Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What are the two inflammatory bowel diseases?

A

Crohn’s disease

Ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the pattern of inflammation in Crohn’s disease?

A

Patchy inflammation anywhere from the mouth to the anus (skip lesions).

It is transmural (goes through the whole thickness of the bowel wall)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What cells / features are present in the bowel wall in Crohn’s disease?

A

White aphthous ulcers
Deep aggregates of lymphocytes in the bowel wall
Granulomas (collection of epithelioid macrophages surrounded by lymphocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the typical appearance of the bowel mucosa in Crohn’s disease?

A

Cobblestone

Fibrosis and strictures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the layers of the bowel wall?

A

mucosa
submucosa
muscularis propria
fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the aetiology of Crohn’s Disease?

A

Inappropriate immune response against the gut flora in a genetically susceptible individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What age does Crohn’s disease typically present?

A

20-40 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the symptoms of Crohn’s disease?

A 
**Diarrhoea 
May be bloody
May become chronic (more than 6 weeks at a time) 
**Abdominal Pain
**Weight loss
Failure to thrive 
Fatigue
Fever
Malaise
Anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How may children present in Crohn’s disease?

A

Poor growth
Delayed puberty
Malnutrition
Bone demineralisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the typical course or presentation of Crohn’s

A

Typically there are periods of acute exacerbation interspersed with remissions or less active disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the signs of Crohn’s disease?

A 
Bowel ulceration 
Abdominal tenderness/palpable mass
Perianal abscess/fistulae/skin tags (characteristic) 
Anal strictures 
Beyond the gut 
- Clubbing 
- Skin, joint and eye problems 
- Mouth ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 1 systemic complication of Crohn’s disease?

A

Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name 5 complications that occur in the bowel as a result of Crohn’s disease?

A

Malabsorption - caused by damage to the mucosal surface in the small bowel.

Obstruction - acute swelling, chronic fibrosis.

Perforation due to deep fissuring ulcers

Fistula formation caused by deep fissuring ulcers

Anal (skin tags, fissure, fistula)

Neoplasia - there is an increased risk on developing colorectal cancer but the risk depends on the duration and severity of the Crohn’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is toxic dilation classed as ?

A

When the colonic diameter exceeds 6cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What tests do you do in a patient with suspected Crohn’s disease?

A

Blood tests

  • FBC
  • CRP
  • U&Es
  • LFTs
  • Ferritin
  • B12
  • Folate

Stool sample

Faecal calprotectin

Colonoscopy and biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is CRP a useful indicator in Crohn’s diease?

A

Useful for assessing a patient’s risk of relapse as high levels are indicative of active disease or a bacterial complication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why do you do a stool sample in patients with Crohn’s?

A

MC&S to exclude C.diff, campylobacter, E.coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is faecal calprotectin a good test to do in Crohn’s patients?

A

The concentration of calprotectin in faeces has been shown to correlate well with the severity of intestinal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the three kinds of treatment options you can offer a patient with Crohn’s disease to induce remission?

A

Monotherapy
Add on therapy
Biologics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What monotherapy can you offer to Crohn’s patients to induce remission?

A

Prednisolone or methylprednisolone

If CI or isn’t tolerated : budesonide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What add on therapy can you offer to patients with Crohn’s patients that have had 2 or more inflammatory exacerbations in the last 12 months?

And if these cannot be tolerated?

A

azathioprine or mercaptopurine

Methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What biologic drugs are there that can help to induce remission in Crohn’s patients?

Name an example of a drug in each class?

A

Anti-TNF-alphas : Infliximab / adalimumab

Anti-integrin :Vendolizumab

Anti-IL-12/23 : Ustekinumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do anti-TNF-alpha drugs help in Crohn’s disease?

A

These block the action of the cytokine tumour necrosis factor alpha which mediates inflammation in Crohn’s
Severe active disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do anti-integrin drugs help in Crohn’s disease?

A

Monoclonal antibodies that target adhesion molecules involved in gut lymphocyte trafficking

Reduces disease activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What treatments are there to maintain remission in Crohn’s patients?

A

Stop smoking
Azathioprine
6-mercaptopurine
Methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the side effects of the drug treatments used to maintain remission in Crohn’s disease?

A

abdominal pain, nausea, pancreatitis, leucopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What non-pharmacological treatment is used in Crohn’s disease? When is it indicated?

A 
Surgery 
To resect the affected areas 
Indications 
Drug failure
GI obstruction from stricture 
Perforation 
Fistulae 
Abscess

Psychological support and nutritional advice.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What nutrition advice can be given to Crohn’s patients?

A

No evidence to suggest that dietary modification can prevent flares or induce remission. A healthy, balanced diet including a variety from all food groups is recommended.

A low-FODMAP diet can be used in patients who report IBS symptoms during remission periods of IBD

Calcium and vitamin D supplementation should be considered in particular during flare ups.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the pattern of inflammation in ulcerative colitis?

A

Relapsing and remitting inflammation of the colonic mucosa

Inflammation is all mucosal (i.e does not extend deeper into the bowel). It starts in the rectum and is continuous but is only confined to the colon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Can there be inflammation of the terminal ileum in ulcerative colitis?

A

Yes, but this is only caused due to backwash of inflammatory cells caused by an incompetent ileocaecal valve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Aetiology of ulcerative colitis?

A

Inappropriate immune response against potentially abnormal colonic flora in genetically susceptible individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What genetic association is there in ulcerative colitis?

A

HLA-B27

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Symptoms of ulcerative colitis?

A
  • Episodic or chronic diarrhoea + blood (blood may be brighter/fresher than in Crohn’s as it is colonic inflammation only)
  • Crampy (colicky) abdominal discomfort
  • Bowel frequency (relates to severity)
  • Urgency
  • Tenesmus (a feeling of incomplete defecation with an inability or difficulty to empty bowel at defecation

Systemic symptoms during attacks

  • Fever
  • Malaise
  • Anorexia
  • Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Signs of ulcerative colitis

A

Depends on disease severity
Patient may be clearly unwell, pale, febrile, dehydrated
May have tachycardia or hypotension
Abdominal examination may reveal tenderness, distension or palpable mass (toxic megacolon)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What extra-intestinal disease may present in patients with ulcerative colitis?

