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Diseases of the human systems > Gastrointestinal disease > Flashcards

Gastrointestinal disease Flashcards

1
Q

What drug eliminates formed acids

A

Antacids

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2
Q

What drugs reduce acid secretion

A

H2 receptor blockers/antagonists

Proton pump inhibitors

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3
Q

How do H2 receptor blockers work

A

They reduce acid production by preventing the histamine activation of acid production

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4
Q

Why do H2 receptor antagonists have limited benefit

A

They only limit 1 of the pathways there is still 2 other; Acetylcholine and Gastrin

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5
Q

Name a H2 receptor blocker

A

Cimentanide

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6
Q

Name a proton pump inhibitor

A

Omeprazole

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7
Q

What is dysphagia

A

Difficulty swallowing

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8
Q

What are the causes of dysphagia

A

External compression e.g. the aorta

Dysmolity

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9
Q

What is dysmolity

A

Condition in which the muscles of the digestive system dont work as they should

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10
Q

Name 2 causes of dysmolity disorders

A 
Fibrosis (e.g. Scleroderma)
Nueromuscular dysfunction (e.g. parkinsons)
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11
Q

What is GORD

A

GORD (Gastro-oesophageal reflux disease) is when acid from the stomach leaks up into the oesophagus

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12
Q

What are the 3 main causes of GORD

A

Defective lower oesophageal sphincter
Impaired lower clearing
Impaired gastric emptying

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13
Q

What are the effects of GORD

A

Ulceration, Inflammation, metaplasia, barretts oesphagitis

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14
Q

What are the signs and symptoms of GORD

A

Epigastric burning, Dysphagia, GI bleeding, severe pain that mimics a MI

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15
Q

What treatment is there for GORD

A

Antacids, H2 receptor blockers, proton pump inhibitors

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16
Q

What is a hiatus hernia

A

When part of the stomach is in the Thorax

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17
Q

What site is affected by peptic ulcer disease

A

ANY acid affected site- oesophagus, stomach, duodenum

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18
Q

What is the main problem of peptic ulcer disease

A

The ulcer fully erodes through the lining and into a artery causing a major bleed or straight through the viscous wall into the periotineum

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19
Q

What is a perforated ulcer

A

A ulcer that has gone straight through the viscous wall into the periotineum

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20
Q

What type of ulcers would high acid secretion make

A

oesphageal and duodenal ulcers

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21
Q

How can a normal acid secretion cause peptic ulcers

A

If there is a reduced protective layer in the stomach

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22
Q

What can cause a loss of the mucosal barrier in the stomach

A

Heliobacter Pylori bacteria infection

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23
Q

What does the loss of the mucosal barrier in the stomach lead to

A

Ulceration and the chronic inflammation of the gastric mucosa which could then cause the lymphoma of the stomach

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24
Q

How can you eliminate a H. pylori infection

A

through triple therapy

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25
Q

What does triple therapy encompass

A

2 antibiotics (amoxicillin, metronidazole) and 1 proton pump inhibitor (omeprazole)

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26
Q

What are the symptoms and signs of peptic ulcer disease

A

Normally asymptomatic but can have epigastric burning pain

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27
Q

What nvestigations is there for peptic ulcer disease

A

Endoscopy, radiology, Anemia(FBC test)

H. pylori test- breath, antibodies,mucosa

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28
Q

What are the systemic complications of peptic ulcer disease

A

Anaemia

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29
Q

What are the local complications of peptic ulcer disease

A

Perforation, Haemorrhage, stricture, malignancy

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30
Q

What treatment is there for peptic ulcer disease

A

Medical: stop smoking, ulcer healing drugs, small regular meals, eradication therapy

Surgical: Endoscope, vagotomy, surgical repair(gastectomy)

