ASSCC Flashcards
Why do you hyperglycaemia and hypocalcaemia in acute pancreatitis?
Hyperglycaemia: pancreatic enzymes destroy B cells of islet of langerhans and stress response both increase glucose
Hypocalcemia: in early phase autodigestion of mesenteric fat by pancreatic enzymes allows FFA release which chelate Ca to form Ca salts but then as sepsis develops there is increased circulating catecholamines which drive Ca into intracellular compartment - ARF also contributes
Describe a pancreatitis scoring system.
Glasgow score (PANCREAS) estimates severity
PO2 <8
Age >55
Neutrophils >15
Ca <2
Renal (urea) >16
Enzymes (LDH) > 600
Albumin <32
Sugar >10mmol/L
At least 3 = severe episode & consider ITU
Ransons criteria estimates mortality
At time of admission:
Age >55
WCC >16
Glucose >11
AST >250
LDH >350
After 48h of admission:
HCT drops 10% or >
Fluid sequestration >6L
Ca <2
PO2 <8
BUN rises more than 5mg/dl after IVD
BE >4
0-2 points = 1%
3-4 points = 16%
5-6 points = 40%
7-11 points = almost 100%
What are the CT findings of pancreatitis?
Inflammation & oedema
Peripancreatic collection
Fat stranding
Pseudocyst
Necrosis
When would amylase be normal in acute pancreatitis?
Too early
Too late - returns to normal >48h after onset of attach
Does not correlate with severity and is not specific
What is a pseudocyst and when would it present? What is the clinical presentation of a pseudocyst?
Collection of amylase-rich fluid enclosed in wall of granulation tissue often in lesser peritoneal sac occuring 4 weeks or more after onset of attach - pseudo as it isnt closed and is not lined by epithelial cells seperating it from nearby tissues
Signs/symptoms:
Epigastric swelling/tenderness
Dyspepsia
N&V
Mild fever
Why might a pancreatitis patient be tachypnoeic?
Pain causing poor expansion of chest/ventilation
Splinting of diaphragm if large collection/cyst
ARDS development
Sympathetics activated due to stress response in sepsis
How do you investigate pancreatitis?
Bedside: obs & ABG
Bloods: FBC,CRP, U&Es, LFTs, amylase/lipase, Ca, LDH, coag & G+S/CM
Imaging: USS & CTAP + IV contrast
How to manage acute pancreatitis?
A-E as per CCRISP
Analgesia as per WHO pain ladder (pethidine is drug of choice, no NSAIDs to prevent renal injury & also no morphine to prevent SOO spasm but can consider PCA/epidural)
Aggressive IVF
O2
Catheter & consider NGT
IV PPI
Abx to be considered
Corticosteroids
Octreotide to decrease secretions
ERCP within 72h if due to gallstones
Escalate to HDU for CVP (hydration, monitoring & TPN) & potential organ support
How does paracetamol cause liver injury?
Toxic metabolite NAPQI produced when paracetamol taken which is normally neutralised by glutathione but this system will become overwhelmed so it accumulates in liver effecting vital function
What are the different ways to assess pain?
Pain score
Description
Visual analog scale
Smiley faces in children
Why should codeine be avoided?
CYP2D6 metabolises it converting it into morphine in liver - ultra-metabolisers with high amounts can get lifethreatening intoxication over days & 10% population lack enzyme to metabolise who get no analgesic effect but get SEs
SEs inc. constipation, sedation, N&V & resp depression
What are the physiological effects of pain?
CVS: increased HR/BP + myocardial consumption leading to MI or DVT from immobility
GIT: delayed gastric emptying, reduced bowel motility & paralytic ileus
Resp: limited chest movements leading to atelectasis & pneumonia
Also psychological impacts such as trauma, depression and anxiety
What are the safety features of a PCA?
Lock out time
Measured dose
Locked unit to cannot be tampered with
One way valve preventing opiate backflow into infusion chamber causing OD when re-delivered
What are the complications of pancreatic pseudocyst?
Enlargement: pressure effects on biliary system causing obstructive jaundice and BO
Infection: abscess or systemic sepsis
Rupture into gut causing GI bleeding/fistula or into peritoneum causing peritonitis
Erosion into vessel causing haemorrhage into cyst or haemoperitoneum
What is SIRS criteria? When does it become sepsis?
Systemic inflammatory response syndrome where 2 or more present of:
Temp >38 or <36
Tachycardia
WCC raised
RR/PaCO2
+clear source of infection = sepsis
+lactic acidosis = severe sepsis
Why would you get a metabolic acidosis in sepsis?
Lactate produced as B2 adrenergic receptors stimulated by adrenaline (stress response) increasing glycolysis producing more pyruvate than can be used so excess converted to lactate + impaired clearance of it
This causes acidosis and a decreased BE
What is HDU admission criteria?
Requiring support for single failing organ e.g. vasoactives required but not needing advanced respiratory support i.e. mechanical ventilation
More detailed monitoring required than on ward - needs 1:1 nursing care
ITU step downs
If post op monitoring needed for more than few hours