A

Liver

  • Fatty change
  • Sclerosing cholangitis - fibrosis of bile ducts

Colorectal cancer

Joints

  • Ankylosing spondylitis
  • Arthritis

Eyes

  • Iritis
  • Uveitis
  • Episcleritis

Skin

  • Erythema nodosum
  • Pyoderma gangrenosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is an acute complication of ulcerative colitis?

A

Toxic dilatation of colon with risk of perforation

Venous thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is a chronic complication of ulcerative colitis?

A

Colonic cancer. Risk is related to duration and severity of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What investigations do you do in ulcerative colitis?

A

Limited flexible sigmoidoscopy if acute to assess and biopsy, full colonoscopy once controlled to define disease extent

Bloods
FBC, renal function, LFTs, ESR, CRP, iron studies, vitamin B12, folate

Stool microscopy culture and sensitivity
Exclude campylobacter, C.diff
Faecal calprotectin

Abdominal X-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What may an abdominal x-ray show/be used to show in a patient with ulcerative colitis?

A

To exclude colonic dilatation
May also help assess disease extent in UC
Mucosal thickening / islands
No faecal shadows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What drug treatment is used in patients with mild-moderate ulcerative colitis?

A

Topical mesalazine 5-aminosalicylic acid
Oral aminosalicylate e.g mesalazine
Oral/topical corticosteroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the treatment for patients with severe ulcerative colitis?

A

Unwell + 6 or more motions a day
IV hydration
IV steroids
Rectal steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What other treatment options are there if the patient has not responded to conventional drug therapy used in ulcerative colitis?

A

Immunomodulation
Biologic agents
Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When is immunomodulation therapy indicated in ulcerative colitis patients?

Name a drug used

A

Immunomodulation is indicated if the patients flare on steroids or require 2 or more courses of steroids in a year
Azathioprine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What biologic agents can be used to treat ulcerative colitis?

A

Infliximab

Adalimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What surgery may be needed in patients with ulcerative colitis?

A

May need emergency treatment for severe UC that does not respond to drug treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the pathology of irritable bowel syndrome

A

Seems to involved abnormal smooth muscle activity +/- visceral hypersensitivity and abnormal central processing of painful stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the aetiology of irritable bowel syndrome?

A

No organic cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the age of onset of irritable bowel syndrome?

A

less than 40 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the symptoms of irritable bowel syndrome?

How long must they have had these symptoms to be able to diagnose IBS?

A

6 month history of either
Abdominal discomfort/pain
Bloating
Change in bowel habit

Plus the recurrent abdominal pain is associated with at least 2 of
Relief by defecation
Altered stool form
Altered bowel frequency (constipation and diarrhoea may alternate)

AND at least 2 of the following 
Altered passage of stool 
Abdominal bloating, distension or hardness
Symptoms are aggravated by eating 
Passage of mucus rectally 
Other symptoms 
Lethargy 
Nausea
Backache 
Bladder symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What can make IBS symptoms worse?

A

exacerbated by stress, menstruation or gastroenteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Signs of IBS?

A

Examination may be normal but general abdominal tenderness is common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do you diagnose IBS?

A

Diagnosis should be made positively on symptom based criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What tests do you when investigation IBS?

A

FBC
ESR
CRP
Coeliac screen
CA 125 (for women with symptoms that could be ovarian cancer)
Faecal calprotectin (in patients with symptoms that could be IBD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Female patient presents with IBS type symptoms but they say that their pain is cyclical - what may this suggest?

A

Endometriosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What advice would you give to a patient with IBS who has

  1. constipation
  2. diarrhoea
A
  1. adequate water and fibre intake. Physical activity, avoid insoluble fibre like bran. If this fails then can try simple laxatives
  2. avoid sorbitol sweetners, alcohol and caffeine. Reduce dietary fibre content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What medication can you give to a patient with IBS who experiences colic or bloating?

A

Oral antispasmodics

medbevrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

how is surface area in the intestine increased?

A

mucosal folds
villi
brush border of microvilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what are the role of crypts in the intestine?

A

proliferative cells that replace higher up epithelial cells as they come to the end of their lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the 5 main reasons why malabsorption may occur?

A
  1. Defective intraluminal digestion
  2. Insufficient absorptive area
  3. lack of digestive enzymes
  4. defective epithelial transport
  5. lymphatic obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Name 3 things that can cause malapsorption by causing defective intraluminal digestion.

A
  1. Pancreatic insufficiency
  2. Defective bile secretion
  3. Bacterial overgrowth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Name 2 diseases that cause pancreatic insufficiency leading to malabsorption? Why?

A

Chronic pancreatitis
- repeated bouts of inflammation leads to insufficient pancreatic tissue to produce digestive enzymes

Cystic Fibrosis
- viscous secretions block the duct, the pancreas atrophies and there are insufficient enzymes for digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Why can defective bile secretion cause malabsorption?

In what conditions may this occur?

A

Bile salts are needed for fat absorption. If there are not enough of these bile salts then fats cannot be absorbed.

Biliary obstruction (gallstones) 
Ileal resection - because the ileum absorbs and recirculates the bile salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

where are bile salts absorbed?

A

ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Name 4 conditions that may cause malabsorption by insufficient absorptive area

A
  1. Coeliac disease
  2. Crohn’s disease
  3. Extensive surface parasitisation
  4. Small intestinal resection or bypass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Why may extensive parasitusation cause malabsorption?

A

Giardia lamblia

When you have a large infestation they carpet the villi and digested food cannot be absorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Why can Crohn’s cause malabsoprtion?

A

Cobblestone mucosa and inflammation reduce the surface area for absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is a common digestive enzyme deficiency that can cause some degree of malabsorption ?

A

Disaccharidase deficiency (lactose intolerance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Why do symptoms of lactose intolerance manifest?

A

Lactose arrives at the colon undigested where there are lots of microbes that use lactose as energy. When they digest the lactose they produce gas, causing distension, wind and bloating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Name two conditions that cause defective epithelial transport leading to malabsorption and why?

A
  1. Abetalipoproteinemia
    - genetic mutations that cause a particular protein to not be produced so a particular nutrient cannot be absorbed
  2. Primary bile acid malabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What can cause lymphatic obstruction leading to malabsoption and why?

