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GI Flashcards

1
Q

|what are the three causes of bowel obstruction

A

problems in the lumen
obstruction in teh wall
obstruction pressing onteh bwel from teh outside

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2
Q

what are the three main cuases of small bowel obstructions

A

adhesions
hernias
cancers

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3
Q

what s teh test you need to do for small bowel instruction

A

CT scan! xrya is not good enough

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4
Q

what are teh common causes of diahorrhea that come on after

2 hours
6 hours
12 hours

A

bacterial toxins
virus
bacteria

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5
Q

what is teh difference between functional and orgaic disease

A

Organic disease is one in which measurable changes are detected in cells, tissues, or organs of the body. In contrast, a functional disease causes symptoms, but the disease process is either unknown or it can’t be measured by an agreed-upon scientific method or standard.

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6
Q

chrons disease definition

A

Transmural granulomata’s infection affecting any part of the gut

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7
Q

chrons disease epidemiology

A

Northern europe and nrthen america

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8
Q

chrons disease pathophysiology

A

It originates in the mucosa and moves through the layers of the bowel, its most common in the ilium and colin, macroscopically there are skip lesions (it causes patches of inflammation not consistent), cobblestone appearance due to ulcers and fissures in the mucosa.

Microscopically it is transmural (affects all layers of the bowel) and causes non-caseating granulomas and goblet cell number decreases!!!

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9
Q

chrons disease key oresintations

A

CHRISTMAS

Cobblestones
Hight temp
Reduced lumen
Intestinal fistulae
Skip lesions
Transmural
Malabsorption
Abdominal pain
Submucosal fibrosis

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10
Q

chrons disease signs

A

Blood in the stool
Malabsorption
Mouth ulcer
Extra intestinal features - anal fissures erytherma nodosum, episcleritis

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11
Q

chrons disease symptoms

A

Diahrrhea
RUQ pain
Fatigue fever N&V
Tenderness

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12
Q

chrons disease 1st line test

A

Colonoscopy
Biopsy
Barium enema
Stool sample
FBC - raised ESR/CRP
Faecal calprotectin

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13
Q

chrons diseases differential

A

Alternative causes of diarrhoea - salmonella, giardia intestinalis, rotavirus
Chronic diarrhoea
IBS

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14
Q

chrons disease complications

A

Malabsorption
Obstruction - access
Acute swelling
Chronic fibrosis
Perforation
Fistula
Anal - fistula, fissure skin tag
Neoplasia - colorectal cancer
Systemic - amyloidosis

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15
Q

Ulcerative collitis defornition

A

Inflamatory condistion o the colon mucosa up t the ilioceacal valcve. Ulcers form in the lumen.

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16
Q

Ulcerative collitis epidemiology

A

Affects males and females equally
Ages 15-30

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17
Q

Ulcerative collitis risk factors

A

NSAIDS
Chronic stress
Family history
SMOKING RELIVES UC

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18
Q

Ulcerative collitis pathophysiology

A
  • Remains in the mucosa - doesn’t go though the walls of the bowel
  • Only affects the colon
  • Macrosoicalli - continous inflamtion, Ulcers, Psudopolyps
  • Microsopically - muclsoal inflamtion
  • No granuomata
  • Depleted goblet cells
  • Inceased crypt abcesses
    Paneth cells are part of the innate immune system and suggest inflamation when they are presant in the colon
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19
Q

Ulcerative collitis key presintations

A

ULCERATIONS
Ulcers
Large itestine
Carcinoma risk
Extra intestinal anifestations
Remenrnats of old ulcers - pseudopolyps
Abcess in the crympts
Toxic megacolon
Inflamed granular mucosa
Originates at rectum
Neutrophil invasion
Stool is blood and has mucous

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20
Q

Ulcerative collitis signs and symptoms

A
  • Rectal tenesmus - urgency, bleeding, incontance
  • Tender distended abdomen
  • Clubbing
  • Erythema nodosim
  • LLQ pain
  • Fever
  • Diarrhoea
  • Cramps
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21
Q

Ulcerative collitis tetst

A

Colonoscopy - diagnostic test
Biopsy

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22
Q

Ulcerative collitis differentials

A

Alternative causes of diahorreah - salmonella, giardia intestinalis, rotavirus

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23
Q

Ulcerative collitis treatment

A
  • Antiinflamatorys - sulfalazine, 5 aminosalisylic acid is absorbed in the small intesine
  • Immunosuppressors - corticosteroids, azathioprine
  • Anti TNF drigs - infiximab
  • Colectormy with ileoanal anastamosis indicated in patiens with severe UC not responding to treatment
  • Surgery - if severe
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24
Q

Ulcerative collitis complications

A

Liver - fatty change
Chronic pericholangtis
Sclerosing cholangitis
Blood loss
Toxic dilation
Colerectal cancer
Erythesma nodosum
Pyoferma gangrenosum
Ankylosing spondylitis
Arthitius
Iritis
Uvitis
Episcleritis

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25
Q

IBS definition

A

A group of abdominal symptoms for which no organic cause can be found.

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26
Q

IBS epidemiology

A

<40
F>m
Western world
Symptoms exacerbated by stress, food, gastroenteritis, menstruation

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27
Q

IBS causes

A

Psychological - stress, depression, anxiety, trauma
GI infection - gastroenteritis
Sexual, physical, verbal abuse
Eating disorders

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28
Q

IBS risk factors

A

Female
Stress
Gastroenterisis
Sever and long diarrhoea
Hypochondrial anxiety

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29
Q

IBS pathophysiology

A

Dysfunction of the brain gut axis resulting in disorder of intestinal motility and enhanced visceral sensitivity.
Recurrent abdominal pain with NO inflammation
There are 3 different types….

