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Therapy > Alagala > Flashcards

Alagala Flashcards

1
Q

What is Gastronemia
How does Hpylori cause Gastronemia?

A

Gastronemia is excessive production of gastrin.
D-Antral Cells produce gastrin

Somatostatin regulates gastrin production.
It can inhibit or promote the production of gastrin
D-Antral Cells also produce Somatostatin.

H. Pylori doesn’t play- it goes to the grass root and attack.
H.pylor causes the death of D- Antral cells
Which will inhibit the amount of Somatostatin produced.

Since Somatostatin is not available to inhibit gastrin production there will be excessive production.

Also- inflammatory processes also have a stimulatory effect on gastrin

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2
Q

Explain the rationale approach for managing NSAID induced Ulcer

A
  1. NSAID discontinuation
  2. Review on Patient
  3. Treatment options
    First line of treatment: PPI’s - Omeprazole
    Dose regimen
    1 tab of Omeprazole 20mg b.d .
    OR
    1 tab of Omeprazole 40mg nocte

Other treatments options available:
H2 Antagonist: Ranetidine
Misoprostol
Sulcrafate.

Dose regimen for Ranetidine
Ranetidine 150mg Bd
Ranetidine 300mg nocte

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3
Q

Management of GERD,.. 3 steps

A
  1. Lifestyle modification
  2. Drug related GERD
  3. Pharma treatment
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4
Q

Lifestyle modif of gerd

A

Smoke cessation
Weight loss

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5
Q

Drug related GERD

A

Drugs that affects muscle tone - relax them

Ccb
TCA’s
Atc’s

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6
Q

Drug related GERD

A

Drugs that affects muscle tone - relax them

Ccb
TCA’s
Atc’s

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7
Q

Rx treatment GERD

A
  1. PPI’S OMEPRZOLE 20MG B.D 2/52

SEVERE PPIS + RÀNETIDINE 150 MG NOCTE

V.SEVERE- PPIS + RANETÍDINE + ANTACID….,.. EXCELLENT RESULT

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8
Q

Management of Nsaids

A
  1. Drug treatment evaluation - Nsaids
    2 Q& A- drug history check
  2. Rx treatment
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9
Q

Rx treatment of NSAIDS

A
  1. PPIS - 1ST LINE TREATMENT
    Omeprazole 20mg Bd ….. Most efficient 80%
    40mg o.d for 8/52 79%
  2. H2 ANTAGONIST - RANETIDINE
    150mg b.d ……… 63%

MISOPROSTOL
SULCRÀFATE

NSAIDS + PPI’ OR H2 ANTAGONIST

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10
Q

Hpylori management

A

“Radical treatment”

2 antibiotics+ 1 conventional ulcer healing frug

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11
Q

Ocm used to ensure?

A
  1. Symptomatic relief
    Healing of ulcer
  2. Increase pH by decreasing HCL production in the stimach
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12
Q

OCA
OCM?

A

Omeprazole 20mg
Clarithromycin 500mg
Amoxicillin - 1000mg

Omeprazole 20mg
Clarithromycin 250mg
Metronidazole 400mg

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13
Q

Why is OCA MORE EFFECTIVE THAN OCM

A

Hpylori has developed resistance to metronidazole

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14
Q

Ocm instead of o use?

A

Ranetidine 300mg.

Ranetidine bismuth citrate used in addition to treatment

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15
Q

Faliure in combination equals?

Or add what?

A

Switch in combination

4th drug Ranetidine 300mg nocte

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16
Q

Antacids?

A

They neutralise gastric acid in the stomach and therefore increase pH and relief dyspepsia symptoms

17
Q

Antacids interfer w?

A

Interfere or block absorption of fluoroquinolones - antibiotics

18
Q

Eg of antacids

A
  1. Mg based - diarrhoea winner

Al based - constipation - loser

19
Q

GERD COMPLICATION?

