Liver Flashcards

Question

What's the liver blood flow? % from PV & HA?

Answer 1

1.5L/min, 80% & 20%

Answer 2

Not likely as if loose blood it's a sudden major bleed & need products ready (vs steady trickle)

Answer 3

10%, 20-30%

Answer 4

running the pt dry- UO 0.5mL/kg/hr

Answer 5

sux actual, others ideal (which is 22 x (height in m^2))

Answer 6

0.1mg/kg & 0.01mg/kg

Answer 7

induction lean body weight & maintenance infusion total body weight

Answer 8

Acute hepatocellular dysfunction with coagulopathy & encephalopathy in a pt without prior known liver disease

Answer 9

30, 33 & 14%

Answer 10

``` Paracetamol excess (up to 70% of cases) Viral hepatitis (Heps A-G, CMV, EBV, HSV) Autoimmune hepatitis Toxins (eg. carbon tetrachloride) Acute fatty infiltration of pregnancy HELLP syndrome Wilson's disease Reye's syndrome ```

Answer 11

Encephalopathy, cerebral oedema Severe coagulopathy with active fibrinolysis Metabolic acidosis, hypokalaemia, hypoglycaemia, hyponatremia High cardiac output state with reduced SVR, risk of raised ICP, ARDS & renal failure

Answer 12

No. It's a contraindication to elective surgery due to high periop mortality. Delay (unless true emergency) until 30d after LFTs have normalised.

Answer 13

A: pts w grade 3/4 encephalopathy require intubation to protect their airway B: at risk of ARDS C: high CO state Hypotension & hypovolaemia- Mx w IVT, vasopressors/inotropes (NAdr= first line) Maintain BP within 10-20% of pre-op baseline D: encephalopathy May require ICP monitoring (?+/- bicarbonate-buffer haemofiltration) E: temp management (coagulopathy) hyponatremia, hypokalaemia, metabolic acidosis (correct), risk of renal failure G: hypoglycaemia common- need to correc H: severe coagulopathy with active fibrinolysis- reverse for surgery. May need ICU K: renal failure with hepatic failure confers high mortality- up to 50% of pts w ALF also have ARF. Avoid intra-op hypoT, maintain UO 1mL/kg/hr, avoid nephrotoxins. Personnel: hep B/C contagious- universal precautions Discuss w specialist liver unit (?considering transplantation) Require management of cause: delivery if pregnancy-related, NAC if paracetamol OD, orthotropic liver transplant may be definitive Rx

Answer 14

Noradrenaline

Answer 15

``` Paracetamol: pH <7.3 of ALL of: PT>100 or INR >1.5 Cr >300 Grades 3-4 encephalopathy Non-paracetamol: PT>100 OR any 3 of: age<10 or >40 PT>50 bili >300 ```

Answer 16

Any hepatitis lasting >6/12. Inflammation can --> fibrosis & may lead to nodular regeneration & disruption of liver architecture (cirrhosis) which may lead to portal HTN. Compensated= liver function maintained decompensated (eg. triggered by infection)= deterioration in liver function. If unable to remain compensated w Rx of the cause (which can sometimes reverse fibrosis), consider transplantation.

Answer 17

ETOH, HBV, HCV & fatty liver disease Less common: Inherited (haemachromatosis, Wilson's disease, alpha-1 antitrypsin deficiency) Immune-mediated (primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis) Vascular disease (budd-chiari, veno-occlusive) Drugs (isoniazid, methyldopa)

Answer 18

Vertical transmission- falling numbers due to routine vaccination of babies 95% risk developing chronic HBV if infected @ birth, when infected as an adult 3% chance developing chronic HBV

Answer 19

75%. IVDU (less common w blood products now all donors screened)

Answer 20

Non-ETOH liver disease w rising obesity levels, esp in pts w T2DM & HTN

Answer 21

Acute intoxication: - Consent issue. Avoid non-emergency surgery. - May have vomiting, hypoglycaemia & delayed gastric emptying: RSI - Binge drinking (associated with vomiting & fasting) may be associated with ketoacidosis - Ensure adequate rehydration, check for electrolyte & glucose disturbance, consider IV vit-B (slow BD for 3-5 days) Chronic ETOH excess: - Tolerance to GA, 2-5x increased risk of postop complications - Anticipate ETOH withdrawal symptoms but don't complicate management by attempting to withdrawal perioperatively; most pts can tolerate 24hr abstinence- monitor & prescribe regular BZD - Seizures are most commonly 6-48hrs after drinking cessation- several fits over a period of days are common & may be predisposed by low K+ & Mg++. May be preceded by disorientation & agitation (DTs). Rx w BZD (eg, diazepam 10mg IV), repeat as required - ETOH cardiomyopathy - ETOH liver disease