IBS - c - constipation
IBS - D - diarrhoea
IBS - M - constipation and diarrhoea

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30
Q

IBS key presintations

A

Mucus in stools
Change in stool frequency
Change in stool consistency
Incomplete emptying
Urgency
Worsening symptoms after food

Abdominal pain and bloating
Alternating bowel habits
Constipation
Diarrhoea

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31
Q

IBS tests

A

There is nothing physical found, so diagnosis is made by ruling out other differentials:

* Faecal calprotectin- raised in IBD 
* Colonoscopy - rule out IBD and colorectal cancer 
* FBC - anaemia 
* ESR and CRP for inflammation 
* Coeliac serology
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32
Q

IBS differentials

A

Coeliac diseases
Lactose intolerance
IBD
Colorectal cancer

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33
Q

IBS manegement

A
  • Lifestyle modification- fluids, avoid caffeine alcohol and fizzy drinks, have fibre for wind and bloating
  • Pain/bloating - Buscopan (muscle relaxer)
  • Constipation - laxative such as senna
  • Diarrhoea - anti motility -loperamide
    If none of the above work - try amitriptyline
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34
Q

coeliac disease definition

A
  • A state of heightened immunological responsiveness to ingested gluten in genetically susceptible individuals
    Ingestion of gluten stimulates the immune system to attack the small intestine
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35
Q

coeliac disease epidemiology

A
  • 40-60 age
  • 1/100 Europeans
  • Associated with other autoimmune conditions - diabetes 1, graves
    Presentation at any age - but normally after infancy
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36
Q

coeliac disease causes

A

Gluten found in wheat, barley and rye

BROWN - barley, rye, oats, wheat NEVER!!!

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37
Q

coeliac disease risk factos

A

Other autoimmune diseases
IgA deficiency
Age of introduction into the diet
Rotavirus infection in infancy increases the risk

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38
Q

coeliac disease pathophysiology

A
  • A- gliadin is the toxic part of gluten that is resistant to proteases in the small intestine
  • Gliadin binds to IgA in the mucosal body
  • The complex I then moved to the lamina propria via HLA DQ2 DQ8
  • It is then taken up by macrophages and expressed on MHCII
  • T helper cells release cytokines and c cells

It causes villous atrophy, crypt hyperplasia, reduced surface area for nutrient absorption, b12, folate and iron deficiencies which causes anaemia

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39
Q

coeliac disease key presintations

A

Classic:
* Diarrhoea
* Statorrhea
* Abdo pain
* Abdo distention
* Weight loss
* Faliure to thrive
* Nutritional deficency

Non classic:
* Dermatitis herpiformis - red raised patches with blisters caused by IgA antibodeies
* IBS symptoms
* Iron deficency aneamia
* Osteoporesis
* Chroic fatigue
* Ataxia
* Peripheral neuropathy
* Hypospleenism
* Amenorema
Infertility

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40
Q

coeliac disease testing

A
  • Serology - anti tissue transglutaminase (tTG) - anti-endomysial antibody (EMA) (IgA)- anti-gliadin IgG/IgA
  • Endoscopies and duodenal biopsies - villous atrophy, crypt hyperplasia, intraepithelial lymphocytes
  • Scalloping of mucosa, duodenal bulb
  • FBC - low B12, low ferratin, low Hb
    Autoimmune condition screening T1DM, Thyroiditis
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41
Q

coeliac disease tx

A
  • BROWN - barley, rye, oats, wheat NEVER!!!
  • Dietitian review to correct deficiencies
  • DEXA scan for the osteoporotic risk
    Treat anaemia
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42
Q

coeliac disease complications

A
  • T cell lymphoma
    • Osteoporosis
    • Anaemia
    • Infertility
    • Hypospleenism (reduced ability to fight infection)
      Vitamin deficient
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43
Q

gastritis defonition

A

Inflammation of the stomach lining associated with mucosal injury

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44
Q

gastritis and ulcers comparison

A

Gastritis is an inflammation of the stomach lining, while ulcers are open sores in the lining of the stomach – and sometimes in the duodenum (the first part of the small intestine). While they are separate issues, the causes and symptoms of gastritis and ulcers are similar.

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45
Q

gastritis causes

A
  • H Pylori
  • Immune gastritis - antibodies to parietal cells and iF
  • Viruses, CMV and HSV
  • Chrons diseassse
  • Incrased acid
  • Alcohol
  • Mucosal ishchemia
  • NSAIDs
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46
Q

gastritis pathophysiology

A
  • H Pylori - lives in the gastric mucosa and secretes urease which splits urea in the stomach into CO2 and ammonia, this then reacts tithe the H+ to mke ammonium which is damaging to the epithelium
  • This causes gastrin release, histamine release, increased parietal cell mass and decreases somatostatin released form d cells which all leads to increased acid secretion
  • Autoimmune gastritis - fundus and body of stomach- loss of parietal cells and intrinsic factor deficiency causing pernicious anaemia

NSAIDS - inhibit COX1

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47
Q

gastritis sign and symptoms

A
  • Anorexia
  • Abdominal bloating
  • Haematemesis
  • Epigastric pain
  • Nausea
  • Vomiting
  • Indigestion
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48
Q

gastritis differntials

A
  • Peptic ulcer
  • GORD
  • Gastric lymphoma
    Gastic carcinoma
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49
Q

gastritis treatment

A

CAP - clarithromycin, amoxicillin, PPI (omeprazole)
Prevention - give PPIs along side chnic NSAID use to prevent ulcers ad gastritis

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50
Q

GORD definition and causes

A

Gastro-oesophogeal reflux disease

Obestity
Hiatus hernia
Lower oesophoguel sphincter hyotension
Overeating

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51
Q

GORD risk factos

A

Obestiy
Male
Regnany
Hiatus hernia
Smoking

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52
Q

GORD pathophysiology

A

There is an increases in lower oesophageal sphincter relaxation which leads to reflux of gastric acid and pepsin back into the oesophagus, this causes pain

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53
Q

GORD sign snad symptoms

A

Chest pain aggravated by stooping
Nocturnal asthma due to aspiration of gastric contents

Heart burn
Painful swallowing - odynophagia
Hoarse throat
Regurgitation
Acidic taste in mouth

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54
Q

GORD tests

A
  • Diagnosed in clinical findings
    Oesophago-gastro- duodenoscopy - may show oesophogitus and hiatus hernia
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55
Q

GORD tx

A
  • Weight loss, stop smoking small regular meals
  • Antacids - gaviscon
  • Proton pump inhibitors - lansoprazole, omeprazole
  • H2 receptors antagonists - cimetedine
    Surgery
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56
Q

