Acute Pancreatitis Flashcards
(114 cards)
1
Q
what is the difinition of acute inflammation of the pancreas ?
A
abdominal pain and elevated pancreatic enzymes
2
Q
what are the two main etiologies behind acute pancreatitis ?
A
gallstones and alcohol consumption
2/3 of cases
3
Q
explain the mechanism behind biliary lithiasis
A
- obstruction of Ambullae Vatter with gallstones
- Transitory obstruction +/- edema of Amp. Vatter
4
Q
Where does alcohol metabolization occur?
A
Liver (oxidative pathway) and Pancreas (non-oxidative pathway)
5
Q
What is produced in the pancreas during alcohol metabolization?
A
Toxic metabolites (acetaldehyde and fatty acid esters)
6
Q
What do these toxic metabolites (acetaldehyde and fatty acid esters) do in the pancreas?
A
accumulate
7
Q
What are four mechanisms by which alcohol contributes to acute pancreatitis?
A
Increased acinar cell sensibility to cholecystokinin (CCK)
Increased pancreatic and lysosomal enzyme synthesis in acinar cells, secondary to toxic metabolite accumulation
Altered calcium homeostasis
Activation of stellate cells - increased
production of collagen and proteins of ECM
8
Q
What are two metabolic causes of acute pancreatitis (AP)?
A
Hypertriglyceridemia and hypercalcemia
9
Q
At what triglyceride level does hypertriglyceridemia (HTG) induce AP?
A
> 1000mg/dL
10
Q
How does hypertriglyceridemia (HTG) lead to AP?
A
Pancreatic lipase metabolizes triglycerides (TRG) into free fatty acids (FFA), which are toxic in high concentrations.
11
Q
What are the two types of hypertriglyceridemia (HTG)?
A
Primary HTG (familial/hereditary) and Secondary HTG
12
Q
Give examples of secondary hypertriglyceridemia (HTG).
A
Uncontrolled diabetes, drugs (estrogen-tamoxifen), pregnancy, alcohol
13
Q
What combination often leads to AP?
A
Primary HTG + Secondary cause
14
Q
How does hypercalcemia contribute to AP?
A
Intraductal calcium deposits + activation of trypsinogen inside acinar cells.
15
Q
What is the typical latency period for drug-induced AP?
A
After weeks/months of exposure
16
Q
What are some mechanisms by which drugs can induce AP?
A
Immune reactions, direct toxic effect on the pancreatic duct, ischemia, ↑ viscosity of pancreatic juice, intravascular thrombosis
17
Q
Give examples of drugs/drug classes and their associated mechanisms for inducing AP.
A
Immune reactions: aminosalicylates, 6MP
Direct toxic effect on pancreatic duct: diuretics
Ischemia, ↑ viscosity of pancreatic juice: diuretics
Intravascular thrombosis: estrogens
low mortality and good prognosis
18
Q
List some viruses that can cause acute pancreatitis
A
Mumps, Coxsackie, CMV
19
Q
What bacteria is associated with acute pancreatitis?
A
Mycobacterium
20
Q
Name a fungus that can cause acute pancreatitis.
A
Aspergillus
21
Q
What parasite is associated with acute pancreatitis?
A
Toxoplasma
22
Q
What toxin is specifically mentioned as a cause of acute pancreatitis?
A
Scorpion venom
23
Q
What conditions can ischemic pancreatitis be associated with?
A
Vasculitis and Hemorrhagic shock
24
Q
Name a congenital defect of the pancreatic ducts that can lead to acute pancreatitis.
A
pancreas divisum
25
Describe the duct formation in Pancreas Divisum.
Formation of a major (dorsal) Santorini duct that drains through papilla minor
26
What does Pancreas Divisum lead to?
**Intraductal hypertension**
27
What genetic condition is associated with Pancreas Divisum?
cystic fibrosis
28
Iatrogenic causes ?
post ERCP
29
How can hereditary pancreatitis present?
AP in childhood, without a clear cause OR Recurrent AP at a young age (<35yo)
30
What does the PRSS1 gene mutation do, and what does it codify?
