pancreas Flashcards
(92 cards)
1
Q
Q: What percentage of the pancreatic mass is made up by the exocrine pancreas?
A
A: About 85%.
2
Q
Q: What percentage of the pancreas is accounted for by extracellular matrix?
A
A: 10%.
3
Q
Q: What percentage of the pancreas is made up of blood vessels and major ducts?
A
A: 4%.
4
Q
Q: What percentage of the pancreas is comprised of endocrine tissue?
A
A: 2%.”Q: How much pancreatic juice does the pancreas secrete daily?
5
Q
Q: What are the characteristics of pancreatic juice?
A
A: Colorless, odorless, alkaline, and isosmotic.
6
Q
Q: What is pancreatic juice a combination of?
A
A: Acinar cell and duct cell secretions.
7
Q
Q: What do acinar cells secrete?
A
A: Amylase, proteases, and lipases.
8
Q
Q: What types of food does pancreatic juice help digest?
A
A: Carbohydrates, proteins, and fats.”Q: In what form is pancreatic amylase secreted?
9
Q
Q: What digestive process does pancreatic amylase complete?
A
A: The process already begun by salivary amylase.
10
Q
Q: What is unique about amylase among pancreatic enzymes?
A
A: It is the only pancreatic enzyme secreted in its active form.
11
Q
Q: What does amylase hydrolyze starch and glycogen into?
A
A: Glucose, maltose, maltotriose, and dextrins.
12
Q
Q: How is trypsinogen activation within the pancreas prevented?
A
A: By the presence of inhibitors secreted by the acinar cells.
13
Q
Q: What does pancreatic lipase hydrolyze triglycerides into?
A
A: 2-monoglyceride and fatty acid.
14
Q
Q: In what form is pancreatic lipase secreted?
A
A: In an active form.
15
Q
Q: What is the hallmark of acute pancreatitis?
A
A: Acute pancreatic inflammation associated with little or no fibrosis.
16
Q
Q: What is the range of severity in acute pancreatitis?
A
A: From mild self-limiting inflammation to critical disease.
17
Q
Q: What are the severe complications of critical acute pancreatitis?
A
A: Infected pancreatic necrosis, multiple organ failure, and a high risk of mortality.
18
Q
Q: What initiates pancreatitis according to prevalent belief?
A
A: The activation of digestive zymogens inside acinar cells, causing acinar cell injury.
19
Q
Q: What is an important aspect of acute pancreatitis pathophysiology?
A
A: The mechanism by which pancreatic events induce systemic inflammation and multiorgan failure.
20
Q
Q: How is organ failure scored in acute pancreatitis?
A
A: Using the Marshall or Sequential Organ Failure Assessment (SOFA) systems.
21
Q
Q: Which three organ systems are most frequently involved in acute pancreatitis?
A
A: Cardiovascular, respiratory, and renal.
22
Q
A
23
Q
Q: What are the most common causes of acute pancreatitis?
A
A: Gallstones and alcohol, accounting for up to 80% of cases.
24
Q
Q: Is it possible to diagnose acute pancreatitis without gallstones or alcohol?
A
A: Yes, it is not uncommon.
25
Q: What types of trauma can cause acute pancreatitis?
A: External trauma, surgical trauma, and endoscopic retrograde cholangiopancreatography.
26
Q: What ischemic factors can lead to acute pancreatitis?
A: Hypoperfusion, atheroembolic, and vasculitis.
27
Q: What are some causes of pancreatic duct obstruction?
A: Neoplasms, pancreas divisum, and ampullary or duodenal lesions.
28
Q: What viral infections can cause acute pancreatitis?
A: Mumps and Coxsackie B.
29
Q: What other factors can contribute to acute pancreatitis?
A: Venom, drugs, and idiopathic causes.
30
Q: How does the median age of onset of acute pancreatitis vary with etiology?
A: Alcohol and drug-induced pancreatitis typically present in the third or fourth decade, while gallstone and trauma-induced disease present in the sixth decade.
31
Q: What is a significant gender difference in the causes of acute pancreatitis?
A: Males more often have alcohol-induced pancreatitis, while females more often have gallstone-induced pancreatitis.
32
Q: What percentage of patients with acute pancreatitis have gallstones in their feces within 10 days of an attack?
A: 88% compared to 11% in those without acute pancreatitis.
33
Q: What is the 'common channel' hypothesis regarding gallstones and pancreatitis?
A: It suggests a gallstone lodged in the distal common channel allows bile to reflux into the pancreatic duct, but this cannot be reliably reproduced experimentally.
34
Q: How might a gallstone cause acute pancreatitis through duct obstruction?
A: By obstructing the pancreatic duct, leading to ductal hypertension and potential minor ductal disruption.
35
Q: What happens due to ductal hypertension caused by gallstones?
A: It may cause extravasation of pancreatic juice into the interstitium, promoting enzyme activation.
36
Q: What is the role of occult microlithiasis in idiopathic acute pancreatitis?
A: It is probably responsible for up to half of those with idiopathic acute pancreatitis.