A

Lymphoma
TB

Cannot get transported from the lacteal to the rest of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Name 5 symptoms of malabsorption?

A

Diarrhoea Weight loss (despite maintaining a normal calorie intake/diet)
Lethargy
Steatorrhoea
Bloating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the features of steatorrhoea?

A

Unpleasant faeces
Fat isn’t being absorbed
Stools may be bulky and difficult to flush, have a pale and oily appearance and can be especially foul-smelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the signs of malabsorption?

A 
Anaemia 
- Decreased iron
- Decreased B12
- Decreased folate 
Bleeding disorders
- Due to decreased vitamin K
Oedema
- Due to decreased protein 
Metabolic bone disease 
- Due to decreased vitamin D
Neurological features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What tests do you do in malabsorption?

A 
FBC 
Decreased or increased MCV
Decreased calcium
Decreased iron 
Decreased B12 and folate 
Increased INR
Lipid profile
Coeliac serology 
Stool 
Breath hydrogen analysis 
Endoscopy and small bowel biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What stain would you use on a stool sample to look for fat globules?

A

Sudan stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What does breath hydrogen analysis show?

A

For bacterial overgrowth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Name 2 causes of infective malabsorption?

A

Giardia
Cryptosporidium
Tropical sprue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How many people does coeliac disease affect?

A

1% of the adult population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

When does coeliac disease often develop?

A

Commonly presents between the 4th and 6th decade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the pathology of coeliac disease?

A
  1. Gluten peptides in the intestinal lumen cross the lumen and reach the lamina propria
  2. They activate innate and adaptive immunity
  3. IL-15 promotes lymphocyte growth and can play a role in intestinal damage
  4. Tissue transglutaminase is involved in the cross linking of collagen and tissue
  5. tTG operates a deamidation process to gluten peptides.
  6. These peptides become negatively charged and have a high affinity to binding to the HLA-DQ2 / HLA-DQ8 molecules that are expressed on antigen presenting cells.
  7. The HLA-DQ2 and HLA-DQ8 molecules are able to present these gluten peptides to CD4+ cells and trigger an immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What genetic molecules are associated with coeliac disease?

A

HLA-DQ2/DQ8 molecules

HLA-DQ2 molecules are expressed in 95% of patients and HLA-DQ8 molecules are expressed in 5%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

If a person has the genetic molecules that are seen in coeliac does that mean they will have coeliac disease?

A

No, they are necessary for development of the disease but are not definitive for getting the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the negative predictive value of HLA-DQ2 and HLA-DQ8 when diagnosing coeliac?

A

Have a negative predictive value of 100%

i.e if you do not have them then you will not get the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the aetiology of coeliac disease?

A 
Gluten 
Glidans
Glutenins 
Individual factors 
Genetic predisposition 
- HLA-DQ2 and HLA-DQ8 
- Tissue transglutaminase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What immune response do the coeliac antigens cause?

A

TH1- natural killed cells release cytokines leading to mucosal inflammation and cause villous atrophy

TH2 - B cells, antibodies are formed (anti-gliadin, anti-endomysial and anti-tissue transglutaminase). This causes autoimmunity and presents with intestinal and extraintestinal symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What antibodies are formed in coeliac disease?

A

anti-gliadin,
anti-endomysial and
anti-tissue transglutaminase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Name a risk factor that increases your risk of developing coeliac?

A

Relative risk in first degree relatives is 6 fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the symptoms of coeliac disease?

A

Steatorrhoea
Diarrhoea
Weight loss
Failure to thrive in children

Abdominal pain 
Bloating 
Nausea + vomiting 
Aphthous ulcers 
Angular stomatitis 
Fatigue 
Weakness

Or patient can be asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What complications can arise from coeliac?

A 
Anaemia 
Dermatitis herpetiformis 
Osteopenia/osteoporosis 
Hyposplenism 
GI T cell lymphoma 
Increased risk of malignancies 
-Lymphoma 
-Gastric
-Oesophageal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What investigations do you do in coeliac disease?

A

Serology
Positive IgA tissue transglutaminase
IgA anti- endomysial antibody

Upper GI endoscopy and duodenal biopsy 
Villous atrophy 
Crypt hyperplasia
Flat mucosa 
Increased intraepithelial lymphocyte count
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the histological features of the intestine in a person with coeliac?

A

Villous atrophy
Crypt hyperplasia
Flat mucosa
Increased intraepithelial lymphocyte count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What important thing do patients need to do before they are tested for coeliac disease?

A

Before testing patients NEED to keep gluten in their diet! Need to eat some gluten in their diet in more than 1 meal every day for at least 6 weeks before testing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the treatment for coeliac disease?

A

Gluten-free diet lifelong

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What foods do patients with coeliac have to avoid?

A

Avoid bread, cakes, pasta, cereals, wheat flour, meat pies, sausages, fish fingers, wheat, rye, barley

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the pathology of GORD?

A

Backflow of gastric acid from the stomach into the oesophagus due to incompetent oesophageal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the normal histology of the oesophagus?

A

stratified muscle

non-keratinized squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Name 5 causes of GORD?

A

Most causes are due to an increase in intra-abdominal pressure

-Lower esophageal sphincter hypotension
-Inadequate cardiac sphincter for anatomical reasons or factors that reduce tone and also poor esophageal peristalsis
-Hiatus hernia
-Esophageal dysmotility
-Obesity
-Gastric acid hypersecretion
-Delayed gastric emptying
-Smoking
-Alcohol
-Pregnancy
-Fatty meals
Relaxes the tone of the cardiac sphincter
-Drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Why can smoking cause GORD?

A

reduces the tone of the cardiac sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What drugs relax the tone of the cardiac sphincter and can cause GORD?

A

Tricyclic antidepressants
Anticholinergics
Nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the oesophageal symptoms of GORD?

A 
Heartburn 
- Burning, retrosternal discomfort after meals, lying, stooping or straining 
Belching 
Acid brash 
- Acid or bile regurgitation 
Waterbrash 
- Increased salivation 
Odynophagia 
- Painful swallowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

When can heartburn be felt?

A

Burning, retrosternal discomfort after meals, lying, stooping or straining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the extra-oesophageal symptoms of GORD?

A

Nocturnal asthma
Chronic cough
Laryngitis
Sinusitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Name three differential diagnoses from GORD?