Codifies TRIPSINOGENUL and causes premature activation of pancreatic zymogens inside the pancreas.
31
What does the CFTR gene mutation do, and what does it stand for?
Cystic Fibrosis Transmembrane Conductance Regulator, leads to viscous pancreatic juice causing ductal obstruction.
32
What does the SPINK1 gene mutation affect?
Pancreatic secretory trypsin inhibitor.
33
Why is pancreatic duct injury rare?
Retroperitoneal localization of the pancreas
34
What can abdominal trauma cause
Can injure the pancreas
35
What can rupture of the pancreatic duct lead to?
Ascites
36
What can healing after pancreatic duct injury result in?
Ductal strictures
37
What are zymogens?
Inactive digestive enzymes secreted by the pancreas
38
How are zymogens deposited?
As vacuoles
39
Where are zymogens secreted?
In the duodenum through the pancreatic duct
40
What influences zymogen activity
pH-dependent activity
41
What are the mechanisms for neutralization of prematurely activated pancreatic enzymes?
Pancreatic secretory trypsin inhibitor (PSTI/SPINK) - neutralizes 20% of trypsin activity
Autolysis of premature form (deficient in hereditary forms of AP)
Mesotrypsin and Y enzyme: lytic proteases of trypsin
Nonspecific antiproteases: alpha-1
antitrypsin and alpha-2 macroglobulin
42
What is the first step in the pathophysiology of pancreatitis?
Increased lysosomal synthesis
43
What is inhibited at the apical pole in the pathophysiology of pancreatitis?
Zymogen exocytosis
44
What cytokine independently activates zymogens?
TNF-alpha
45
What enzyme from lysosomes activates trypsinogen?
Cathepsin B
46
What do Cathepsin B and trypsin activate when released in the cytosol?
Protein-kinases
47
What is a consequence of activated protein-kinases?
Cytochrome c mediated apoptosis (Mithocondria)
Membrane rupture, enzymatic leakage and necroptosis
48
What does Ca2+ released from ER promote physiologically
Apical exocytosis of zymogens and mitochondrial ATP synthesis
49
ow is accumulation of Ca2+ prevented?
SERCA - ATP-dep: reintroduces Ca2+ in the SER
PMCAs - ATP-dep: lowers intracellular Ca2+
50
What is a pathological consequence of intraacinary hypercalcemia
Premature activation of trypsinogen
51
What are the causes of intraacinary hypercalcemia?
Toxic effect of alcohol and biliary salt on SERCA and PMCA
Ductal hypertension (activation of mechanoreceptor-PIEZO1) - Ca2+ influx
52
What does intraacinary hypercalcemia produce?
Premature activation of trypsinogen
Perturbed membrane potential -> decreased ATP production
Hypofunction of ATP-dep SERCA and PMCAs, accumulation Ca2+
Acinar necrosis/apoptosis due to low ATP reserve
53
Acute pancreatitis evolution:
Intraacinary activation of proteolytic enzymes
Local microcirculation lesions
Leucocyte chemotaxis, cytokine secretion și ROS
SIRS
Bacterial translocation
54
What is a primary symptom in acute pancreatitis
Abdominal pain
55
What are the possible onsets of abdominal pain in acute pancreatitis
Acute (biliary AP) or progressive (alcoholic, metabolic, hereditary AP
56
What is the typical localization of abdominal pain in acute pancreatitis?
epigastric
57
What are the possible radiations of pain in acute pancreatitis?
Posterior, left hypochondrium, right hypochondrium
58
What antalgic position may a patient with acute pancreatitis assume?
Thorax anteflexion, orthostatism (standing upright)
59
What are some other symptoms that may accompany abdominal pain in acute pancreatitis?
Nausea and vomiting
60
What respiratory symptom can occur in acute pancreatitis?
Dypnea
61
What is the cause of dyspnea in acute pancreatitis
Diaphragm inflammation
## Footnote
restrictive syndrome
62
What thoracic condition can occur in acute pancreatitis
Left pleural effusion
63
What severe respiratory condition can develop as a result of SIRS in acute pancreatitis?