Answer 22

Dilated, hypokinetic LV & reduced EF May have CCF & oedema, exacerbated by low serum Alb Consider echo

Answer 23

Reversible fatty liver, then ETOH hepatitis (abdo pain, wt loss, jaundice, fever) later cirrhosis (jaundice, ascites, portal HTN, hepatic failure)

Answer 24

sepsis, bleeding, renal failure, worsening hepatic failure with encephalopathy

Answer 25

``` Bilirubin Albumin PT Ascites Encephalopathy ```

Answer 26

Decreased synthesis of clotting factors Decreased clearance of activated clotting factors Quantitative & qualitative platelet abnormalities Hyperfibrinolysis Vitamin K deficiency (due to obstructive jaundice- this will prolong the PT. No vit K assay so a trial IV vit K may improve PT if it's the cause, no improvement if the coagulopathy due to impaired liver synthetic function)

Answer 27

Buildup of toxins (esp ammonia due to deranged amino acid metabolism), may be precipitated by sedatives, GI bleed, infection, surgery, trauma, postop ileus (HENCE PRESCRIBE CONCURRENT LACTULOSE W POSTOP OPIOIDS as constipating agents may precipitate encephalopathy), hypokalaemia. Grade 0= alert & oriented 1= drowsy & oriented 2= drowsy& disoriented 3= rousable stupor, restless 4= coma Intubate if Gd 3/4 or if cerebral oedema develops

Answer 28

Impaired glycogen storage. Monitor BGL, give 30mL of 50% glucose (15g) as slow IV push 15-minutely until BGL >4, monitor plasma potassium.

Answer 29

Fibrotic changes-->portal HTN, in combo with salt/water retention secondary to hyperaldosteronism, splanchnic VD & low serum Alb--> fluid accumulation in peritoneal cavity

Answer 30

Spironolactone--> aldosterone antagonist @ CCD limits Na+ reabsorption but limits K+ secretion, risk hyperK+ acidosis

Answer 31

immunoglobulins

Answer 32

Hyperdynamic circulation with high CO state (up to 50%), contributed by portosystemic, pulmonary & cutaneous shunting. See low SVR, low MAP, tachycardia, increased contractility BUT blunted response to pharmacologic, physiologic or pathological stress which may--> overt HF. RAAS activation--> volume expansion. May have ETOH excess if cardiomyopathy. Care w periop IV fluids to avoid volume overload but ensure urine output >1mL/kg/hr Portopulmonary HTN may occur so cirrhotic pts undergoing major surgery should be screened with an echo

Answer 33

50%, concurrent renal & liver failure has high mortality.

Answer 34

dehydration, sepsis & nephrotoxic drugs.

Answer 35

A diagnosis of exclusion Occurs exclusively in pts w cirrhotic liver disease Due to altered renovascular tone. Type 1= rapidly progressive Type 2= slower onset, diuretic-resistant ascites Both types poor prognosis, liver transplant may be the only cure Criteria: CLD & ascites urine Na+ <10 urine:plasma osmolality & Cr ratios >1 Normal CVP & no diuresis on volume expansion Prevent w adequate hydration/renal blood flow Avoid intra-op hypotension, maintain UO >1mL/kg/hr, avoid nephrotoxic drugs

Answer 36

1. Ascites- diaphragm splinting basal atelectasis 2. Hepatopulmonary syndrome- in 0.5-4% of pts w cirrhotic liver failure. Arterial hypoxaemia due to intrapulmonary vascular dilatations thought due to bacterial translocation & toxins from portal HTN which stimulate vasoactive mediators or failure of liver to clear circulating vasodilators (eg. N2O) 3. Portopulmonary syndrome- pulm HTN (type 1) due to circulating vasoactive substances usually degraded by the liver, reaching pulm circn through portosystemic collaterals, may cause RV failure/intraop cardiac arrest * pulm VC occurs while systemic VD predominates

Answer 37

Low PPs- oedema/ascites & higher unbound fraction of some drugs which may--> toxicity of drugs which normally high BP (eg. bupivacaine) Anaemia- from chronic blood loss, hypersplenism, haemolysis, chronic illness, malnutrition

Answer 38

Initially oxidised or reduced by the CYP450 system in phase 1, then conjugated to enhance water solubility & excretion in bile or urine in phase 2.

Answer 39

Early the CYP450 system induced so drug metabolism quicker but in end-stage liver disease drug metabolism prolonged. The liver has a large functional reserve so drug metabolism usually preserved until end-stage disease.

Answer 40

End-stage liver disease may have higher sensitivity to sedative agents (w encephalopathy)

Answer 41