A

Oesophagus
- barrette oesophagus
Oesophageal structure

Ulceration

20
Q

Complications of Pud

A

Aneamie
Perforation
Heamorrhage

21
Q

Symptoms of gerd

A

Heart burn
Acid regurgitation
Dsyphagia

22
Q

GERD OCCURS AS A REULT IF WHAT?

A

Result of acid regurgitation into the oesophagus

Bile acid too
Pepsin regurgitation

23
Q

GERD OCCURS AS A REULT IF WHAT?

A

Result of acid regurgitation into the oesophagus

Bile acid too
Pepsin regurgitation

24
Q

Pud causes?

A

Cigarette
Caffeine
Alcohol
Use of corticosteroids
Emotional trauma

25
Q

Enzymes that produce bacteria

A

Neuramidase
Urease
Haemolysin
Fucosidase

26
Q

How Hpylori cause Gastronemia

A

D antral cells - somatostatin
G cells. - gastrin

Somatostatin inhibits the release of gastrin

Hpylori attacks and kills d antral cells.
Reduces the number

Therefore reduced or no somatostatin available.
Consequently without adequate somatostatin there is less inhibition of gastrin - gastrin is not inhibited leading to excessive production of gastrin

Gastrin stimulates the parietal cells to produce more HCl leading to pud

Gastronemia.🙂

27
Q

CAP
VAC

A

Jj

28
Q

How is NSAID implicated in Pud?

A
  1. Local - weak acid
    Remains non ionized
    penetrates cell of stomach lining - mucosa
    They attract leukocytes
    Initiates inflammatory response
    Cause direct damage on stomachs epithelial lining
    Weakens protective stomach layer
  2. Systemic - Cox 1and 2

Cox 1 produce prostaglandin that protects the stomachs lining
Stimulates mucuius and bicarbonate

Cox 2 prostaglandin involved in inflammatory response.

Nsaids inhibits both Cox 1 and 2

Reduce protective prostaglandin - increased ulcer risk

29
Q

Crohn’s disease

A

Chronic inflammation characterised by inflammation of the bowel of the GIT.
XTERISED by flare ups and remissions.
And increasing disease severity can affect anywhere from mouth to anus in GIT

30
Q

Management of Crohn’s
What
Treatment factors

A
  1. MDT
  2. Site of action and clinical presentation
  3. Aim is to induce and maintain remission
  4. Avoid risk factors
  5. Psychosocial support and patient edu
31
Q

Medical interventions of Crohns

A
  1. Dietary advive- take vitamin supplement
  2. Diarrhoe management - antidiarrhoe - loperamide
  3. To induce remission -
    Corticosteriods
    Infliximab
    Aminosalicylates
  4. Maintain remission
    Don’t smoke
32
Q

Complications of Crohns

A

Structures that can lead to Blockages
Fistula foation
Hemorrgoids
Cancer
Colorectal carcinoma

33
Q

Diagnosis of Crohns

A

Radiology and imaging colonoscopy, ultra sound
Stool culture : faecal calprtectin shows inflammatory activity
Blood test hematological test cbc

34
Q

Symptoms of Crohn’s

A

Abdominal pain
Diarrhoea- can be bloody
Weight loss
Anotexia, vomitting

Depends on site of action

35
Q

Aetiology of Crohn’s disease

A
  1. Environmental - diet drugs, smoking
  2. Genetics- card 15 gene 16- mutation occurs. This gene helps regulate the immune system response to bacteria int he gut. When mutation occurs- immune system may not recognize normal gut bacteria and initiate inflammatory process
  3. Hist immune system
    Mucosal immunity is dyregulated in CD leading to a prolonged inflammatory response
36
Q

3 reasons for death in crohns

A

Sepsis
Pulmonary embolism
Surgery complications

37
Q

Crohn’s pathology

A
  1. Inflammation but why? - patchy transmural inflammation…. Causes what?
    Causes thickening of the bowel
    Thickening cause narrow lumen
    Aphthoid ulcerations and cobble stoning

Therapy (11 decks)

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