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W3 GI Flashcards

1
Q

other name for jaundice and what is it

A

icterus

yellowing of sclera and skin due to increased levels of bilirubin in the blood

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2
Q

Branches of bile duct and what it drains into

A

branches of bile duct= cystic duct and common hepatic duct

bile duct drains into 2nd part of the duodenum

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3
Q

What drains into the 2nd part of the duodenum

A

the bile duct and the pancreatic duct

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4
Q

how does bile move from liver to gall bladder

A

bile moves down common hepatic duct, up the cystic duct into gall bladder

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5
Q

Journey of bile duct to reach the duodenum

A

Bile duct descends posterior to 1st part of duodenum to connect with the main pancreatic duct forming the ampulla of vater/ hepatopancreatic ampulla which drains into the 2nd part of the duodenum through the major duodenal papilla

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6
Q

Name the sphincters where the bile duct and pancreatic duct connect with the duodenum

A

Bile duct sphincter
pancreatic duct sphincter
Sphincter of Oddi

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7
Q

What is endoscopic retrograde cholangiopancreatography used to do

A

view the biliary tree and pancreas

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8
Q

Extra-hepatic causes of jaundice

A

Obstruction of the biliary tree by gallstone or carcinoma at the head of the pancreas

causes backflow of bile to the liver and bile overspills into the blood

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9
Q

Anatomical parts of the pancreas

A

Head and uncinate
neck
body
tail

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10
Q

Nerve supply of the pancreas

A 
Vagus nerve (P)
Abdominopelvic splanchnic nerves (S)
both form a plexus around the celiac trunk

superior mesenteric ganglia hitch a ride with the arteries to get to the pancreas

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11
Q

What influences pancreatic secretion

A

hormones from duodenum epithelium and proximal intestinal epithelium which is stimulated by stomach acid

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12
Q

Arterial blood supply of the pancreas

A

Splenic artery gives rise to pancreatic arteries

anterior and posterior superior pancreaticoduodenal artery arises from the gastroduodenal artery

anterior and posterior inferior pancreaticoduodenal artery arises from the superior mesenteric artery

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13
Q

Describe a cause of pancreatitis

A

Blockage of ampulla by gall stone

Bile can’t get into duodenum - backs up into pancreas - irritation and inflammation of pancreas

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14
Q

Describe pain due to pancreatitis

A

Pancreas is a foregut and midgut organ so could cause epigastric and/or umbilical pain

can also radiate to the back

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15
Q

How is SI split into foregut and mid gut

A

foregut- 1st and 2nd part of duodenum=foregut

the rest of SI=midgut

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16
Q

Four parts of duodenum, where it begins, and what it secretes into blood

A

superior, descending, horizontal and ascending
begins at the pyloric sphincter
peptide hormones

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17
Q

Where would pain from a duodenal ulcer present

A

epigastric

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18
Q

Effect of Autonomic innervation of the duodenum

A

P- relaxation

S-contraction

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19
Q

Blood supply of the Duodenum

A

Branches of anterior and posterior superior pancreatoduodenal artery supply proximal duodenum (1st and 2nd part of duodenum)
Branches of the inferior pancreatoduodenal artery supply horizontal and ascending duodenum (3rd and 4th parts)
This is embryological and marks division between foregut and midgut

superior pancreatoduodenal artery arises from the gastroduodenal artery

inferior pancreatoduodenal artery arises from the splenic artery

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20
Q

where does the jejunum begin

A

duodenaljejunal flexure

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21
Q

where does the ilium end

A

ileocecal junction

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22
Q

Differences in jejunum and ilium

A

jejunum mucosa has plicae circulares whereas the ileal mucosa is much smoother

Jejunum is quite wide, distal ileum is quite narrow
Proximal jejunum is very highly folded
PC increase SA
PC more sparse at ileum than jejunum

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23
Q

Arterial blood supply of jejunum and ileum

A

superior mesenteric artery via jejunal and ileal arteries

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24
Q

Venous drainage of jejunum and ileum

A

jejunal and ileal veins to the superior mesenteric veins to hepatic portal vein

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25
Q

Where does the superior mesenteric artery arise from

A

SMA is the 2nd of the midline branches of the abdominal aorta

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26
Q

what are the jejunal and ileal arteries and veins in

A

within the mesentary

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27
Q
  • what do jejunal and ileal arteries give rise to

- describe the difference in the ileal and jejunal arteries

A

Loop and join to form arterial arcades which then give rise to straight arteries (vasarecta) that go to walls of jejunum and ileum

Jejunum has less arcades and longer recta, ileum has more arcades and shorter vasarecta

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28
Q

how contents of SI reach liver

A

Venous drainage absorbs proteins and carbohydrates from SI back into portal venous system to go back to the liver by jejunal and ileal veins which feed back into superior mesenteric vein to the hepatic portal vein to the liver

