Week 13: Acute Hepatic Dysfunction Flashcards

Question

sentaken-blakemore placement

Answer 1

cause pressure to stop bleeding

Answer 2

* both exocrine (most of cells in pancreas, produc and release pancreatic juice to digest fat, carbs, protein) and endocrine functions (much smaller in number, clusters of islets. produce insulin (reduce amount of sugar in blood) and glucagon (increases sugar available in blood when bs is low)) * neutralize chyme * digestive enzymes * hormones

Answer 3

* specialized cells which synthesize, store, and secrete digestive enzymes * These digestive enzymes are stored in zymogen granules which serve as a compartment for inactive pro-enzymes thus preventing auto-activation.

Answer 4

* The more proximal the nutrient infusion…the greater the pancreatic stimulation (dog studies) * _stomach_ – maximal stimulation * _duodenum_ – intermediate stimulation * _jejunum_ – minimal / negligible stimulation * Elemental formulas tend to cause less stimulation than standard intact formulas * intact protein \> oligopeptides \> free amino acids * Intravenous nutrients (even lipids) do not appear to stimulate the pancreas

Answer 5

* COMPARTMENTALIZATION - digestive enzymes are contained within zymogen granules in acinar cells * REMOTE ACTIVATION - digestive enzymes are secreted as inactive proenzymes within the pancreas * PROTEASE INHIBITORS – trypsin inhibitor is secreted along with the proenzymes to suppress any premature enzyme activation * AUTO “SHUT-OFF” – trypsin destroys trypsin in high concentrations

Answer 6

* Acute inflammatory process involving the pancreas * Usually painful and self-limited * Isolated event or a recurring illness * Pancreatic *function* and *morphology* return to normal after (or between) attacks etiology * usually due to gallstones or alcohol abuse *

Answer 7

* Cholelithiasis * Ethanol abuse * Idiopathic * Medications * Hyperlipidemia * ERCP * Trauma * Pancreas divisum * Hereditary * Hypercalcemia * Viral infections: Mumps, Coxsackievirus * End-stage renal failure * Penetrating peptic ulcer

Answer 8

* _AIDS therapy_: didanosine, pentamidine * _Anti-inflammatory_: sulindac, salicylates * _Antimicrobials_: metronidazole, sulfonamides, tetracycline, nitrofurantoin * _Diuretics_: furosemide, thiazides * I**_BD_**: sulfasalazine, mesalamine * _Immunosuppressives_: azathioprine, 6-mercaptopurine * _Neuropsychiatric_: valproic acid * _Other_: calcium, estrogen, tamoxifen, ACE-I

Answer 9

* Autosomal dominant with 80% phenotypic penetrance * **Recurrent** acute pancreatitis, chronic pancreatitis, and **50-fold increased risk of pancreatic cancer** * Mutation in cationic trypsinogen gene (R122H) * Other genetic defects: CFTR, SPINK1

Answer 10

* acinar cell injury causes premature enzyme activation causing failed protective mechanisms--\>autodigestion of pancreatic tissue--\>local vascular issufficiency, activation of white blood cells, release of enxymes into the circulation--\>local complications and distant organ failure * failure of compartmentalization, premature activation, and overwhelming or absence of inhibitors

Answer 11

* STAGE 1: Pancreatic Injury * Edema * Inflammation * STAGE 2: Local Effects * Retroperitoneal edema * Ileus * STAGE 3: Systemic Complications * Hypotension/shock * Metabolic disturbances * Sepsis/organ failure

Answer 12

Abdominal pain * Epigastric * Radiates to the back * Worse in supine position Nausea and vomiting Fever

Answer 13

non-hemorrhagic * Short duration * Pancreatic edema and swelling * Little to no necrosis * Local inflammation * Reversible * Good prognosis hemorrhagic * Long duration * Pancreatic hemorrhage * Extensive necrosis * Extra-pancreatic * Irreversible damage * Poor prognosis- sepsis MOSF

Answer 14

Symptoms * Abdominal pain Laboratory * Elevated amylase or lipase * \> 3x upper limits of normal Radiology * Abnormal sonogram or CT

