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CP - JL > Diseases of the GI tract > Flashcards

Diseases of the GI tract Flashcards

1
Q

What are the majority of normal flora in the fut

A

Majority anaerobes

Some are facultative anaerobes e.g. E. Coli

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2
Q

What viruses generally cause gastroentertisi

A

Commonly norovirus

Very infectious due to aerosols

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3
Q

Parasites causing gastroenteritis

A

Cryptosporidium, giardia and entamoeba

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4
Q

Why do we get antibiotic associated dirarhoea

A

Disrupts the microflora - changes the metabolism of carbs/bile acids
C. Diff is 10-25% of cases and 99% of pseudomembranous colitis

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5
Q

Complications of antibiotic associated diarrhoea

A 
Diarrhoea
Pseudomembranous Colitis
Toxic Megacolon
Perforation
Shock
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6
Q

High risk antibiotics for diarrhoe

A

Cephalosporins and clindamycin

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7
Q

Medium risk antibiotics for diarrhoea

A

Ampicillin/amoxicillin, macrolides, co-trimoxazole, fluiroquinolones e.g. E. Coli

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8
Q

How do we treat C. Diff

A

Vancomycin and Oral Metronidazole

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9
Q

How do bacterias produce disease

A

Either by toxins or adherence

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10
Q

What type of bacteria is E. Coli

A

Gram - ve

Produces toxins

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11
Q

Hoe does salmonella cause disease

A

Adherence

Can be typhoidal (invades outside the GI tract or non-typhoidal)

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12
Q

Who do we give antibiotics to for gastroenteritis

A

Generally try to avoid giving unless v young, old or invasive campylobacter

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13
Q

Protective and increasing factors in UC and Crohns

A

Smoking and appendectomy protective in UC
Smoking and female are both risk factor in Crohns

Oral contraceptive, MMR, childhood infections increase risk of both

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14
Q

Presentation of UC

A 
Diarrhoea - urgency/tenesmus but small amount have constipation
Rectal bleeding
Abdo pain
Weight loss
Anorexia
Anaemia
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15
Q

Presetantion fo crohns

A 
Diarrhoea (may be bloody)
Colicky abdomen pain
Palpable abdominal mass
Oral Ulcers
Fever
WEigth loss
Anaemia
Peri-anal disease
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16
Q

Complications of UC and Crohns

A

Both: Toxic megacolon and perforation, haemorrhage, stricture (rare in UC, common in Crohns), Carcinoma

Crowns: Fistula, short bowel syndrome

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17
Q

Pathology of Crohns

A 
All GI tract
Skip Lesions
Cobblestone appearance - athoid and fissuring ulcers
Serositis
Transmural
Crypt abscesses and distortion less common
Sarcoid like granulomas
Inflammatory polyps less common
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18
Q

Pathology of UC

A 
Affets colon, appendix and terminal ileum
Continuous disease
Granular red mucose with flat underlying ulcers
Normal serosa
Mucosal inflammation
Crypt abscess and distortion common
No granulomas
Common inflammatory polyps
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19
Q

IBD Extra-intestinal manifestations: Hepatix

A

Fatty Change
PSC
Granulomas
Bile duct carcinoma

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20
Q

IBD Extra-intestinal manifestations: Muco-cutaneous

A

Oral apthoid ulcers
Pyoderma gangrenosum
Erythema nodosum

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21
Q

IBD Extra-intestinal manifestations: Ocular

A

Iritis/Uveitis
Episoleritis
Retinits

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22
Q

IBD Extra-intestinal manifestations: Renal

A

Kidney and bladder stones

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23
Q

IBD Extra-intestinal manifestations: Haematological

A

Anaermia
Leucocytosis
Thrombocytosis
Thrombo-embolic disaese

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24
Q

IBD Extra-intestinal manifestations: Skeletal

A

Polyarthritis
Sacro-ilietis
Ankylosing Spondylitis

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25
Q

IBD Extra-intestinal manifestations: Systemic

A

Amyloid

Vaculitis

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26
Q

Risk factors for CRC in UC

A

1) Early onset
2) Had for over 10 years
3) Total or extensive colitis
4) PSC
5) Family history of CRC
6) Severity of inflammation
7) Presence of dysplasia

