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Surgery > Medbear Pancreas and Spleen > Flashcards

Medbear Pancreas and Spleen Flashcards

1
Q

Describe the embryology of the pancreas

A
  • Developed from the dorsal and ventral buds (with the bile duct), ventral bud rotates around the 2nd part of duodenum, majority of pancreatic duct (duct of Wirsung) from ventral bud and accessory duct (duct of Santorini) from dorsal bud
  • Main pancreatic duct - segment of the dorsal duct proximal to dorsal-ventral fusion point

Duct of Wirsung - segment in ventral duct between dorsal-ventral fusion point

Duct of Santorini - portion of the dorsal duct distal to the dorsal-ventral fusion point

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2
Q

Describe the anatomy of the pancreas based on the following heading
- Head
- Neck
- Body
- Tail

A
  • Head = lie within C-shaped concavity of duodenum
  • Neck = lie in front of the portal vein and overlie origin of SMV
  • Body = runs upwards and to the left across the midline
  • Tail = passes forward in the splenorenal ligament, anterior to left adrenal gland contacting hilum of the spleen
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3
Q

State the blood supply of the pancreas

A

Arterial supply
- Celiac artery give rise to SPLENIC ARTERY (TAIL) and SUPERIOR PANCREATICODUODENAL ARTERY (HEAD)
- Superior mesenteric artery -> INFERIOR PANCREATICODUODENAL ARTERY (HEAD)

Venous drainage (head and uncinated)
- PANCREATICODUODENAL VEINS -> Posterolateral surface of the portal vein

*Splenic artery runs superior to pancreatic body
*Splenic vein runs posterior to pancreatic body

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4
Q

Define acute pancreatitis

A
  • Reversible pancreatic parenchymal damage of varying severity owing to an acute inflammatory disease of the pancreas
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5
Q

Which 3 features are required in the diagnosis of acute pancreatitis?

A
  • Abdominal pain consistent with epigastric pain
  • Serum lipase/amylase activity of at least 3X greater than the upper limit of normal
  • Characteristic findings of acute pancreatitis on CECT, MRI or trans-abdominal US
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6
Q

State the causes of acute pancreatitis

Hints: I GET SMASHED

A
  • Idiopathic (15-25%)
  • Gallstones (40-70%)
  • Ethanol (25-35%)
  • Trauma
  • Steroids
  • Mumps and other infections
  • Autoimmune (increase in IgG4)
  • Scorpion toxin and other toxins
  • Hypertriglyceridemia, hypercalcemia (metabolic causes)
  • ERCP (2-5%)
  • Drugs (1-2%)

Others: Neoplasm, Congenital, Familial Pancreatitis

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7
Q

Explain on the pathophysiology of acute pancreatitis

A
  • Caused by unregulated activation of TRPSIN within pancreatic acinar cells -> activating pro-enzymes leading to AUTO-DIGESTION and inflammatory cascade
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8
Q

How gallstones causes acute pancreatitis?

A
  • Obstruction of the pancreatic duct -> Increased pressure in the pancreatic duct -> EXTRAVASATION of pancreatic juice -> Injury of the gland
  • Interstitial edema impairs blood flow to pancreatic cells -> ischemic cellular injury -> activation of pro-enzymes -> destruction of pancreatic acinar cells
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9
Q

How alcohol causes acute pancreatitis?

A
  • Direct toxic effect and/or its metabolites on acinar cells -> gland autodigestive injury
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10
Q

State the (3) common clinical presentation of acute pancreatitis

A
  • Acute and constant pain at the EPIGASTRIC area or RUQ
  • Unable to get comfortable when lying supine
  • Pain last for several days associated with NAUSEA and VOMITING
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11
Q

State (5) complicated symptoms of acute pancreatitis

A
  • Respiratory failure (e.g dyspnoea secondary to diaphragmatic inflammation, pleural effusion, ARDS)
  • Renal failure (e.g OLIGURIA)
  • GI failure (e.g nausea, vomiting, abdominal bloatedness)
  • Fever +/- hypotension
  • SIRS response (e.g tachycardia, tachypnea, fever)
  • Obstructive jaundice

*SIRS - Systemic Inflammatory Response Syndrome

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12
Q

What other differential diagnosis you should rule out for a case of acute pancreatitis?

