GIT 1 Flashcards

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1
Q

what is the gut ?

A

continuous tub from mouth to anus

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2
Q

which organs feed into the GIT?

A

liver
gall bladder
pancreas

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3
Q

what is the livers role in the GIT?

A

feeds into gall bladder

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4
Q

What is the role of the gall bladder?

A

secrets bile into duodenum

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5
Q

what is the role of the pancreas in GIT?

A

secrets pancreatic juices into the duodenum

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6
Q

where is the appendix situated ?

A

end of the ileum and beginning of colon just above the right hip bone

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7
Q

what is the role of the appendix

A
  • blind ended tube
  • evolutionary vestige - used to need when we were primitive (used to eat more vegetation)
  • has bacteria that breaks down cellulose and gets nutrition from cellulose
  • we don’t need it anymore
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8
Q

what happens when the appendix becomes blocked?

A

becomes necrotic
inflamed
pain and sepsis
needs removal

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9
Q

describe the lining of the mouth

A

stratified squamous epithelium

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10
Q

describe the lining of the stomach

A

mucus producing epithiulm and enzyme secreting

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11
Q

describe the lining of the small intestine

A

mucus
needs to absorbs nutrients so need high SA so have vili

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12
Q

describe the lining of the large intestine

A

less mucus
needs to absorbs nutrients so need high SA so have vili

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13
Q

describe the stomach

A

has mucous glands which secret acid too

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14
Q

what does the GIT tube have around it ?

A

layers of muscle which produce peristaltic waves which pushes food from one end to the other (to get water and nutrients removed)

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15
Q

what does the liver produce ?

A

bile salts - allows emulsification of fats to be more easily absorbed

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16
Q

where are bile salts stored ?

A

gall bladder

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17
Q

how is gall bladder contraction stimulated?

A

food leaving the stomach and entering the duodenum is mixed with bile via this contraction

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18
Q

why are our faeces brown?

A

bile is red and green

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19
Q

where does the pancreas release its secretions to ?

A

duodenum

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20
Q

what does the pancreas release?

A

an alkali solution which neutralises the acid from the stomach
releases pro enzymes

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21
Q

what are pro enzymes ?

A

inactive enzymes

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22
Q

why does the pancreas secrete pro enzymes instead of enzymes?

A

-there are a lot of proteases and lipases
- proteases break down protein and lipases break down fat
- if ur pancreases secreted these as active enzymes the pancreas would ingest itself

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23
Q

what is pancreatitis ?

A

auto digest pancreas

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24
Q

what else does the pancreas secrete?

A

insulin into the circulation in response to food in the GIT

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25
Q

describe the gut

A
  • big blood supply to absorb nutrients from gut into portal venous system
  • vili to maximise SA
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26
Q

describe the blood supply of the gut

A
  • arterial blood flows from the aorta to the mesenteric arteries
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27
Q

what are the mesenteries ?

A

layers of tissue that connect the gut to the posterior abdominal wall

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28
Q

what would happen if the blood drained straight back into the vena cava?

A

we would have fat droplets, partially digested proteins, bacteria, toxins that would go straight into the circulation

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29
Q

where does the blood drain into from the gut?

A

into the portal venous system towards liver

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30
Q

what is the role of the liver once it receives nutrient rich blood?

A

liver hepatocytes filter and metabolise drugs, nuteinrts and vitamins before releasing them into systemic circulation

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31
Q

describe the parasympathetic stimulation of the gut

A
  • promotes gut motility and gut secretion (increases capacity fro digestion with peristaltic waves and increases gut function)
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32
Q

describe the sympathetic stimulation of the gut

A
  • reduces gut motility and secretion ( fight or flight, autonomic nervous system, increase BP, vasoconstriction, increase pulse rate and blood flow, decrease blood to gut so decreases its function)
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33
Q

list the signs and symptoms of GIT

A
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34
Q

what is a change in bowel habit?

A

no of times you go to the toilet for a no 2

35
Q

what Is a normal bowel habit ?

A
  • 3 times a day to once in 3 days
36
Q

what do we mean by sustained change in bowel habit ?

A

any change longer than 2 weeks

37
Q

why is learning about ones bowel habit useful?

A

it can be indicative of a gut condition

38
Q

what are the causes of a painful bowel motion?

A
  • severe constipation
  • inflammation around lining of rectum or anus
  • blood or mucus in bowel motions
  • tenesmus - feeling of not having emptied bowel
39
Q

why can the rectum feel?

A
  • pressure or experience inflammation
  • doesn’t have somatic nerves so it can’t detect exactly WHERE there is pain = can lead to tenesmus
40
Q

what can give one tenesmus?

A
  • tumour in rectum
  • ulcerative colitis - inflammation can give one sensation of tenesmus
41
Q

what does the stomach contain?

A

Low PH
enzymes

42
Q

how is the stomach protected from low ph and enzymes to prevent it from being digested ?

A

the lining is protected by mucus

43
Q

how does the lining produce mucus?

