sided abdo pain and bloody diarrhoea

Investigations - GI endoscopy + CT

Management - Fluid replacements + antibiotics + resuscitation - resection and STOMA :(

143
Q

Complications of chronic colonic ischaemia?

A

Ischaemic stricture

Gangrenous ischaemic colitis - peritonitis and hypovolaemic shock

144
Q

Mallory Weiss tears?

A

Most common cause of upper GI bleeding

Tears at the OG junction due to persistent retching, vomiting or coughing resulting in haematemesis

SYMPTOMS - Haematemesis, melena, dizziness and abdo pain

INVESTIGATIONS - Endoscopy

MANAGEMENT - Heal on its own or endoscopic injection therapy :

  • Epinephrine injection
  • Haemoclipping

Embolization

Cauterization

145
Q

Haemorrhoids pathophysiology?

A

Anus is surrounded by anal cushions which contribute to the anal closure

Cushions are attached by smooth muscle and elastic tissue which are prone to displacement and they protrude through the tight anus and become congested - hypertrophy and strangulation

146
Q

causes of haemorrhoids?

A

Constipation with prolonged straining

Congestion - pelvic tumour or pregnancy

147
Q

Signs and symptoms of haemorrhoids?

A

Bright red blood coating stool, tissue and pan

Mucus discharge and pruritus discharge

Anaemia, weight loss and tenesmus

148
Q

Management of haemorrhoids?

A

Fluid and fibre

Stool softener

Topical analgesics

Rubber band ligation

Sclerosant injection - vessels dilate and cut off flow which in turn then causes the vessels to shrink

Infrared coagulation

149
Q

Pruritus ani?

A

Itchy anus - avoid scratching, have good hygiene and avoid food that softens stools

150
Q

Anal fissure?

A

Painful tear of the squamous lining of the lower anal canal caused by hard faeces or spasms constricting blood flow meaning it takes longer for the fissures to heal

(SYPHILIS, CROHNS, HERPES, TRAUMA OR ANAL CANCER)

MANAGEMENT: Lidocaine, GTN ointment, Topical diltiazem, fibre and fluids or stool softener

151
Q

Anal fistulae?

A

Abscess forms due to anal crypts being infected - then they rupture and a fistula (track route) between skin and anal canal is formed

(CROHNS AND DIVERTICULAR DISEASE)

152
Q

Pilonidal sinus?

A

(small hole in the skin)

obstruction of the natal cleft 6cm above the anus - hair follicles become clogged with debris and it excites a foreign body reaction forming an abscess with a foul-smelling discharge

MANAGEMENT - Excision of sinus tract, primary closur, antibiotics or cover with skin flaps

153
Q

Rectal prolapse?

A

Mucosa (1) or all the layers (2) of the rectum protrudes through the anus due to a lax sphincter (or neurological or prolonged straining)

MANAGEMENT- Rectoplexy - fix the rectum to the sacrum

154
Q

Proctalgia Fugax?

A

Idiopathic cramping rectal pain often worse at night

MANAGEMENT - reassurance, salbutamol (shortens attacks of pain), topical GTN or Diltiazem

155
Q

What staging system is used to measure the severity of colon cancer?

A

Duke’s stages of colon cancer - How much of the GI wall has been invaded

156
Q

T/F proximal cancer have a worse prognosis?

A

T

157
Q

T/F majority of cancers are in the distal colon?

A

T

158
Q

Key features of coeliac?

A

Atrophic villi and hypertrophic crypts graded using marsh stages

159
Q

Symptoms of C.diff?

A

Spore forming bacteria

Watery diarrhoea, abdo pain, bloody, Increased WBC and toxic megacolon

160
Q

What things would increase if a patient had PBC compared to PSC?

A

PBS - Increased ALP and bilirubin

  • Fatigue, pruritus, xathelasma, +ve AMA + IgM, intrahepatic duct

PSC - Increased ALT and AST

  • Fatigue, pruritus, jaundice, ANCA, intra and extrahepatic
161
Q

How would a patient with a paracetamol overdose present?

A

Metabolic acidosis, Increased PTT, Increased creatinine, hypoglycaemia, Increase ALT, Coagulopathy and renal failure

<8 hours - activated charcoal

>8 hours - acetylcysteine

162
Q

Wernicke’s encephalopathy?

A

Decreased thiamine causes ataxia, nystagmus, Ophalmoplegia (paralysis of muscles surrounding the eye) and confusion

If untreated it develops into korsakoff’s which is untreatable

163
Q
A

Phase 2a (7 decks)

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