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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
IBD Extra-intestinal manifestations: Systemic
Amyloid | Vaculitis
26
Risk factors for CRC in UC
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
27
What is a polyp
Mucosal projectio
28
Types of polyps
Neoplastic Hamartamous Reactive Infectious
29
Where are hyper plastic polyps common
Located in rectum and sigmoid colon | 1-5mm in size
30
Do hyperplastic polyps have malignant potential
Small distal HP's have no malignancy potential | Large right sided polyps may cause micro satellite carcinoma
31
Type of hamartamous polyps
Juvenile polyps | Peutz-Jeughers syndrome
32
What are juvenile plyps
``` Common in children In the rectum and distal colon 10-30mm of spherical, pedunctulated polyps Sporadic ones are not malignant!! Get diarrhoea/some bleeding ```
33
What is peutz-jeugher syndrome caused by
Autosomal dominant | Mutatino in STK11 gene on chromosome 19
34
What is peutz-jeugher syndrome
Multiple GI polyps predominantly small bowel Muco-cutaneous pigmentation Presents clinical in teens/20s Increase risk of cancer in stomach, small bowel and pancreas
35
What is the most common benign epithelial tumour
Adenoma | Commonly polypoid but flat!
36
Higher risk of malignancy in adenoma if
``` Flat adenomas Large size over 10mm Villous and tubulo/villous structure High grade dysplasia HNPCC associated carcinomas ```
37
Colorectal cancer risk factors
``` Dietary i.e. fat red meat Obesity NSAIDS HRT and oral contraceptives Schistosomiasis Pelvic radiation UC and Crohns disease ```
38
What is FAP
Autosomal dominant Mutation in APC tumour suppressor gene Multiple benig adenomatous polyps in colon - 100% lifetime risk of large bowel cancer
39
What is HNPCC
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
40
How do we stage bowel cancer
Dukes staging
41
What is diverticulosis
Outpouchings of the mucosa/submucosa Commonly in sigmoid colon Between the mesenteric taenia coli and the anti-mesenteric taenia coli
42
How does diverticulosis progress
Thickening of muscular propr. | Elastosis of the taenia coli - shortens the colon --> redudant mucosal folds and secular --> saculatino and diverticula
43
Features of diverticulosis
90 % asymtpmatic Abdo cramping pain ALternation constipation/diarrhoea
44
Acute complications of diverticulosis
Dierticulitis, peridiverticular abscess Perforation Haemorrhage
45
Chronic complications of diverticulosis
Strictures Fistulas Collitis (segmental and granulomatous) Polypoid Prolapsing Mucosal Folds
46
How do we test for H. Pylori
Urease breath test
47
How do we treat H. Pylori
PPI and 2 antibitoics | (Omeprazole) + Amoxicilin/clarithomycin
48
What is the commonest form of oesophagitis
Reflux oesophagitis
49
Changes in reflux oesophagitis
Increased basal cell layer Increased cell turnover Eosinophils, neutrophils and inflammatory cells Elongated lamina papillae
50
Risk factors for reflux oesophagitis
Defective LOS Hiatus Hernia Raised Intra abdominal pressure Increased gastric fluid volume due to outflow stensosi
51
What are the risk factors for squamous carcinoma of the oesophagus
Tobacco and alcohol | Occurs in lower and middle oesophagus
52
Risk factors for adenocarcinoma of oesophagus
Barrett, tobacco, smoking Higher incidence in males and caucasians Lower oesophagus - plaque like, can get stricturing due to fibrosis around the tumour
53
What occurs in barret's oesophagus
Longstanding reflux Proximal extension of the squamo-columnar junction - glandular metaplasia Often get goblet cells Causes increased risk of developing adenocarcinoma
54
Autoimmune causes of chronic gastritis
Anti-parietal cell and anti-intrinsic factor antibodies Sensitised T lymphocyes Glandular atrophy in the body mucosa INtestianl metaplasia
55
Bacteria causes of chronic gastritis
H. Pylori Produces cytokines, mucolytic enzymes, ammonia Tissue damage due to immune response Multi-focal atrophy more in antrum then body and intestinal metaplasia
56
Chemical causes of chronic gastritis
Direct - fovealor hyperplasia NSAIDS - disrupts the mucous layer --> oedema Bile reflux - degranulates mast cells - vasodilation Alcohol - paucity of inflammatory cels
57
What is Coeliacs disease
Sensitivity to gliadin in gluten
58
Pathogenesis of coeliacs
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
Silent coeliacs disease
Positive serology Villus atrophy No symtpoms
60
Latent coeliacs disease
Positive serology Villous atrophy No symptoms
61
Associated coeliacs disaese