A

goblet cells and mucus glands

44
Q

does the oesophagus secrete mucus?

A

NO

45
Q

what causes GORD?

A

diet, stress and NSAIDs

46
Q

what is the problem with GORD?

A
  • contents of stomach can enter oesophagus to pharynx and damage it
47
Q

what can protect the oesophagus ?

A
  • lower oesophageal sphincter
  • which passes through diaphragm at an angle
  • if sphincter weakens it can cause reflux
48
Q

list GORD symptoms

A
49
Q

what can acid in the larynx and pharynx cause?

A
  • thickening
  • hoarse voice
  • lump in throat (gp usually gives antacids to rule out reflux)
50
Q

what are the risk factors for GORD ?

A
  • Reduced tone of the lower oesophageal sphincter
  • Increased intra-abdominal pressure (pregnancy, overweight and lying flat)
  • Decreased stomach pH
  • Increased stomach contents (alcohol, caffeine, fat in food)
51
Q

what are the 3 factors for GORD?

A
  • Lifestyle- stress, diet, overweight, alcohol and caffeine
  • Mechanical
  • Drugs- NSAIDs, serotonin inhibitors
52
Q

how do we manage GORD

A

Address risk factors
Neutralise stomach contents (avoid risks and big fatty meals)
Gaviscon (Bicarbonate Physical barrier, Alginate)
Surgery to tighten lower oesphageal sphincter

53
Q

what is an ulcer?

A

a pathological break in epithelial lining

54
Q

what is peptic ulcer disease?

A

inflammation and break in epithelial lining of stomach and duodenum

55
Q

what is the cause of peptic ulcer disease?

A

acid/ enzyme attack mucus caused by stress, steroids, NSAIDs, SSRIs, H.Pylori
pain in upper abdominal and epigastric

56
Q

lis the symptoms of peptic ulcer disease

A
57
Q

how do we manage PUD?

A
  • upper GI endoscopy
  • biopsy
  • correct risk factors = increase stomach PH, PPI, eradicate H.pylori with clindamycin + metradiazole / amoxicillin
58
Q

What is an inflammatory bowel disease?

A

A group of conditions characterised by inflammation of the intestine:
* Small intestine (ileum)
* Large intestine (colon)
* Rectum
* Anus
inflammation, ulcerations, variable thickness.

59
Q

describe the symptoms of IBD?

A

Abdominal pain
change in bowel habit
blood loss
anaemia
oral signs
RAS
15-30 yrs peak
M=F

60
Q

what are the extra- intestine effects of IBD?

A

fever, malaise
arthritis
skin lesions
eye lesions

61
Q

what are the generalised features of IBD?

A

Abdominal pain
Weight loss
Change in bowel habit
Blood in poo
Fever

62
Q

whats more common UC or Crohn’s?

A

UC

63
Q

where does UC start at?

A

anus/ rectum and may affect more proximal large bowel

64
Q

what does UC never affect?

A

ileum

65
Q

what are the symptoms for UC?

A

rectal inflammation
bleeding
tenesmus
bloody diahorrea
smoking reduces the risk

66
Q

where can crohns affect?

A

any part of small our large bowel

67
Q

crohns aka?

A

regional ileitis

68
Q

what are the main symptoms of crohns?

A

abdominal pain
diarrhoea
constipation
smoking can increase the risk

69
Q

how much involvement is crohns ?

A

full thickness
can stick loops of bowels together
may lead to fistula formation

70
Q

how would we diagnose IBD?

A

endoscopy
biopsy
CT scan

71
Q

Tx of IBD

A
  • Steroids - prednisolone
    Sometimes be rectal but not systemically used
  • Methotrexate
  • Azathioprine
  • Aminosalicylates (Sulphasalazine and Mesalazine) related to asprin
  • Biological response modifiers (Infliximab monoclonal antibody if no response to above)
72
Q

what is coeliac disease?

A
  • autoimmune Rxn to gluten
  • wheat grain
  • inflammation of small bowels
73
Q

symptoms of coeliac?

A

abdominal pain
bloating
skin and mouth vesicles (extreme)

74
Q

how are the vili affected ?

A

reduces height of vili
loss of SA
malabsorption

75
Q

management of coeliac

A

avoid gluten

76
Q

diagnosis of coelic

A

blood test, endoscopy, biopsy

77
Q

Is IBS = IBD ?

A

NO, IBS isn’t an inflammatory disease but shares similar symptoms to IBD
important to exclude IBD and Bowel cancer

78
Q

what is IBS ?

A

very common 20-50% ppl don’t tend to go GP
bloating, urgency or straining, abdominal pain
relieved by bowel movement
worse after eating
some have bladder urgency, lethargy, tired

79
Q

risk factors of IBS?

A

Diet and lifestyle

80
Q

what q’s can we ask to differentiate IBS to IBD or cancers

A

Do you have any blood or mucus in your poo?
Have you lost any weight?
Check for anaemia

81
Q

Crohns disease summary

A
82
Q

UC summary

A
83
Q

coeliac disease summary

A
84
Q
A