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29
Q

Describe absorption of fats

A

Bile helps absorption of fat into intestinal cells and then go into lacteal cells of intestinal cells

travel in lymphatic system to the left venous angle

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30
Q

where do celiac nodes drain

A

foregut organs

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31
Q

where do superior mesenteric nodes drain

A

midgut organs

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32
Q

where do inferior mesenteric nodes drain

A

hindgut organs

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33
Q

where do lumbar nodes drain

A

kidneys, posterior abdomen wall, pelvis and lower limbs

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34
Q

where do superficial lymph vessels drain to

A

Deep lymph vessels

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35
Q

Two places that lymph will ultimately drain to

A 
Thoracic duct (3/4)
Right lymphatic duct (1/4)

to the venous angles i.e. junctions between the subclavian veins and internal jugular vein

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36
Q

Risk factors of oral cancer

A

Smoking, alcohol, diet, tobacco chewing, HPV, UVL, previous oral cancer, Candida, Syphilis drugs

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37
Q

Recommended Upper weekly limit of alcohol intake for men

A

14 units

2 units per day

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38
Q

What is binge drinking

A

At least 8 units for men and at least 6 units for women

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39
Q

How does alcohol cause oral cancer

A

Ethanol is converted to acetaldehyde by ADH
Acetaldehyde is a carcinogen
acetaldehyde is converted into acetate (harmless) by ALDH

ADH is found in the mouth, ALDH isnt

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40
Q

Dietary components which increase risk of Oral Cancer

A

Low in vitamin A and C and Iron

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41
Q

Why may oral sex have link to oral cancer

A

HPV 16 and 18

association with oropharyngeal cancer

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42
Q

Presentation of oral cancer

A 
Red patches
White patches
Red/White patches (erythroleukoplakia) 
Ulceration
Bleeding
Induration (hard feeling)
Exophtosis
Lymphadenopathy
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43
Q

What type of cancer does oral cancer tend to be

A

Invasive squamous cell carcinoma

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44
Q

High risk sites of oral cancer

A
  • Soft, non-keratinising sites eg ventral tongue, floor of mouth
  • Lateral tongue

rarer sites= dorsal tongue and hard palate

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45
Q

read only

potentially malignant lesions

A

erythroplakia- Red patch
Erythroleukoplakia-Red-white patch
Leukoplakia-White patch
Erosive lichen planus
submucous fibrosis- mucous fibrosis, associated with bidy chewing
Dyskeratosis Congenita- Rare syndrome of white patch in the mouth, increased skin pigmentation and nail dystrophy

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46
Q

Signs of oral cancer

A 
Red/White/Red-white lesions
Ulcer
Numbness of lips or face
unexplained pain in mouth or neck
change in voice
dysphagia
Drooping eyelid or facial palsy (tumour in parotid gland through facial nerve)
Fracture of mandible (osteosarcoma)
Double vision- tumour has disturbed position of globe of the eye
Blocked or bleeding from nose
Facial swelling
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47
Q

Four questions you should ask patient with ulcer on tongue

A

How long have had it? (normal would heal in 7-10 days)
Painful?
Smoke/drink?
Colour? (red or red/white are more dangerous)

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48
Q

in what part of the mediastinum is the oesophagus located

A

in the posterior mediastinum

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49
Q

Type of epithelium in oesophagus

A

squamous stratified epithelium

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50
Q

Describe the two inflammatory disorders of the oesophagus and their causes

A

acute oesophagitis: rare

corrosion following chemical ingestion, infective in immunocompromised patients
can be caused by candidiasis, herpes, CMV

chronic oesophagitis: common

reflux disease, crohn’s disease

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51
Q

Reflux Oesophagitis-what is it, causes, pathology

A

inflammation of the oesophagus due to reflux of low pH gastric contents

may be due to defective sphincter, hiatus hernia
abnormal oesophageal activity and increased intra-abdominal pressure (pregnancy)

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52
Q

Microscopic appearance of reflux oesophagitis

A

basal zone epithelial hyperplasia, elongated papillae
intra-epithelial neutrophils, lymphocytes, eosinophils
increased cell proliferation to compromise for increased cell desquamation

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53
Q

Complications of Reflux

A

Ulceration and bleeding
Stricture (narrowing)
Barrets oesophagus

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54
Q

What is Barrets oesophagus

A

type of metaplasia- replacement of stratified squamous epithelium by columnar epithelium due to acid reflux or bile

protective response, faster regeneration
red, velvety mucosa

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55
Q

why is barretts oesophagus dangerous

A

pre-malignant, unstable mucosa

increased risk of dysplasia and carcinoma of oesophagus

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56
Q 
What is allergic oesophagitis
History
investigations
who is likely to get it
appearance
A

Rare form of oesophagus inflammation

Eosinophilic inflammation (increased Eos blood)
history of allergy, asthma
young, more males than females 
pH probe - for reflux 
ridged, spotty oesophagus
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57
Q

