PUD Flashcards

1
Q

PUD clinically

A
  • Loss of the mucosal surface
  • Seen by endoscope and radiologist
  • < 5mm in diameter
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2
Q

PUD pathologically

A

Loss of surface epith.
+
Muscularis Mucosa penetration

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3
Q

HCl secretion stimulus

A
  • Ach (Mainly)
  • Histamine
  • Gastrin
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4
Q

Under the normal conditions there is a balance between

A
  • Defensive mechanisms
  • Aggressive mechanisms
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5
Q

Defensive mechanisms

A
  • Mucos
  • Good mucosal blood flow (rich in HCO3)
  • Tigh intercellular junction
  • Gastric mucosal renewal
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6
Q

Aggressive mechanisms

A
  • NSAIDs
  • Smoking
  • H.pylori
  • Pepsin
  • Bile salts & acids
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7
Q

General C/P of PUD

A

Epigastric pain
Dyspepsia
GERD symptoms
Gastric outlet obstruction (Finally as a complication)

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8
Q

GU C/P
(Rhythmic)

A

Absent during fasting
occurs shortly after eating –> weight loss
Relived by fasting (Stomach emptying)
Rare at night
Radiation to the back
Periodic (Recur at intervals)

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9
Q

DU C/P

A

Relived by food intake
Returns after eating
Usually awakens at night
Radiation to the back
Peridoic

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10
Q

PUD complications

A

Bleeding
penetration
Perforation
Obstruction
Gastric carcinoma

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11
Q

PUD COMP.
1. Bleeding

A

May be the first presentation
The most common presentation
Forms:
1- stool ( Melena / Occult blood )
2- Vomitus ( Coffee ground emesis / Hematemesis )
3- Sudden collapse and shock

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12
Q

PUD COMP.
2. Perforation

A

Less common
Mostly in the elderly patients and those who takes NSAIDs / corticos
C/P:
- Loss of bowel sounds
- Board like rigidity of AW
- Diffuse Abdominal pain
- Usually followed rapidly by bowel sounds cessation and development of rebound tenderness (surgical abdomen)

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13
Q

PUD COMP.
3.Penetration

A

Penetration into an adjacent structure
C/P:
- Gradual exacerbation of pain
- Increase in local tenderness
- Features of an additional diseases (Pancreatitis)

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14
Q

PUD COMP.
4. Obstruction

A

D.2 :
- Edema & inflammation surrounding the ulcer
- Permanent scarring with fibrosis

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15
Q

PUD INVES.
1. LAB

A

Uncomplicated cases= Normal
Perforation= polymorphonuclear leucocytsosis
Zollinger- Ellison $ = Serum Gastrin

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16
Q

PUD INVES.
2. Radiological

A

X-ray on abdomen = free air in cases of perforation

Barium meal = A permanent record of the findings

17
Q

The gold standard in DX of PUD

A

UGIE

18
Q

DU (Biopsy)

A
  • Mostly benign
  • Require biopsy only in the case of CROHN’S disease
  • Du patients should have biopsy (Antral) to diagnose H.Pylori
19
Q

GU (Biopsy)

A

Gu patients over 40 should have biopsy to exclude Gastric carcinoma

20
Q

H.Pylori Inves.

Serology

A

Abs declined gradually in the serum after eradication of the organism

21
Q

H.pylori Inves.

Urea breath test

A
  • Principle: The orally given urea, isotopically labelled with 14C or 13C, is hydrolyzed by the enzyme urease of H. pylori and *CO2 is expired in breath
  • Non-invasive test
  • positive test establishes the presence of current infection.
22
Q

PUD DD

A
  • Esophageal (GERD)
  • Stomach (Cancer)
  • Billiary system (Obstruction - Chronic cholecystitis)
  • Pancreatic (Chronic pancreatitis- Cancer)
  • Intestinal (Mesentric A Ischemia - T. colon disease)
23
Q

PUD TTT

A
  • Therapeutic
  • Non pharmacological interventions
  • Medication management
24
Q

PUD Medical TTT

A
  • Antacids
  • Mucosal protective agents
  • H2-receptor antagonist
  • PPI
25
Q

PUD medical TTT
1. Antacids

A
  • 2 MOA
  • AL (constipation)
  • Mg (Diarrhea)
  • Actions after 15-30 min if taken in empty stomach.
  • Renal damage: Al can cause Al toxicity.
26
Q

PUD medical TTT
2. Mucosal protective agents

A
  • Colloidal bismuth compounds.
  • Sucralfate:
    Needs acidic PH to be converted into viscus gel that adhere to ulcer crater
    Taken 1 h before meals
27
Q

PUD medical TTT
3. H2-Recptors antagonist

A
  • Reversible
  • Highly selective (x on H & H3)
  • More effective in inhibiting nocturnal acid secretion.
  • Cimetedine
  • Inhibits CYP450 (so increase conc. of WETP)
  • Causes gynecomastia and galactorrhea (anitandrogenic & increase prolactin)
28
Q

PUD medical TTT
4. PPI

A
  • Most effective anitulcer drug.
  • Omeprazole, Pantoprazole, Rabeprazole
  • DU: 4 WEEKS
  • GU: 8 WEEKS
  • T1/2: 1.5 hrs
  • Given 0.5-1 hr before meals
  • Inhibit CYP 450 (WETP) except panto and rabe.
29
Q

H.pylori
Related diseases

A

Esophagus: Reflux esophagitis

Gastric:
- Carcinoma
- Lymphoma
- PUD
- Chronic gastritis

30
Q

H.pylori
Pathogenesis

A

Infection
Mucous colonization
Urease action – neutralization of the acidic medium – rebound acid production
Protease – mucous break down
Acid & pepsin digestion
Chronic ulceration

31
Q

H.pylori
Eradication
1. Drug management

A

Triple
Amoxicillin + clarithromycin + PPI

consider metronidazole instead of amoxicillin in case of penicillin-allergic patients..

32
Q

H.pylori
Eradication
2. Surgical management

A
  • Vagotomy
  • Pyloroplasty
  • Antrectomy