37
Q: How is alcohol ingestion related to acute pancreatitis?
A: Alcohol ingestion is associated with acute pancreatitis, while sustained ingestion can lead to recurrent acute pancreatitis and chronic pancreatitis in susceptible individuals.
38
Q: What effect does ethanol have on pancreatic acinar cells?
A: Ethanol is a metabolic toxin that causes a brief secretory increase followed by inhibition.
39
Q: How does ethanol affect ductal permeability?
A: Ethanol induces ductal permeability, allowing prematurely activated enzymes to damage the pancreatic parenchyma.
40
Q: What changes does ethanol cause in pancreatic juice composition?
A: Ethanol increases protein content, decreases bicarbonate levels, and reduces trypsin inhibitor concentration.
41
Q: What are some treatments that can result in acute pancreatitis?
A: Pancreatic biopsy, exploration of the extrahepatic biliary tree and ampulla of Vater.
42
Q: Which surgical procedures are associated with the risk of acute pancreatitis?
A: Distal gastrectomy, splenectomy, colectomy, nephrectomy, aortic aneurysm repair, and retroperitoneal lymphadenectomy.
43
Q: What should be considered in any patient with idiopathic acute pancreatitis?
A: A pancreatic or periampullary tumor.
44
Q: What percentage of patients with acute pancreatitis have a pancreatic tumor?
A: Approximately 1% to 2%.
45
Q: What can an episode of acute pancreatitis indicate regarding a pancreatic tumor?
A: It can be the first clinical manifestation of the tumor.
46
Q: What types of drugs are known to cause acute pancreatitis?
A: Certain drugs, including thiazide diuretics, furosemide, estrogens, and azathioprine.
47
Q: Name some additional drugs that can lead to acute pancreatitis.
A: L-asparaginase, 6-mercaptopurine, methyldopa, sulfonamides, tetracycline, pentamidine, procainamide, nitrofurantoin, dideoxyinosine, valproic acid, and acetylcholinesterase inhibitors.
48
Q: What scoring systems are used to identify high-risk patients with acute pancreatitis?
A: Ranson’s Criteria and Modified Glasgow criteria.
49
Q: How are Ranson’s Criteria and Modified Glasgow criteria assessed?
A: They use clinical and biochemical parameters scored over the first 48 hours of admission.
50
Q: What is considered 'predicted severe' disease in these scoring systems?
A: When there are 3 or more positive criteria.
51
Q: What does the Bedside Index for Severity of Acute Pancreatitis (BISAP) include?
A: Blood urea nitrogen (> 25 mg/dl), impaired mental status (GCS <15), presence of SIRS, age >60 years, and pleural effusion.
52
Q: What are the four categories of severity in acute pancreatitis?
A: NO ORGAN FAILURE: MILD, TRANSIENT ORGAN FAILURE: MODERATE, PERSISTENT ORGAN FAILURE with NO/LOCAL COMPLICATION: SEVERE, PERSISTENT ORGAN FAILURE with INFECTED LOCAL COMPLICATION: CRITICAL.
53
Q: What is the cardinal symptom of acute pancreatitis?
A: Pain.
54
Q: How quickly does pain develop in acute pancreatitis?
A: It develops quickly, reaching maximum intensity within minutes.
55
Q: How long does the pain associated with acute pancreatitis persist?
A: It can persist for hours or even days.
56
Q: How is the pain in acute pancreatitis characterized?
A: The pain is frequently severe, constant, and refractory to usual doses of analgesics.
57
Q: Where is the pain usually experienced in acute pancreatitis?
A: It is usually first felt in the epigastrium but may localize to either upper quadrant or felt diffusely throughout the abdomen.
58
Q: How often does the pain in acute pancreatitis radiate to the back?
A: It radiates to the back in about 50% of patients.
59
Q: What position may provide relief for some patients with acute pancreatitis?
A: Sitting or leaning forwards.
60
Q: What are the diagnostic criteria for acute pancreatitis?
A: Abdominal pain consistent with acute pancreatitis and elevation of serum amylase or lipase (>3 times upper limit of normal).
61
Q: When is imaging required for the diagnosis of acute pancreatitis?
A: When the diagnostic criteria are not met, imaging (usually by contrast-enhanced CT) is required.
62
Q: When does serum amylase concentration increase in acute pancreatitis?
A: It increases almost immediately with the onset of the disease and peaks within several hours.
63
Q: How long does serum amylase remain elevated?
A: It remains elevated for 3 to 5 days before returning to normal.
64
Q: What can happen with increasing severity of acute pancreatitis?
A: Intravascular fluid loss may become life-threatening due to sequestration of edematous fluid in the retroperitoneum.
65
Q: What is a consequence of hemoconcentration in severe acute pancreatitis?
A: It results in an elevated hematocrit.
66
Q: What bleeding manifestations can occur in severe cases?
A: Bleeding may occur into the retroperitoneum or peritoneal cavity, leading to Cullen’s sign (bluish discoloration around the umbilicus) or Grey Turner’s sign (in the flanks).