Treatment of allergic oesophagitis

A

Steroids, Montelukast, Cromoglicate

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58
Q

Benign tumours of the oesophagus

A

Squamous papilloma (rare, HPV related)
leiomyomas, lipomas
fibrovascular polyps
granular cell tumours

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59
Q

Two types of malignant oesophageal tumours and who do they occur in

A
  • Squamous cell carcinoma (more common in males, S. Africa, Brazil, central china)
  • Adenocarcinoma (more common in Caucasians, in males and obese, most common in lower 1/3 oesophagus)
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60
Q

Causes of squamous cell carcinoma

A 
Vitamin A or Zinc deficiency
Tannic acid/strong tea
smoking, alcohol
HPV
Oesophagitis
Genetic
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61
Q

main risk factor of adenocarcinoma

A

Barrets oesophagus

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62
Q

Stepwise progression of adenocarcinoma of oesophagus

A 
chronic reflux oesophagitis
barrets oesophagus (metaplasia)
low grade dysplasia
high grade dysplasia
adenocarcinoma
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63
Q

Presenting symptoms of oesophageal carcinoma

A

dysphagia due to obstruction (local)

metastases
Anaemia
weight loss
loss of energy

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64
Q

mechanisms of oesophageal carcinoma metastases

A

Direct invasion
Lymphatic
Vascular

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65
Q

why may oesophagus tear

A

prolonged vomiting

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66
Q

effect of liver cirrhosis on oesophagus

A

oesophageal varices

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67
Q

what is the most commo type of oral cancer

presentation

A

Squamous cell carcinoma (90%)

white, red, ulcers

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68
Q

High risk areas of mouth for oral cancer

A 
Soft palate 
floor of mouth
lateral and ventral tongue
retromolar pad
tonsils
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69
Q

Rare sites of oral cancer

A

dorsum of tongue, hard palate

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70
Q

Pathology of oral cancer

A

Malignant squamous epithelium

invasion and destruction of local tissues

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71
Q

Variation in grades of SSC

A

well differentiated- obviously squamous, prickles and keratinisation

poor differentiation- difficult to identify

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72
Q

Acute gastritis cause

A

chemical injury

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73
Q

Chronic gastritis causes

A

autoimmune (rarest)
bacterial (H pylori)
chemical

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74
Q

Antibodies involved in Autoimmune Chronic Gastritis
Type of disease
complications

A

anti-parietal and anti-intrinsic factor antibodies

multi-system disease (gastric, bone marrow, spinal cord)

atrophy and intestinal metaplasia in stomach body-increased risk of malignancy

pernicious anaemia, macrocytic due to Vitamin B12 deficiency -SACDC

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75
Q

SACDC

A

Subacute combined degeneration of spinal cord= degeneration of the posterior and lateral columns of the spinal cord as a result of vitamin B₁₂ deficiency, vitamin E deficiency, and copper deficiency. It is usually associated with pernicious anaemia.

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76
Q

H pylori associated with Chronic gastritis

where it inhabits, appearance, what is produced against it

A

Bacteria inhabits between epithelium and mucus barrier

G- curvilinear rod

early acute inflammatory response- if not cleared will turn into chronic inflammatory response

IL8 released in response to H pylori infection

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77
Q

why is H pylori dangerous

A

Lamina propria produces antibodies against H pylori

increases risk of duodenal and gastric ulcer and of Gastric carcinoma or lymphoma

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78
Q

Causes of Chemical gastritis

A

due to NSAID, alcohol, bile reflux
direct injury to mucus layer by fat solvents
epithelial regeneration, hyperplasia, congestion and inflammation

produces erosion and ulcers

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79
Q

what is peptic ulceration and its casue

A

Breach in GI mucosa due to acid or pepsin attack

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80
Q

Sites of chronic peptic ulcers

A

1st part of duodenum
stomach (body and antrum junction)
oesophago-gastric junction

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81
Q

Causes of Chronic peptic ulcers

A

Synergism

  • Failure of mucosal defence
  • Increased acid production

causes gastric metaplasia then H pylori infection, inflammation and epithelial damage and ulceration

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82
Q

Macroscopic Appearance of peptic ulcers

A

2-3cm

characteristic clear cut edges, punched out

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83
Q

Microscopic appearance of peptic ulcers

A

layered appearance
floor of necrotic fibrinopurulent debris
base of inflammed granulomatous tissue
deepest layer is fibrotic scar tissue

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84
Q

Complications of peptic ulcers

A

perforation, penetration, haemorrhage, stenosis, pain

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85
Q

what are polyps

A

benign tumours

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86
Q

three types of malignant gastric tumours

A

carcinomas
lymphomas
GI stromal tumours

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87
Q

Role of H Pylori in Gastric Adenocarcinoma

A

anti-H Pylori antibodies give higher risk of cancer

H. Pylori causes chronic gastritis, causing intestinal metaplasia/atrophy-dysplasia-carcinoma

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88
Q

Diseases which contribute to gastric cancer

A 
H pylori
Pernicious anaemia
Partial gastrectomy 
Lynch syndrome
Menetriers Disease
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89
Q