``` alfentanil morphine benzodiazapines vecuronium, rocuronium succinylcholine, mivacurium, ester LAs (lack of plasma cholinesterase) ```

Answer 42

Absorption reduced w PO due to slowed gastric emptying VD higher for hydrophilic drugs due to Na+/water retention hypoalbuminemia/low PPs may increase free fraction & activity of highly PB drugs (eg. bupivacaine) Reduced hepatic blood flow may reduce first-pass metabolism (prolong action drugs with high HER eg. lignocaine, propofol) reduced liver mass & biotransformation enzymes alters metabolism obstructive jaundice reduce biliary excretion of drugs using primary biliary route (eg. rocuronium)

Answer 43

Falsely low due to decreased hepatic production

Answer 44

2-17micromol/L, raised in haemolysis, Gilbert's syndrome, acute & chronic liver failure, biliary obstruction

Answer 45

0-35IU/L, non-specific (found in liver, heart, muscle, rbc), raised in hepatocellular injury

Answer 46

0-45IU/L, specific indicator of hepatocellular injury Degree of elevation suggests aetiology, >1000 acute viral hepatitis, drugs, autoimmune, ischemia 100-200 acute viral hepatitis, ETOH & NAFLD

Answer 47

``` 30-120IU/L Elevation may be physiological (pregnancy, adolescents, familial) BILIARY OBSTRUCTION (stones, drugs, Ca) PBC metastatic liver disease bone disease ```

Answer 48

0-30IU/L non-specific (heart, pancreas, kidney) Useful to confirm a hepatic source of raised ALP (always raised if an increased ALP is due to a liver source) raised in ETOH liver disease

Answer 49

40-60g/L. Non-specific (reduced in chronic liver disease, catabolism, nutritional state, urinary & GI losses) Prognostic in chronic liver disease

Answer 50

1-1.2 (with normal PT 10-9-12.5s), nonspecific (elevated in vit K deficiency, warfarin therapy, DIC) but is best prognostic marker in acute liver failure

Answer 51

PT, albumin & bilirubin

Answer 52

No as they are sensitive to even mild liver damage & levels may decrease in severe disease

Answer 53

electrolyte abnormalities may precipitate arrhythmia high bilirubin may cause bradyarrhythmias ETOH excess may precipitate AF & cardiomyopathy prol QTc relatively common

Answer 54

desflurane (also it's least metabolised). Halothane > enflurane the worst for decreasing HBF & inhibiting drug metabolism.

Answer 55

``` Lorazepam Propofol, thio, etomidate des/sevo/iso/nitrous atrac & cisatracurium remifentanil ```