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27
Q

What is a polyp

A

Mucosal projectio

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28
Q

Types of polyps

A

Neoplastic
Hamartamous
Reactive
Infectious

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29
Q

Where are hyper plastic polyps common

A

Located in rectum and sigmoid colon

1-5mm in size

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30
Q

Do hyperplastic polyps have malignant potential

A

Small distal HP’s have no malignancy potential

Large right sided polyps may cause micro satellite carcinoma

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31
Q

Type of hamartamous polyps

A

Juvenile polyps

Peutz-Jeughers syndrome

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32
Q

What are juvenile plyps

A 
Common in children
In the rectum and distal colon
10-30mm of spherical, pedunctulated polyps
Sporadic ones are not malignant!!
Get diarrhoea/some bleeding
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33
Q

What is peutz-jeugher syndrome caused by

A

Autosomal dominant

Mutatino in STK11 gene on chromosome 19

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34
Q

What is peutz-jeugher syndrome

A

Multiple GI polyps predominantly small bowel
Muco-cutaneous pigmentation
Presents clinical in teens/20s
Increase risk of cancer in stomach, small bowel and pancreas

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35
Q

What is the most common benign epithelial tumour

A

Adenoma

Commonly polypoid but flat!

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36
Q

Higher risk of malignancy in adenoma if

A 
Flat adenomas
Large size over 10mm
Villous and tubulo/villous structure
High grade dysplasia
HNPCC associated carcinomas
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37
Q

Colorectal cancer risk factors

A 
Dietary i.e. fat red meat
Obesity
NSAIDS
HRT and oral contraceptives
Schistosomiasis
Pelvic radiation
UC and Crohns disease
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38
Q

What is FAP

A

Autosomal dominant
Mutation in APC tumour suppressor gene

Multiple benig adenomatous polyps in colon - 100% lifetime risk of large bowel cancer

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39
Q

What is HNPCC

A

Mutation in DNA mismatch repair gene
50-70% lifetime risk of large bowel cancer

Increased risk of endometrial, ovarian, gastric, small bowel, urinary tract and biliary tract caner

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40
Q

How do we stage bowel cancer

A

Dukes staging

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41
Q

What is diverticulosis

A

Outpouchings of the mucosa/submucosa
Commonly in sigmoid colon
Between the mesenteric taenia coli and the anti-mesenteric taenia coli

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42
Q

How does diverticulosis progress

A

Thickening of muscular propr.

Elastosis of the taenia coli - shortens the colon –> redudant mucosal folds and secular –> saculatino and diverticula

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43
Q

Features of diverticulosis

A

90 % asymtpmatic
Abdo cramping pain
ALternation constipation/diarrhoea

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44
Q

Acute complications of diverticulosis

A

Dierticulitis, peridiverticular abscess
Perforation
Haemorrhage

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45
Q

Chronic complications of diverticulosis

A

Strictures
Fistulas
Collitis (segmental and granulomatous)
Polypoid Prolapsing Mucosal Folds

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46
Q

How do we test for H. Pylori

A

Urease breath test

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47
Q

How do we treat H. Pylori

A

PPI and 2 antibitoics

(Omeprazole) + Amoxicilin/clarithomycin

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48
Q

What is the commonest form of oesophagitis

A

Reflux oesophagitis

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49
Q

Changes in reflux oesophagitis

A

Increased basal cell layer
Increased cell turnover
Eosinophils, neutrophils and inflammatory cells
Elongated lamina papillae

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50
Q

Risk factors for reflux oesophagitis

A

Defective LOS
Hiatus Hernia
Raised Intra abdominal pressure
Increased gastric fluid volume due to outflow stensosi

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51
Q

What are the risk factors for squamous carcinoma of the oesophagus

A

Tobacco and alcohol

Occurs in lower and middle oesophagus

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52
Q

Risk factors for adenocarcinoma of oesophagus

A

Barrett, tobacco, smoking
Higher incidence in males and caucasians

Lower oesophagus - plaque like, can get stricturing due to fibrosis around the tumour

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53
Q

What occurs in barret’s oesophagus

A

Longstanding reflux
Proximal extension of the squamo-columnar junction - glandular metaplasia
Often get goblet cells

Causes increased risk of developing adenocarcinoma

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54
Q

Autoimmune causes of chronic gastritis

A

Anti-parietal cell and anti-intrinsic factor antibodies
Sensitised T lymphocyes
Glandular atrophy in the body mucosa
INtestianl metaplasia

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55
Q

Bacteria causes of chronic gastritis

A

H. Pylori
Produces cytokines, mucolytic enzymes, ammonia

Tissue damage due to immune response

Multi-focal atrophy more in antrum then body and intestinal metaplasia

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56
Q

Chemical causes of chronic gastritis

A

Direct - fovealor hyperplasia
NSAIDS - disrupts the mucous layer –> oedema
Bile reflux - degranulates mast cells - vasodilation
Alcohol - paucity of inflammatory cels

57
Q

What is Coeliacs disease

A

Sensitivity to gliadin in gluten

58
Q

Pathogenesis of coeliacs

A

Gliadin causes epithelial cells to produce IL-15
IL-15 activates/proliferation of CD8+ IEL
Cytotoxic and kill enterocytes
Atrophy of bill and secondary malabsorption!