A
  • Gastric cause (PUD, perforated viscus)
  • Hepatobiliary cause (hepatitis, GB/CBD disease)
  • Medical cause (AMI, DKA, lower lobe pneumonia)
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13
Q

What are the diagnostic investigations (Biochemical) done to confirm a case of acute pancreatitis?

A

Investigations for diagnosis -> investigation for severity stratification

Diagnostic:
(Levels >3 times the normal upper limit)
- Serum amylase (Normal = 30-100U/L)
- Serum lipase (Normal = 10-140U/L)

Assess severity and prognosticate disease
- Full blood count (Leukocytosis, Hematocrit levels)
- Renal panel, calcium panel, glucose (Assess hydration status and degree of renal impairment, hypocalcemia, hyperglycemia)
- Liver function test (AST, Albumin, LDH)
- ABG (Assess base deficit and arterial oxygenation)
- CRP (>150mg/L within 48 hrs associated with severe pancreatitis)

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14
Q

What are the diagnostic investigations (Imaging) done to confirm a case of acute pancreatitis?

A
  1. Erect CXR and supine AXR
  2. Hepatobiliary US
  3. CTAP
  4. MRCP
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15
Q

What to look for in the erect CXR and supine AXR of acute pancreatitis?

A

Erect CXR
- Air under the diaphragm (Perforated viscus)
- Complete whiteout (ARDS)

Supine AXR -> Look for
- Sentinel loop sign - focal area of adynamic ileus close to an intra-abdominal inflammatory process
- Colon cut-off sign - distended colon from ascending to mid-transverse with narrowing of splenic flexure
- Pancreatic calcification (chronic pancreatitis from alcohol abuse)

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16
Q

State (3) indications for CTAP in a case of acute pancreatitis

A
  • Useful in confirming the diagnosis of pancreatitis if hematological result is inconclusive
  • Useful in severely ill patients with suspicion of necrotizing pancreatitis
  • Patient with persisting organ failure, signs of sepsis, or deterioration in clinical status 6-10 days after admission
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17
Q

State the (3) categories of the modified CT severity index

A
  • Pancreatic inflammation
  • Extra-pancreatic complication
  • Pancreatic necrosis
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18
Q

State (3) advantages of MRCP in diagnosing acute pancreatitis

A
  • Higher sensitivity for diagnosis of early acute pancreatitis
  • Substitute for CT scan in patients allergic to iodinated contrast and in acute renal failure
  • Good for visualizing cholelithiasis, choledocolithiasis, congenital anomalies of the pancreas
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19
Q

According to Atlanta Classification for acute pancreatitis, state the characteristic features of moderate severity.

A
  • Transient organ failure (resolves within 48 hours)
  • Local complications or exacerbation of comorbid disease
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20
Q

State Ranson’s criteria (On admission and initial 48 hours)

Hints:
On admission (LEGAL)
Initial 48 hours (CAlvin & HOBBES)

A

A score of >3 indicates severe pancreatitis

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21
Q

What are the shortfalls of Ranson’s criteria?

A
  • Validated for alcoholic pancreatitis only -> revised Ranson’s criteria is for gallstone pancreatitis
  • Cumbersome to wait for 48 hours and difficult to assess for negative fluid balance
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22
Q

State all components of Imrie’s criteria

Hints: PANCREAS

A
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23
Q

How do we diagnose SIRS?

A
  • Based on temperature, HR, RR, and WBC
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24
Q

Describe the management of acute pancreatitis

A

Supportive treatment
1. Fluid resuscitation - with CRYSTALLOIDS (lactated ringer)
2. Monitoring (after resuscitating)
3. Pain control with analgesia -> Use opioid analgesia (TRAMADOL) other than morphine. Also, do not give NSAIDs
4. Nutrition
5. Antibiotics
6. Support for organ failure - with presence of organ failure, manage patient in ICU

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25
Q

List the early local complication of acute pancreatitis.