Dermatitis herpetiformis Lymphocytic gastritis/cells Enteropathy associated T cell lymphoma small intestine adenocarcinoma
62
When are we worried about Enteropathy associated T cell lymphoma small intestine adenocarcinoma in coeliacs
IF symptoms are persisting despite a gluten free diat
63
Morphology in coeliacs disease
Villous atrophy Crypt elongation Increased lamina propr. inflammation Increased IEL
64
What type of bacteria is H. Pylori
Gram -ve spiral bacteria
65
How does h pylori damage the epithelium
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
What is the most frequent gastric cancer
Adenocarcinoma
67
Carcinoma of the GOJ
No association with H, Pylori Diet Associated with GO reflux White males
68
Carcinoma of body/antrum
Associated with diet and H. Pylori | No association with GO reflux
69
INtestinal gastric carcinoma
Well differentiated Intestinal metaplasia Adenoma steps
70
Diffuse gastric carcinoma
Poorly differentiated Scattered growth Cadherin Loss Signet ring
71
Hereditary diffuse type gastric cancer
Germiline E. Cadherin mutation Precursor lesions Likely to be young diffuse type gastric cancer
72
Complication of peptic ulcers
Haemorrhage - anaemia Perforation Penetration Stricturing
73
What is peptic ulcer disease
Extends to atleast submucos!
74
Acute gastric ulcers
Full thickness coagulative necrosis of the mucose Covered with ulcer slough Granulation tissue at the ulcer floow
75
Chronic gastric ulcers
Clear cut edges Extensive granulation/scar Bleeding Scarring often throughout the entire gastric wall breaching the muscular propria
76
Features of duodenal ulcers
``` More common In younger Elevated or normal acid levels Almost always H. Pylori associated Bulbus Blood group O ```
77
Features of gastric ulcers
``` Less common Older Normal or low acid H Pylori in 70% Lesser curve/ antum-corpus unction Blood group A ```
78
What is an intra-abdominal infection
Micro-organisms in normally-sterile sites within the abdominal cavity i.e. the peritoneal cavity and the hepatobiliary tree
79
Why is gasto-enteritis not an intra-abdominal infection
As the bowel lumen is a non-sterile site
80
Is the stomach sterile
Yes Primal small intestine also considered relatively free of bacteria as growth inhibited by bile - a few aerobic bacteria and candida are there
81
Normal flora of small intestine
Majority anaerobic | Some aerobic e.g. enterobacteriaceae and gram +ve cocci
82
Sources if intra-abdominal infection
GI contetns - main cause Blood External i.e. post op infection
83
Mechanism of intra-abdominal infections
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
Translocation across a wall causing intra-abdominal infections
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
Tranlocation along a lumen causing intra-abdominal infections
Blockage - cholecystitis etc | Iatrogenic - instrumentation
86
Perforated appendix
``` 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
What are perforated ficerticulum
Herniation of mucosa/submucosa through muscular layer in the sigmoid and descending colon Asymptomatic common Complications of diverticulitis, perforation and pericolic abscess
88
What bugs are associated with bowel cancer
``` Clostridium septicum Streptococcus gallolyticus (aka S. Bovis) ```
89
How does ischaemia cause intra-abdominal infections
Interruption of intestinal blood supply - strangulation ARterial occlusion Gut wall loses its structural integrity --> allows translocation of luminal contents
90
Mechanisms of post operative infections intra-abdominally
Seeding at operation - reduce with prophylactic antibiotics Anastomic leak Acute infection - abdominal pain and tenderness, shock Intrapertioneal abscess
91
What causes cholecystitis
Gall stones majorty | Also malignancy, parasitic worms, surgery, occasionally no obstruction
92
Presentation of cholecystitis
Fever RUQ pain Mild jaundice
93
What is emphysematous cholecystitis
Intramural gas in the gallbladder wall
94
What is empyema of the gall bladder
Complication of cholecystitis | Pus in gallbladder
95
presentation of empyeme of the gall bladder
Same as cholecystitis BUT SEPTIC PRESENTATION Sever pain, high fiver, chills and rigors
96
What is cholangitis
Inflammation/infectin of the biliary tree | Same causes as cholecystitis
97
Presentation of cholangitis
RUQ pain Fever (rigors) Jaundice May have a non-specific presentation
98
Routes of infection causing pyogenic liver abscesses
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
What is a pyogenic liver abscess
Abscess with collection of pus in the liver parenchyma