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31
Q

How can you improve the mucosal barrier of the stomach

A

eliminate heliobacter

Inhibit Prostagaldin removal- avoid NSAIDs and steroids

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32
Q

What are the 2 PUD surgerys and what happens in them

A

Bilroth1- Top half of stomach is atatched to the duodenum

Bilroth2- Top half of the stomach is attached to the small bowel

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33
Q

What is the small intestine compromised of

A

duodenum, Jejunum, Ileum

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34
Q

What diseases/ conditions can lead to malabsorption

A

Coeliac disease, prenicious anemia, crohns, infections, tumours

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35
Q

What is coeliac disease caused by

A

Sensitivity to the aplha-gliaden component of Gluten

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36
Q

What does coeliac disease lead to

A

Villous atrophy of the jejunum

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37
Q

What is villous atrophy

A

When the villi in the intestines erode away leaving a virtualy flat surface

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38
Q

What are the clinical effects of Jejunal atrophy

A

Growth failure, oral ulceration

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39
Q

What are the ‘classical’ symptoms of coeliac disease

A

Weight loss, lassitude, weakness, abdomail pain, dirrhoea, oral aphthae, toung papillary loss

40
Q

What is oral aphthae

A

An ulcer that forms on the mucous membrane

41
Q

What investigations are there for coeliac disease

A

Autoantibody test- Serum Transglutaminase(TTG) and anti-glidan antibodies
Jejunal biopsy- capsule, endoscopic biopsy
Haematinics- B12, Folate, Ferrin levels

42
Q

In coelaic disease what would cause reversal of the jejunal villi atrophy

A

A gluten free diet

43
Q

What skin disease is associated with coeliac disease

A

Dermatitis Herpetiforms

44
Q

What happens in dermatitis herpetiformis

A

Granular IgA deposits in the skin and mucosa

45
Q

What is pernicious anaemia caused by

A

Vit. B12 deficency

46
Q

What helps the intestines absorp Vit. B12

A

Intrinsic factor

47
Q

What is the only Vit. B12 absorption site in the bowel

A

Terminal Ilium

48
Q

How do you diagnose Pernicious anaemia

A

carry out a blood test for antibodies to intrisnic factor

49
Q

Causes of Pernicious anaemia

A

lack of B12 in diet
disease of the gastric parietal cells
Inflammation bowel disease of the terminal ileum(Crohns)
Bowel cancer at the ilei-coecal junction

50
Q

What are the age ranges of Inflam. bowel disease

A

15-25yrs 50-80yrs

51
Q

What gender is Crohns more prelevant in

A

Male

52
Q

What gender is ulcerative colitis more prelevant in

A

Female

53
Q

Aetiology of IBD

A

Food inolerance, persisting viral infection, smoking, genetic

54
Q

What is thought to be a possible aetiology of Crohns

A

Infection with Mycobacteria

55
Q

Where does Crohns affect

A

Any part of the GI tract

56
Q

Where does ulcerative colitis affect

A

Colon and rectum

57
Q

What is IBD

A

Chronic inflam. of the GI tract

58
Q

What are the differences between crohns and ulcerative colitis

A

Crohns:
Disontinous, rectum involved 50%, Anal fissures 75%, Ileum involved 30%, mucosa cobbled and fissures, Non-vascular, Serosa inflamed.

Ulc. Col:
Continous, Rectum always involved, Anal fissures 25%, Ileum involved 10%, Mucosa granuloma and ulcers, Vascular, Serosa normal

59
Q

What are the microscopic diffrences between Crohns and Ulc. Col.

A

Crohns:
Transmural, Oedematous, granulomas

Ulc. Col:
Mucosal, Vascular, mucosal abcesses

60
Q

What is meant by saying Ulc col. is continous

A

The disease spreads in one way si it starts at the rectum and can spread continously through the colon

61
Q

What are the symptoms of Ulc. Col.

A

Dirrhoea, abdominal pain, PR bleeding

62
Q

What are the symptoms of Crohns

A

Colonic- Dirrhoea, abdominal pain, PR bleeding
Small bowel disease- Pain from obstruction and malabsorption
Mouth- OFG

63
Q

Investigations for IBD

A 
Blood tests (anaemia, C reactive protien- a inflam. marker)
Faecal calprotectin
Endoscopy 
Leukocyte scan 
Barium studies 
Bullet endoscopy
64
Q

What does Ulc. Col. have the risk of developing

A

carcinoma

65
Q

What is the medical treatment for IBD

A

Systemic steroids
Local steroids
Anti inflam. drugs
Non steroid immunosuppressants

66
Q

What is the cure for Ulc Col.