59
Q

Silent coeliacs disease

A

Positive serology
Villus atrophy
No symtpoms

60
Q

Latent coeliacs disease

A

Positive serology
Villous atrophy
No symptoms

61
Q

Associated coeliacs disaese

A

Dermatitis herpetiformis
Lymphocytic gastritis/cells

Enteropathy associated T cell lymphoma small intestine adenocarcinoma

62
Q

When are we worried about Enteropathy associated T cell lymphoma small intestine adenocarcinoma in coeliacs

A

IF symptoms are persisting despite a gluten free diat

63
Q

Morphology in coeliacs disease

A

Villous atrophy
Crypt elongation
Increased lamina propr. inflammation
Increased IEL

64
Q

What type of bacteria is H. Pylori

A

Gram -ve spiral bacteria

65
Q

How does h pylori damage the epithelium

A

Lives on epithelial surface protected by the overlying mucosa
Damages the epithelium - causing chronic inflammation - causes gland atrophy
Replacement fibrosis - intestinal metaplasia
More common in antrum than body

Can predispose to gastric cancer and MALT lymphoma

66
Q

What is the most frequent gastric cancer

A

Adenocarcinoma

67
Q

Carcinoma of the GOJ

A

No association with H, Pylori Diet
Associated with GO reflux
White males

68
Q

Carcinoma of body/antrum

A

Associated with diet and H. Pylori

No association with GO reflux

69
Q

INtestinal gastric carcinoma

A

Well differentiated
Intestinal metaplasia
Adenoma steps

70
Q

Diffuse gastric carcinoma

A

Poorly differentiated
Scattered growth
Cadherin Loss
Signet ring

71
Q

Hereditary diffuse type gastric cancer

A

Germiline E. Cadherin mutation
Precursor lesions
Likely to be young diffuse type gastric cancer

72
Q

Complication of peptic ulcers

A

Haemorrhage - anaemia
Perforation
Penetration
Stricturing

73
Q

What is peptic ulcer disease

A

Extends to atleast submucos!

74
Q

Acute gastric ulcers

A

Full thickness coagulative necrosis of the mucose
Covered with ulcer slough
Granulation tissue at the ulcer floow

75
Q

Chronic gastric ulcers

A

Clear cut edges
Extensive granulation/scar
Bleeding
Scarring often throughout the entire gastric wall breaching the muscular propria

76
Q

Features of duodenal ulcers

A 
More common
In younger
Elevated or normal acid levels
Almost always H. Pylori associated
Bulbus 
Blood group O
77
Q

Features of gastric ulcers

A 
Less common
Older
Normal or low acid
H Pylori in 70%
Lesser curve/ antum-corpus unction
Blood group A
78
Q

What is an intra-abdominal infection

A

Micro-organisms in normally-sterile sites within the abdominal cavity i.e. the peritoneal cavity and the hepatobiliary tree

79
Q

Why is gasto-enteritis not an intra-abdominal infection

A

As the bowel lumen is a non-sterile site

80
Q

Is the stomach sterile

A

Yes
Primal small intestine also considered relatively free of bacteria as growth inhibited by bile - a few aerobic bacteria and candida are there

81
Q

Normal flora of small intestine

A

Majority anaerobic

Some aerobic e.g. enterobacteriaceae and gram +ve cocci

82
Q

Sources if intra-abdominal infection

A

GI contetns - main cause
Blood
External i.e. post op infection

83
Q

Mechanism of intra-abdominal infections

A

Translation of micro-organisms from FI tract limen to peritoneal cavity - intraabdominal infections
Translocation along a lumen - hepatbiliary infections
Translocation from extra-intestianl source - penetrating and haematogenous spread

84
Q

Translocation across a wall causing intra-abdominal infections

A

Perforation - e.g. appendix, ulcer, diverticulum, malignancy –> this is the most common cause of perforation
Loss of integrity - ischaemie, strangulation
Surgery - seeding at operation, anatomic leak