100
Presentation of intraperiotneal abscess
Non-sepcific | Sweating, anorexia, wasting, high swinging pyrexia
101
Presentation of a subphrenic abscess
``` Pain in shoulder on affected side Persistent Hiccups Intercostal tenderness Apparent hepatomegaly Ipsilateral lung collapse with pleural effusion ```
102
Pelvic abscess presentation
Urinary frequency | Tenesmus
103
Predisposing factrs for intra-peritonral abscesses
Perforation, chlecystitis, mesenteric ischaemia, pancretitis, penetrating trauma, postopertaive anastomic leak
104
What is spontaneous bacterial peritonitis
Infected ascots fluid | Usually in patients with chronic liver disease - no evidence of perforation
105
What is an amoebic abscess caused by
entamoeba histolytica
106
What causes hydatid cysts
Echinococcus granulosus | This si parasitic condition where the worm enter the liver causing cysts
107
Desrive ileo-caecal tuberculosis
Mycobacterium tuberculosis Presents with systemic TB symptoms Diagnose with abdomen CT
108
What usually causes liver abscsses
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
What are the major mortalities after trauma
Head injury then haematological shock then acute respiratory distress syndrome then multi-gan failure
110
Consequences of a RTA
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
Immediate effects of physical trauma
Intravascular fluid loss Extravascular fluid volume Tissue destruction Obstructed/impaired breathing
112
Later effects of physical trauma
Starvation Infection inflammation
113
What does clinical shock occur due to
Due to a lack of blood
114
Describe phase 1 of trauma - clinical shock
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
Describe phase 2 ot trauma - catabolic state
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
Primary aim of phase 2 of trauma
Avoid sepsis and provide adequate nutrition
117
Phase 3 of trauma - anabolic state
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
Inflammatory response at a trauma site
Pathogens enter wound Platelets activate clotting factors Mast cells secrete factors - vasodilation Neutrophisl and macrophages recruited Macrophages secrete cytokines to attract immune cells
119
What are the inflammatory mediators
Cytokines IL1, IL6, TNF alpha
120
What occurs due to capillaries due to inflammatory mediators
Systemic capillar leak - lose H20, NaCl, albumin and energy substrates
121
What are the endocrine effects of the inflammatory cytokines
Secretion of catabolic hormones (by IL1 and TNF) --> catecholamines, glucagon and ACTH Inhibitor of anabolic hormones --> growth hormone and insulin
122
How long do we have glycogen stores for
24 horus | Brain has NO glycogen stores - will not survive more than 2 minutes of circulatory fail
123
Why can kidneys and liver survive hours of interrupted blood supply
Capable of glucneogenesis
124
How much glucose does 1kg of muscle make
200g of protein which = 120g of glucose
125
What rate do we lose nitrogen in gluconeogenedid
About 60-70g a day but can be unto 300g in sever burns
126
What happens in lipolysis and ketogenesis
FFA--> Acetyl CoA --> Acetoacetate and hydroxybutyrate | Gradual change to ketones by the CNS to spare protein stores
127
What happens with low ATP
Loss of Na/K pump --> cellular swelling and loss membrane integrity --> lysosomal enzyme release Decreased pH Increased H+ and increased lactate
128
How much of the bodies protein is readily available as a source of energy
30%
129
Why does giving food solve protein breakdown in starvation but not for trauma/sepsis patients
As in trauma the primary stimulation for protein breakdown is due to the cytokine stimulation form activated macrophages
130
Why is latte produced in hypoxia
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
What can immobilisation cause the loss of
Minerals
132
What is primary malnutrition
Protein calroie undernutrition
133
What is secondary malnutrition
Nutrients present in adequate amounts but appetite is supressed
134
Consequences of malnutrition
Negative nitrogen balance MUscle wasting Widespread cellular dysfunction Poor wound healing etc.
135
What happens in referring system
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
What is CFTR
A cAMP dependent chloride channel
137
Why do you get lung disease n cystic fibrosis
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
What does diabetes decrease
Lipases hence lipid malabsorption
139
What do we treat cF with
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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