GI Pharmacology Flashcards

1
Q

Discuss the drugs that are used to treat liver failure
think about the 4 main common conditions and how you would treat them !
(4)

A

1-Treating Ascites= build up of fluid in abdomen = diuretics ( spironolactone and furosemide)
2-Hepatic Encephalopathy ( mental confusion etc = Ammonia is systemic curation to the Brain and increase in GABA . For this treat the bleeding , give laxative lactulose , give vitamins, antibiotics )
3-Coagulopathy = give clotting factors and vitamin K
4-Hepatorenal syndrome = fluid and blood in the Wrong place due to vasodilation so give ADH to vasoconstrict.

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2
Q

Describe the principles of peptic ulcer disease therapy

a) what is a peptic ulcer and how is it caused

A
Peptic Ulcer =defect in duodenal mucosa 
-Due to acid and mucosal defence imbalance 
TREATMENT:
1-remove irritants (NSAIDS)
2-Antacids 
3-Proton Pump Inhibitors
4-H2 receptor antagonist 
5-Antibiotics

(blood in ur faeces called malaenia = black old blood from higher up the GI tract = darker blood from peptic ulcers)

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3
Q

List the potential areas of the parietal cell peptic acid secretion control that can be targeted by drugs in both predisposing and treating peptic ulcer disease

A

Gastric Parietal cell :
1-ACH receptor increases H+ secretion, hence more acidic in stomach
2-PGE2= Less secretion of H+ from the Lumen
3-Histamine 2 receptor = increases the H+ released to lumen
4-Gastrin increases H+ too

H+/K+ ATPase is a proton pump which can be inhibited

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4
Q

Compare proton pump inhibitors with histamine2-receptor antagonists in terms of mode of action, efficacy and adverse effects
(5)

A

-H2 blocks receptor which is acid producing stimuli , PPI block production at the source!
-H2 = decreases production for 8Hr, PPI= decreases production x>24hr
-Both = heart burn
-H2 = starts working in 15-30 min.PPi= begins working in 1hr but peak effect in 1-4hrs
-H2= relief for 12hr. PPI= relief for 24hr
PPI= irreversible , whereas H2 is a competitive antagonist

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5
Q

Discuss the diagnosis and treatment of helicobacter pylori infection relative to peptic ulceration

What is it ?
How do we test for this ?
How do we do Helicobacter Eradication ?

A

Peptic ulcer can be causes by gram negative Bacillus (Helicobacter pylori)= secrets inflammatory proteins , toxins which can cause Ulceration .

-urease enzyme in H.pylori which makes urea–>NH4 and CO2

HOW DO WE TEST FOR THIS?
1-C13 test + Urea breath test
2-Serology , to currently used by NICE
3-Upper GI endoscopy with biopsy , rapid urease test
4- Helicobacter Eradication Regimens ( 2 antibiotics + PPI) = triple therapy for 7 days

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6
Q

Apply the knowledge of peptic ulcer disease treatment to hypothetical clinical scenarios
(4)

A

If your stomach ulcer is caused by a Helicobacter pylori (H. pylori) bacterial infection, a course of antibiotics and a medication called a proton pump inhibitor (PPI) is recommended.

  • Anti-inflammatory drugs (NSAIDs).
  • H2 Receptor Antagonist
  • Antacids
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7
Q

Proton pump inhibitor
(ends in ? what does it do and when is it used ?)
one really important precaution !?

A

Ends in -prazole
- Blocks the H+/K+ ATPase pump in the cell
-used in dyspepsia (indigestion)
+PUD
+GORD
-Be careful when prescribing ! can mask gastric cancer !!!
- vomiting , abdominal pain, diarrhoea, constipation , headache

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8
Q

Omeprazole
(normal side effects - name 3 )

Adverse drug reactions

INTERACTIONS

A

Proton pump inhibiter
-can mask gastric cancer , vomiting , abdominal pain, diarrhoea, constipation , headache

ADR:
1-increases risk of clostridium difficile
2-Hyponatraemia and Hypomagnesaemia
3-Hepatitus, Intestinal nephritis , blood disorders
4-increased risk of community acquired and hospital acquire pneumonia

Interactions :
1- Warfarin ( omeprazole and esomeprazole are weak CYP450 = increasing ANTI coagulant effect)

2-Clopidogrel( Hepatic pro-drug)= CYP450 inhibitors which have anti platelet effect