Sometimes Intra-abdominal infection is the primary presentation of malignancy

85
Q

Tranlocation along a lumen causing intra-abdominal infections

A

Blockage - cholecystitis etc

Iatrogenic - instrumentation

86
Q

Perforated appendix

A 
Mainly affects children and young adults
obstruction of lumen and vermiform appendix --> results in stagnation of liminal contents, bacterial growth and recruitment of inflammatory cells
Build of pressure causes perforation
Severe, generalised pain
Shock
May locales to from appendix maaa
87
Q

What are perforated ficerticulum

A

Herniation of mucosa/submucosa through muscular layer in the sigmoid and descending colon

Asymptomatic common
Complications of diverticulitis, perforation and pericolic abscess

88
Q

What bugs are associated with bowel cancer

A 
Clostridium septicum
Streptococcus gallolyticus (aka S. Bovis)
89
Q

How does ischaemia cause intra-abdominal infections

A

Interruption of intestinal blood supply - strangulation
ARterial occlusion
Gut wall loses its structural integrity –> allows translocation of luminal contents

90
Q

Mechanisms of post operative infections intra-abdominally

A

Seeding at operation - reduce with prophylactic antibiotics
Anastomic leak
Acute infection - abdominal pain and tenderness, shock
Intrapertioneal abscess

91
Q

What causes cholecystitis

A

Gall stones majorty

Also malignancy, parasitic worms, surgery, occasionally no obstruction

92
Q

Presentation of cholecystitis

A

Fever
RUQ pain
Mild jaundice

93
Q

What is emphysematous cholecystitis

A

Intramural gas in the gallbladder wall

94
Q

What is empyema of the gall bladder

A

Complication of cholecystitis

Pus in gallbladder

95
Q

presentation of empyeme of the gall bladder

A

Same as cholecystitis BUT SEPTIC PRESENTATION

Sever pain, high fiver, chills and rigors

96
Q

What is cholangitis

A

Inflammation/infectin of the biliary tree

Same causes as cholecystitis

97
Q

Presentation of cholangitis

A

RUQ pain
Fever (rigors)
Jaundice
May have a non-specific presentation

98
Q

Routes of infection causing pyogenic liver abscesses

A

Biliary obstruction
Direct spread from other intra-abdominal infections
Haematogenous (mesenteric vis hepatic portal vein or from systemic via hepatic artery)
Penetrating trauma
Idiopathic

99
Q

What is a pyogenic liver abscess

A

Abscess with collection of pus in the liver parenchyma

100
Q

Presentation of intraperiotneal abscess

A

Non-sepcific

Sweating, anorexia, wasting, high swinging pyrexia

101
Q

Presentation of a subphrenic abscess

A 
Pain in shoulder on affected side
Persistent Hiccups
Intercostal tenderness
Apparent hepatomegaly
Ipsilateral lung collapse with pleural effusion
102
Q

Pelvic abscess presentation

A

Urinary frequency

Tenesmus

103
Q

Predisposing factrs for intra-peritonral abscesses

A

Perforation, chlecystitis, mesenteric ischaemia, pancretitis, penetrating trauma, postopertaive anastomic leak

104
Q

What is spontaneous bacterial peritonitis

A

Infected ascots fluid

Usually in patients with chronic liver disease - no evidence of perforation

105
Q

What is an amoebic abscess caused by

A

entamoeba histolytica

106
Q

What causes hydatid cysts

A

Echinococcus granulosus

This si parasitic condition where the worm enter the liver causing cysts

107
Q

Desrive ileo-caecal tuberculosis

A

Mycobacterium tuberculosis
Presents with systemic TB symptoms
Diagnose with abdomen CT

108
Q

What usually causes liver abscsses

A

Polymicrobial - may be sterile on culture but usually just hard to grow bacteria
Infections secondary to haematogenous spread or trauma that may not involve normal GI flora
Hepatobiliary tract infection s- usually invovle lower GI flora despite duodenal origin

109
Q

What are the major mortalities after trauma

A

Head injury then haematological shock then acute respiratory distress syndrome then multi-gan failure

110
Q

Consequences of a RTA

A

Blood loss + impaired breathing
Descresed circulating volume/RBC/WBC’s –> impaired immune response, decreased CO and organ perfusion, decreased substrate delivery to cells

Major organ dysfunction
Infection barrier penetration leads to sepsis

111
Q

Immediate effects of physical trauma

A

Intravascular fluid loss
Extravascular fluid volume
Tissue destruction
Obstructed/impaired breathing

112
Q

Later effects of physical trauma

A

Starvation
Infection
inflammation

113
Q

What does clinical shock occur due to

A

Due to a lack of blood

114
Q

Describe phase 1 of trauma - clinical shock

A

2-6 hours after injury, last 24-48 hours
Cytokines, catecholamines and cortisol secreted
Tachycardia, tachypnoea and peripheral vasconstriction to rpeserve vital organisms
Hypovolaemia