Two types of gastric adenocarcinoma

which has a poorer prognosis

A

Intestinal type-exophytic/polypoid mass (volcano)

Diffuse type-expands/infiltrates stomach wall (poorer prognosis)

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90
Q

Spread of gastric adenocarcinoma

A

locally to other organs
lymph nodes (omental)
haematogenous (liver ect)
transcoelomic (into peritoneal cavities and ovaries, (Kruckenburg)

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91
Q

Gastric lymphoma

A

Solid mucus associated lymphoid tumours

associated with H Pylori

Continuous inflammation- B cell proliferation- low grade lymphoma-high grade lymphoma

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92
Q

Histological appearance of Gastric lymphoma

A

sheets of lymphoid cells which attach to epithelial gastric pits

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93
Q

what does GI stromal tumour produce, mutation involved

A

produce spindle cell masses driven by mutations in KIT oncogene

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94
Q

what are the haematinic deficiencies

A

Vitamin B12, Folate, Iron

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95
Q

what is angular cheilitis and its causes

A

cracking at the corners of the mouth
Causes: candida infection, with or without bacteria, usually Staph Aureus

inflammation of upper muscoa-is present it may be denture stomatitis (type of candida infection)
recurring condition- underlying anaemia or haematinic deficiency
(If swab of skin doesnt show Staph Aureus or underlying pathology or full serum count, serum B12 folate ect is normal- consider deficiency)

can be caused by anaemia or hematinic deficiencies

96
Q

what can recurrent oral ulcers be a sign of

A

celiac disease (caused by anaemia or folate deficiency)

97
Q

Describe recurrent aphthous like stomatitis minor and major and their potential causes

A

minor- halo, yellow centre, up to 10, 1-2 weeks to heal
major-larger, up to 3, 4 weeks to heal, scarring

anaemia/haematinic deficiencies

98
Q

recurrent aphthous like stomatitis- herpetiform

A

Small ulcers, sometime coelesce to form larger ulcers, painful
Numerous, up to 100
7-14 days to heal

99
Q

underlying causes of anaemia and haematinic deficiencies

A

Gi bleeding

Malabsorption

100
Q

Describe two types of IBD

A

Crohns Disease-can affect anywhere in GI tract, blood loss, malabsorption

Ulcerative colonitis-blood loss

101
Q

Crohns disease and its facial features

A

Affects anywhere from mouth to anus

chronic granulomatous condition

orofacial granulomatosis:
oral ulceration, mucous tags, cobblestone mucosa, swollen lips, angular cheilitis, gingival erythema

102
Q

Mouth disease that affects type II diabetes

A

Thrush- acute pseudomembranous candidosis

103
Q

What medications cause dry mouth

A

PPI
Anti-muscarinics
Tricyclic antidepressants
opioid analgesia

104
Q

what medications cause angioedema

A

ACE inhibitors

105
Q

Causes Osteonecrosis of the jaw

A

Bisphosphonates for osteoporosis

metastases

106
Q

what medications cause oral ulceration

A

methotrexate used in rheumatoid arthritis

Nicorandil (ulceration of other parts of GI tract, fistula)

107
Q

Lichen planus- where does it present and type of reaction?

A

affects oral mucosa, oesophagus, skin, genitals ect

Oral Lichen lesions can be a type IV hypersensitivity reaction to dental restorative materials and mercury in restoration

presents in mouth and on skin

108
Q

name of lichen planus skin lesions

A

violaceous papules (itchy)

109
Q

mucus membrane pemphigoid- type of reaction and symptoms

A

Oral, nasal, genital mucosa, conjunctiva

Autoimmune condition - antibodies target BM of epithelium so epithelium separates from underlying connective tissue producing vesicles (small blister) and bullae (blister)

Scarring in eye can lead to blindness

Gingivae eyrthema
Red eye
Superficial ulceration of buccal mucosa

110
Q

Sjogrens and its symptoms

A

Autoimmune condition- dry mouth/eyes due to damage to exocrine glands

(Rheumatology-Type of connective tissue disease)

111
Q

Oral manifestations of HIV/AIDS

A

Candidosis
Hairy leukoplakia (white patch, lateral tongue)
Herpes simplex virus infection
Kaposi’s Sarcoma (malignant)

112
Q

Trigeminal neuralgia

A

sharp, ‘electric shock’ short lived burst of pain of less than 2 minutes of areas innervated by trigeminal nerve and its branches
recurrent
Usually unilateral, mostly areas innervated by maxillary and mandibular division

Lots of secondary causes eg tumour pressing nerve, MS

113
Q

investigation for trigeminal neuralgia

A

MRI

MRI will show vascular loop in close proximity to trigeminal nerve in posterior cranial fossa, pressure from which results in morphological changes affecting the nerve