ARDS (Acute Respiratory Distress Syndrome)
64
What might jaundice indicate in acute pancreatitis?
Biliary AP or edema of the head
65
What do subcutaneous nodules indicate in acute pancreatitis
Fat tissue necrosis
66
What are the characteristics of subcutaneous nodules?
Red, painful, upper extremities
67
What do xanthelasma/xanthoma suggest in acute pancreatitis
Metabolic AP (Hypertriglyceridemia - HTG)
68
What conditions can cause parotid hypertrophy?
Alcoholic AP, Epidemic parotitis (Mumps)
69
What liver condition might be present in alcoholic AP?
hepatomegaly
70
What is a common sign of inflammation in acute pancreatitis?
Fever
## Footnote
in Severe AP
71
What change in blood pressure can occur in acute pancreatitis?
Hypotension (hTA)
## Footnote
in severe AP
71
What change in respiration rate can occur in acute pancreatitis?
Tachypnea
## Footnote
in severe AP
72
What skin discoloration can occur in severe cases of acute pancreatitis?
Cyanosis
## Footnote
Severe AP
73
What might abdominal enlargement suggest in acute pancreatitis?
Pancreatic ascites (pancreatic cyst rupture or pancreatic duct rupture)
73
What abdominal sign is associated with "paralitic" ileus?
Meteorism
74
What is the name of the paraumbilical ecchymoses seen in acute pancreatitis
Cullen sign
75
What is the name of the ecchymoses seen on the flanks in acute pancreatitis
Grey Turner sign
76
What might be noted on palpation of the abdomen in acute pancreatitis
Sensibility/pain at profound palpation in the epigastrum
77
What might dullness on percussion indicate?
Ascites
78
What might a hyperresonant sound on percussion indicate?
Ileus
79
Paraclinic explorations
Serology
Imagistic investigations
- Abdominal x-ray
- Abdominal US
- Abdominal CT
- ColangioMRI
80
What are the key characteristics of serum amylase in diagnosing acute pancreatitis?
Low specificity
Increases 6-12h from onset
T ½ short, 10h
81
What are the key characteristics of serum lipase in diagnosing acute pancreatitis?
High sensitivity and specificity
Increases 4-8h from onset
T ½ long, 8-14 days
82
What inflammatory markers are elevated in acute pancreatitis, and what does a high CRP at 48 hours indicate
CRP (>150mg/L at 48 h **severe AP**)
IL-6
IL-8
TNF
83
What is the typical abdominal x-ray finding in acute pancreatitis?
normal
83
What is a "sentinel loop" on an abdominal x-ray, and what does it indicate?
Dilation of a segment of the intestine secondary to ileus
Helps localize the inflammatory process (e.g., upper abdomen in AP)
84
What are other common lab findings in acute pancreatitis, besides amylase and lipase?
Leucocytosis and Ht (hemoconcentration)
Hypo/hyperglycemia
Elevated urea, creatinine
Low SpO2
84
What is the cause of hemoconcentration in acute pancreatitis?
Extravasation of intravascular fluid into surrounding tissue
85
What are common chest x-ray findings in acute pancreatitis?
Ascended left hemidiaphragm
Left pleural effusion
Basal atelectasis
86
What are the advantages and limitations of abdominal ultrasound in evaluating acute pancreatitis?
Widely spread and easy to use, but possible difficulty in evaluating the pancreas due to abdominal meteorism.
87
What are typical ultrasound findings in acute pancreatitis
Enlargement of the pancreas, nonhomogeneous echotexture, hyperechogenicity/hypoechogenicity (edematous AP).
Peripancreatic liquid.
88
When is an abdominal CT scan indicated in acute pancreatitis?
Only used if diagnosis is uncertain.
Mandatory if clinical deterioration after 48-72h to assess local complications (collections/necrosis).
88
What are the advantages and disadvantages of abdominal and cholangio-MRI in evaluating acute pancreatitis?
Pricy, not routinely used.
