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Case 1 > Dyspepsia And GORD > Flashcards

Dyspepsia And GORD Flashcards

1
Q

What age range do gastric ulcers occur at

A

55-65

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2
Q

Wat age range do duodenal ulcers occur between

A

25-75

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3
Q

Hat are the genetic and family factors for peptic ulcers

A

Increased acid production, weaker mucosa and abnormal mucus production

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4
Q

What are lifestyle factors for peptic ulcers

A

Caffeine, smoking, alcohol NSAIDs, stress, H. Pylori

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5
Q

Which type of ulcer is accosicted with, weight loss, anorexia and nausea

A

Duodenal ulcers

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6
Q

What are the causes of peptic ulceration

A

Infection with H. Pylori
Long term use of NSAIDs
Stress ulcers

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7
Q

How many COD enzymes are there?

A

2, cox-1 and cox-2

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8
Q

What happens when COX is inhibited

A

Decrease in prostaglandins
Increases gastric acid secretion
Decrease mucus production and blood flow
Increased expression of intracellular adhesion molecules in gastric vascular endothelium
Increased neutrophil adherence to vascular endothelial cells
Mucosal damage due to neutrophil derived free radicals and protease

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9
Q

Which neutralisation medications are used for treatment

A

Antacids
Alginates
Sucralfate

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10
Q

Which reduction of acid secretion medications are used for treatment

A

Proton pump inhibitors

Histamine H2 receptor antagonist

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11
Q

What are the adverse effects of antacids?

A

Constipation, laxative properties, bloating/flatulence, renal calculi,

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12
Q

How do antacids work?

A

Binding of other drugs = reduced bioavailability
Chemical inactivation of drugs
Increased gastric pH, decreased drug absorption and excretion

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13
Q

What do alginates do

A

They are usually combined with antacids, they form protective barriers on top of gastric contents

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14
Q

Which cells do proton pump inhibitors work on?

A

Parietal cells (produce HCL)

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15
Q

Give examples of PPIs

A

OmepraZOLE, lansopraZOLE, enteric coated to resist gastric metabolism and allow GI absorption

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16
Q

How do H2 histamine receptor antagonists work?

A

Block competitively
Histamine stimulates acid production by parietal cells through histamine H2 receptor
Drugs end in “ine” = cimetidine and ranitidine

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17
Q

Which peptic ulcers do sucralfate treat?

A

Benign gastric and duodenal ulcers

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18
Q

What are the 5 features of inflammation?

A 
Rubor (redness) 
Tumour (swelling)
Calor (heat) 
Dolor (pain) 
Loss of function
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19
Q

What is the rapid host response to acute inflammation?

A

Vasodilation, increased vascular permeability and leukocyte migration

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20
Q

Which two mediators are involved in inflammation?

A

Cell derived meditators, plasma protein derived mediators

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21
Q

Which enzyme relseases arachidonic acid?

A

Phospholipids A2 from membrane phospholipids

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22
Q

What do COX-1 and COX-2 convert arachidonic acid into?

A

Prostaglandins

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23
Q

What does extended injury result in?

A

Fibrosis

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24
Q

Which cells are in chronic inflammation?

A

Macrophages, lymphocytes and plasma cells

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25
Q

What are the pathogenic effects of autoantibodies?

A

Affect molecular function
mediate cell destruction
Immune consoles mediated reactions (type III hypersensitivity)

26
Q

Which cells circulate and bind to self antigens released from injured cells?

A

B cells

27
Q

Which conditions are included in IBS (irritable bowel syndrome)

A

Ulcerative colitis, Crohn’s disease

28
Q

What are the causes of IBS

A 
Stress 
Diet 
Abnormal GI motility 
Infections 
Overgrowth of intestinal flora
29
Q

Treatment for IBS

A 
Antidepressants
Dietary fibre supplementation 
Loperamide/laxative 
Antibiotics 
Analgesics
30
Q

What are the symptoms of Crohn’s disease?

A

Pain
Diarrhoea
Weight loss
Anaemia

31
Q

What are the symptoms of UC (ulcerative colitis)

A

Bloody diarrhoea
Colicky abdominal pain
Urgency
Fever

32
Q

In which genes, are mutations a sign of early onset IBS

A

IL10RA, IL10RB, TGFBR1, TGFBR2

33
Q

Which drug treatments are available for IBS

A

DMARDS -> aminosalicylates, methotrexate

Immunosuppressant drugs —> glucocorticoids, azathioprine, cyclosporin

34
Q

What are the side effects of aminosalicylates?

A

Diarrhoea, salicylate sensitivity and interstitial nephritis

35
Q

Does methotrexate have a in UC

A

No

36
Q

What is methotrexate an antagonist of?

A

Folic acid

37
Q

What is the mechanism of action of glucocorticoids?

A

Reduce transcription of genes encoding COX-2, phospholipids A2, pro-inflammatory cytokines and iNOS

38
Q

What is the mechanis of action of azathioprine?

A

Interferes with purine synthesis

Inhibits cell mediated and antibody medicated immune reactions

39
Q

What is the mechanism of action of cyclosporin?

A

Inhibitor of IL-2 gene transcription
Binds to cyclophilin in lymphocytes
Reduction of of T cell dependent B cell responses

40
Q

What is the mechanism of action of biologics?

A

Monoclonal antibodies directed against TNF

Immunosuppressant activity

41
Q

What is the difference between IBD and IBS

A

IBD - structural problem

IBS - functional problem

42
Q

How is IBS diagnosed

A

Discomfort for 3 days a month for 3 months minimum, especially intolerance to food (lactose)

43
Q

How is IBS treated

A

Treatment dependent on the pathogenesis

44
Q

What is the main factor that lead to the development of IBD

A

Defects in the epithelial barrier, microbiota is able to get through the barrier which causes inflammation

45
Q

What predisposes you to IBD

A

NOD2 polymorphisms, less macrophages are produced

46
Q

Diagnosis of IBD

A

Stool tests
Blood tests
GI Investigation

47
Q

Which two types of drugs can be used for treatment IBD

A

DMARDS

Immunosuppressant drugs

48
Q

What does methotrexate antagonise

A

Folic acid

49
Q

Example of glucocorticoids

A

Prednisolone

50
Q

Why is CTZ triggered easily

A

Outside the blood brain barrier, easily stimulated, more permeable to cytotoxic agents

51
Q

What do NSAIDS inhibit

A

COX enzyme

52
Q

How does mucous protect the stomach

A

Traps HCO3

53
Q

How does stress lead to gastric ulcers

A

Reduces the amount of bicarbonate ions

The mucous isn’t protecting the epithelium

54
Q

What is the treatment for damage caused by NSAID us

A

Misoprostol, analogue of prostaglandins

55
Q

Which cox enzyme is turned on when there is inflammation

A

COX 2

56
Q

Which treatments are there for dyspepsia

A

Antacids and alginates
PPIs
H2RAs

57
Q

Give two examples of H2Ra

A

Cimetidine

Ranitidine

58
Q

When are PPIs activated

A

In acidic conditions

59
Q

What is the the difference between IBS and IBD

A 
IBD = structural disorder 
IBS = functional disorder
60
Q

When is IBS diagnosed

A

When a patient has had discomfort 3 times a month for three months

61
Q

What is loperamide used for

A

Diarrhoea

Case 1 (3 decks)

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