A
  1. Acute peripancreatic fluid collection (30-50%)
    - Due to increased vascular permeability
    - Only applied to area of peripancreatic fluid seen within the first 4 weeks after onset of interstitial edematous pancreatitis and without the feature of pseudocyst
  2. Acute necrotic collection (10-20%)
    - A collection containing fluid and necrosis associated with necrotizing pancreatitis
    - It can be divided into STERILE necrosis or INFECTED
    - Sterile necrosis -> SUPPORTIVE CARE
    - Infected necrosis -> IV ANTIBIOTICS + DRAINAGE PROCEDURES
26
Q

State the late local complications of acute pancreatitis (>4 weeks)

A
  1. Pancreatic Pseudocyst (10-20%)
    - Present as persistent pain, mass on examination, persistent increase in amylase and lipase
    - Pancreatic pseudocyst contains pure pancreatic juice (suggesting a communication with the pancreatic duct)
    - It occurs at the lesser sac, anterior wall of pseudocyst (posterior aspect of stomach), inferior wall of pseudocyst (transverse mesocolon)
  2. Walled-off Pancreatic Necrosis (WOPN)
    - A mature, encapsulated collection of pancreatic or extra-pancreatic necrosis with a well-defined inflammatory wall

Other complications:
- Hemorrhage
- Enteric fistulation
- Venous thrombosis

27
Q

List the complications associated with pseudocyst

A
  • Fistula formation
  • Hemorrhage -> Angioembolization
  • Rupture (Pancreatic ascites)
  • Obstruction, GOO
  • Infection (Pancreatic abscess)
28
Q

State the early systemic complications of acute pancreatitis

A
  • Multiple organ failure
  • Hematological (DIVC)
  • Intra-abdominal hypertension
  • Metabolic complications -> hypocalcemia, hyper/hypoglycemia
29
Q

State (2) late systemic complications of acute pancreatitis

A
  • Sepsis -> can also lead to multiple organ failure
  • Venous complications
    1. Venous thrombosis
    2. Intra-abdominal hemorrhage
30
Q

Define chronic pancreatitis

A

Inflammation, fibrosis and loss of acinar and islet cells

31
Q

State (5) etiology for chronic pancreatitis

A
  • Toxic-metabolic factors
  • Hypertriglyceridemia
  • Genetic
  • Autoimmune - Type 1 (IgG4-related) and Type 2
  • Recurrent and severe acute pancreatitis
  • Chronic obstruction of main pancreatic duct by tumors
  • Idiopathic
32
Q

Describe about the pathogenesis of chronic pancreatitis

A
  • Progressive destruction of the pancreas by repeated flare-ups of mild and subclinical types of acute pancreatitis
  • Characterized by diffuse scarring and strictures in the pancreatic duct

*Islet of Langerhans (endocrine function) have a greater resistance to injury

33
Q

State the clinical presentation of chronic pancreatitis

A
  • Abdominal pain (epigastric pain radiating to the back) - associated with nausea/vomiting
  • Pancreatic insufficiency symptoms
    1. Fat malabsorption (e.g STEATORRHEA, Vitamin ADEK and B12 deficiency)
    2. Pancreatic diabetes (late) - usually requires INSULIN, increased risk of hypoglycemia
34
Q

State (5) complications of chronic pancreatitis

A
  1. Local complications
    - Pseudocyst
    - Pancreatic ductal stones
    - Pancreatic ascites
    - Pancreatico-pleural fistula
    - Pancreatico-enteric fistula
    - Head of pancreas mass
  2. CBD Obstruction (Due to transient obstruction from pancreatic inflammation)
  3. Duodenal Obstruction (Occur due to acute pancreatic inflammation, chronic fibrotic reaction, pancreatic pseudocyst or neoplasm)
  4. Pancreatic cancer (Chronic pancreatitis -> increase risk by 2-3X)
  5. Pancreatic insufficiency (Type 1 DM)
35
Q

State the radiological investigations you would order to diagnose a case of chronic pancreatitis