A 
Oesophagitis 
NSAIDs
Herpes
Candida
Duodenal or gastric ulcers
Non-ulcer dyspepsia
Oesophageal spasm
Cardiac causes
104
Q

How can you differentiate GORD from angina?

A

In GORD there is no relationship with exercise and pain

105
Q

Name three complications of GORD?

A 
Oesophagitis 
Ulcers
Benign stricture
Iron-deficiency
Metaplasia → dysplasia → neoplasia 
GORD may lead to Barrett’s oesophagus
106
Q

What investigations do you do in GORD?

A

Endoscopy

FBC - to exclude significant anaemia

Esophageal 24 hour pH monitoring to assess if symptoms coincide with acid in the oesophagus
- Used if the endoscopy is normal

107
Q

What are the different grades of GORD based on the endoscopy?

A

Grade 1
Single or multiple erosions on a single fold

Grade 2
Multiple erosions on multiple folds

Grade 3
Multiple circumferential erosions

Grade 4
Ulcer, stenosis or esophageal shortening

Grade 5
Barrett’s epithelium. Columnar metaplasia in the form of circular or non-circular extensions

108
Q

What lifestyle advice would you give to someone with GORD?

A 
Weight loss
Stop smoking 
Small, regular meals 
Reduce
-Hot drinks 
-Alcohol 
-Citrus fruits 
-Tomatoes
-Onions
-Fizzy drinks
-Spicy foods
-Caffeine 
-Chocolate 
Avoid eating less than 3 hours before bed
Raised the bed head
Avoid drugs that affect oesophageal motility or damage the mucosa
109
Q

What are the pharmacological treatment options used in GORD?

A

Antacids to reduce symptoms
- Magnesium trisilicate mixture
Proton pump inhibitor

Avoid drugs that affect esophageal motility or damage the mucosa (e.g NSAIDs)

110
Q

Name 2 examples of a proton pump inhibitor?

A

Lansoprazole

Omeprazole

111
Q

Mechanism of action of PPIs?

A

Inhibit the proton pump on the parietal cells decreasing the concentration of HCl in the stomach, increasing pH

112
Q

Mechanism of action of NSAIDs?

A

COX-1 enzyme inhibitor inhibiting prostaglandin synthesis decreasing inflammation

113
Q

What surgical treatment options are there for GORD patients?

How do they work?

A

Laparoscopic fundoplication surgery

  • Narrowing the hiatus where the oesophagus enters the stomach
  • Wrapping the upper part of the stomach around the lower oesophagus to recreate the valve at the lower end of the oesophagus

Magnetic bead band

  • Encircles the distal oesophagus at the gastro-oesophageal junction
  • Ring of interlinked titaniumbeads, each with a weak magnetic force which holds the beads together to keep the distal oesophagus closed
  • When patient swallows the magnetic force is overcome allowing the ring to open
114
Q

What are the red flag symptoms for cancer?

A 
unexplained weight loss
anaemia
evidence of GI bleed
Dysphagia
Upper abdominal mass
Persistent vomiting
115
Q

define Barrett’s oesophagus?

A

A premalignant condition.
Oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium.

116
Q

Pathology of Barrett’s oesophagus?

A

Long-standing reflux of acid causes the normal squamous epithelium that lines the oesophagus to die.

There then may be gaps in the epithelial lining leading to ulceration which can cause pain and indigestion.

If reflux continues then the oesophagus has intestinal metaplasia and consists of columnar epithelium with goblet cells and tall intervening mucus-producing cells that secrete intestinal-type mucins.

117
Q

What is the oesophageal lining seen in Barrett’s oesophagus?

A

columnar epithelium with goblet cells and tall intervening mucus-producing cells

118
Q

What are the risk factors for Barrett’s oesophagus?

A 
Chronic GORD 
- Risk increases with longer duration and increased frequency of gastro-oesophageal symptoms 
Hiatus hernia
Obesity 
Alcohol 
Smoking
119
Q

What are the symptoms of Barrett’s oesophagus?

A

May be asymptomatic
Dysphagia
Weight loss
Retrosternal chest pain

120
Q

What are the signs of Barrett’s Oesophagus?

A

Hoarseness

Cough

121
Q

What investigation do you do in Barrett’s oesophagus?

A

Endoscopy and biopsy

122
Q

What will the biopsy show in a patient with Barrett’s oesophagus?

A

Columnar epithelium with goblet cells and mucus producing cells in the oesophagus
Red islands

123
Q

What are the management options for patients with Barrett’s oesophagus who have dysplasia?

A

Endoscopic mucosal resection
- Removal of small polyps or growths from the lining of the oesophagus

Radiofrequency
- Burn away the abnormal cells

Surgery
- Oesophagectomy is recommended when there is severe dysplasia

124
Q

What is the first line treatment for a patient with dysplasia in Barrett’s oesophagus?

A

Radiofrequency

Burn away the abnormal cells

125
Q

What is the management for patients with Barrett’s oesophagus and no dysplasia?

A 
Lifestyle 
Weight loss
Reduced alcohol intake 
Stop smoking 
Reduce portion sizes 
Avoid eating within 3 hours of going to bed

Medications
Long term PPI

126
Q

What does Barrett’s oesophagus increase the risk for?

What should you look for that may indicate they could be developing this?

A

oesophageal adenocarcinoma

Persistence of reflux
Difficulting swallowing 
Unexplained weight loss 
Bringing up blood 
Hoarse voice
127
Q

What are the two main types of oesophageal cancers?

A

Squamous carcinoma

Adenocarcinoma

128
Q

What is the pathology of squamous carcinoma (oesophagus)

A

Develops from squamous epithelium and may come before any dysplastic changes.

129
Q

What is dysplastic squamous epithelium characterised by?

A

lack of maturation of cells towards the surface and immature cells are seen close to the surface. Degree of dysplasia can be low or high grade

130
Q

Where are squamous carcinoma tumours usually found?

A

usually found in the middle and upper third of the oesophagus

Can have a superficial cancer, a polypoid into the lumen or it can become invasive going through the mucosa.

131
Q

What are the risk factors for developing squamous carcinoma of the oesophagus?