GORD complications

A

Barrets oesophogus - epitelium of the oesophogus undergoes metaplasia and changes from squampus into columnar epithelium with goblet cells, tjs causes an increasde rosk fof oesophogeal cancer, its premalognant for adenocarcinoma of the oesohphogus

Peptic stricture - inflamation of the oesophogus resulting from gastric exposr

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57
Q

Peptic Ulcer Disease definition

A

A break in the epithelium cells which penetrate down into the muscularis mucosa of the stomach/duodenum

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58
Q

Peptic Ulcer Disease epeidmeiology

A
  • More common in eldery
  • Developing cuntries due to H Pylori
  • Duodenal ulcers are the most common, they are relived by eating, they are 2-3x more common than gastric
  • Gastric ulcers are worstened by eating and are assocoaited with asptin and other NSAIDS
    Risk factors for gastric cancer due to chronic inflammation - gastric carcinoma and lymphoma
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59
Q

Peptic Ulcer Disease causes

A
  • H pylori lives in the gastric mucas and creass urease which splits the urea in the stomach into CO2 and amonia
  • This causes amonnia and H to react to make amonium
  • Amonium is damading to the mucsa which leads to ulscer forrmation
  • It also cuases more gastirn, more histamin and more parietal cell mass which all leads to more acid to secretion
  • NSAIDs - inhibit COX1 one which is needed or prostoglandin synthesis. Prostoglandins are what causes mucus secretion
  • Ischemia -stomach cells don’t have surficant blood which means that they die off and gastric acid attacks the cells
  • Increased acid - overwhels the mucosal defence

Bile reflux - regurgitated bile strips away the mucas

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60
Q

Peptic Ulcer Disease pathophysiology

A
  • Ulcers lead to gastritis
    Mucin is protective and produced by the gastric cells
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61
Q

Peptic Ulcer Disease signs and symptoms

A
  • Gastric ulcer pain often occurs when hungry or eating or at night
  • Duodenal pain occurs several hours after meals, causes weight gain and is relieved by eating
  • Anorexia
  • Burning epigastric pain
  • Vomiting
  • Bloating
  • Dyspepsia
  • Flatulence
  • Haematemesis
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62
Q

Peptic Ulcer Disease tx

A
  • Reduce smoking, reduce stress, less alcohol
  • Stop NSAIDs
  • Antibiotics for H Pylori (clarithromycin, amoxicillin)
  • H2 antagonists (cimetidine)
  • Surgery for complications
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63
Q

Peptic Ulcer Disease complications

A

There are some red flags for cancer - unexplained weight loss
Anaemia
GI bleeding
Dysphagia
Upper abdominal mass
Persistent vomiting

Duodenal ulcers caan eerode into arterys and causes massive hemmorage and shock 
It can cause perforation, obstruction, peritonitus is stomach acid enters the peritoneum 
Acute pancreatitis is ulcer reaches the pancreas
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64
Q

Mallory Weiss tear definition, risk factors and epidemiology

A

Linear muclosal tear occurring in the oesophagitis junction produced by a sudden increase in intraabdominal pressure

More common in men
20-50

Alcoholism
Forceful vomiting
Eating disorder
Male

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65
Q

Mallory Weiss tear pathophysiology

A
  • Vomiting, coughing, increases intraabdminal oressure awhihc forced the stomach contents inot the oesophgus, dilating ti and causing a tear
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66
Q

Mallory Weiss tear key presintations

A

Vomiting, abdominal pain
Haematemesis
Retching
Melena
Dizziness
Postural hypotension

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67
Q

Mallory Weiss tear test

A

Endoscopy

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68
Q

Mallory Weiss tear differentials

A

Gastroenteritis
Cancer
Peptic ulcer
Oesophageal varices - there are ruptured veins in the oesophogus caused by portal hypertension!

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69
Q

mally weis tear treatment

A

Most bleeds are minor and heal within 24 hours
Might need surgery to repair a tear
ADH analouge - Vasporessin - Constircts the blood vessles and so reduced the bleeding
Adrenaline- It is enjected using an endoscope to helop close the blood vessles around the tear

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70
Q

achalasia difinition and causes

A

The oesophagus doesn’t contract or open properly so you can’t swallow.

  • The nerves stop working properly
  • Autoimmune condition
  • Viral infection
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71
Q

achalasia risk factors

A

Having certain genes.
Having a problem with your immune system that causes it to attack nerve cells in your oesophagus.
Having herpes simplex virus or other viral infections.
Having Chagas disease. This is an infection caused by a parasite.

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72
Q

achalasia key presintations

A
  • Dysphagia
  • Bring back up undigested food
  • Heartburn
  • Chest infections
  • Weight loss
  • Chest pain
    Choking and coughing fits
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73
Q

achalasia first line tests

A

Manometry – a small plastic tube is passed through your mouth or nose into your oesophagus to measure the muscle pressure along it at different points.
Barium swallow – you drink a white liquid containing the chemical barium and X-rays are taken. The barium shows up clearly on X-ray so the doctor can see how long it takes to move into your stomach.
Endoscopy – a thin, flexible instrument called an endoscope is passed down your throat to allow the doctor to look directly at the lining of your oesophagus, the ring of muscle and your stomach.

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74
Q

achalasia tx

A
  • Nitrase and nifedipine - relax the muscels in the oesophogus and make swallowing easier
  • Ballon dialation- endoscope is put in and a baloon is inflated to stretch open the muscles, but this caus canses oesophogeusl ruptre which requires emergancy surgery
  • Botow injection - cuases it to relax
    Surgery - laproscopic surgeyr to cut the ring of muscles, this is called hellers myotomy
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75
Q

ischeamic colitis epidemiology

A

Elderly
Underlying atherosclerosis and vessels occlusion

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76
Q

ischeamic colitis causes

A
  • Atherosclerosis
  • Thrombosis
  • Emboli
  • Decreased co and arrhythmia
    Vasculitis
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77
Q

ischeamic colitis risk factors

A
  • Contraceptive pill
  • Vasculitis
    Thrombophilia
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78
Q

ischeamic colitis pathophysiology

A

Occlusion of a branch - often superior mesenteric artery or inferior mesenteric artery
Results in a watershed area of the colon - normally the splenic flexure