114
Q

Treatment for trigeminal neuralgia

A

Treatment= carbamazepine/gabapentin (anti-epileptic)

115
Q

what is apthous ulceration a sign of

A

Vit B12, folate and iron deficiency

116
Q

Cause of angular cheilitis

A

iron deficiency

117
Q

cause of swollen tongue

A

iron deficiency

118
Q

Oral manifestations of crohns disease

A

Orofacial granulomatosis (non-caseating)

oral ulceration
mucosal tags
angular chelitis 
cobblestone mucosa (raised areas)
swollen lips
gingival erythema
119
Q

what is Pseudo-membrane candidosis and in what condition do you get it?

A

Thrush

Type II diabetes

120
Q

First line treatment for squamous cell carcinoma of the upper oesophagus

A

Radiotherapy and chemotherapy

121
Q

What is dyspepsia

A

indigestion

upper abdominal pain, often after eating drinking

122
Q

what is peptic ulcer disease

A

break in mucosa in stomach, duodenum or lower oesophagus

123
Q

Criteria of dyspepsia

A

epigastric pain/burning, postprandial fullness, early satiety

124
Q

where does dyspepsia come from

A

foregut organs

125
Q

Causes of dyspepsia

A

Organic (25%)
Peptic ulcer disease, drugs (NSAIDs), gastric cancer

Functional (75%)
Idiopathic, no evidence of structural disease but associated with functional gut disorders like IBS

126
Q

Examination results in uncomplicated dyspepsia

A

Epigastric tenderness only

127
Q

Examination result of complicated dyspepsia

A

Cachexia, mass, evidence of gastric outflow obstruction, peritonism

128
Q

Steps in Dyspepsia management

A
  1. Treat if reflux, check that it isnt from liver, heart, GB, Pancreas, NSAID
  2. Check for alarm features
  3. Consider lifestyle, Antacids/ H2RA
  4. Hp test

if + treat, if - and less than 55 treat as functional dyspepsia, if more than 55 consider hospital

129
Q

Presentation of peptic ulcer disease

A

Pain in epigastric region, radiates to back

also nocturnal, relapsing and remitting

130
Q

Causes of peptic ulcer disease

A

H pylori, NSAID, gastric motility/obstruction

131
Q

Microbiology of H pylori

A

G- flagellate, microaerophilic bacilli

132
Q

Transmission of H pylori

A

oral-oral and faecal-oral route

acquired in infancy, can cause issues later in life

133
Q

Consequences of H pylori

A
  1. nothing (majority)
  2. peptic ulcers
  3. gastric cancer (non-cardia adenocarcinoma)
134
Q

Draw the negative feedback loop of gastrin production in the stomach

A

acid in the stomach inhibits the release of gastrin by G cells, gastrin release will initiate parietal cells to release HCl

135
Q

Investigations of H pylori

A

Gastric biopsy
urease test
histology, culture/sensitivity
Faecal antigen test

136
Q

How does H pylori increase the pH of its environment

A

H pylori uses urease to break urea down into ammonium and bicarbonate

137
Q

Treatment of Peptic ulcer disease

A

ALL get PPI and test for H pylori

Treat cause: stop NSAIDs, lifestyle measures, treat any H pylori (if H pylori -, antacids)

138
Q

Anti-secretory therapy for Peptic ulcer disease

A

Omeprazole 20mg/day= PPI (better)

Ranitidine 300mg/day= H2RA

139
Q

Treatment of H pylori

A

PPI+ amoxicillin 1g bd+ clarythromycin 500mg bd

PPI+ metronidazole 400mg bd+ clarithromycin 250mg bd

140
Q

Complications of Peptic ulcer disease

A

anaemia/bleeding, perforation, scarring

141
Q

presentation of appendicitis

A

Right iliac fossa pain

142
Q

presentation of appendicitis

A
  • Begins with central colicky pain that then shifts to the right iliac fossa
  • sore on coughing and laughing, guarding, rebound
  • loss of appetite, may vomit, may not have opened bowels that day due to inflammation
  • look flushed (rosy red cheeks), mild tachycardia, mild pyrexia (never over 39 degrees, 37.8-37.9 degrees),
143
Q

what is mcburneys point

A

near the most common location of the appendix

Point over the right side of the abdomen that is one-third of the distance from the anterior superior iliac spine to the umbilicus

144
Q

who gets appendicitis

A

children and young adults, another peak in the early

in adult 40-60 presents with appendicitis like pain, CT scan for tumour

145
Q

who gets appendicitis

A

children and young adults, another peak in the early

in adult 40-60 presents with appendicitis like pain, CT scan for tumour

3:2 male to female until age of 25, then equal

146
Q

what happens inside appendix in appendicitis?