A

Heavy smoking
Alcohol
Achalasia - oesophagus has a reduced/no ability to do peristalsis
Vitamin deficiencies
Repeated therapy injury due to hot beverages

132
Q

What are the symptoms of squamous carcinoma of the oesophagus?

A

Usually asymptomatic until advanced disease stage.

Dysphagia (at first with solids then liquids)

Weight loss

133
Q

What type of dysphagia is seen in squamous carcinoma of the oesophagus?

A

at first with solids then liquids)

134
Q

What is the investigations in squamous carcinoma of the oesophagus?

A

Endoscopy and biopsy

CT for staging
Identifies primary tumour in most cases as well as any spread to the lymph nodes or other organs such as the live, lungs and bone

135
Q

What is the radical treatment for squamous carcinoma of the oesophagus?

A

Nutritional assessment and support
Offer people with resectable non-metastatic squamous cell carcinoma of the oesophagus the choice of…
- Radical chemotherapy
- Chemoradiotherapy before surgical resection (only a low number of cases can be offered surgical resection)

136
Q

What is the palliative care for squamous carcinoma of the oesophagus?

A

Chemotherapy

Local tumour treatment including stenting or palliative radiotherapy

137
Q

what is the difference in location of squamous carcinoma of the oesophagus and adenocarcinoma of the oesophagus?

A

squamous carcinoma: occurs in the upper 2/3

adenocarcinoma: occurs in the lower 1/3

138
Q

What is the difference in presenting dysphagia between malignant and benign disease

A

benign : dysphagia to solids and liquids from the start

malignant: dysphagia starts with solids then moves onto liquids

139
Q

What cells does adenocarcinoma of the oesophagus primarily arise frrom?

A

columnar-lined epithelium in the lower oesophagus

140
Q

What are 3 risk factors that increases the likelihood of developing adenocarcinoma of the oesophagus?

A

Barrett’s oesophagus
GORD
Smoking
Obesity

141
Q

What is the clinical presentation of adenocarcinoma of the oesophagus?

A

Usually there are no physical signs and the cancer is typically extremely advanced when it is found

Dysphagia
Starting with solids and moving onto liquids

Weight loss
Lymphadenopathy
Anorexia
Pain due to impaction of food or infiltration of cancer into adjacent structures

142
Q

What investigations are used in adenocarcinoma of the oesophagus?

A

Oesophagoscopy with biopsy
Histological proof of the carcinoma

Barium swallow - to see strictures

CT for staging

143
Q

What are the treatment options for adenocarcinoma of the oesophagus?

A

Surgical resection
Best chance of cure if the tumour has not infiltrated outside the oesophageal wall
Combined with chemotherapy before surgery

If locally incurable or metastatic - systemic chemotherapy

Treatment of dysphagia
Endoscopic insertion of expanding metal stent across tumour to ensure oesophageal patency

Palliative care may be the only option
70% of patients have widespread local disease or metastatic disease at presentation and cannot be cured by surgical resection
May receive palliative chemotherapy, chemoradiation or treated with a stent to improve dysphagia

144
Q

how do malignant tumours of the stomach arise

A

The change from normal gastric mucosa to intestinal metaplasia and then dysplasia.

Can be early or locally advanced

Normal gastric mucosa → intestinal metaplasia → dysplasia → intramucosal carcinoma → invasive carcinoma

145
Q

What are the two different pathologies of malignant cancers of the stomach?

What are their differences

A

Intestinal
Well formed and differentiated glandular structures
More likely to involve distal stomach

2. Diffuse
Poorly cohesive undifferentiated cells 
Tend to infiltrate the gastric wall 
Can involve any part of the stomach
Worse prognosis that intestinal
146
Q

Aetiology of malignant tumours of the stomach?

A

Helicobacter pylori infection Dietary - high salts and nitrates
Smoking
Obesity
Previous gastric surgery for benign disease
Hereditary diffuse gastric cancer
Presence of a CDH1 germline mutation
Deletion of tumour suppressor gene p53

147
Q

Why does H.pylori infection have a role in early stages of gastric cancer?

A

Can lead to atrophic gastritis and pre-malignant intestinal metaplasia

Appears to have a role in the early stages of gastric cancer development as it binds to the surface of the normal gastric epithelial cell

Given the high prevalence of H.pylori infection and the comparative rarity of gastric cancer it is highly unlikely that the organism or its products are directly acting mutagens

148
Q

What are the risk factors for malignant tumours of the stomach?

A 
Pernicious anaemia 
H. pylori infection 
Atrophic gastritis 
Adenomatous polyps 
Lower social class
Smoking 
Diet
149
Q

What are the symptoms of stomach cancer?

A

Usually non-specific.
Most patients that have gastric carcinoma have advanced disease at the time of presentation.

Dyspepsia
Weight loss
Vomiting 
- Frequent and can be severe if the tumour encroaches on the pylorus 
Dysphagia 
Anaemia
150
Q

What is pernicious anaemia?

A

Large immature nucleated cells circulate in the blood and do not function as RBC.

This is caused by the impaired uptake of vitamin B12 due to lack of intrinsic factor in the gastric mucosa.

151
Q

What are the signs of an incurable gastric mass?

A 
Epigastric mass
Virchow’s node
Hepatomegaly
Jaundice (liver mets) 
Ascites
152
Q

What is Virchow’s node?

A

Lies near to the junction of the thoracic duct and the left subclavian vein.

Tumour embolisation of the GI cancers via the thoracic duct usually leads to the enlargement of this node

153
Q

What investigations are used for malignant tumours of the stomach?

A

Gastroscopy and biopsy multiple ulcers
Aim to biopsy all ulcers

Endoscopic ultrasound can evaluate the depth of the invasion of the carcinoma

Staging laparoscopy is recommended for locally advanced tumours

154
Q

What are the different stages of gastric cancer?

A

In situ intramucosal : likely to develop into invasive but currently is unlikely to have spread

Early gastric cancer: limited to the mucosa or submucosa

Locally advanced gastric cancer: spreads into the muscular wall of the stomach

If it has spread into the peritoneal cavity then it cannot be cured

155
Q

Treatment of early stomach cancer?

A

Surgical resection is likely
Chemotherapy before
Nutritional support

156
Q

Treatment / management of more advanced stomach cancer?