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79
Q

ischeamic colitis key presintations

A
  • LLQ pain
    Bloody diarrhoea
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80
Q

ischeamic colitis test

A
  • CT/MRI
  • Stool analysis
  • Ultrasou and abdominal CT
    Colonoscopy and biopsy - gold standard
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81
Q

ischeamic colitis differential

A

IBD

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82
Q

ischeamic colitis

A
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83
Q

ischeamic colitis tx

A
  • Symptomatic manegement
  • Fluid replacement
  • Antibiotics - reduce infectio risk due to translocation of bacteria across dying gut wall
    Surgery - for gangrene, perforation, stricture
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84
Q

mesenteric ischeamia epidemiology

A

> 50
Usually involved the small bowel

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85
Q

mesenteric ischeamia causes

A
  • Superior mesenteric artery thrombosis
  • Superior mesenteric artery embolism
  • Mesenteric vein thrombosis
  • Volvulus - loop of intestine twists round itself and causes bowel obstruction
    Non occlusive diseases - severe hypotension, vasospasm
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86
Q

mesenteric ischeamia key presintations

A

Triad of:
* Acite severe abdominal pain
* No abdominal sign
Rapid hypovolemia resulting in shock - pale skin, rapid weak pulse, reduced urine output, confusion

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87
Q

mesenteric ischeamia test

A

Laparotomy - diagnostic test
Bloods - metabolic acidosis and high lactate

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88
Q

mesenteric ischeamia treatment

A
  • Surgery to remove dead bowel
  • Fluid resuscitation
  • Antibiotics - IV gentamycin and vancomycin
    IV heparin to clot the blood
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89
Q

appendicitis defonition

A

Inflammation of the apendix, it should be consdered for all right sided pain. The appendix is located ag mcburnys point which is 2/3 of yeh way along from the umbilicus to the ASIS

90
Q

appendicitis epidemiology

A
  • Most common surgical emergency
  • More common in males
    10-20 years
91
Q

appendicitis causes

A
  • Feacolth - stones made of feaces
  • Filaral worms
  • Undigested seeds
  • Lymphoid hyperplasia - obstruction of tube, they can grow durng viral infection
    Bacteria - campylobacter jejuni, salmonella, yersinia, bacillus cerueus
92
Q

appendicitis pathophysiology

A
  • The lumen of the appendix becomes obstructed, as the intestnal lumen is always producing fluid and mucus, it leads to a build uo and this causes incrased pressure ot build up
  • This pressure presses on afferent visceral nerves nearby causing pain
  • Bacteria become trapped and multiply leading to invasion of gut organisms into the mucal wall
  • This leads to oedema, ischaemia, perforation and inflammation
93
Q

appendicitis signs

A
  • Tender mass in RIR
  • Guarding
  • Rebound tenderness
    Pyrexia
94
Q

appendicitis symptoms

A
  • Acute pain in umbilicus and Right illiac region
  • N&V
    Fever
95
Q

appendicitis test

A
  • CT abdomen
  • Bloods - FBC shows raised WBC count, elevated CRP and ESR
  • Ultrasound - women and children especially
  • Pregnancy test
    Urinalysis
96
Q

appendicitis differentials

A
  • Acute terminal ileitis due to crones
  • Ectopic pregnancy
  • UTI
  • Diverticulitis
  • Perforated ulcer
  • Food poisoning
97
Q

appendicitis treatment

A
  • Laproscpoic appendectomy
    Drainage of apensdix abcess
98
Q

appendicitis compliations

A

f the apendix ruptures, infected feacal matter will enter the peritoneum resulting in life threataning peritonitus and rebound tenederness

Apendix abcess - can be on the appendix or subphrenic - under the diaphragm, this is a collection of pus.

99
Q

Diverticula disease definition

A

When diverticula causes symptoms such as intermittent lower abdominal pain without inflammation and infection

100
Q

Diverticula disease epidemiology

A
  • Increaseing age, between 50-70
    Mainly in the sigmoid colon
101
Q

Diverticula disease risk factors

A

Risk Factors

  • Increasing age
  • Low dietary fibre
  • Obesity
  • Sedentary lifestyle
  • Smoking
  • NSAIDs
102
Q

Diverticula disease pathophysiology

A

Diverticula form in the sigmoid maily because it has a small diameter which mean that there is more pressure.

103
Q

Diverticula disease key presintations

A
  • Pain relived by defecation on the left lower side
  • Flatulence
  • Erratic bowel habits
    Constipation and diarrhoea
104
Q

Diverticula disease test

A
  • FBC - anaemia, leucocytosis and neutrophilia
    Colonoscopy
105
Q

Diverticula disease treatment

A
  • High fibre diet
    Paracetamol
106
Q

Diverticulosis definition

A

When the diverticula become inflames and infected, causing sever lower abdominal pain, fever, general malaise and occasionally rectal bleeding

107
Q

Diverticulosis pathophysiology

A

Inflamtion that occurs when feacal matter or feacaliths become lodged in the diverticula or when there is erosion of the diverticula wall due to higher luminal pressure

108
Q

Diverticulosis key presintations

A
  • Fever
  • Left lower quadrant tenderness and guarding
  • Rigidity, guarding and tendernes suggests perforation
  • Fresh blood and pelvic tenderness on rectal exam
  • Tachycardia and hypotension if there is septicaemia
  • Pain in left lower quadrant, but right colon in Asian people as well!
  • N&V
  • Rectal bleeding
    Palpable abdominal mass
109
Q

Diverticulosis 1st line test

A
  • U&E - if significantly dehydrated or septic
  • CRP and ESR - elevated
  • Venous blood gas - raised lactate in significant PR bleed
    Colonoscopy
110
Q

Diverticulosis tx

A

Oral co-amoxiclav (at least 5 days)
Analgesia (avoiding NSAIDs and opiates, if possible)
Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
Follow-up within 2 days to review symptoms

If severe pain and in hospital:
Nil by mouth or clear fluids only
IV antibiotics
IV fluids
Analgesia
Urgent investigations (e.g., CT scan)
Urgent surgery may be required for complications