A

Colectomy

67
Q

What are ASA drugs and what are they used for

A

They are anti inflam. drugs used to treat IDB as they are not absorbed in the small intestine and pass through the bowel and effect the surface mucosa topically

68
Q

Name 2 ASA based drugs

A

Pentasa, Mesalazine, Suphasalazine

69
Q

What surgical treatment is there for Crohns

A

Remove obstructed bowel segments, drain abcesses, close fistulae

70
Q

in bowel cancer what do most carcinomas arrise in

A

Polyps

71
Q

What is acute liver failure

A

Sudden loss of liver function (In days or weeks)

72
Q

What will a patient die from in acute liver failure

A

bleeding and encephalopathy

73
Q

Can a liver recover from acute liver failure

A

Yes, if given time and patient still alive

74
Q

What can cause chronic Liver failure

A

Cirrhosis, primary liver cancer and secondary liver cancer

75
Q

What is cirrhosis

A

A mixed picture of damage, fibrosis and regeneration of liver structure

76
Q

What is chronic liver failure

A

It is a progressive deterioration of liver functions for more than six months

77
Q

What is the aetiology of cirrhosis

A

It is multifactorial:

Alcohol, primary biliary cirrhosis, viral disease, autoimune chronic hepatitis, haemachromatosis and cystic fibrosis

78
Q

What viral disease can cause cirrhosis

A

Chronic active hepatitis

79
Q

Wha are the signs and symptoms of cirrhosis

A

Normally NONE but a large or small liver

Acute bleed (Oespahgeal varices), portal hypertension, jaundice, oedema and ascites, encephalopathy, spider naevi and palmar erythema

80
Q

What causes the spider naevi and palmar erythema in cirrhosis

A

The high levels of oestergen from reduced metabolism

81
Q

What causes oesophageal varices

A

Blood entering the portal system has no exit route as the portal vein cannot communicate with the hepatic vein due to disordered portal triads in liver cirrhosis

Blood engorges as passes through vessels at the end of the embryological gut – lower oesophagus – getting from the portal vein to the systemic circulation

Veins dilated and fragile(thin walled) and Protrude into oesophageal lumen

82
Q

What are the 2 functions lost in liver failure

A

Synthetic and metabolic

83
Q

What does the loss of synthetic action affect

A

Plasma proteins, clotting factors

84
Q

What does the loss of metabolic function affect

A 
Drug metabolism (esp. first pass)
Detoxification
Conjugation of RBC breakdown products
85
Q

What tests are there for liver function

A

Hepatic cell enzyme levels(ALT,GGT)- which in liver inflam. is raised

INR test, which is most useful

86
Q

What INR level is high for none warafin patients

A

1.3

87
Q

As a dentist, when treating someone with liver failure what must you avoid and why

A

Intravenous sedation as with thte metabolic changes it will have prolonged effect

88
Q

Is there a problem with LA with patients of liver failure

A

NO as metabolised in the plasma not liver

89
Q

What are the 3 types of jaundice

A

Pre-Hapatic, Hepatic, Post-Hepatic

90
Q

what is the cause of prehepatic jaundice

A

Due to factors BEFORE liver metabolism

-usually excessive quantities of red blood cell breakdown products

91
Q

What is the cause of hepatic jaundice

A

Liver failure

92
Q

What is the cause of post-hepatic jaundice

A

obstruction to bile flow (e.g. gal stone)

93
Q

What treatment is there for Prehepatic jaundice

A

identify the cause and treat it

94
Q

What treatment is there for post-hepatic jaundice

A

Remove the obstruction

95
Q

What treatment is there for liver failure

A

Supportive
Transplant(only cure)
Artifical liver systems
-Molecular Adsorbent Recirculating System (MARS)

Diseases of the human systems (3 decks)

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