A

Partial gastrectomy for more advanced distal tumours
Surgery and combination chemotherapy
Just chemotherapy can increase quality of life survival
Surgical palliation is often needed for obstruction, pain or haemorrhage
Nutritional support

157
Q

What are the two types of small intestine tumours?

A

Adenocarcinoma

Lymphomas

158
Q

What are the risk factors for developing small intestine tumours?

A

Coeliac

Crohn’s

159
Q

Are small intestine tumours common?

A

No, they are relatively resistant to the development of neoplasia

160
Q

What are the symptoms of small intestinal tumours?

A 
Pain 
Diarrhoea
Anorexia
Weight loss
Anaemia
161
Q

Sign of a small intestinal tumour?

A

May be a palable mass

162
Q

What investigations do you do for a small intestinal tumour?

A

Ultrasound

Endoscopic biopsy to histologically confirm a diagnosis

CT scan

163
Q

What may the CT scan show a small intestinal tumour?

A

May show small bowel wall thickening and lymph node involvement

164
Q

What is the treatment for a small intestinal tumour

A

Surgical resection

Radiotherapy

165
Q

What are polyps

A

abnormal growth of tissue projecting from the colonic musoca. Most are asymptomatic and found by chance.

Can be epithelial or mesenchymal

166
Q

What type of cancer do colorectal cancers tend to be?

A

adenocarcinoma

167
Q

What is the usual progression for colorectal cancer development?

A

Usually progresses from :

Normal epithelium → adenoma → colorectal carcinoma

168
Q

What are colonic adenomas?

A

benign dysplastic tumour of columnar cells or glandular tissue

169
Q

What causes adenomas to progress to carcinomas?

A

Activation of oncogenes
Loss or mutations of tumour suppressor genes
Defects in DNA repair

170
Q

Aetiology of colorectal cancer?

A

Diet
Inherited genetic factors
Long standing ulcerative colitis

171
Q

What inherited genetic factors can cause colorectal cancer?
What is the pattern of inheritance?
How do they increase likelihood of developing colorectal cancer?

A

Familial adenomatous polyposis

Autosomal dominant pattern of inheritance that causes mutations in the APC tumour suppressor gene

Numerous adenomas develop at an early age mainly in the large intestine and subsequently undergo malignant change

172
Q

What impact does diet have on the colon?

A

affects the flora of the large bowel, the bowel transit time and the amount of cellulose, amino acids and bile acids in bowel contents

173
Q

What type of diet is associated with colorectal cancer? Why?

A

High fat, high protein, low fibre diet is linked to colorectal cancer

High fat increases bile salt production leading to a higher load of faecal bile acids

High protein leads to transformation of amino acids by bacteria

Low fibre reduces the number of volatile fatty acids which prolongs intestinal transit time leading to more time for bacterial action on the content. There is prolonged contact between any carcinogen generated and the mucosa

174
Q

Name three predisposing factors that can increase risk of developing colorectal carcinoma?

A 
Neoplastic polyps 
IBD
Increased alcohol consumption 
Smoking 
Family history 
Previous cancer
175
Q

Where do the majority of colorectal cancers present?

A

rectum

176
Q

What features are more visible the closer the cancer is to the outside?

A

The closer the cancer is to the outside the more visible the blood and mucus will be

177
Q

What is the clinical presentation of left sided colorectal cancer?

A 
Stenosing type 
Obstruction 
Bleeding/mucus in the stools
Altered bowel habit 
Tenesmus
Mass PR
Diarrhoea or alteration constipation and diarrhoea 
Colicky abdominal pain
Less advanced disease at presentation
178
Q

What is the clinical presentation of right sided colorectal cancer?

A

Iron deficiency anaemia
Weight loss
Decreased haemoglobin
Abdominal pain
Occult bleeding (not visible to the patient or doctor)
Disease is more likely to be advanced at presentation

179
Q

What can be a feature of either right or left sided colorectal cancer?

A 
Abdominal mass
Perforation 
Haemorrhage
Fistula
Jaundice and hepatomegaly indicate advanced disease with extensive liver metastases
180
Q

What investigations do you do in colorectal cancer?

A

Colonoscopy is the gold standard investigation
Biopsy
Removal of polyps

FBC - microcytic anaemia

Faecal occult blood
It checks blood in the faeces
Home kit is used for screening

181
Q

When would you do a barium enema in a patient with suspected colorectal cancer?

A

If patient cannot tolerate a colonoscopy or if the colonoscopy fails to visualise the caecum can do a barium enema
Avoids perforation risk
More limited in detecting small lesions

182
Q

How can you help to prevent colorectal cancer?

A

increase the fibre in the diet

  • wholegrain bread and oats
  • wholewheat pasta
  • berries, pears, melon
  • broccoli, carrots, sweetcorn
  • peas, beans and pulses
  • potatoes with skin
183
Q

What is the treatment options of colorectal cancer?

A

Surgery
Radiotherapy
Chemotherapy

184
Q

What surgery can you do to treat colorectal cancer?

A

Aims to cure or relieve symptoms
Laparoscopic surgery to

(hemi) colectomy

185
Q

When would you use radiotherapy in the treatment of colorectal cancer?

A

Locally advanced rectal cancer
Palliation of colonic cancer
Post-op radiotherapy is used in patients with rectal tumours that are at high risk of local recurrence

186
Q

What type of colorectal cancer do you use chemotherapy?

A

Adjuvant chemotherapy in stage 3 disease (cancer is invading the subserosa and beyond but not other organs)

187
Q

What is more common duodenal or gastric ulcer?

A

Duodenal ulcer is 4 x more common

188
Q

What is a peptic ulcer?

A

a localised defect extending at least into the submucosa.

189
Q

What is the pathophysiology behind a H. pylori infection causing a peptic ulcer?

A

A bacteria that lives in the mucin layer of the stomach
Causes a decrease in duodenal HCO3-. This increases the acidity of the stomach as there is less alkali to buffer the acid
Bacteria secretes urease splitting urea into CO2 and ammonia
Also secrete proteases which attack the gastric epithelium
Increases gastrin released from G cells, increasing acid secretion
Decreases somatostatin leading to increased acid secretion
Inflammatory response
Increased acidity overwhelms the protective mucin resulting in mucosal damage.

190
Q

What is the pathophysiology of NSAIDs causing a peptic ulcer?