111
Q

Diverticulosis complications

A

Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction

112
Q

small bowel obstruction causes

A
  • Adhesions due to a previous surgery
  • Hernia
  • Malignancies
  • Gallstone illuis
    Volvulus
113
Q

small bowel obstruction pathophysiology

A
  • There is obstruction, this causes bowel distention above the block and increased secretion of fluid into the distended bowel
    This causes vessels to be compressed leading to ischaemia, necrosis, and perforation
114
Q

small bowel obstruction signs and syptoms

A
  • Obstipation - constipation wth no wind
  • Incrases bowl sounds
  • Typanic percussion
  • Tenderness - suggests strangulation
  • Less distention compared o LBO

Vomiting - if green it’s probably an obstruction as that’s the bile
Colic pain - comes in waves
Localised pain - more likely to be pericarditis as the bowel is dying
Vomiting following pian
Nausea
Anorexia

115
Q

small bowel obstruction test

A

CT scan! - not Xray
FBC

116
Q

small bowel obstruction tx

A
  • Analgesia for pain
  • Asses fluid balance, urinary catheter, nasogastric tube
  • Resuscitate - IV fluids
  • Alleviate nausea - antiemetics
  • Nutrition - if more than 5 days without intake, they may need parenteral feed into the vein.
    Surgery for decompression
117
Q

large bowel obstruction causes

A
  • Colorectal malignancy
    Volvulus
118
Q

large bowel obstruction signs and symptoms

A

Abdo distention
Palpable mass
Constipatio
Fullness/bloating

  • Acute onset - on average 5 days, the stmpis persnet lateras the large bowl can stretch so much
  • Voting faeces
  • Constant abdominal pain
119
Q

large bowel obstruction pathophysilolgy

A
  • Obstruction causes dilation
  • Increased colonic pressure and decreased mesenteric blood flow
    Mucosal ulceration, necrosis and perforation
120
Q

large bowel obstruction etst

A

CT scan
* DRE - empty rectum, hard stool, blood
* FBC - low Hb is a sign of chronic occult blood
Occult blood - blood not visible to the naked eye

121
Q

large bowel obstruction tx

A
  • Aggressive fluid resuscitation
  • Bolwel decompression
  • Anaglesia and anti emetic
  • Abtibiotics
  • Surgery
  • NG tube for feeding
  • Colostomy potentially
    Laproscpic exploration
122
Q

pseudo obstruction definition

A

Clinical picture mimicking colonic obstruction but no mechanical causes - also called oglivie syndrome

123
Q

pseudo obstruction causes

A
  • Postpartum - the organs are shifting back
  • Postoperative - the organs are moving back
  • Intraabdominal trauma
  • Intra-abdominal sepsis
  • Pelvic spinal and femoral fractures
  • Cardiorespiratory and neurological disorders
  • Antidepresants
  • Opoids
124
Q

pseudo obstruction symptoms

A
  • Abdominal pain and disternion - rapid onset
125
Q

pseudo obstruction test

A

x ray for gas
CT scan

126
Q

pseudo obstruction tx

A
  • Withdraw causative agents - drugs stop
  • Correcnt U&E
  • IV neosigmine - a choliesterase inhibitor to encourage motility
    Endoscopic colonic decompression
127
Q

diharrhoea definition

A
  • Diarrhoea - abnormal passage of loose or liquid stools more than 3 times daily
    Acute - less than 2 weeks
128
Q

diarrhoea causes

A
  • Viral -rotavirus, noravirus
  • Bacterial - campylobacter, shigella, salmonella, c.perfingens, s.aures, b.cereus, e.coli, c.difficil, parasites - giadia
  • The most common cause in children is rotavirs, the most common in adults is noravirus and campylobacter
  • Antibiotics can give rise to C.diff diarrhoea bcuases it kills all the other bacteria in the gut so it overgrows and causes an infection of its own! The main antibiotic that causes this are the 4 Cs - clindamycin, ciprofloxican (the group of quinolones genrally), co-amoxicolav (penicillins group genrally) cephalosporins.
  • Intraluminla infections (caused by cannulas) and systemic infections
    Non infective causes - cancer, chemicals - poisens, sweetners, drug side effects, IBS, endocrine, radiation.
129
Q

diarrhoea risk factors

A

Immuno suppressed - especially for CMV, HSV, mycobacteria.
recent travel

130
Q

Diarrhoea history

A

HISTORY IS KEY:
* Onset and duration - acute more likely to be virla or bacterial, chronic more likely to be parasites and non-infections
* Family history
* Characteristic of stools - floating means high fat content, blood or mucus - inflammatory, invasive infection, cancer, if it is watery it means a small bowl infection
* Food and drink - meat & BBQs campylobacter
* Travel
* Immunocompromised? Diabetes, chemo, steroids, HIV (crypto and CMV)
* Fresh water swimming - cryptosporidina, giardia
* Medications - C. diff caused by antibiotics or side effects of medications
* Neuro signs - clostridium botulinum, C.jejuni (they both causes descending weakness paralysis)

131
Q

Diarrhoea gold standard tets

A

Stool tests - faecal calprotectin, faecal occult blood, microscopy, toxin detection, stool culture
FBC, inflammatory markers, blood cultures

132
Q

infective Diarrhoea epifdemiology

A

2nd leading causes of child dath after pneumonia

133
Q

infective Diarrhoea causes

A
  • Enterotoxigenic e.coli (30-70%)
  • Campylobacter (5-20%)
  • Shigella (5-20%)
  • Non-typhoidal Salmonella (5%)
  • V.parahaemolyticus (shellfish)
  • Viral (10-20%)

Cholera:
* Vibrio cholerae
* Contaminated food/water
* Cholera toxin
* Profuse watery “rice water” diarrhoea 🡪 up to 20L a day
* Vomiting
* Rapid dehydration
* Doxycycline and fluids

Parasites:
* -Protozoal (5-10% more chronic)
* Cyrpto
* Giardia
* Entamoeba
* -Worms
* Schistosomiasis
* Strongyloides

Many are asymptomatic but can become a problem if the normal gut flora is alterd normally due to broad spectrum antobiotics.