A

lumen may or may not be occluded
mucosal inflammation
lymphoid hyperplasia
mucus, exudate

147
Q

Rosvings sign

A

Sign of appendicitis where pushing down on the left side causes pain or the right side

148
Q

psoas sign

A

sign of appendicitis where the patient flexes their right hip to lift inflamed appendix off the psoas

149
Q

Obturator sign

A

sign of appendicitis where flexing the right hip and internal rotation causes pain (appendix touches obturator internus)

150
Q

*Investigations of appendicitis

A

Ultrasound
Bloods- CRP, WCC
Urinalysis
AXR to exclude other causes

151
Q

Score used for appendicitis

A

Alvarado score

Migration of pain to RLQ
Anorexia
Nausea and vomiting
Tenderness of RLQ
Rebound pain
Elevated temperature
Leukocytosis
Shift on WBC to left
Sore to move/laugh/cough
Flushed red face
Foetor oris (bad breath due to rotting appendix)
152
Q

Management of appendicitis

A 
Antipyretics 
Analgesia
Theatre
Antibiotics
Appendicectomy
153
Q

Treatment of appendix mass

A

antibiotics

theatre if it gets more complicated

154
Q

Treatment of appendix abscess

A

Radiological drain

155
Q

Causes of small bowel obstruction and what happens

A

lumen-gall stone, food, bezoar
wall-tumour, crohns, radiation
outside wall-adhesions, hernia

colicky central pain, absolute constipation, vomiting, burping, abdominal distension, vomiting stool, boborygmi

156
Q

Investigations of small bowel obstruction

A

Urinalysis, bloods, gases

AXR, contrast CT of abdomen, gastrograffin studies

157
Q

Treatment of small bowel obstruction

A

‘Drip and Suck’

ABC, Analgesia
IV fluid with potassium (hypokalaemia, alkalosis)
Catheterise, NG tube (Ryles tube)
Antithromboembolic measures

only drip and suck adhesional bowel obstructions

158
Q

What is malabsorption

A

defective mucosal absorption

159
Q

Causes of malabsorption

A

Defective luminal digestion, mucosal disease, structural disorders

160
Q

Causes of malabsorption and examples

A

Defective luminal digestion, mucosal disease, structural disorders

Celiac disease, Crohns disease, post-infection, biliary obstruction, cirrhosis, pancreatic cancer…

161
Q

Digestive and absorptive causes of protein malabsorption

A

digestive-gastrectomy (poor mixing), exocrine pancreatic deficiency, trypsinogen deficiency, congenital

absorptive-celiac disease, short bowel syndrome ect

162
Q

causes of fat malabsorption

A

digestive: issues with lipolysis (pancreas) or bile salts (liver)
absorptive: issues in jejunal mucosa
post-absorptive: issues with lacteal delivery

163
Q

Causes of carbohydrate malabsorption

A

digestive: pancreatic a-amylase deficiency
absorptive: Celiac disease, Crohns disease…

164
Q

Coeliac Disease

  • cause
  • pathology
  • symptoms
  • diagnosis
  • treatment
A
  • exposure to wheat, barley, rye will cause lesions on mucosa
  • individuals with antigen presenting cells expressing HLA-DQ2 or HLA-DQ8, bind to dietary gluten peptides and activate mucosal T lymphocytes, cytokines cause mucosal damage
  • can be asymptomatic, diarrhoea, weight loss, abdominal discomfort
  • IgA anti-tissue transglutaminase biopsy
  • Gluten free diet
165
Q

What is lactose malabsorption caused by?

A

Deficiency of lactase

166
Q

What is lactose malabsorption caused by?

symptoms of lactose malabsorption

A
  • Deficiency of lactase

- Diarrhoea, abdominal discomfort, excess flatulence following ingestion of dairy products

167
Q

What is lactose malabsorption caused by?
symptoms of lactose malabsorption
How to diagnose lactose malabsorption

A
  • Deficiency of lactase
  • Diarrhoea, abdominal discomfort, excess flatulence following ingestion of dairy products
  • lactose breath hydrogen test or oral lactose intolerance test
168
Q

What is lactose malabsorption caused by?
symptoms of lactose malabsorption
How to diagnose lactose malabsorption
Treatment of lactose malabsorption

A
  • Deficiency of lactase
  • Diarrhoea, abdominal discomfort, excess flatulence following ingestion of dairy products
  • lactose breath hydrogen test or oral lactose intolerance test
  • lactose free diet
169
Q
  • What is tropical sprue
  • Symptoms of tropical sprue
  • Treatment of tropical sprue
A

Colonisation of intestine by infectious agents or alterations in gut flora by exposure to another env agent

  • diarrhoea, steatorrhea, nausea, anorexia, weight loss, anaemia
  • Tetracycline and folic acid
170
Q