Superior to CT in evaluating biliary cause and local complications
89
**Positive diagnosis**
Clinic criterion: characteristic abdominal pain
Biologic criterion: Amylase or Lipase x3 normal value
Imagistic criterion: characteristic aspect (US, CT, IRM)
2/3 criteria are needed for diagnosis
90
Differential diagnosis
1. Peptic ulcer
No radiation, intermittent , normal amylase/lipase
2. Biliary colic/ acute cholecystitis
Radiation in RH, right shoulder
Murphy sign: pain when palpating the cystic point
Vesicular hydrops
3. Appendicular colic
Epigastric pain (Initially), later- right iliac fossa
4. Intestinal occlusion
Fecaloid vomit, absent intestinal sounds
Amylase, lipase <3x NV
Abdominal x-ray: hydro-aeric levels and intestinal distension
5. Mesenteric ischemia
Intense periumbilical pain
Risk factors: elderly, systemic atheromatosis, arrythmia
Amylase, lipase <3x NV (CT for positive diagnosis)
6. Intestinal perforation
Acute onset of pain
Signs of peritoneal irritation: abdominal guarding
Amylase <3x NV
Abdominal x-ray: pneumoperitoneum (air in the peritoneum)
7. Acute hepatitis
Pain in RH ( painful hepatomegaly due to Glisson capsule distension)
AST,ALT> 1000 UI
8. Inferior acute myocardial infarction
9. Lower left inferior lobe pneumonia
10. Renal colic
90
treatment
hospitalization
fluid replacement
pai control
mandatroy fasting
91
What is the recommended fluid replacement strategy for acute pancreatitis?
"Aggressive" hydration (5-10mL/kg/h crystalloid solution - normal saline or Ringer Lactate).
91
What are the benefits of aggressive hydration in acute pancreatitis?
Accelerates enzymatic and inflammatory clearance.
Maintains effective circulating plasma volume.
Most important initial management.
Reduces mortality in the first 24h (reduces SIRS, MSOF incidence).
92
What are the risks associated with aggressive hydration in acute pancreatitis?
Risk of pulmonary edema in cardiac patients.
Risk of compartment syndrome (aggressive hydration no more than 48-72h).
92
What are the therapeutic goals of fluid replacement in acute pancreatitis?
HR < 120 bpm, mAP > 65 mmHg, lowering BUN and Hct, normal diuresis.
## Footnote
revaluation after 6-24 h
93
When should Ringer Lactate be avoided during fluid replacement in acute pancreatitis?
In metabolic AP (hypercalcemia) due to its calcium content.
94
What class of medications is used for pain management in acute pancreatitis?
Opioid analgesics.
95
What is a preferred opioid analgesic in acute pancreatitis, and why
Fentanyl (25-50 μg) due to its safe renal profile
95
What are the potential drawbacks of using morphine for pain management in acute pancreatitis?
It can induce **spasm of the Oddi sphincter,** potentially aggravating acute pancreatitis.
96
What is an alternative opioid analgesic to morphine in acute pancreatitis, and why is it preferred?
Meperidine/Pethidine is preferred due to its higher safety profile (low T ½, no Oddi spasm).
97
What is a significant potential side effect of opioid analgesics?
Respiratory depression
98
Why is fasting mandatory in acute pancreatitis?
To stop stimulating pancreatic secretion.
99
When is a nasogastric tube indicated in acute pancreatitis?
To reduce gastric secretion or in patients with ileus.
100
What are the criteria for reinitiating oral alimentation in acute pancreatitis?
No pain (without analgesics)
No nausea or vomiting
No ileus
Hunger sensation
101
What is the preferred order of nutritional support in acute pancreatitis?
Oral nutrition > enteral nutrition > parenteral nutrition.
102
What is the initial diet progression after reinitiating oral alimentation in acute pancreatitis?
Initially, liquid diet, followed by a hypolipidic diet, low quantity meals.
103
When is enteral nutrition via naso-jejunal tube indicated in acute pancreatitis?
In severe forms of AP (without digestive tolerance).
104
Treatment of local complication
Treatment of necroses
Treatment of pseudocysts
Treatment of pseudoaneurysms
Treatment of thromboses
Treatment of pancreatic ascites
105