134
Q

infective Diarrhoea symptoms

A
  • Recurrent diarrhoea
  • V&N
  • Fever
  • Fatigue
  • Muscle pain
    Steatorrhea
135
Q

infective Diarrhoea test

A

Diarrhoea and 3 of the following:
* Abdo pain
* Cramps
* Nausea
* Vomiting
* Dysentry
* Blood - e.coli and shigella

Stool sample
If chronic - sigmoidoscopy and bloo test

136
Q

infective Diarrhoea differntial

A

Appendicitis
IBD
UTI
Coeliac disease
Volvulus

137
Q

infective Diarrhoea tx

A
  • Rehydration
  • Antibiotics - metronidazole or vancomycin
  • Barrier nursing - in a side room, gloves and apron
  • Fluid and electrolytes
  • Antiemetics
  • Antimotility agents - ONLY IF NOT INFLAMATORY DIARRHOEA
  • C.difficil - vancomycin
  • E.Coli - fluroquinolones such as ascprofloxican or andlevofloxican
  • Shigella - azithromycin and ciprofloxacin
  • Salmonella -fluoroquinolones, such as ciprofloxacin, and azithromycin
    Campylobacter jejuni - Macrolides (e.g., azithromycin, erythromycin) are generally the treatment of choice in both children and adults, owing to increasing resistance to fluoroquinolones (e.g., ciprofloxacin)
138
Q

infective Diarrhoea complications

A

Red flags:
* Dehydration
* Electrolyte imbalance
* Renal failure
* Immunocompromised
* Severe abdominal pain

Cancer risk factors:
* Over 50
* Chronic diarrhoea
* Weight loss
Blood in stool

139
Q

infective Diarrhoea risk factors

A

Forgn travel
PPI or H2 antagonist us
Crowded area

139
Q

h pylori test

A
  • ‘Clo test’ (rapid urease test) during biopsy to check for H.pylori presence
  • Pylori urea breath test - breath into a bag to measure CO2, you take a urea tablet, then breathe into a bag again, if Pylori are present it causes and increase in CO2 as they have the urease enzyme.
    Pylori stool antigen test - looks for Pylori associated proteins in the faeces
140
Q

h pylor treat,ent

A
  • It is triple therapy
    • PPI for acid suppression (lansoprazole or omeprazole
    • Plus two of metronidazole, clarithromycin, amoxicillin, tetracycline, bismuth. If no penicillin allergy do amoxicillin plus another one.
      Quinolines - ciprofloxacin, furazolidone, rifabutin are used when the other have failed as a last ditch attempt
141
Q

small bowel cancer epdemiology

A

1% of all malignancies
Adenocarcinoma most common

142
Q

small bowel cancer risk factors

A
  • Family history
  • Coeliac disease
    Chronns diseases
143
Q

small bowel cancer key presintations

A
  • Abdominal pain
  • Diarrhoea
  • Weight loss
  • Anorexia
  • Anaemia
    Palpable mass
144
Q

small bowel cancer test

A

Ultrasound
Endoscopic biopsy
CT/MRI

145
Q

small bowel cancer treatmen

A

Surgical resection
Radiotherapy

146
Q

oesophagael cancer epidemiology

A
  • More common in men
  • 60-80 age group
    Adenocarcinoma is the most common in the UK
147
Q

oesophagael cancer risk factors

A

lder age
Smoking
Achlasia
smoking

For adenocarcinoma;
* Barrettes oesophagus
* Obesity
* Male
* Coeliac disease

For SSC:
* Alcohol
* Caustic strictures
* Hot beverages
Palmoplantar keratoderma - thick patches of skin on hands and skin

148
Q

oesophagael cancer pathophysiology

A

quamous cell carcinoma (cancer of the flat lining cells):
* Arises from squamous epithelium, most commonly in the upper 2/3ds
* When the epithelium is repeatedly exposed to toxins such as alcohol, soke, hot fluids it gets damaged do the cells divide to make more
* With each division there is more risk of mutation

Adenocarcinoma (cancer of glandular tissue):
* Arises from the columnar glandular epithelium, this is in the lower third of the oesophagus and develops as a consequence of GORD, the acid leads to barrettes oesophagus (squamous to columnar)
Over time these cells turn into metaplastic and result in a tumour

149
Q

oesophagael cancer key presintations

A
  • Lymphadenopathy
  • Vocal cord paralysis
  • Meleana
  • Progressive dysphagia
  • Regurgitation
  • Pyrosis
  • Pain in chest and back
  • Odynophagia (painful swallowing)
  • Hoarse voice
  • Vomiting
    Weight loss
150
Q

oesophagael cancer test

A
  • Upper GU endoscopy and biopsy
  • Barium swallow for staging
  • CT of chest abdomen and pelvic to look for metastatic disease
  • PET scan to look for metastasis
    Staging laparoscopy
151
Q

oesophagael cancer differenctials

A

Benign oesophageal tumours - they are smooth muscle tumours that arise from the wall and are very low growing, treated by endoscopic removal and surgery.

152
Q

oesophagael cancer tx

A
  • Surgical resection - is the patients fir, age, co morbidities, severity of cancer, is it respectable?
  • Chemo and radiotherapy
    Palliative care
153
Q

gastric cancer epidemiology

A

Males
Eastern Europe and Asia more

154
Q

gastric cancer risk factors

A

Smoking
H pylori

155
Q

gastric cancer pathophysiology

A

Adenocarcinoma, lymphoma, carcinoid tumour (slow growing neuroendocrine tumours of the bowel), leiomyosarcoma (cancer of smooth muscle)

156
Q

gastric cancer key presintations

A
  • Epigastric pain
  • N&V
  • Anorexia
  • Weight loss
  • Dysphagia
  • Anaemia
    Liver metastasis - jaundice
157
Q

gastric cancer test

A
  • Gastroscopy with biopsy
  • Endoscopic ultrasound
  • CT/MRI
    PET scan
158
Q

how are you doing

A

hang in there !

159
Q

gastic cancer tx

A
  • Surgcial removal
  • Radiation therapy
  • Chemoterapy
  • Immunotherapy
  • HER-2 targert theraypy (herceptin) - if people test poeiitve for the gene the it can be used as a treatment
    Palliative care
160
Q

large bowel cancer epidemiologyy

A
  • Colorectal cancer is the fourth most common UK cancer behind breast prostate and lung
  • Males
    Western countries
161
Q

large bowel cancer risk factors

A

Sporadic mutation
* FAP - familial adenomatous polyposis, where you have thousands and thousands of polyps which can turn malignant. It is autosomal dominant.
* Lynch syndreome (hereditary non-polyposis colorectal cancer (HNPCC)) - genetic predisposition to developing different cancers, especiallt colerectal, utrine, gastric, overian, pancreatic, prostrae, kidney, bile duct and brain.