Name of pathogen and Antigen involved in whipples disease

A

Tropheryma whipple

HLA-B27

171
Q

Name of pathogen and Antigen involved in whipples disease

A

Tropheryma whipplei

HLA-B27

172
Q

How to diagnose whipples disease

A

micorscopy showing tropheryma whipplei in tissues

173
Q

How to diagnose whipples disease

A

microscopy showing tropheryma whipplei in tissues

174
Q

Treatment of whipples diease

A

anti-microbials

175
Q

Symptoms of crohns disease

A

mostly RLQ discomfort and abdominal pain, diarrhoea, fever, weight loss

176
Q

Diagnosis of crohns disease

A

endoscopy, barium swallow, CT, MRI

177
Q

Treatment of crohns disease

A

Steroids, immunosuppressants, azathioprine 6-MP, anti-TNF

178
Q

What is Giardia lamblia and how it it transmitted

A

parasitic infection, contaminated water

179
Q

Symptoms of Giardia lamblia infection and diagnosis

A

Diarrhoea, flatulence, abdominal cramps, epigastric pain, nausea

1/3 vomiting

diagnosed by stool sample

180
Q

Treatment of Giardia lamblia

A

metronidazole, 1 week

181
Q

small bowel bacterial overgrowth

a) causitive organisms
b) signs
c) what does the disease cause
d) diagnosis
e) what test will diagnosis bacterial overgrowth
f) Treatment

A

a- E. Coli, Bacteroides
b- diarrhoea, steatorrhea, macrocytic anaemia
c- fistulas, diverticula, strictures related to crohns disease
d- low cobalamin, high folate levels
e-Schilling test
f- surgical correction of abdominal blind loop, tetracyclines for 2-3 weeks

182
Q

Important aspects of GI history

A

GI symptoms, Travel history, PMH, Dietary history, Drugs history, Social history (alcohol, water supply)

change in bowel habits, eg pale colour, steatorrhea

183
Q

In what disease states should malabsorption be suspected?

A

diseases of the liver, pancreas and small bowel

184
Q

Questions to ask about relating to diarrhoea

A

Duration, fat globules, floating/hard to flush away, offensive

185
Q

Causes of easy bruising

A

Vitamin K deficiency

186
Q

Cause of scurvy

A

Vitamin C deficiency

187
Q

what is acrodermatitis enteropathica caused by? treatment? how it is acquired? symptoms?

A

autosomal recessive
impaired zinc uptake so treatment= zinc supplements

rash, perioral, acral, alopecia

188
Q

Cause of Dermatitis herpetiformis

what disease may it indicate

A

Sub-epithelial deposition of IgA at extensor surface causing itchy blisters
may indicate coeliac disease

189
Q

Cause of glossitis and angular stomatitis

A

Vitamin B and iron deficiency

190
Q

Cause of spooning of nails

A

Iron deficiency (thyroid)

191
Q

Tests in suspected malabsorption

A

FBC, coagulation, LFTs, albumin, Ca/Mg, stool culture

endoscopy, histology, X ray, CT

192
Q

Three causes of Gastro-oesophageal reflux disease

A
  1. incompetent LOS
  2. poor oesophageal clearance
  3. barrier function/visceral sensitivity
193
Q

Symptoms of GORD

A

Heartburn, Acid reflux, chest pain
waterbrash (acid taste)
weight loss, coughing
dysphagia, odynophagia, hoarseness

194
Q

Investigations of GORD

A

Endoscopy
Barium swallow
oesophageal manometry (LOS function)
pH studies

195
Q

Alarm symptoms in dyspepsia

A

should prioritise patients with these signs as they may have oesophageal carcinoma

Hx cancer, anaemia, pernicious anaemia, PUD >20 years, dysphagia, weight loss, vomiting,

196
Q

what is the Z line

A

normal marking between the oesophagus and stomach

197
Q

How do we grade oesophagitis

A

Severity of errosive disease

198
Q

Complications of GORD

A

Oesophagitis, schatzki ring causing sticturing, metaplastic change

199
Q

Which oes cancer is associated with barretts oes?

A

Adenocarcinoma

normal>oesophagitis>barrets>adenocarcinoma

200
Q

3 lifestyle modifications for GORD

A

smoking cessation
lose weight
prop up bed head

201
Q

Can antacids heal/prevent GORD?

A

no- will neutralise acid, but wont heal/prevent

202
Q

Name two H2RA

Why do HR2A have a worse outcome than the placebo in GORD

A

Ranitidine, Cimetidine

Block H2RA so body increases gastrin and ACh production to maintain acid output- sometimes patient will forget to take H2RA- rebound acid production

203
Q

First line treatment of GORD

A

PPI

204
Q

Nissen fundoplication and who it is used in

A

tighten LOS by wrapping the fundus around it

used in young people who want to come off PPI

205
Q

Grading Barrets oesophagus

Management of BO/Dysplasia

A

irreversible Intestinal metaplasia
Graded as low/high

3 month surveillance, optimise therapy to 40mg x2
remove by endoscopic resection (EMR) and ablate rest of BO with HALO technique

