Acute Pancreatitis Flashcards

A 45-year-old, diagnosed & managed for acute pancreatitis 2 weeks ago. Now presents with vomiting, SOB & epigastric pain which is not improved with PPIs. Examination revealed tachycardia & tachypnoea.

1
Q

A 45-year-old, diagnosed & managed for acute pancreatitis 2 weeks ago.
Now presents with vomiting, SOB & epigastric pain which is not improved
with PPIs. Examination revealed tachycardia & tachypnoea.

Q. Causes of Acute pancreatitis?

A

, The mnemonic “I GET SMASHED” is used to remember the causes of acute pancreatitis:

I: Idiopathic
G: Gallstones
E: Ethanol (alcohol)
T: Trauma
S: Steroids
M: Mumps (and other infections)
A: Autoimmune diseases
S: Scorpion sting
H: Hypercalcemia/Hyperlipidemia
E: ERCP (Endoscopic Retrograde Cholangiopancreatography)

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Q1. Which enzymes to be checked apart from Amylase & lipase? Are amylase & lipase valuable? Why?

A

LDH , Urinary amylase
less valuable
as they are increasing late not early, and may increase in chronic cases and other conditions

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3
Q

Q2. What are Causes of post-cholecystectomy pancreatitis ?

A

Missed stone, infec. , stricture of CBD or injury

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Q

Q3: Patient comes with jaundice and ascending cholangitis 6 months after surgery, reason?

A

Missed stone, stricture, malignancy, remenant of long cystic duct( incr. risk of infection)

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5
Q

Q4. 5 weeks after the initial attack patient presented with epigastric fullness, vomiting and dyspcpsia, diagnosis?

A

Pancreatic pseudocyst

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Q

Q5. Define pseudocyst and what are its contents?

A

Amylase risch fluid that surrounded by fibrous mesh which called psuedocapsule
content; fluid rich in amylase

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7
Q

Q6.Difference between cancer & pseudocyst?

A

Pseudocyst; rich for amylase, No tumor markers, fluid is less viscus
Cancer; Fluid is more viscous and positive tumor markers and there is no pseudocyst

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8
Q

Q7. In case of pancreatic Necrosis, what investigation of choice ?

A

CT angio for the abdomen and pelvis
Q8. What are the findings to look for in CT?
According to Belhazard classification; Edema, Necrosis, Abscess, Pseudocyst, collection.

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Q9. What are the biochemical findings ?

A

Increase in glucose and less albumen and Ca.
ABG – > Hypoxemia

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9
Q

Q12: How could you classify obstructive jaundice according to cause?

A

Obstruction from inside lumen like Stone or parasite
Itralumenal; tumors of CBD
Outside; Cancer head of pancrease or LN enlargement

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10
Q

Q11.Why is there hyperglycemia?

A

Due to autodigestion of beta cells leading to decrease insuline level and increase glucose in blood. Also Stress response in sepsis leading to release of chatecholamines and increasing glucose in blood.

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10
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Q10. Why is the calcium level is low?

A

Early stages due to destruction of mesenteric fat and presence of free fatty acid that attached to Ca with chelation of calcium
Transient hypoTH and HypoMg
Late stage due to sepsis leading to increase catecholamines and shifting of Ca intracellular

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11
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Q13. Whal could the cause for silent obstructive jaundice?

A

According to courvsier law it most commonly Ca head of Pancr.

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Q14. How would you manage a patient with acute pancreatitis? Does steroids have a role in acute pancreatitis?

A

CCRISP
Admission to HDU/ICU
Analgesia
Aggressive fluid rehydration
Supplemental oxygen
Invasive monitoring of vital signs, central venous pressure, urine output, blood gases
Frequent monitoring of haematological and biochemical parameters (including liver and renal function, clotting, serum calcium, blood glucose)
Nasogastric drainage (only initially)
Antibiotics if cholangitis suspected; prophylactic antibiotics can be considered
CT scan essential if organ failure, clinical deterioration or signs of sepsis develop
ERCP within 72 hours for severe gallstone pancreatitis or signs of cholangitis
Supportive therapy for organ failure if it develops (inotropes, ventilatory support, haemofiltration, etc.)
If nutritional support is required, consider enteral (nasogastric) feeding
Corticosteroids suppress the release of inflammatory cytokines in AP.
Corticosteroid therapy can benefit SAP (severe acute pancreatitis) patients by reducing the length of hospital stay, the need for surgical intervention and the mortality rate

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13
Q

Q15.What scoring for pancreatitis do you know? Talk about each of them.

A

READ Glascow, Ranson’s, Belhazard’s

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14
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Q16.What are the early and delayed complications of acute pancreatitis?

A

Early; MOF , Hyperglycemia, Hypovolumic shock, ARDS, AKI
Late; Abcess formation, Pseudocyst, Choronicity.

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Q17.How to treat splenic vein thrombosis in a patient with Haemorrhagic pseudocyst?

A

Coiling by interventional Radiology.

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Q

Q18. Complications of coiling ?

A

Bleeding and Injury to surrounding tissue, infection

17
Q

Q. when to use Abx?

A

Infected pseudocyst, Sepsis and prophylaxis before major intervention ERCP

17
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Q. which Abx to use?

A

Quinolones

18
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Q. when to go for TPN?

A

If entral is not accessible/ Pt is in sever sepsis or sever pancreatitis/ Complicated by formation of high output fistula.

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Q

Q. Which analgesia to give?

A

According to WHO ladder
If mild – > Paracetamol. (No NSAIDs – Incr. PU/Renal injury)
Sever – > PCA or Epidural ( Admit to ITU )