* Male 
* Smoking
* Pbeses
* Precoessed/red meats 
* Polyps  Older age
162
Q

large bowel cancer pathophysiology

A
  • There are some cancers sure to inherited genetic mutations such as APC which shoud causes apoptoasis of damaged cells, but is mutated so doesn’t which causes the formation of polyps
163
Q

large bowel cancer dukes criteria

A

The cancer is in the inner lining of the bowel. Or it is slightly growing into the muscle layer.

Diagram showing Dukes’ A bowel cancer
Dukes’ B
The cancer has grown through the muscle layer of the bowel.

Diagram showing Dukes’ B bowel cancer
Dukes’ C
The cancer has spread to at least 1 lymph node close to the bowel.

Diagram showing Dukes’ C bowel cancer
Dukes’ D
The cancer has spread to another part of the body, such as the liver, lungs or bones.

In the number staging system, this is the same as stage 4. It is also called advanced bowel cancer.

164
Q

large bowel cancer kery presintations

A
  • Right sided tumours are often asymptomatic but pressnt with iron deficency aneamia .
  • Abdominal discomfort
  • Bowel obstruction symptoms
  • Constitutional symptoms dysponea and fatigue
  • Left sided are associated with a change in bowel habits and have high rates of rectal bleeding and large bowel obstruction
  • Rectal mass
  • Diarrhoea or constipation
  • Abdomonal consipation
  • Colicky pain, vomiting, blood streaked stools
    Rectal bleeding and tenesmus (the feeling of needing a poo when you don’t actually)
165
Q

large bowel cancer tests

A
  • FBC - microcytic aneamia
  • U&E - renal function may be alter in advanced pevic disease
  • Colonoscopy and biopsy - gold standeard investigation may demonstrate an ulcerating lesion
  • CT colonography - CT bowel preop and contrast to visulise the colon
  • CT chest abdomen and pelvis (CAP) - if a biopsy is diagnostic of malinancy, this is used for staging
    MRI - sometimes better for staging rectal cancers
166
Q

large bowel cancer differentail

A
  • IBS
  • Ulcerative colitis
  • Chrons
  • Haemorroids
  • Anal fissure
    Diverticular disease
167
Q

large bowe cancer tx

A

There are screening tests to look for straces of blood in the stool - Fealcal occlut blood (FOB) and Faecal immunochemical test (FIT).
If these come back positive there is a colonoscopy does to have a further look.

* Iron replacement for the aneamia 
* Chemotherapy
* Radiotherapy - for rectal cancer as it is extraperitoneal 
* Surgical resection
168
Q

Pseudomembranous colitis definition

A

Pseudomembranous colitis (PMC) is a manifestation of severe colonic disease that is usually associated with Clostridium difficile infection, but can be caused by a number of different etiologies. Prior to the use of broad-spectrum antibiotics, PMC was more frequently related with ischemic disease, obstruction, sepsis, uremia, and heavy metal poisoning

169
Q

Pseudomembranous colitis causes

A

Brad spectrum antibiotics - can kill off all bacteria apart form c.dificcil so it takes over and causes an infection.

170
Q

Pseudomembranous colitis pathophysiology

A

pathophysiologyThere are yellow fatty lumps growing on top of the mucosa

171
Q

Pseudomembranous colitis test

A

Stool sample
Blood tests
Imaging tests
Colonoscopy

172
Q

Pseudomembranous colitis treatment

A

Antibiotics agsint c.difficile
Fecal microbial transplant
Repeat antibiotics
Surgery - orgen faliue or rupture

173
Q

Haemorrhoids definition

A

Haemarroids are normal spongy vascular structeus that cision the stool as it passes through. In heamarroids disease, they gaet disrupted swollen and inflamed.

174
Q

Haemorrhoids causes

A
  • Chronic or reoccuring increase in abdominal pressure such as straing for poos, diahrroea or constipation
  • congestion fomr tumour, pregnancy, portal hypertension
    Anal intercourse
175
Q

Haemorrhoids risk factors

A

Obesity
Older age

176
Q

Haemorrhoids pathophysiology

A

nternal ones are above the dentate line. Internal ones fall into 4 classifications -

Grade I: no protrusion outside the anal canal.

Grade II: protrusion outside the anus during bowel movement, but they retract spontaneously.

Grade III: prolapsed haemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.

Grade IV: prolapsed haemorrhoids that cannot be manually pushed back in.

* Hemmaroids are vunerable to trauma (hard stools) so will bleed easily on impact 
* Internal hemmaorids arent painful unless they get caught in the anal sphincter 
* Exteral haemorrhoids are painful  There is a vicious circle; the vascular cushions protrude through a tight anus → become more congested and hypertrophy → protrude again more readily
177
Q

Haemorrhoids ke presintations

A

NTERNAL:
Itching
* Burning
* Bright red blood in stool

External:
* Painful hemarroids
* Thrombosed with purplish hue
* Sweling
* Mucus discharge
Itching

178
Q

Haemorrhoids test

A
  • Abdo investigation
  • Rectal exam
  • Protoscopy to look for intenal haemorrhoids
    Flexible sigmoidoscopy ot colonoscpy to exclude pathology
179
Q

Haemorrhoids tx

A

st
* - incrases finre and fluid
* Stool softners
* Topical analgesia
* Topical steriods
* Topical analgesia
2nd
* Rubber band ligation
- Sclerotherapy: injection of drugs causes coagulation
- Infrared coagulation
- Bipolar diathermy and direct current electrotherapy: local heat causes coagulation
Surgical excision

180
Q

Fistula definition

A

An abnormal connection between the anal canal and skin

181
Q

Fistula causes

A

Perineal Sepsis
Tb
Chrons
Rectal carinoma

182
Q

Fistula pathophysiology

A

Blockedge of deep intramusclea glan duct thought to predispose to the formation of abcess

183
Q

Fistula key presintation

A

Pain
Dischareg of blood or mucus
Itchy bum
Systemic abcess

184
Q

Fistula test

A
  • Palpation on digital exam
  • MRI - to exclude sepsis, will show contrast material in fistula
  • Endoanal ultrasoud
185
Q

