Term
| 95% of ingested lipids are what? |
|
Definition
| Triacyglycerol (TAG), the others are phospholipids and cholesterol. |
|
|
Term
| What two fatty acids must be gained from diet as they cannot be produced? |
|
Definition
| Linoleic acid and linolenic acid. |
|
|
Term
| In what form do lipids enter the duodenum? |
|
Definition
|
|
Term
| Pancreatic lipolytic enzymes degrade TAGs into what? |
|
Definition
| 2 Free fatty acids (FFA's) and 1 Monoacylglycerol (MAG) by lipase and Co-lipase |
|
|
Term
| Pancreatic lipolytic enzymes degrade phospholipids into what? |
|
Definition
| Phosphoglycerol and 2 FFA's by phospholipase A2 |
|
|
Term
| Pancreatic lipolytic enzymes degrade cholesterol into what? |
|
Definition
| Cholesterol by cholesterol esterase. |
|
|
Term
| Products of degraded lipids aggregate into what and are then transferred into what? |
|
Definition
| Aggregate into Multilamellar vesicles and are transferred into mixed micelles (lipid core, amphipathic bile acid skin) |
|
|
Term
| Where are bile salts ionised into acids? |
|
Definition
|
|
Term
| Where and how are bile acids degraded? |
|
Definition
| Degraded by flora in the duodenum from 1ry to 2ry acids. |
|
|
Term
| What are the functions of bile acids? |
|
Definition
| Excretion route for cholesterol, emulsify lipids and form mixed micelles. |
|
|
Term
| Bile salts are amphipathic, what does that mean? |
|
Definition
| One end hydrophobic, the other hydrophillic, hence mixed micelle formation. |
|
|
Term
| Where are bile salts reabsorbed and how are they transported back to the liver? |
|
Definition
| 95% reabsorbed in the terminal ileum, transported by albumin back to the liver for re-synthesis if needed. |
|
|
Term
| What are the functions of the pancreas? |
|
Definition
Endocrine - Metabolic control (insulin & glucagon)
Exocrine – Digestive enzyme secretion & neutralisation of duodenum through HCO3- secretion |
|
|
Term
| What controls the exocrine function of the pancreas? |
|
Definition
| Vagus nerve in cephalic phase, hormones (CCK – enzyme secretion in response to low duodenal pH and Secretin – HCO3- secretion in response to lipids & proteins), inhibitory hormones amylin and pancreatic polypeptide and somatostain/ghrelin. |
|
|
Term
| What is the cephalic phase of pancreas stimulation? |
|
Definition
| Sight/taste/smell of food stimulates hypothalamus & vagus nerve, stimulates approx 40% of maximum pancreas secretion. |
|
|
Term
| What is the duodenal phase of pancreatic function? |
|
Definition
| Endocrine cells secrete secretin in response to low pH and CCK in response to lipids and proteins. Vagal nerve afferents monitor pH |
|
|
Term
| What are the hormonal actions of secretin? |
|
Definition
| Secreted by duodenal endocrine cells in response to low pH and causes duct cells to secrete HCO3- increasing pH resulting in +ve feedback. |
|
|
Term
| What are the hormonal actions of CCK? |
|
Definition
| Secreted in response to lipids and proteins in duodenum, causes gall bladder contraction, oddi relaxation and acinar cell excretion. |
|
|
Term
| What are the hormonal actions of amylin? |
|
Definition
| Secreted by beta cells, slow gastric emptying and pancreatic secretions and inhibits glucagon production. |
|
|
Term
| What are the hormonal actions of Pancreatic polypeptide? |
|
Definition
| Produced in the islets and inhibit both gall bladder secretions and pancreatic secretions. |
|
|
Term
| Which pancreatic cells are exocrine? |
|
Definition
| Acinar cells 80% (enzymes) and duct cells 10% (HCO3-) |
|
|
Term
| What are the endocrine cells of the Pancreas? |
|
Definition
| α-Cells (Glucagon), β-Cells (Insulin & Amylin) and δ-Cells (Somatostatin) |
|
|
Term
| Aetiology of acute pancreatitis? |
|
Definition
| Gallstones, alcohol, post ERCP complication, pregnancy and auto-immunity (rare) |
|
|
Term
| How does acute pancreatitis present? |
|
Definition
| Sudden/gradual onset of epigastric severe pain radiating to back which is relieved sitting forwards, vomiting, bruising (severe, cullens sign, grey-turners sign), tenderness, guarding and shock (severe) |
|
|
Term
| What are Cullens sign and Grey-Turners sign, how do they differ and what are they suggestive of? |
|
Definition
Bruising as a symptom of acute pancreatitis.