A

Mucus secretion by mucosal cells is stimulated by prostaglandins
Cyclo-oxygenase 1 is needed for prostaglandin synthesis
NSAIDs inhibit COX-1 enzyme
Reduced mucosal defence
Cells are not protected from the HCl of the stomach which can cause cell death and can develop a micro ulcer
Acid can then get into the micro ulcer and damage the adjacent cells

191
Q

Causes of a duodenal ulcer?

A 
H.pylori infection 
NSAIDs
Smoking
Steroids
Increased gastric acid secretion
192
Q

Causes of a gastric ulcer?

A 
H.pylori infection 
Smoking 
NSAIDs
Reflux or duodenal contents 
Delayed gastric emptying 
Stress
Alcohol - usually only spirits
193
Q

Symptoms of a duodenal ulcer?

A

May be asymptomatic
Epigastric pain relieved by antacids
Pain usually presents 1-3 hours after food
Can wake patients at night
Pain is worse when the patient is hungry
May present with weight loss
Nausea

194
Q

sign of a duodenal ulcer?

A

Epigastric tenderness

195
Q

Symptoms of a gastric ulcer?

A

May be asymptomatic
Epigastric pain relieved by antacids
May present with weight loss
Nausea

196
Q

What type of bacteria is H.pylori?

A

Gram negative spiral bacillus

197
Q

Where is H.pylori most prevalent?

A

In poor socioeconomic and overcrowded areas

198
Q

How is H.pylori infection acquired?

A

Faecal-oral or oral-oral route

199
Q

Investigations in peptic ulcers?

A

C-urea breath test for H.pylori
Stool antigen test for H.pylori
Endoscopy

200
Q

What is the treatment for a H.pylori infection?.

A

Lansoprazole (PPI)
Amoxicillin
Metronidazole

201
Q

What lifestyle advice can you offer to a patient with a peptic ulcer?

A

Reduce alcohol intake

Reduce tobacco consumption

202
Q

What drugs can reduce stomach acid where the cause of the peptic ulcer is not H.pylori?

A

PPI

H2 blockers e.g ranitidine

203
Q

Name an example of a H2 blocker drug?

A

ranitidine

cimetidine

204
Q

How do H2 receptor blocking drugs work?

A

Block the H2 receptor on the parietal cell
Histamine cannot bind to the receptor
Decreasing the proton pump activity
Decreasing the concentration of HCl in the stomach

205
Q

When do acute ulcers tend to develop?

A

Develop as part of acute gastritis as a complication of a severe stress response due to mucosal ischaemia or as a result of extreme hyperacidity

206
Q

Where do chronic ulcers most frequently develop?

A

Mucosal junctions

207
Q

What are 2 complications of peptic ulcers?

A
  • Haemorrhage - ulcer erodes deeper, can erode into a large blood vessel (most commonly the gastroduodenal artery)
  • Perforation - causes an acute abdomen with epigastric pain
    Peritonitis - as acid enters the peritoneum
  • Scarring of the duodenum may lead to pyloric stenosis
  • Malignancy
  • Reduced gastric outflow
208
Q

Pathology of appendicitis?

A

Sudden inflammation of the appendix, usually initiated by the obstruction of the lumen of the appendix

Lumen of the appendix becomes obstructed resulting in the invasion of gut organisms into the appendix wall

Leads to oedema, ischaemia, necrosis and inflammation

209
Q

Name 3 causes of appendicitis?

A 
Faecolith 
Lymphoid hyperplasia
Filarial worms
Normal stool blocking the lumen 
Infective agents
210
Q

Symptoms of appendicitis?

A

Pain in the umbilical region that migrates to the right iliac fossa

  • Early inflammation irritates the structure and walls of the appendix so a colicky pain is referred to the mid-abdomen around the umbilical area
  • As the inflammation continues it irritates the parietal peritoneum and the pain settles at McBurney’s point

Anorexia
Nausea and vomiting
Constipation is usual but may also have diarrhoea

211
Q

What are 3 signs of appendicitis?

A

Tenderness in the right iliac fossa with guarding due to localised peritonitis
May be a tender mass in the right iliac fossa
Low grade pyrexia

212
Q

Name 2 complications that can arise from appendicitis?

A

Perforation
Wound infection
Appendix mass
- Omentum and small bowel adhere to the appendix
- Usually presents with a fever and palable mass
Appendix abscess

213
Q

What investigations do you do for appendicitis? What is the gold standard?

A

Essentially a clinical diagnosis

Blood tests
Raised WCC
Neutrophil leukocytosis
Elevated ESR and CRP

Ultrasound can detect an inflamed appendix

CT is the gold standard for diagnosis and will show an enlarged appendix

214
Q

Treatment for appendicitis?

A

Laparoscopic appendectomy

IV prophylaxis antibiotics

215
Q

What is gastritis?

A

Lining of the stomach becomes inflamed after mucosal damage

216
Q

How does H.pylori infection cause gastritis?

A

Bacteria that live in the mucin layer of the stomach and are ingested
Bacteria produce chemicals which attract acute inflammatory cells to the mucin which damage cells

217
Q

How does an autoimmune reaction cause gastritis?

What does it lead to?

A

Affects the fundus and body

Atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia

218
Q

How do NSAIDs cause gastritis?

A

Inhibit prostaglandin synthesis via the inhibition of COX enzyme leading to less mucus production and therefore gastritis

219
Q

Name 3 causes of gastritis?

A 
H.pylori infection 
Autoimmune
NSAIDs
Viruses (CMV, herpes simplex) 
Duodenogastric reflux - bile salts enter the stomach and damage mucin protection 
Mucosal ischaemia 
Increased acid 
Alcohol
220
Q

How does gastritis present?

A

Epigastric pain
Vomiting
Abdominal bloating
Indigestion

221
Q

Investigation for gastritis?

A

Upper GI endoscopy

222
Q

Treatment for gastritis?

A

Remove any causative agents e.g alcohol

Reduce stress

H.pylori eradication therapy
PPI
Amoxicillin
Metronidazole

H2 antagonist e.g ranitidine or cimetidine

Antacids

223
Q

What is a consequence of bowel obstruction?

A

If you have an obstruction food will begin to accumulate which causes bacterial growth

224
Q

What are the three different types of bowel obstruction?

