Which enzymes to be checked apart from amylase & lipase?

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Lactate dehydrogenase

Is amylase and lipase valuable? and why?

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Lipase levels are more specific to the pancreas.
While amylase is not specific and can be normal if measured too early or too late because of its short half-life.

What are Causes of post-cholecystectomy pancreatitis ?

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Iatrogenic injury
infectious
retained stones
stricture.

Patient comes with jaundice and ascending cholangitis 6 months after surgery, reason?

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Retained stone causing obstruction
Stricture

5 weeks after the initial attack patient presented with epigastric fullness, vomiting and dyspepsia, diagnosis?

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Pancreatic pseudocyst

Define pseudocyst and what are its contents?
Collection of amylase-rich fluid enclosed in a wall of fibrous or granulation tissue.

Difference between cancer & pseudocyst?
Tumour- Pseudocyst
Fluid viscosity: Elevated -Low
Tumour marker CA19-9: High -Low
Amylase: Low- High

What is the difference between true cyst and pseudocyst?

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Pseudocyst is not closed and doesn't have a lining of epithelial cells separating it from the nearby tissue, instead its wall made up of fibrous and granulation tissue.

In case of pancreatic necrosis, what investigation of choice?

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CT abdomen with IV contrast pancreatic protocol (thin CT slices).

What are the findings to look for in CT?

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Fat stranding
Oedema
Collection
Pseudocyst
Abscess
Necrosis

What are the biochemical findings?

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Hyperglycaemia
Hypocalcaemia
Hypomagnesemia
Hypoalbuminemia.

Why is the calcium level low?

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In early stages
Auto-digestion of mesenteric fat by pancreatic enzymes and release of free fatty acids (chelate calcium), which form calcium salts (saponification of fat).
Later stages, due to complication like:
-Sepsis
-Hypoalbuminemia
-Transient hypoparathyroidism

Why is there hyperglycaemia?

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Destruction of B cells of islets of Langerhans that normally secret insulin.
Could be due to stress response (cortisol and catecholamines).

How could you classify obstructive jaundice according to cause?

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Intra-luminal: stone
Trans-luminal: cholangiocarcinoma
Extra-luminal: cancer of head of pancreas

What could the cause for silent obstructive jaundice?

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Carcinoma of head of pancreas

How would you manage a patient with acute pancreatitis?

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CCrISP protocol using the ABCDE approach
Admission to HDU/ICU.
Analgesia
Aggressive fluid rehydration
Supplemental oxygen
Monitoring
-Central venous pressure
-Urine output
-Blood gases
-Liver function, U&E
-Clotting profile
-Serum calcium
-Blood glucose
-Nasogastric drainage (only initially)
Antibiotics if
-If suspected cholangitis
-Sepsis
-Necrosis
-Pre-invasive intervention (ERCP).
Octreotide → decrease pancreatic secretions
PPI → prevent stress ulcers
CT scan if
-Organ failure
-Clinical deterioration
-Signs of sepsis
ERCP within 72 hours for
-Severe gallstone pancreatitis
-Or signs of cholangitis
Supportive therapy for organ failure if it develops → (inotropes, ventilatory support, hemofiltration, etc.)
If nutritional support is required → nasojejunal tube.

What scoring for pancreatitis do you know? Talk about each of them
Glasgow criteria: PANCREAS

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PaO₂ < 8 kPa (normal: 10–13 kPa)
Age > 55
Neutrophils > 15,000
Calcium < 2 mmol/L (after 48h)
Renal (urea) > 16 mmol/L (normal: 2.5–6.7)
Enzymes (LDH) > 600 (after 48h)
Albumin < 32 g/L (after 48h)
Sugar (glucose) > 10 mmol/L
(at least 3 of the above = severe episode = ITU admission)

Ranson's criteria

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Estimates mortality of patients with pancreatitis, based on initial and 48-hour lab values.
Criteria at time of patient admission to hospital
Age > 55
WBC > 16,000
Glucose > 11 mmol/L (> 200 mg/dL)
AST > 250 IU/L
LDH > 350 IU/L
Within 48 hours
Hct drops 10% or greater
Fluid sequestration > 6 L
Calcium < 2.0 mmol/L (< 8 mg/dL)
PO₂ < 60 mmHg (< 8 kPa)
BUN rises more than 1.98 mmol/L (> 5 mg/dL) after IV fluid hydration
Base deficit > 4 mmol/L
Mortality prediction
0–2 points: Mortality is 1%
3–4 points: Mortality is 16%
5–6 points: Mortality is 40%
7–11 points: Mortality almost 100%

What are the early and delayed complications of acute pancreatitis?
Early

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Necrosis
ARDS
Pleural effusion
Electrolyte disturbance:
Hyperglycaemia
Hypocalcaemia
Hypomagnesemia
Hypoalbuminemia
Late
!Pseudocyst
Splenic vein thrombosis

How to treat splenic vein thrombosis in a patient with haemorrhagic pseudocyst?

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Multidisciplinary approach including:
-Gastroenterologist/hepatologist
-Haematologist
-Interventional radiologist
→ For radiological intervention (coiling)

Complications of coiling?
Injury to surrounding structures
Haemorrhage
Failure
Infection

Abx in pt with acute pancreatitis?

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Quinolones or according to Trust guidelines

Management of pain?

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According to WHO analgesic ladder but I will try to avoid morphine and NSAID.
Starting with non-opioid like paracetamol, then weak opioid like (codeine), then strong opioid (pethidine), then PCA (patient-controlled analgesia), and epidural analgesia.

Why not morphine?

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Causes constriction of sphincter of Oddi.

Is it true or theoretical?

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Theoretical

What is CRP?

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Nonspecific acute phase reactant protein made by the liver released into the blood in response to inflammation.

Causes of tachypnoea in this patient?

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ARDS as complication
Sympathetic overactivation
Compression of diaphragm by pseudocyst

Exocrine enzymes of the pancreas?

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Amylase: breaks down carbohydrates into simple sugars like glucose.
Proteases: break down proteins into amino acids. The main proteases are trypsin, chymotrypsin, and carboxypeptidase.
Lipase: breaks down fats into fatty acids and glycerol.

Other than the enzymes what is present in pancreatic juice?

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Bicarbonate: neutralizes the acidic chyme from stomach, creating an alkaline environment that is optimal for the activity of pancreatic enzymes.
Water: helps to dilute the chyme and facilitate transport of nutrients.
Electrolytes: such as sodium, potassium. The secretion of pancreatic juice is stimulated by factors including:
-Acetylcholine: released by the vagus nerve, stimulates the secretion of pancreatic enzymes.
-Cholecystokinin (CCK): a hormone released by the duodenum in response to the presence of fatty acids and amino acids, stimulates the secretion of pancreatic enzymes and contraction of the gallbladder.
-Secretin: a hormone released by the duodenum in response to the presence of acid, stimulates the secretion of bicarbonate-rich fluid by the pancreas.

How is the pancreatic secretion stimulated?

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Acid load in the duodenum plays a crucial role in stimulating pancreatic secretion. When acidic chyme enters the duodenum from the stomach, it triggers the release of secretin, which stimulates the pancreas to secrete bicarbonate-rich fluid. This fluid neutralizes the acid, creating an alkaline environment that is necessary for the activity of pancreatic enzymes.