Cullens: Periumbilical bruising
Grey-Turners: Flank bruising
Both suggest necrotising pancreas +/- haemorrage. |
|
|
Term
| What blood investigations would you do for acute pancreatitis? |
|
Definition
| Serum amylase >3x normal range, serum lipase (more sensitive and specific than amylase), U&Es (hypovolaemia, Hyponatraemia, hypokalaemia, hypocalcaemia & hypomagnesaemia may develop) BM's, ABGS and FBCs. |
|
|
Term
| Why might hypovolaemia show on U&Es in response to acute pancreatitis? |
|
Definition
| Renal failure - May occur due to inflammatory response causing ↑capillary permeability & third-space sequestration |
|
|
Term
| What imaging would you use to investigate acute pancreatitis? |
|
Definition
| Erect CXR (exclude preforation), abdo X-ray (find calcifications), abdo USS (gallstones) and CT/MRI (severity shows oedematous and necrosis) |
|
|
Term
| What factors make up the PANCREAS scoring system, having >3 of which allows the diagnosis of severe pancreatitis. |
|
Definition
PaO2<8KPa
Age >55
Neutrophils Raised WCC
Calcium ,2.0mmol/L
Raised urea >16mmol/L
Enzymes- LDH.600iu/L, AST >200iu/L
Albumin- <32g/L
Sugar >10mmol/L |
|
|
Term
| How do you treat mild pancreatits (85%)? |
|
Definition
| Supportive care: Fluids - Lots of 0.9% Saline, to maintain BP/HR & urine output >30mls/kg/hr, O2, NG Tube - To relieve pressure from ileum, NBM - To rest pancreas (JEJ or TPN feed if necessary)and Analgesia - Pethidine or Morphine |
|
|
Term
| How do you treat severe pancreatitis? |
|
Definition
| ITU, Pre-emptive ABX – to stop necrosis becoming infected, Surgical Intervention - to drain abcesses/remove necrosis etc and ERCP if gallstones present |
|
|
Term
| Aetiology for chronic pancreatitis? |
|
Definition
| Alcohol, malnutrition, hereditary and cystic fibrosis |
|
|
Term
| What is the pathophysiology of chronic pancreatitis? |
|
Definition
| Hypersecretion of proteins leading to plug formation and blockage of duct, premature activation of enzymes, Loss of pancreatic tissue and pancreatic insufficiency, Fibrosis, scarring & Calcification occur |
|
|
Term
| Presentation of chronic pancretitis? |
|
Definition
| Epigastric pain, pancreatic insufficiency, weight loss, steatorrhea, flatus, diabetes and jaundice. |
|
|
Term
| Chronic pancreatitis investigations? |
|
Definition
| Low faecal elastase, low PABA (urine), USS, CT, MRI/Endoscopic USS |
|
|
Term
| How is chronic pancreatitis treated? |
|
Definition
| Analgesia, enzyme supplements, diabetic control, surgery if pain unbearable/ cysts/acites. |
|
|
Term
| Risk factors of carcinoma of pancreas? |
|
Definition
| Age >60, smoking/alcohol, chronic pancreatits, family Hx (BRAC2) |
|
|
Term
| How does carcinoma of pancreas present in head of pancreas and tail of pancreas? |
|
Definition
Head of pancreas : early presentation, obstructive jaundice painless.
Tail of pancreas: Late presentation, epigastric pain, weight loss. |
|
|
Term
| Carcinoma of pancreas investigation? |
|
Definition
| USS, CT, Tumour markers CA19-9 and CA125. Biopsy only when surgery not planned. |
|
|
Term
| Carcinoma pancreas treatment? |
|
Definition
| Usually palliative, stenting of CBD, chemo/radiotherapy. 10% suitable for attempted curative surgery. |
|
|
Term
| What are the most common type of gall stones and how are they formed? |
|
Definition
| Cholesterol stone, formed by cholesterol supersaturation, reduced bile salt, stasis and promoting factors. |
|
|
Term
| What two types of pigment stone are there and what forms them? |
|
Definition
Black pigment stones: Calcium billirubinate (associated with haemolytic disease)
Brown pigment stones: Calcium/ FA salts+ calcium billirubinate (due to bile stasis/infection. |
|
|
Term
| Predisposing factors of gall stones? |
|
Definition
FAT, FEMALE, FERTILE, FAIR & FORTY.
Age, female gender, obesity, drugs, chrons and diabetes. |
|
|
Term
|
Definition
| Gallstone lodged in cystic duct/CBD. Causes mucocele of GB, exits blocked so salts build up causing distended GB (full of mucous). |
|
|
Term
| What is acute cholecystitis? |
|
Definition
Obstruction of cystic duct causing inflammation/infection.
Complications Empyema of GB and Perforation of GB. |
|
|
Term
| What is obstructive jaundice? |
|
Definition
| Hepatic duct obstruction caused by stone or mass in head of pancreas causing billirubin in blood. |
|
|
Term
| What occurs in ascending cholangitis? |
|
Definition
| Infection spreads up static bile from duodenum |
|
|
Term
| What is a gallstone ileus? |
|
Definition
| Large gallstone erodes from GB to duodenum and occludes ileocaecal junction. |
|
|
Term
| How does biliary cholic present? |
|
Definition
Pain in Rt Upper Quadrant, Restless, Constant & Crescendo-ing pain Lasts hrs, radiates to rt shoulder/subscapular reg, Precipitated by fatty food, Nausea & Vomiting
o Jaundice. |
|
|
Term
| Biliary cholic investigations? |
|
Definition
| Bloods, USS, MRCP and HIDA scan. |
|
|
Term
| How does acute cholecystitis present? |
|
Definition
| RUQ pain, nausea&vomiting, guarding&tenderness, fever +ve murphys sign. |
|
|
Term
| In acute cholecystitis what is murphys sign? |
|
Definition
| Pain on inspiration when hand pushed into abdo due to GB pushing on hand. |
|
|
Term
| Acute cholecystitis investigation? |
|
Definition
| Bloods (CRP, ESR and WCC), USS, MRCP and HIDA. |
|
|
Term
| Acute cholecystitis treatments? |
|
Definition
| Cefuroxime of infective, cholecystectomy. |
|
|
Term
| Obstructive Jaundice/Cholangitis presentation? |
|
Definition
| RUQ pain, Nausea&vomiting, Jaundice, Fever and charcots triad (fever, jaundine & RUQ pain) |
|
|
Term
| Obstructive Jaundice/Cholangitis investigations? |
|
Definition
Bloods (elevated billirubin)and LFTS, obstructive pattern (increased ALP and Gamma GT)
Imaging: Dilation/masses in CBD/pancreas, USS, MRCP, HIDA. |
|
|
Term
| Obstructive Jaundice/Cholangitis treatment? |
|
Definition
| Cefuroxime if infective, ERCP (drainage, stone removal, stenting). |
|
|