A
  • CT, MRI, US -> May show calcifications, ductal dilatation, enlarged pancreas, fluid collection
  • MRCP (Diagnostic investigation of choice)
  • ERCP (Characteristic “CHAIN OF LAKES” of main pancreatic duct
  • EUS (Diagnosis of chronic pancreatitis based on ROSEMONT criteria)
36
Q

State the biochemical test to be done in evaluation of a case of chronic pancreatitis

A
  • Pancreatic secretin stimulation test
  • Postprandial pancreatic polypeptide hormone
  • Pancreatic endocrine function
  • 72hrs faecal collection for the estimation of daily faecal fat (Note for any steatorrhea)
37
Q

State the management principles of chronic pancreatitis

A
  1. Lifestyle modification
  2. Medical therapy
  3. Surgery
  • Treat underlying etiology (Stop alcohol drinking and smoking)
  • Supportive treatment (Give supplementation, diabetes management and pain relief)
  • Treat complications
38
Q

How would you treat the following complications seen in chronic pancreatitis?
1. Pancreatic pleural effusion
2. Pancreatic ascites
3. Ductal complication
4. Pseudocyst, aneurysm, fistula, local obstruction

A

Management:
1. TUBE THORACOSTOMY
2. PARACENTESIS
3. ERCP (If fail then we proceed with surgical intervention)
4. SURGICAL MANAGEMENT

39
Q

State the most common pancreatic tumour

A

ADENOCARCINOMA (95%)

40
Q

What are the modifiable risk factors of pancreatic CA?

A
  • Smoking (2.5X increased risk)
  • Diet (e.g Obesity, High fat, High meat diet, Diet low in vegetable, Alcohol)
  • Occupational exposure (e.g Chlorinated hydrocarbon solvent, Asbestos)
41
Q

State the non-modifiable factors of pancreatic CA

A
  • Family history
  • Age/Gender (e.g Age>60, male)
  • Personal history (Chronic pancreatitis, DM, IPMN)
  • Genetic predisposition
  • Others (e.g H. pylori infection, Periodontal disease, Cystic fibrosis, ethnicity, blood group)
42
Q

State the pathogenesis of pancreatic CA

A

It involves progressive genetic mutations:
- Telomere shortening -> contributing to chromosomal instability
- Mutational activation of K-RAS oncogene (early)
- Inactivation of tumor suppressor gene (p16/CDKN2A, tp53, SMAD4)

43
Q

List the symptoms of pancreatic CA

A
  • Classical Courvoisier sign
  • Obstructive jaundice symptoms +/- pain
  • New onset of DM in elderly patients
  • Endoscopy negative epigastric pain
  • Signs of malabsorption (e.g steatorrhea)
  • LOW and anorexia
  • Nausea/vomiting
  • Upper BGIT (hematemesis and/or melena) - tumour invasion into stomach/duodenum
44
Q

List the signs of advanced malignancy in pancreatic CA

A
  • Malignant pleural effusion
  • Virchow’s node (left supraclavicular node enlargement)
  • Trousseau sign (Migratory superficial thrombophlebitis) paraneoplastic
  • Sister Mary Joseph Nodule (umbilical metastatic lesion via falciform ligament)
  • Hepatomegaly (underlying liver metastasis)
  • Non-bacterial thrombotic (marantic) endocarditis
45
Q

What are the investigations to be done to diagnose pancreatic CA?

A

Biochemical
- FBC -> Look for any occult blood loss and sepsis (Increase TWC)
- U/E/Cr -> assess electrolyte abnormalities
- LFT -> confirmation of obstructive jaundice
- Amylase/Lipase -> any ongoing pancreatitis
- PT/INR -> evidence of hepatic dysfunction
- Random blood glucose test -> assess for DM
- CA19-9 (Useful as a marker for tumour recurrence during post-op follow up

Imaging
- Transabdominal US
- Tri-phasic “pancreatic protocol” CT scan
- MRI pancreas with MRCP (Use as an adjunct to CT)
- Endoscopic US + FNA Biopsy
- ERCP (KIV stenting)
- Staging laparoscopy

46
Q

How would you manage a case of pancreatic CA?

