Diseases of the GI tract Flashcards Preview

CP - JL > Diseases of the GI tract > Flashcards

Flashcards in Diseases of the GI tract Deck (139):
1

What are the majority of normal flora in the fut

Majority anaerobes
Some are facultative anaerobes e.g. E. Coli

2

What viruses generally cause gastroentertisi

Commonly norovirus
Very infectious due to aerosols

3

Parasites causing gastroenteritis

Cryptosporidium, giardia and entamoeba

4

Why do we get antibiotic associated dirarhoea

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

5

Complications of antibiotic associated diarrhoea

Diarrhoea
Pseudomembranous Colitis
Toxic Megacolon
Perforation
Shock

6

High risk antibiotics for diarrhoe

Cephalosporins and clindamycin

7

Medium risk antibiotics for diarrhoea

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

8

How do we treat C. Diff

Vancomycin and Oral Metronidazole

9

How do bacterias produce disease

Either by toxins or adherence

10

What type of bacteria is E. Coli

Gram - ve
Produces toxins

11

Hoe does salmonella cause disease

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

12

Who do we give antibiotics to for gastroenteritis

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

13

Protective and increasing factors in UC and Crohns

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

Oral contraceptive, MMR, childhood infections increase risk of both

14

Presentation of UC

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

15

Presetantion fo crohns

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

16

Complications of UC and Crohns

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

Crowns: Fistula, short bowel syndrome

17

Pathology of Crohns

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

18

Pathology of UC

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

19

IBD Extra-intestinal manifestations: Hepatix

Fatty Change
PSC
Granulomas
Bile duct carcinoma

20

IBD Extra-intestinal manifestations: Muco-cutaneous

Oral apthoid ulcers
Pyoderma gangrenosum
Erythema nodosum

21

IBD Extra-intestinal manifestations: Ocular

Iritis/Uveitis
Episoleritis
Retinits

22

IBD Extra-intestinal manifestations: Renal

Kidney and bladder stones

23

IBD Extra-intestinal manifestations: Haematological

Anaermia
Leucocytosis
Thrombocytosis
Thrombo-embolic disaese

24

IBD Extra-intestinal manifestations: Skeletal

Polyarthritis
Sacro-ilietis
Ankylosing Spondylitis

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