Answer 15

_amylase _ _ lipase_ Pancreatitis ↑ ↑ Parotitis ↑ Normal Biliary stone ↑ ↑ Intestinal injury ↑ ↑ Tubo-ovarian disease ↑ Normal Renal failure ↑ ↑ Macroamylasemia ↑ Normal

Answer 16

* _EtOH_: history * **_Gallstone_**s: abnormal LFTs & sonographic evidence of cholelithiasis * _Hyperlipidemia_: lipemic serum, Tri\>1,000 * _Hypercalcemia_: elevated Ca * _Trauma_: history * _Medications_: history, temporal association

Answer 17

PANCREATIC * _Mild_: edema, inflammation, fat necrosis * _Severe_: phlegmon, necrosis, hemorrhage, infection, abscess, fluid collections PERIPANCREATIC * Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinum * _Adjacent viscera_: ileus, obstruction, perforation SYSTEMIC * _Cardiovascular_: hypotension * _Pulmonary_: pleural effusions, ARDS * _Renal_: acute tubular necrosis * _Hematologic:_ disseminated intravascular coag. * _Metabolic_: hypocalcemia, hyperglycemia

Answer 18

* Cytokine release, 48 hrs, organ failure, 72 hrs * In the early stages ofpancreatic injury and inflammation, proinflammatory cytokines, such as interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor (TNF)-A, appear to be released from tissue macrophages within the pancreas. * Neutrophil activation likely results from release of IL-8 from macrophages and endothelial cells and release of platelet-activating factor (PAF) from endothelial cells. * Later in theprocess, release of cytokines from T-helper lymphocytes (eg, IL-2, interferon-C) may also participate in the inflammatory response [3]

Answer 19

Why are they needed? * appropriate patient triage & therapy * compare results of studies of the impact of therapy When are they needed? * optimally, within first 24 hours (damage control must begin early)

Answer 20

_Ranson and Glasgow Criteria (1974)_ * based on clinical & laboratory parameters * scored in first 24-48 hours of admission * poor positive predictors (better negative predictors) _Computed Tomography Severity Index_ * **much better diagnostic and predictive tool** * optimally useful at 48-96 hours after symptom onset

Answer 21

At admission * Age \> 55 years * WBC \> 16,000 * Glucose \> 200 * LDH \> 350 IU/L * AST \> 250 IU/L Within 48 hours * HCT drop \> 10 * BUN \> 5 * Arterial PO2 \< 60 mm Hg * Base deficit \> 4 mEq/L * Serum Ca \< 8 * Fluid sequestration \> 6L higher point values=higher mortality rates less than 2=1% mortality rate 3-4= 16% 5-6=40% 7-8=100%

Answer 22

Glasgow prognostic score: (NOTE PANCREAS ACRONYM) * **P**aO2 \< 8kPa (60mmhg) * **A**ge \> 55 years * **N**eutrophils: (WBC \>15 x109/l * **C**alcium \< 2mmol/l * **R**enal function: (Urea \> 16mmol/l) * **E**nzymes: (AST/ALT \> 200 iu/L or LDH \> 600 iu/L) * **A**lbumin \< 32g/l * **S**ugar: (Glucose \>10mmol/L) score \> 8 points predicts 11% to 18% mortality

Answer 23

* score \> 8 points predicts 11% to 18% mortality * Online calculator * Hemorrhagic peritoneal fluid * Obesity * Indicators of organ failure * Hypotension (SBP \<90 mmHG) * tachycardia \> 130 beat/min * PO2 \<60 mmHg * Oliguria (\<50 mL/h) * Increasing BUN and creatinine * Serum calcium \< 1.90 mmol/L (\<8.0 mg/dL) * serum albumin \<33 g/L (\<3.2.g/dL)

Answer 24

looking at the results of looking at the pancreas itself, giving a grade and a score. **Best way to judge severity** appearance: * normal: grade A, score 0 * enlarged:grade B, score 1 * inflamed: grade c, score 3 * 1 fluid collection: D, score 4 * 2 or more collections: E, score 5 Necrosis: * None: score 0 * \<33%: score 2 * 33-50%: score 4 * \>50%: score 6 Score 1-2: 4% morbidity, 0% mortality Score 7-10: 92% morbidity, 17% mortality

