Scenario 1 Harry Flashcards

1
Q

What is hematemesis?

A

The Vomiting of blood

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2
Q

How does ibuprofen help Harry’s back pain?

A

When cells are damaged they release arachidonic acid. The two enzymes that break it down are cox-1 and cox-2 and convert it into prostaglandin H2 which then convert it into many other chemicals which increase temperature, lower pain threshold, and inflammation. The ibuprofen comes in and is absorbed through the stomach wall to our blood stream. It attaches to cox-1 and cox-2 and prevents the enzymes from breaking arachidonic acid down which prevents pain. Then eventually Cox-1 and Cox-2 reject the ibuprofen then you need to see if you want more.

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3
Q

What is dyspepsia?

A

Pain in the upper gut: stomach oesophagus and duodenum

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4
Q

How does Gaviscon work?

A

When Gaviscon hits the stomach acid it goes into a foam barrier and surrounds the stomach contents and keeps them in the stomach rather than in the oesophagus where is hurts.

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5
Q

What is a side effect of Gaviscon?

A

Constipation or diarrhoea

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6
Q

What is an endoscopy?

A

An upper gastrointestinal (UGI) endoscopy is a procedure that allows your doctor to look at the interior lining of your esophagus , your stomach, and the first part of your small intestine (duodenum ) through a thin, flexible viewing instrument called an endoscope. It relays it onto a TV

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7
Q

What is a biopsy?

A

Taking a small tissue sample and examining it under a microscope

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8
Q

What is the pathophysiology of H.pylori?

A

H.pylori could be in your stomach as 50 per cent of people have it in them or you may have got through and infection which could be through contaminated foods. The H.pylori changes the chemical urea to carbon dioxide and ammonia because it has the enzyme urease. Ammonia is an alkaline so it neutralizes the acidity and makes it thin and watery therefore the h.pylori moves down using its flagella. Once it has moved to the stomach cells it can adhere to the stomach cells using liposachride. Once it has stuck to the stomach cells it can secrete dangerous exotoxins like Cag A and Vac A. Cag A disrupts cell integrity and breaks down tight juntions between stomach cells . Also stimulates the production of cytokins such as interlukin A which promotes imflation. Vac A causes death to stomach cells. This combined causes the breakage of the stomach cells which causes the hydrochloric acid comes in which damages the surrounding area causing the stomach ulcer.

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9
Q

When the H.plylori causes inflammation what does that do? And what can it cause?

A

The H.pylori infection will promote inflammation will result in a lot more hydrochloric acid being produced by the parietal cells. This is because inflammation promotes hydrochloric acid in the stomach due to histamine. With so much hydrochloric acid being produced it could leak into the duodenum causing a duodenal Ulcer.

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10
Q

What is the pharmacodynamics of amoxicillin?

A

antibiotic stops the H pylori from making its cell wall. The cell wall is protective - it prevents the bacterial cell contents from spilling out and prevents stuff in the bactrium’s environment that might be harmful to the bacterium from getting into the bacterium. - in this case - the clarithromycin

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11
Q

What does Clarithromycin do?

A

works inside the bacterium - inhibits ribosomes’ ability to make proteins - so the bacterium can’t carry out its norma; cell functions and dies

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12
Q

Define gastric ulcer

A

A break in the protective mucosal line of the stomach wall and underlying muscularis mucosa layer

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13
Q

Discuss the pathophysiology of gastric ulceration

A

Hcl and pepsin penetrate the mucosal barrier which will be right up to the muscularis mucosa. This strong acid inflamed and destroys the cells and pepsin digests the proteins in the cells plasma membranes and inside the cells so kills the cells etc.

Blood vessels in the stomach wall are eroded which means bleeding.
Ulceration thru thickness of stomach wall means perforation

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14
Q

Pharmacokenetics of amoxicillin

A

Absorbed rapidly
Bioavailability 80 percent

Distribution: most bodily fluids/ csf less than 1 percent / protein bound 20 percent

Metabolism: heptic

Excreted 60 percent in 8 hours
Half life: 61.3 mins

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15
Q

What shouldn’t you take gaviscon with?

A

Antacids may impair absorption of many drugs eg

ACE inhibitors, antibacterials, digoxin

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16
Q

Why is a mixture of 2 antibiotics used off triple therapy

A

One is ineffective- H.pylori is tough

Resistance - easily develops to just one antibiotic so needs two

17
Q

What happens if the infection persists?

A

Retreat with quadruple therapy including antibiotics not used before and taken for 14 days

18
Q

Why is a proton pump inhibitor used? And what does it do?

A

Esomeprazole block the H+/ k+ part of the pump so therefore HCL cannot be formed this means:

Less acid formed so less corrosion/inflammation
Less acid so less peosinogen activated to pepsin so
Less breakdown of structural proteins in gut wall cells
Less cell necrosis
Ulcer able to heal

19
Q

Why should Harry cut down smoking

A

Increases the risk of getting h.pylori
Slows the process of the ulcer healing
Increases the likelihood that stomach ulcers will reoccur
Increases the production of substances that may harm the mucosal layer such as pepsin
Decreases factors that protect and heal the lining, including blood flow and secretion of mucus

20
Q

Why should Harry stop taking ibuprofen?

A

It blocks cox-1 and cox-2 and cox-1 carries out the “housekeeping functions” which are:
Increase blood flow to stomach wall so stimulate mucus producing cells
enables platelets to stick together when blood clot production required
enables production of macrophages

If these are blocked it means:
Bleeding
Less mucus barrier
Chronic inflammation due to reduced immune cell function in the stomach wall

21
Q

Pharmacokinetics of amoxicillin

A

Absorbed rapidly

Distribution: most bodily fluids/ csf less than 1 percent / protein bound 20 percent

Metabolism: heptic metabolism accounts for 30 percent of most penicillins

Excreted 60 percent in 8 hours
Half life: 61.3 mins

22
Q

Pharmacokinetics of clarithromycin

A

Absorbed: clarithromycin is well absorbed acid stable and may be taken with food
Protein binding 70 percent
Metabolised: heptic - metabolised using cytochromes to 14-hydroxyclarithromycin and N-desmethylclarothromycon
Excretion: 30 percent after 12 hours
Half life: 3-4 hours

23
Q

Pharmacokinetics of I ibuprofen

A
Absorbed: 80 percent GI tract 
Protein binding: 90 percent
Metabolised: by oxidation to 2 inactive metabolised 
Elimated: urine
Half life: 3 hours
24
Q

Pharmacokinetics of esomeprazole?

A

Absorption: 90 percent
Protein binding: 97 percent
Mainly heptic. Completely metabolised by the cytochrome p450 system.
Elimation: 80 percent excreted as metabolites in the urine and 20 percent in feces
Half life: 1houurs
Bioavailability 65 percent

25
Q

Side effects of triple therapy?

A

Diarrhoea, nausea, inflammation in the bowel. Could mean clostridium difficile

26
Q

Side effects of amoxicillin

A

Breathing problems, dark urine and allergic reactions e.g. Redness of the skin

27
Q

Side effects of ibuprofen

A

Nausea, vomiting, diarrhoea

28
Q

Side effects of esomeprazole

A

Dizziness, diarrhoea, tachycardia

29
Q

Progression after gastric ulceration

A

Bleeding/ small scale/chronic- malena - haemorrhage -shock - death

Perforation - heck and pepsin enter the peritoneal cavity and digest any tissue there - peritonitis - shock - death

30
Q

What tests could you see if Harry still had h.pylori

A

Urea breath test and stool antigen test