67
Q: What severe fluid loss can lead to prerenal azotemia?
A: Elevated blood urea nitrogen and creatinine levels.
68
Q: What metabolic imbalances may occur in acute pancreatitis?
A: Hyperglycemia, hypoalbuminemia, and hypocalcemia, which can produce tetany.
69
Q: What three factors can predict 'harmless' acute pancreatitis upon admission?
A: Absence of rebound tenderness or guarding, normal hematocrit, and normal serum creatinine.
70
Q: Why should morphine be avoided in acute pancreatitis?
A: Because it can cause sphincter of Oddi spasm.
71
Q: What is the most important intervention in the early management of acute pancreatitis?
A: Fluid therapy to restore and maintain circulating blood volume.
72
Q: What type of fluid is probably best for resuscitation in acute pancreatitis?
A: A balanced crystalloid.
73
Q: What should fluid therapy aim to restore in acute pancreatitis?
A: Normal blood volume, blood pressure, and urine output.
74
Q: What is the established practice regarding antibiotics in acute pancreatitis?
A: The use of broad-spectrum antibiotics to treat established infection.
75
Q: What controversy surrounds the use of antibiotics in acute pancreatitis?
A: The use of prophylactic antibiotics.
76
Q: What has the overuse of antibiotics been associated with?
A: A rise in fungal infections and resistant organisms.
77
Q: What is the current approach to nutrition in acute pancreatitis?
A: It is no longer acceptable to 'rest the pancreas' by avoiding enteral nutrition.
78
Q: When should enteral nutrition be commenced in acute pancreatitis?
A: After initial fluid resuscitation and within the first 24 hours of admission.
79
Q: How can enteral nutrition be introduced?
A: Through a nasogastric tube.
80
Q: How should enteral nutrition be increased?
A: In a step-wise fashion over 2 to 3 days.
81
Q: What are the local complications of acute pancreatitis?
A: Local complications include pancreatic phlegmon, pancreatic abscess, pancreatic pseudocyst, pancreatic ascites, and involvement of adjacent organs (hemorrhage, thrombosis, bowel infarction, obstructive jaundice, fistula formation, mechanical obstruction).
82
Q: What are the systemic complications of acute pancreatitis?
A: Systemic complications include pulmonary issues (pneumonia, atelectasis, acute respiratory distress syndrome, pleural effusion), cardiovascular issues (hypotension, hypovolemia, sudden death, nonspecific ST-T wave changes, pericardial effusion), hematologic issues (hemoconcentration, disseminated intravascular coagulopathy), GI hemorrhage (peptic ulcer, erosive gastritis, portal vein or splenic vein thrombosis with varices), renal issues (oliguria, azotemia, renal artery/vein thrombosis), metabolic issues (hyperglycemia, hypocalcemia, hypertriglyceridemia, encephalopathy, sudden blindness), central nervous system issues (psychosis, fat emboli, alcohol withdrawal syndrome), and fat necrosis (intra-abdominal saponification, subcutaneous tissue necrosis).
83
Q: What is chronic pancreatitis?
A: An incurable, chronic inflammatory condition that is multifactorial in etiology, highly variable in presentation, and challenging to treat.
84
Q: What are some etiologies of chronic pancreatitis?
A: Genetic mutations, alcohol exposure, duct obstruction (due to trauma, gallstones, tumors), metabolic diseases (hyperlipidemia, hyperparathyroidism), and autoimmune disease.
85
Q: What does the TIGAR-O scheme categorize?
A: Chronic pancreatitis according to risk factors and etiologies.
86
Q: What are the categories in the TIGAR-O scheme?
A: a) Toxic-metabolic, b) Idiopathic, c) Genetic, d) Auto-immune, e) Recurrent and severe acute pancreatitis, f) Obstructive.
87
Q: What is chronic calcific (lithogenic) pancreatitis?
A: The largest subgroup in the classification scheme proposed by Singer and Char.
88
Q: What characterizes chronic obstructive pancreatitis?
A: Chronic inflammatory changes caused by compression or occlusion of the proximal ductal system by tumors, gallstones, posttraumatic scars, or inadequate duct caliber (e.g., pancreas divisum).
89
Q: What is chronic inflammatory pancreatitis?
A: Characterized by diffuse fibrosis and a loss of acinar elements with predominant mononuclear cell infiltration throughout the gland.
90
Q: What is tropical (nutritional) pancreatitis?
A: A form of chronic pancreatitis prevalent among adolescents and young adults in tropical regions, characterized by abdominal pain, brittle pancreatogenic diabetes, and large pancreatic duct stones.
91
Q: What is asymptomatic pancreatic fibrosis?
A: Pancreatic fibrosis seen in some asymptomatic elderly patients, in tropical populations, or in asymptomatic alcohol users.
92
Q: What defines idiopathic pancreatitis?
A: When a definable cause for chronic pancreatitis is lacking, typically seen in young adults and adolescents without a family history but possibly with spontaneous gene mutations.