206
Q

What is a hiatus hernia

A

part of stomach pushes up into the thorax through a weakness in the diaphragm

207
Q

Gastroparesis

A

poor emptying of stomach without physical blockage in pylora, when vagus nerve is damaged and pyloric sphincter closes

208
Q

Symptoms of gastroparesis

A

Bloating, loss of appetite, nausea, vomiting, weight loss, upper abdominal pain

209
Q

Causes of gastroparesis

A

Think nerve damage

Cannabis, idiopathic, diabetes, medications (opioids, anti-cholinergics), systemic disease

210
Q

Investigations of gastroparesis

A
  • Gastroscopy (ensure no obstruction or malignancy or pylorus/antrum)
  • gastric emptying study (isotope consumed, calculate t1/2 of emptying)
211
Q

Management of gastroparesis

A

Gastric pacemaking (particularly useful for diabetes)
liquid/sloppy diet, eat little and often, promotility agents
remove cause eg drugs

212
Q

Hallmark of achalasia

A

Oesophageal beaking

213
Q

What is achalasia

A

The LOS cant relax, so oesophagus will have reduced peristalsis and become dilated

214
Q

1st line investigation of achalasia and other

A

1st line= oesophageal manometry

also endoscopy, barium swallow (shows beaking)

215
Q

Treatment of achalasia

A

balloon dilation, cardia myotomy, botox (older patients), oesophagectomy (end stage)

216
Q

what GI diseases is weight loss a sign of?

A

colorectal cancer, gastric cancer, oesophageal cancer crohns disease, celiac disease
impaired GI motility, intra-abdominal infection, acute liver disease

217
Q

How to identify malnutrition

A

MUST score (malnutrition Universal screening tool)

  1. Calculate BMI
  2. % unplanned weight loss
  3. acute disease effect (no intake >5 days)
  4. Calculate overall risk of malnutrition from 1,2,3
  5. Use guidelines and local policy to make a plan

0: Routine care
1: Observe
2+: Treat

218
Q

What is Anthropometry

A

nutritional assessment- mid arm muscle circumference, triceps, grip strength

219
Q

Usefulness of Albumin in nutritional assessment

A

50% protein in plasma, non-specific marker of illness

220
Q

Usefulness of Transferrin in nutritional assessment

A

synthesis reduced in protein reduction- affected by APR, anaemia, liver disease

221
Q

Usefulness of Urinary creatine in nutritional assessment

A

assessment of renal function

222
Q

Transthyretin

A

recent dietary intake- increased in ureamia and dehydration, decreased by fasting and APR

223
Q

Retinol binding protein

A

effected by energy
increased by increased GFR and alcoholism
decreased by chronic liver disorders, vitamin A and zinc deficiency

224
Q

IGF1

A

reduced in acute and chronic malnutrition, liver disease and renal failure

225
Q

Order of nutritional support

A
  1. food first
  2. oral nutritional support (snacks, sip feeds)
  3. Enteral tube feeding
  4. Parental tube feeding (IV)
226
Q

who needs nutritional support

A

BMI <18.5
Unintentional weight loss >10%
BMI <20 and unintentional weight loss of >5%
having eaten nothing for >5days
poor absorptive capacity, nutritional loses, , increased nutitional needs

227
Q

Enteral Tube feeding

A

Delivery of nutritionally complete feed via tube into stomach, duodenum or stomach

nasogastric, nasoduodenal, nasojejunal tube
percutaneous endoscopic gastrostomy
percutaneous jejunostomy
surgical jejunostomy

228
Q

Indications for EFT

A

Inadequate or unsafe oral intake but a functional accessible GI tract

eg unconscious, NM swallowing disorder, upper GI obstruction

229
Q

Contra-indications of EFT

A 
Lower GI obstruction
Prolonged intestinal ileus
severe diarrhoea/vomiting
high enterocutaneous fistula
intestinal ischaemia
230
Q

What is parental feeding

A

admin of nutrition via central or peripheral vein

last resort

231
Q

What is Refeeding syndrome and its metabolic consequences

A

When someone is rapidly refed after a period of under nutrition

refeeding leads to increased insulin- increased uptake of Glucose, thiamine, K+, Mg2+, PO4

hypokalaemia, hypomagnesaemia, hypophosphataemia, thiamine deficiency, salt and H2O retention, oedema

232
Q

when is refeeding syndrome more likely to occur?

A

feeding PN or EN

oral feeding, less likely

233
Q

Physiological consequences of refeeding syndrome

A

seizure, arrhythmia, altered level of consciousness, respiratory failure, cardiovascular collapse, death

234
Q

moderate risk of refeeding syn

A

little/no nutrition for >5 days

235
Q

extremely high risk of refeeding syn

A

BMI <14, no intake >15 days

236
Q

Tumour associated with lump at left supraclavicular fossa

A

Gastric adenomacarcinoma

GI (7 decks)

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