A

Best managed by a multidisciplinary approach

  1. Chemotherapy and radiotherapy
    - Neoadjuvant chemotherapy -> Used for borderline resectable pancreatic CA
    - Adjuvant chemotherapy (GEMCITABINE + oral CAPECITABINE)
    - Adjuvant radiotherapy
  2. Surgery - Curative resection
    - Pre-operative biliary drainage -> Done for patients with cholangitis or symptomatic liver dysfunction
    - Pancreaticoduodenectomy (Whipple operation)

Alternative: Pylorus-preserving Pancreaticoduodenectomy resection

47
Q

Since about 80% of patients are not suitable for curative resection, state the palliative management of pancreatic CA

A

Indication:
- Obstructive jaundice
- Upper GI tract obstruction

Surgical measures:
- Surgical bypass of obstruction -> DOUBLE BYPASS INVOLVING ANASTOMOSIS

Non-surgical palliative measures
- Palliative chemotherapy (e.g GEMCITABINE)
- Stenting

48
Q

State the complications of late stage pancreatic CA and how would you manage it

A
  • Obstructive jaundice
  • GOO
  • Pain from coeliac plexus infiltration
  • Venous thromboembolism
49
Q

List the early and late complications of Whipple’s operation

A

Early complication
- Delayed gastric emptying
- Pancreatic fistula
- Wound infection

Late complication
- Long-term exocrine insufficiency
- Gastric stasis with pylorus-preserving Whipple
- Diarrhoea resulting from autonomic nerve injury during lymph node dissection
- Endocrine insufficiency resulting in DM

50
Q

State the differentials for cystic pancreatic mass

A
  • Pancreatic pseudocyst
  • Serous cystadenoma
  • Mucinous cystadenoma and cystadenocarcinoma
  • Intraductal Papillary Mucinous Neoplasm (IPMN)
  • Solid Pseudopapillary Tumour
51
Q

State the differentials for solid pancreatic mass

A
  • Pancreatic adenocarcinoma
  • Pancreatic neuroendocrine tumours
  • Pancreatitis
  • Lymphoma (rare)
52
Q

State the weight and measurement of splenomegaly

A
  • Spleen >500g
  • > 15cm in length
53
Q

State the weight and measurement of a case of massive splenomegaly

A
  • Spleen >1000g
  • > 22cm in length
54
Q

List the ligament support of spleen with its associated organs

A
  • Splenocolic ligament - colon
  • Gastrosplenic ligament - stomach
  • Splenophernic ligament - diaphragm
  • Splenorenal ligament - kidney, adrenal and tail of pancreas
55
Q

List the blood supplies of the spleen

A
  • Splenic artery - Distributive type (70%) and Magistral type (30%)
  • Short gastric vessels
56
Q

State the differentials for splenomegaly

A
  • Infection - viral, bacterial, parasitic (e.g Schistosomiasis0, others (e.g TB)
  • Hematological - leukemia, lymphoma
  • Portal hypertension
  • Neoplastic - lymphoma, myeloproliferative disorders
  • Inflammatory - rheumatoid, systolic lupus, amyloidosis
57
Q

What are the indications for splenectomy?

A
  • Splenic trauma/Splenic rupture
  • Splenic abscess
  • Splenic cyst
  • Neoplasm
  • Hematological disorders
58
Q

What are the vaccinations given prior to a splenectomy?

A
  • Streptococcus pneumoniae
  • H. influenzae
  • N. meningitidis

Given at least 2 weeks prior or within 7-10 days after emergent splenectomy

59
Q

What post-operative splenectomy patient should be vaccinated on?

A
  • Yearly influenza vaccine
  • Vaccinate against pneumococcus, maningococcus C (both repeated every 5 years) and Hib (repeated every 10 years)
  • +/- long term oral penicillin prophylaxis
60
Q

List the complications of splenectomy based on the following classification
- Intra-operatively
- Early
- Late

A

Surgery (13 decks)

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