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9
Q

H2 receptor inhibitor

A

1-Cimetidine and Ranitidine

( stop the H2 receptor being activated , hence no cAMP –>NO pKA–>No Hydrogen potassium ATPase PUMP WORKING = LESS ACID

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10
Q

Constipation

treated by ?
causes ( the drugs which can cause this )

A
Treated by non pharmacological treatment :
1-increase fluid intake
2-imporve mobility
3-increase fibre intake
4-stop Constipating drugs 
5-exclude the underlying pathology 

CAUSES (DRUG WISE)
1-opoids, antacids including Ca2+, Al, anti depressants , anti musarinics
2-Anal fissure , peri anal absceses
3-benign colorectal disease
4-endocrine/ metabolic = hypercalacemia , hypothyroidism
5-Malignancy ( tumours )

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11
Q

LAXATIVES

3 main types

A

1) Osmotic laxative = draws in water to stool ie : Macrogois, Microvil
2) Stimulants = causes peristalsis = Senna
3) Bulk forming =causes stool to get bigger and softer = decussate

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12
Q

what is the phase 1 reaction of liver

what is phase 2 reaction of liver :
2

A

1-P450 monooxygenase & CYP450 2D6 enzymes =REDOX and they make drugs more reactive and hydrolytic reaction to make is WATER SOLUBLE and sticky

2) add the inactive groups to conjugate the groups = even more water soluble

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13
Q

enzyme inducers ?

PC BRAGS

A

1-At a cellular level , induces more Cytochrome enzymes = lasts longer and SLOW = increases enzyme production and hence drug metabolism increases so drug levels drop.

PC BRAGS

Phenytoin
Carbamazepine

Barbituates ( Brussel sprouts)
Rifampicin 
Alcohol 
Glucocorticoids
St. John's warts
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14
Q

CYP450 Enzyme inhibition
(Taehyung wants ON very easily )
(5)

A

FAST
1-Grapefruit juice
2-Protease Inhibition
3- Azoles

Causes the drug to increase as enzyme activity to break it down decreases.

Theophylline 
Warfarin 
Oxycodone 
Verapamil
Erythromycin
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15
Q

cirrhosis signs and symptoms

5

A
1-Ascites 
2-Encephalopathy 
3-Coagulopathy (x>1.7 coagulation time )
4-Hepatorenal Syndrome
5-Varices / portal HT

for every thing you score , you add one mark

CLASS A= 5-6 points ( easy )
B= 7-9 Points
C=10-15 points ( hard to treat )

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16
Q

How to treat ascites due to cirrhosis ?

A

1-Non -pharmacological measures
( Na+ restriction, parcel

2-Diuretics= spironolactone ( blocks aldosterone in DCT) or Furosemide = loop diuretics inhibits Na/K/2Cl transporter

17
Q

How do you treat Encephalopathy due to liver failure ?

what is it due to ? and how do we treat it ?

A
Due to build up of the excess of ammonia from bacteria in the GIT ( no urea )
Excess GABA ( inhibitory substance ) 

Treatments:
1-avoid protein , GI bleeding and avoid constipation
2- 3rd line laxative = Lactulose
3-Vitamin B+c
4-Antibiotics to reduce Bacteria and Blocks RNA transcription

18
Q

how to treat coagulopathy

4

A

increases in blood clotting time and bleeding time

1-Increase thrombin time
2-Vitamin k Increase ( vitamin K makes clotting proteins )
3-Increase clotting factors and increase platelets
1972 ( 10,7,9,2)

19
Q

How to increase Hepatorenal Syndrome ?

3

A

1-Multifactorial - one issue is splanchnic vasodilation
2- Blood is going to the wrong place and wrong direction

Give ADH = try to increases BV

20
Q

Heart burn syndrome ? GORD ( Gastricoesophagul Refluc disease)
(3)

A

1) antacids – these neutralise the effects of stomach acid
2) alginates – these produce a coating that protects the stomach and oesophagus (gullet) from stomach acid
3) low-dose proton-pump inhibitors and H2-receptor antagonists

21
Q

How do we treat colycistituis ( gall bladder infection due to e.coli ) ?
(2)

A

1- Co-amoxiclav
( clauvidonic acid = beta lactamase inhibitor
Beta lactate = enzyme of bacteria which breaks down our cells , so we use inhibitor and an antibiotic to stop them )
Amoxicillin = Beta lactam antibiotic