A

Intraluminal - material inside the lumen

Intramural - something in the wall of the bowel that is causing bowel to constrict causing obstruction

Extraluminal - something on the outside of the intestinal wall pushing down on the bowel and decreasing it’s size

225
Q

Name three causes of intraluminal bowel obstruction?

A

Tumour (carcinoma or lymphoma)

Meconium ileus
- SI obstruction resulting from thickening and desiccation of the vicious meconium. Commonly seen in cystic fibrosis

Gallstone ileus
- caused by impaction of a gallstone within the lumen of the small intestine. Commonly caused by a fistula

226
Q

What is the difference in presentation between a RHS and LHS intraluminal tumour causing obstruction?

A

If on the RHS the material inside the bowel is more liquid so will cause less of an obstruction

If on the LHS the faecal material is more solid

227
Q

Name three causes of intramural intestinal obstruction?

A

Inflammatory - Crohn’s, diverticulitis

Tumours

Neural - Hirschsprung’s disease

228
Q

What is Hirschsprung’s disease

A

Congenital aganglionic megacolon.
Failure of neuroblasts to migrate into the developing gut leading to failure of intramural parasympathetic nerve plexuses to develop.
There is no contraction or circular muscle in the gut wall leading to small bowel obstruction

229
Q

What is the histologocal diagnosis of Hirschsprung’s disease?

A

there are no ganglion cells in the submucosal and myenteric plexuses

230
Q

Name 3 causes of extraluminal intestinal obstruction?

A

Adhesions
Fibrous adhesions between loops of bowel

Volvulus
360 degrees twist in the bowel that occludes it’s lumen
SI or sigmoid (occurs at the part of bowel with mesentery)

Tumour
Mainly ovarian cancer

231
Q

Where do volvulus usually occur?

A

SI or sigmoid (occurs at the part of bowel with mesentery)

232
Q

What are the symptoms of a small bowel obstruction?

A 
Vomiting presents early 
Pain is colicky to constant (diffuse) 
Constipation presents late 
Distension, will probably be less marked
Tenderness
Progress is faster
233
Q

What are the symptoms of large bowel obstruction?

A 
Abdominal discomfort 
Fullness/bloating/nausea
Vomiting 
Late presentation 
Faeculent 
Constipation presents early 
There may be a history of progressive constipation of change in bowel habits 
Abdominal pain
234
Q

What is the presentation of a volvulus?

A

Sudden
Pain
Localised tenderness and distension

235
Q

What are the signs of intestinal obstruction?

A

Distension (more marked the lower the obstruction)
Tympany (hollow sound) due to an air filled stomach
High pitched and irregular bowel sounds
Look for signs of dehydration
If there is strangulation or perforation there will be features of an acute abdomen

236
Q

What are three complications of an intestinal obstruction?

A

Bowel ischaemia
Perforation
Sepsis

237
Q

What investigations do you do in a patient that has an intestinal obstruction?

A 
Fluid charts 
Abdominal X-ray 
Bloods
FBC
U&Es
Creatinine 
Glucose may be high due to stress

CT scan of abdomen

Ultrasound

238
Q

What is the conservative treatment for intestinal obstruction?

A

Fluid resuscitation
Electrolyte replacement
Bowel rest
Intestinal decompression

239
Q

What is the surgical treatment for patients with intestinal obstruction?

A

Laparotomy required without a clear diagnosis
Bowel resection
Prophylactic antibiotics

240
Q

What is a non-surgical treatment of intestinal obstruction?

A

Endoscopic stenting (usually palliative)

241
Q

How do you treat a volvulus?

A

Decompression

242
Q

what is pseudo-obstruction of the intestine?

A

A false obstruction of the intestine

condition characterized by impairment of the muscle contractions that move food through the digestive trac

243
Q

What can cause a pseudo-obstruction of the intestine?

A

Myopathy - there is no peristaltic contractions

Neuropathy

  • Hirschsprung’s disease
  • no innervation so abnormal movement of muscle
244
Q

What can pseudo-obstruction lead to?

A

Sepsis

245
Q

What is a diverticulum?

A

Outpouching of the gut wall

Usually at the sites of perforating arteries

246
Q

What is diverticulitis?

A

Diverticulitis is evidence of diverticular inflammation

247
Q

Where does diverticulitis most commonly occur?

A

Most commonly seen in the sigmoid colon in the taenia coli

248
Q

What is the pathology of diverticulitis?

A
  1. Diverticular form at gaps in the wall of the gut where blood vessels penetrate
  2. Sigmoid motility is sensitive to the bulk of colonic contents - if this is low then abnormally high intraluminal pressures are generated to help move faeces along
  3. Pressure pushes the mucosa into and out of the wall leading to pouches of mucosa being formed
  4. Faeces can become stuck and obstruct these diverticular causing stagnation and allowing the bacteria to multiply producing inflammation
249
Q

What are the causes of diverticulitis?

A

Low fibre diet
Obesity in the young
Smoking
NSAIDs

250
Q

What are the symptoms of diverticulitis?

A 
Left iliac fossa pain 
Pain may be intermittent or constant and may be associated with a change in bowel habits
Fever
Tachycardia
Anorexia
Nausea
Vomiting
251
Q

What are the signs of diverticulitis?

A

Hypotension
Localised tenderness
Guarding and rigidity on the left side of the abdomen
A palpable mass can be occasionally felt
Reduced bowel sounds
Rectal examination may reveal tenderness or a mass

252
Q

Name three complications of diverticulitis?

A

Abscess
Perforation
Fistula
Hemorrhage

253
Q

What investigations do you do in diverticulitis?

A

Blood tests
Polymorphonuclear leukocytosis
ESR raised
CRP raised

CT colonography
Shows colonic wall thickening and diverticula

Abdominal erect X-ray - may identify obstruction of free air

254
Q

What is the treatment for mild attacks of diverticulitis?

A

ciprofloxacin

Paracetamol

255
Q

What is the treatment for diverticulitis and signs of systemic disease?

A

Bowel rest
IV fluids
IV antibiotics
Paracetamol

256
Q

What surgery may be needed for patients with diverticulitis and when is it indicated?

A 
Surgery - bowel resection 
Faecal peritonitis 
Uncontrolled sepsis 
Fistula
Obstruction

Phase 2A (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions