Acute pancreatitis and chronic* Flashcards
Describe the anatomy and location of pancreas
- Retroperitoneal endocrine
& exocrine organ - Lies in the upper
abdomen, in transpyloric
plane (L1) - Divided into head, neck,
body, tail - 2 duct openings –
Santorini and Wirsung
RUQ. Endocrine and exocrine organ.
Just anterior to abdominal aorta and vena cava
Head of pancreas is adjacent to descending duodenum, and just anterior to common bile duct.
Tail is medial to spleen.
Inferior to liver, posterior to stomach.
A retroperitoneal organ, except for tail.
When the pancreas is inflamed it affects both cavities.
anterior: lesser sac, pylorus, D1, SMA AND VEIN, transverse mesocolon, stomach
superior: splenic a
laterall R: D2, ampulla of vater
Lateral eft: spleen hlum
posterior: lcrus diaphragm, psoas, R renal vein, L renal vessels, IVC, bile duct, spleen, L kidney and adrenal, coelaic plexus, IMV, SV, PB, SMA and vien, aorta
Describe pancreas blood supply, lymphatics, embryology
Splenic branches
ant and post superior and inferior pancreaticoduodenals;
drainage by ant and post superior pancretatico, inferior, splenic vein
Lymphatics: splenic, pyloric, pancreatodudoenal , inferior pancreatic and superior pancreatic, superior mesenteric/aortic nodes–> coleoac
Foregut - 2 buds: ventral from hepatic diverticulum, dorasal from dorsal surface of dupdenu,
Describe SIRS and MODS
Heart rate >90
* Temperature <36 or >38
* WCC <4 or >12
* Respiration Rate >20 or PaCO2 <32mmHg
* 2 or more of the above constitutes SIRS
vMulti-Organ Dysfunction Syndrome
* Impairment of 2 or more organ systems whereby homeostasis
cannot be maintained without therapeutic intervention
Describe symptoms and investigations for acute pancreatitis
- epigastric pain, may radiate to back (no radiation in chronic)
- nausea and vomiting
- +- alcohol history
- HR up, temperatuere up, RR up,
- bloods; CT if bloods ambiguous
- assess severity of comps around day 2-3
- ID underlying cause using US, lipid syudoes, calcium
note chrronic present s with adbominal pain, polyuria/dipsisa, steatorrhea
List diagnostic criteria and principels f management
- 2 or more of the following:
– Lipase 3x normal
– Consistent history and clinical findings
– Radiological evidence of pancreatitis - Supportive care, no rx resuscitation
- Look out for complications
- Find and underlying cause
-icu: organs failure, local or systemic comps, cormorbid
Initial treamtnet and remament coyrse
Airway
* Breathing – oxygen
* Circulation – cannulas, IV fluids
* Disposition – admit? Who to call?
* Antibiotics? not ususally unless infiltratied necrotic tissue
* Abnormal LFTs -
Steowise treatment: aggressive fluid resus-> enteral nutrition if no oral tolerance –> antibiotics if documented infection –> minimally invasive therapy for local complications
Suspected infected necrotising pancreatitsi, temposide with Abx —> laparototomy if comps –> percutaneous drain or endoscopic drain, repeat if not resolved –> debridment MIS or endo, VARD –> lapartomoy last resort
Managing pancreatic collections
- Collections usually managed with drains
- Evidence shows that in pancreatitis, delay drainage until
there is a wal
evolution: acute peripancreatic collcection-> acute necrotic -> pseudocyst -> wall ed off necrotsis
Managing pseudocyst
Surgical
* Percutaneous drainage under imaging
guidance
* Endoscopic (US guided cyst-gastrostomy
What does the pancreas do (exocrine)?
Trypsin – cleaves protein (arginine/lysin) into
polypeptides. Peptidases further break down at the brush border. Stored as trypsinogen
(precursor)
Trypsin is able to cleave and activate other
protease and lipase enzymes.
Describe the activation pathway of enzymes
- trypsinogen released first
- enterokinase activates converstion to trypsin
- enterokinase is a duodenal wall enzyme located on the brush border
- it is not the only regulator of trypsin activation; trypsin can auto-activate
- from there trypsin helps convert several enzymes to their active form including
- kallikrein
- chemotrypsin
- elastase
- carboxypeptidase
- phospholipase A2
- as well as activation of acinar cells, duct cells and inflammatory cells via trypsin receptor PAR-2
- the action of trypsin is inhibited by PSTI
Describe digestion breify and how the pancreas is protected from autodigestion
i.e.
Carbohydrates and amylases, fats and lipases, proteins and proteases.
Also… autodigestion.
Pancreas is usually protected from autodigestion by mucus.
In autodigestion protease breaks down muscle, lipase breaks down cell wall and amylase leads to membrane integrity loss.
What is pancreattis?
Pancreatitis is a process of self-digestion
- mild
- severe- + fatty necrosis and haemorrhaage
List common and rare causes of AP
- gallstones
- alcohol
- hypertriglyceridemia
- genetics
- drugs
- autoimmune
- ERCP
Rarer causes of AP
- trauma
- infection
- surgical complication
- obstruction
- associated conditions e.g. diabetes, obesity, smoking
DEscribe the pathophysiology of acute; course of acute and chronic pancreatitis
General pathophysoology:
- duct obstruction e.g. cholelithiasis or chornic alcoholism –> ductal concretion/ampullary obstruction –> interstitial oedema –> impaired blood flow –> oschaemia
- acinar cell injury e.g ischameia drugs alcojhpol viruses –> release of interacellular proenzymes and lysosomal hydrolases –> activation of enxymes either intra or extracellularly
- defective IC trransport e.g. metabolic injury, alcohol, duct obstriction –> delivery of proenzyemes to lysosomes –> IC activation fo enxymes
aLL culminatin in acinar cell injury, activation of enzymes: intetitial infalmmation, oedema, proteolysis, fat necrosis, haemorrage (elastase) = acute pancreatitis
“in pancreatic parenchyma stimulus activates prteolytic enzymes that diggest pancreatic and peri-pancreatic tissuse”
Can be interstitial (85%) or necrotising (15%)
Interstitial – low mortality, transient organ failure, resolution of fluid infiltration or pseudocyst
Necrotising – can be transient or persistent organ failure. Higher mortality.
Treatment – aggressive fluid resuscitation to restore perfusion
Complications – fluid moving to other organs (lungs, stomach, peritoneum) requiring intubation.
Mortality – half of all deaths are in first two weeks due to multiple organ failure. Other half of
deaths occurs after 2 weeks due to pancreatic and extra-pancreatic infections.
chronic
exocrine pancreatic insufficiency. Symptoms include malnourishment, weight loss,
fatigue. Bacteria will eat undigested food causing bacterial overgrowth and excessive gas from fermentation. Give pancreatic enzymes.
Endocrine pancreatic insufficiency. By no remaining islets. Different to type 2 diabetes, in which insulin is plentiful but organs are resistant to effects.
Pain can refer to left shoulder (for tail of pancreas)
Descrube the treatment of AP
- 24h: aggressive fluid resus
- enternal nutrition after day 5 if no tolerance for oral feeding
- from 2 weeks: antibiotics for documented infection
- from 4 weeks minimally invasive therapy for local complications eg infected necrosis