Fistula manegment

A

Surgery - cutting it open fully to heal better
Antibiotics

186
Q

Fissure definition

A

Tearing of squamous lining of lower anal canal on defecation

187
Q

Fissure causes

A
  • Can be isolated due to hard poos
  • Enemas
  • Endoscope
  • Vaginal delivery
  • Anal intercours
    Stis - symphyliss, heres, traums, chrons
188
Q

Fissure pathophysioloy

A

Normal tissues is split apart and cuases invaion of nearby pathogen

189
Q

Fissure key presintations

A

ainful swelling
Tender
Dishcarge

190
Q

Fissure first line test

A
  • The diagnosis can usually be made by physical examination
  • MRI
    Endoanal ultrasound
191
Q

Fissure tx

A

Surgical excision and drainage
- Treatment with antibiotics

192
Q

Pilondial sinus/absess definition

A

A small hole in the skin which haooen in the area where the buttocks divide. It can lead to a pus filled absess

193
Q

Pilondial sinus/absess key presintations

A

Pain
Swelling
Leakage if infected

194
Q

Pilondial sinus/absess tx

A
  • Watch and wait
  • Good hygone
  • Antibiotic
  • Painkillers to reduce swelling
  • Surgery tp drain sinus
  • Surgery to remove sinus - its cut out
195
Q

peritonitis deifinition

A

Definition

Inflammation of the peritoneum - generalised inflammation of the abdominal cavity

Peritonism - tensing of the muscles to prevent movement of the peritoneum

196
Q

peritonitis causes

A

Aetiology

AEIOUP!

* Appendicitis 
* Ectopic pregnancy 
* Infection - E cli and klebsiella, staphylococcus aureus 
* Obstruction - 
* Ulcer - epigastric pain radiating to shoulder 
* Peritoneal dialysis

Causes of inflammation -
* Inflamed organ
* Air - ulcers, stabbings
* Pus
* Feaces
* Lumoncal contents (its not feaces untill it reaches the colcin)
* Blood - spleen problems

Common causes of abdominal pain - gast

197
Q

peritonitis pathophysiology

A

Pathophysiology

Can result from any inflammation of the peritoneum
Perforation of the appendix
Spontaneous bacterial peritonitis

198
Q

peritonitis key presintation s

A

Key presentations

  • Dull pain that become sharp
  • Systemic cymptoms and genrally unwell
  • Pain relived by resting hands on abdome
  • Gaurding and reboud tenderness
  • Abscenc of bowel souds
  • Rigid abdome
  • Pain worse on coughing or moving
  • Wants to lie still
  • Sepsis - hypotension, tachycardia, oliguria
199
Q

peritonitis first line test

A

1st line test

  • CT scan
  • Clinical examination - rigid and guarding, lying still
  • Abdo Xray - dilated bowel, flat fluid level, gas under diaphragm
  • Bloods - FBC, U&E, LTF, clotting factors
  • Ascitic tap - night neutrophil count
200
Q

peritonitis tx

A

Treatment

  • Bread spectrum antibiotics - metronidazole
  • Fluid resuscitation - IV and electrolytes
  • Pain meds
  • Surgery - treat the cause, patch any holes, remove the organ or causes, wash out the infection
201
Q

peritonitis differneital

A

Differential diagnosis

  • Bowel obstruction
202
Q

peritonitis complications

203
Q

common causes of abdominal pain

A

Other notes

Common causes of abdominal pain:
Gastritis – epigastric pain
Cholecystitis – right hypochondrium, mid-clavicular line
Pancreatitis – midway between epigastric and umbilicus
Appendicitis – right iliac fossa
Diverticulitis – left iliac fossa

204
Q

meckles diverticulum definition

A

Definition

A common congenital abnormality that is a small out-pouch of the small bowel which can be asymptomatic.

205
Q

meckles diverticulum pathphysioloy

A

Pathophysiology

RULE OF 2:

* M-f ratio is 2
* 2% of population 
* 2 inches in length 
* 2 age diagnosis
206
Q

meckles diverticulum test

A

1st line test

FBC - anaemia
Technitium-99m scan - meckles scan to look for it
CT of abdomen and pelvis
Ultrasound of the abdomen

207
Q

meckles diverticulum treatment

A

Treatment

If it is found during surgery it might be excised, if it is causing obstruction it will be excised and any adhesions associated fixed.

208
Q

what is teh gold standard test for appendicitis

209
Q

what are the three tests for appendicitis on a physical examination

A

Rosvings sign - press on the left illiac fossa and when released there is pain of teh right

psoas sign - leg is pulled back and this causes pain

obturator sign - hip if flexed and then roated and this cuases pain

210
Q

for apendicitis who shoul have an ultrasoud rathe than a CT

A

women (sespecially preganct) and children - dur to avoiding unecacerry eposure to radiation

211
Q

what is teh treatment for appendicitis

A

IV fluids
pain reief - paracetamol, opioids
antibiotics - metronidazole and ceftriaxone
laprscoic apendectomy

212
Q

complications of apendicitis

A

perforation leading to sepsis and peritonistis

213
Q

where do diverticuli not occur

A

rectume becuases there is an extra muscle band so it can withstand more pressure

214
Q

where is c reascitve proten made

A

in the liver

215
Q

what are the main differenced between gastic and duodenal ulcers

A

gastic - made worse by eating so weight loss

duodenal - relived by eating so weight gain !

216
Q

what are teh red flags for cancer with epigastic pain

A

There are some red flags for cancer - over 55 and then one of these other symptoms:
unexplained weight loss
Anaemia
GI bleeding
Dysphagia
Upper abdominal mass
Persistent vomiting

refer for 2 week endoscopy and biopsy to look for bowel cancer

217
Q

what is teh glasgow blatchford scale

A

A screening tool to assess the likelihood a person with an upper GI bleed will need medical intervention such as blood transfusion or endoscopy .

218
Q

what is teh rockall scre -

A

A system for known upper GI bleeds with a completed endoscopy to estimate re-bleeding and mortality rate due to upper gastrointestinal bleeding

219
Q

what enzyme do ggranulomatas disease cause an incease

Phase 2a (18 decks)

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