Deck 5 Flashcards
Pancreatisis causes
Idiopathic gallstones (lodged at sphincter of oddi) alcohol (increases zymogen secretion and decreases fluid and bicarb, causing obstruction) Trauma Steroids Mumps Autoimmune Spider/scorpion bite Hypercalcaemia/hypertriglyceridaemia ERCP Drugs (azathioprine, furosemide, immunosuppressants, thiazides, ACEi, NSAIDs, sulphonamides)
Pancreatitis general
Can range from mild to severe. 20% are mild and resolve spontaneously.
Males affected more than females. Gallstones and alcohol are biggest causes
Pancreatitis S+S
N&V, epigastric pain, radiating to back, relieves on sitting forward.
Cullen’s sign
Grey turner sign
Hypercalcaemia (due to fat necrosis)
Signs of sepsis (tachycardia, fever, rigid abdomen, shock)
ileus
Pancreatitis investigations
Amylase, lipase (more specific and better after initial phase when amylase decreases), bone profile (hypercalaemia), triglycerides, FBC, U&E, CRP, ABG, lactate and o2
Clinical diagnosis, imaging not needed but may do: AXR to show ileus CXR to exclude other cause USS to exclude gallstones CT abdo if uncertainty MRCP to visualise ductal system
Scoring system for pancreatitis
Glasgow scoring system P (aO2<8) Age (>55) Neutrophils/WCC>15 Calcium <2mmol Renal, urea (>16) Enzymes (LDH >600, AST>200) Albumin (<32) Sugar (glucose >10) 3 or more is severe -HDU/ITU
Can also use Apache II (clinical features, age and comorbidities to give score. >9 is severe)
Randon criteria uses age, lab score on admission and38h to give mortality risk
periductal pancreatitis
Necrosis of acinar cells adjacent to duct- obstruction cause
panlobular pancreatitis
whole acinar lobule necrosis. Drugs, toxins, viruses, metbolic insult
Perilobular pancreatitis
necrosis of peripheries. shock/hypothermia
Pancreatitis management
Fluids (3rd space loss), analgesia (caution with morphine, can spasm sphincter of oddi), NG tube, adeqaute oxygenation, ERCP if gallstones, broad spec Abx
Pancreatitis complications
Pancreatitis necrosis (liquifactive haemorrhagic necrosis), pseudocyst (can be infected and form abscess), abscess formation (pain, anorexia, palpable tender mass - CT visible) Can also lead to hypovolaemic shock (blood vessels rupture), , DIC, ARDS (inflammation causes leaky blood vessels), thrombosis of splenic/gastroduodenal arteries (bowel necrosis), hyperglycaemia, hypokalaemia, hypoalbuminaemia, vitamin deficiency
Primary haemostasis
Platelet mediated.
Injury causes vasoconstriction to allow platelet adhesion to exposed collagen.
VWF binds collagen, Gp2b on platelets bind vWF.
Platelets release ADP/TXA2
Collagen activated platelets expose fibrinogen receptors.
Soft, weak plug formed
Primary haemostasis impairment
Bruising, epistaxis, gum bleeding, menorrhagia, intra/immediate post op bleed
Primary haemostasis impairment cauaes
Thrombocytopoenia, lack of GP1b (Bernard Soullier syndrome), lack of GP2b/a (Glanzmann’s thrombasthaenia), antiplatelet drugs, VWF impairment
Thrombocytopoeania causes
Overuse (septicaemia, DIC, TTP), immune reaction (autoimmune, drug induced), decreased production (alcohol, cytotoxic drugs, bone marrow failure), hyperplenism
Aspirin/NSAIDs block`
COX1 (TXA2), but also COX2
Clopidogrel/tricagrelor block
ADP binding P2Y12
Abciximab/eptifibatide block
Gp2b3b
Secondary haemostasis
Clotting cascade and fibrin mesh (needs tissue factor).
Vitamin K dependent clotting factors
2,7,9,10
Extrinsic pathway
Activation of VII and X
Use PT to measure.
INR is PT corrected - normal is 0.9-1.1
Intrinsic pathway
12->11->9–>8 and 10
APTT meausres.
Measure for unfractionated heparin
APTT
Intrinsic pathway
Symptoms of secondary haemostasis disorder
Haemarthrosis, muscular/soft tissue bleed, extensive bruising, delayed post op bleed/poor wound healing
Causes of secondary haemostasis disorder
Reduced coagulation factors (congenital is haemophilias, acquired through warfarin, liver dysfunction, DIC)