Primary aim to reduce blood loss and prevent infecection

115
Q

Describe phase 2 ot trauma - catabolic state

A

2 days after injury
Catecholamines, glucagon and ACTH secreted
Glucagon causes increased lipolysis and glycolysis
Increased oxygen consumption, metaobolic rate
Negative nitrogen balance ash skeletal muscle broken down to release amin aacids

116
Q

Primary aim of phase 2 of trauma

A

Avoid sepsis and provide adequate nutrition

117
Q

Phase 3 of trauma - anabolic state

A

3-8 days after uncomplicated surgery, may not occur for weeks after trauma sepsis

Conincides with beginnning of dieresis and demand for oral intake

Gradual restoration of body protein synthesis etc.

Obseity paradox

ADEQUATE NUTRTIION VITAL - refeeding syndrome is a risk

118
Q

Inflammatory response at a trauma site

A

Pathogens enter wound
Platelets activate clotting factors
Mast cells secrete factors - vasodilation
Neutrophisl and macrophages recruited
Macrophages secrete cytokines to attract immune cells

119
Q

What are the inflammatory mediators

A

Cytokines IL1, IL6, TNF alpha

120
Q

What occurs due to capillaries due to inflammatory mediators

A

Systemic capillar leak - lose H20, NaCl, albumin and energy substrates

121
Q

What are the endocrine effects of the inflammatory cytokines

A

Secretion of catabolic hormones (by IL1 and TNF) –> catecholamines, glucagon and ACTH

Inhibitor of anabolic hormones –> growth hormone and insulin

122
Q

How long do we have glycogen stores for

A

24 horus

Brain has NO glycogen stores - will not survive more than 2 minutes of circulatory fail

123
Q

Why can kidneys and liver survive hours of interrupted blood supply

A

Capable of glucneogenesis

124
Q

How much glucose does 1kg of muscle make

A

200g of protein which = 120g of glucose

125
Q

What rate do we lose nitrogen in gluconeogenedid

A

About 60-70g a day but can be unto 300g in sever burns

126
Q

What happens in lipolysis and ketogenesis

A

FFA–> Acetyl CoA –> Acetoacetate and hydroxybutyrate

Gradual change to ketones by the CNS to spare protein stores

127
Q

What happens with low ATP

A

Loss of Na/K pump –> cellular swelling and loss membrane integrity –> lysosomal enzyme release
Decreased pH
Increased H+ and increased lactate

128
Q

How much of the bodies protein is readily available as a source of energy

A

30%

129
Q

Why does giving food solve protein breakdown in starvation but not for trauma/sepsis patients

A

As in trauma the primary stimulation for protein breakdown is due to the cytokine stimulation form activated macrophages

130
Q

Why is latte produced in hypoxia

A

Anaerobic metabolism
Pyruvate doesn’t undergo oxidative phosphorylation via the TCA cycle but is reduced to lactate

If lactate is over 5mmol/l then 100% mortality

131
Q

What can immobilisation cause the loss of

A

Minerals

132
Q

What is primary malnutrition

A

Protein calroie undernutrition

133
Q

What is secondary malnutrition

A

Nutrients present in adequate amounts but appetite is supressed

134
Q

Consequences of malnutrition

A

Negative nitrogen balance
MUscle wasting
Widespread cellular dysfunction
Poor wound healing etc.

135
Q

What happens in referring system

A

Changes from starvation to anabolic
Turns of Counterregulatory horomones
Secrete insulins (cortisol and glucagon production stopped)
ATP available due to re-uptake of glucose, thiamine and minerals
BUT LOW ATP BLOOD LEVELS - polarity of neurones and cardiac cells not maintained –> heart failure

136
Q

What is CFTR

A

A cAMP dependent chloride channel

137
Q

Why do you get lung disease n cystic fibrosis

A

High bacteria colonisation
Neutrophils accumulate
Elastase secreted –> digests lung proteins causing tissure damage
Dead neutrophil cells release DNA which increases the viscosity of the sputum
Infection and persistent inflammatory state

138
Q

What does diabetes decrease

A

Lipases hence lipid malabsorption

139
Q

What do we treat cF with

A

Nebuliser for drugs - bronchodilators, antibiotics, mucolytics, steroids

Crean delayed release capsule containing lipase, protease and amylase
Life long nutritional supplements
Fat-soluble vitamines
High calorie diet etc.
Avoid catabolic state and maintain body weight

CP - JL (14 decks)

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