GOO, perfed PU, AF and sepsis Flashcards
What are risk factors for perforation?
-NSAIDs
-H.pylori
-Steroids
-Previous peptic ulcer
-Malignancy
How can NSAIDs cause peptic ulceration?
-Topical irritant effect on epithelium
-Suppression of prostaglandin synthesis (inhibition of cyclooxygenase) which are essential in proteting mucosa
-Reduction of gastric mucosal blood flow
What are the management oprtions for the perfed duodenal ulcer?
-Omental patch repair
-Good wash out
-Intraabdominal drain
Biopsy if gastric ulcer to rule out malignancy
What would you give post op to perfed peptic ulcer?
PPI long term
What is mechanism of PPI?
-Binds irreversibly to hydrogen/potassium ATPase enzyme (proton pump) on gastric parietal cells and blocks secretion of hydrogen ions
-These combine with chloride in stomach lumen to form HCL
What are the actions of HCL?
-Activates pepsinogen to pepsin which help in proteolysis
-Antimicrobial
What are the phases of gastric secretion?
- Cephalic phase (smell/taste of food)
–> 30% acid produced
–> vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells - Gastric phase (distension of stomach)
–> 60% of acid produced
–> stomach distension/low H+/peptides cause gastrin release - Intestinal phase (food in duodenum)
–> 10% acid produced
–> high acidity/distension/hypertonic solutions in duodenum inhibits gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes
NCEPOD classification
1: life or limb threatening (immediate, <2 hrs) (ruptured AAA, torsion, compartment syndrome)
Simultaneous resuscitation and management
2a: urgent: 2-6 hrs: Laparotomy for perforated viscus, critical organ or limb ischaemia
once resustcitation completed
2b Urgent 6-18 hours (appendicitis)
3: expedited >18 hours: repair of tendon and nerve injuries, excision of tumour with potential to bleed/obstruct
4 (elective): lap chole
Scenario: lady with vomiting and epigastric fullness. Hyponatremia, ph 7.5
Cause of this clinical picture?
Benign: pyloric stenosis secondary to chronic peptic ulceration
Malignant: gastric or pancreatic carcinoma
What will ABG show
Metabolic alkalosis
What biochemical abnormalities will there be?
-Hypochloraemia due to loss of chloride in vomitus
-Hypokalaemia due to increased aldosterone in response to hypovolaemia
Why is bicarb raised?
-Increased uptake of bicarbonates in renal tubule in response to loss of chloride in order to maintain neutrality
-Reduction of pancreatic juice secretion (due to loss of acid load in duodenum)–> retention of bicarbonate rich pancreatic juice
Why is there hyponatraemia?
-In metabolic alkalosis, kidneys excrete more NAHCO3 to reduce blood alkalinity –> hyponatraemia
Why is there paradoxical aciduria?
Hyponatraemia –> stimulation of angiotensin aldosterone system –> more Na + and H20 reabsorption in exchange for H+ and K + –> hypokalaemia and the urine becomes acidic due to presence of H+
What is the clinical picture of hyponatraemia?
–< confusion
-Agitation
-Fits
-Reduced GCS