Answer 25

Scoring systems * \>/=3 Ranson criteria * \>/=8 APACHE II points * \>/= 5 CT points Organ failure * shock (SBP \< 90 mmHg) * pulmonary edema / ARDS (PaO2 \< 60 mmHg) * renal failure (Cr \> 2.0 mg/dl) Local complications * fluid collections --\>pseudocysts * necrosis (mortality 15% if sterile, 30-35% if infected) * abscess

Answer 26

* Anorexia * Abdominal rigidity/ tenderness * N/V * Pain – sudden, knifelike * Diminished/ absent Bowel sounds * Diminished breath sounds * Cullen’s sign: bruising around the umbilicus * Grey turner’s sign: flank bruising * Altered LOC * Chvostek’s sign: tapping in front of ear, mouth twitches * Trousseau’s sign: latent tetany is a medical sign observed in patients with low calcium * Non-cardiogenic pulmonary edema heard most often on Left side

Answer 27

* Pancreatic rest * Supportive care * fluid resuscitation – watch BP and urine output * pain control * NG tubes and H2 blockers or PPIs are usually not helpful * Refeeding (usually 3 to 7 days) * bowel sounds present * patient is hungry * nearly pain-free (off IV narcotics) * amylase & lipase not very useful here \*mild panc – support is all that’s needed \*hypotension probably predisposes to necrosis (poor microcirculation)

Answer 28

* Pancreatic rest & supportive care * fluid resuscitation\* – **may require 5-10 liters/day** * careful pulmonary & renal monitoring – ICU * maintain hematocrit of 26-30% * pain control – PCA pump **Why Not Morphine?** * correct electrolyte derangements (K+, Ca++, Mg++) * Rule-out necrosis * contrasted CT scan at 48-72 hours * prophylactic antibiotics if present * surgical debridement if infected * Nutritional support * may be NPO for weeks * TPN vs. enteral support (TEN)

Answer 29

Gallstone pancreatitis * Cholangitis * Obstructive jaundice Recurrent acute pancreatitis * Structural abnormalities * Neoplasm * Bile sampling for microlithiasis Sphincterotomy in patients not suitable for cholecystectomy \* Sedated, scope ran down through mouth to see what's going on

Answer 30

Metabolic stress * catabolism & hypermetabolism seen in 2/3 of patients * similar to septic state (volume depletion may be a major early factor in the above derangements) Altered substrate metabolism * increased cortisol & catecholamines * increased glucagon to insulin ratio * insulin resistance Micronutrient alterations * calcium, magnesium, potassium, etc

Answer 31

Hyperdynamic * Increased cardiac output * Decreased systemic vascular resistance * Increased oxygen consumption Hypermetabolism * Increased resting energy expenditure Catabolism * Increased proteolysis (breakdown) of skeletal muscle

Answer 32

* Abdominal pain with food aversion * Nausea and vomiting * Gastric atony ( decresed motility) * Ileus * Partial duodenal obstruction

Answer 33

mild * Admission 80% * Pancreatitc Necrosis: No * Oral diet within 5 days: 80% * Morbidity: 8% * Mortality: 3% Severe Admission 20% Pancreatitc Necrosis: Yes Oral diet within 5 days: 0% Morbidity: 38% Mortality: 27%

Answer 34

* delay until volume repleted & electrolytes corrected * check triglycerides first – **goal \<400** * lipids are OK to use (possible exception of sepsis) * monitor glucose levels carefully * can see insulin insufficiency and resistance * may need to limit calories at first * separate insulin drip may be needed Benefit or harm? * early uncontrolled studies suggested **benefit** * two retrospective studies (70’s & 80’s) showed **no benefit** with TPN in pancreatitis * 1987 – randomized study of early TPN vs. IVF alone showed **more sepsis**, **longer stays**, & no fewer complications with TPN When to use TPN? * jejunal access is unavailable * ileus prevents enteral feeding * patients in whom TEN clearly exacerbates pancreatitis

Answer 35

* may start as early as possible * when emesis has resolved * ileus is not present * nasojejunal route preferred over nasoduodenal * likely decreases risk of infectious complications by reducing transmigration of colonic bacteria

Week 13: Acute Hepatic Dysfunction Flashcards

(59 cards)