Answer 56

``` Bilirubin overload (eg. transfusion, haematoma resorption) Hepatocellular injury (eg. hypotension/hypovolemia, cardiac failure, sepsis, hypoxia, drug-induced) Cholestasis (intrahepatic eg. drug-induced such as cephalosporins), extra hepatic eg, bile duct injury Congenital (gilbert's syndrome) ```

Answer 57

CSL or NaCl 0.9%. CSL presents a lactate land (28mmol/L, only has 131mmol/L Na) while NaCl (Na 150mmol/L) presents higher Na which may exacerbate ascites. Numan albumin useful esp if low serum Alb.

Answer 58

terlipressin 0.5-2mg IV QDS along with human albumin- this may improve renal function. It's a synthetic vasopressin analogue, causes splanchnic vasoconstriction (specific to the splanchnic circulation), reducing portal pressure. Indicated for acute variceal bleeds & hepatorenal syndrome. May cause low CO state, AF, hyponatremia, angina (but terlipressin causes less coronary constriction & angina than vasopressin).

Answer 59

30%, 40%. 70% within 6/52.

Answer 60

band ligation

Answer 61

PPI for acid suppression/reduction in the risk of ulcer rebleed/reduction of rebleed even if no ulcer (neutralisation of gastric acid may stabilise blood clots) Prokinetic: erythromycin (monitor for prolonged QTc) or metoclopromide which may improve gastric visualisation for endoscopy Somatostatin or it's analogue octreotide- vasoactive (inhibits release of glucagon which is a splanchnic VD) Prophylactic antibiotics ideally pre-endoscopy as reduce infections & possibly mortality(but still effective if given after endoscopy)

Answer 62

No- RCT & meta-analysis of 12,000 pts show no improvement death due to bleeding within 5 days- incr risk venous events & seizures cf placebo

Answer 63

If endoscopic & drug Rx have failed. | Only use in ICU/HDU as high risk fatal complications (eg, aspiration, oes rupture, airway obstruction)

Answer 64

Variceal bleed refractory to banding or ascites refractory to diuretics (the pt should be adequately resuscitated & variceal bleeding controlled w balloon tamponade prior to TIPSS)- achieves shunting without need for surgery

Answer 65

reduce portal pressures & reduce variceal rebleed rate from 70-50% but may mask early signs of hypovolemia & worsen hypoT during rebreeding

Answer 66

radiologically-placed shunt between portal & hepatic veins; prevents blood becoming engorged in the gastric/oeseophageal veins

Answer 67

Airway: RSI w cricoid B: IPPV C: Correct hypovolaemia, reverse coagulopathy, stop bleeding (early endoscopy, cease anticoagulants) 2x large-bore IVC, IV access, consider CVC depending on bleed

Answer 68

clinical or EEG evidence of encephalopathy

Answer 69

PTx (internal jugular used) cardiac arrhythmias catastrophic bleed if damage hepatic art or hepatic capsule (so have large-bore IV access, art line, blood products, vasopressors & inotropes ready, CVC setup ready if indicated) acute heart failure (as increase VR & preload) esp if cardiomyopathy so have a pre-op echo post-prodedural worsening of jaundice or encephalopathy may occur May be prolonged & pt may be unable to tolerate supine or be an aspiration risk (ascites) so GA w RSI may be preferred Remote- limited access to pts head Need 2x lg bore IV access risk bleeding- Ax & correct coagulopathy before start (plt >50 fibrinogen >2 without correcting INR unless think vit K warranted). TEG may be useful. have G&H. If large-vol paracentesis has occurred prior to TIPSS, use Alb vs crystalloid, if significant hyponatremia 25% Alb is preferred since it has less Na+

Answer 70

``` HISTORY: Anorexia Weight loss Fatigue Pruritis Easy bruising/bleeding RUQ pain ``` ETOH use Hx of fever/jaundice following anaesthetic IVDU, hepB/C, tattoos, blood transfusions, multiple partners/STIs, Fox jaundice or liver disease EXAM: Low SpO2, tachypnoea/tachycardia/hypotension may have bibasal creps if pleural effusions Confusion or reduced GCS if encephalopathic Jaundice Metabolic flap Hyperdynamic HS (loud S3) ascites palmar erythema spider naevi caput medusa Hepatosplenomegaly gyanecomastica, testicular atrophy

Answer 71

Child-Pugh C cirrhosis severe chronic hepatitis Severe coagulopathy (prolongation of the PT by >3 seconds despite vit K, plt <50) Severe extra hepatic complications (acute renal failure, cardiomyopathy/heart failure, hypoxia)

Answer 72

``` A= well-compensated disease (score 5-6) B= significant functional compromise (7-9) C= decompensated disease (10-15) ```

Answer 73

100, 85% 80, 60% 45, 35%

Answer 74

APACHE III score (acute physiology, age & chronic health evaluation system)

Answer 75

MELD score + etiology of liver failure, ASA class & age | In a validation score it overestimated mortality

Answer 76

infections, stress ulcers, DIC, wound dehiscence, renal failure

Answer 77

Hct <30% initial bilirubin >11mg/dL malignant cause of obstruction if all 3 factors present, mortality approaches 60% while mortality is 5% if none are present

Answer 78

endotoxins usually have their absorption limited by the detergent effect of bile salts- in obstructive jaundice endotoxin absorption from the gut is increased --> exaggerated renal VC & acute tubular necrosis

Answer 79

MELD score for cardiac surgery, excludes INR since cardiac pts generally anti coagulated. CP of >7 & MELD of >=13.5 generally contraindication to card surg.

Answer 80

Total time on cardiopulmonary bypass Nonpulsatile vs pulsatile cardiopulmonary bypass need for periop pressors

Answer 81

inducing platelet dysfunction, fibrinolysis & hypocalcemia

Answer 82

40% vs 20%

Answer 83

45%. Always postop ICU irrespective of the severity of their injuries.

Answer 84

No, but histologically similar to ETOH-associated hepatitis & pts may not admit to their ETOH ingestion so it's clinically difficult to distinguish; should always advise ETOH abstinence prior to surg for all pts w appearance of steatohepatitis or those w suspected ETOH consumption even if they don't have liver disease, as ETOH use disorder higher risk periop complications (eg. etoh withdrawal, hepatotoxic w paracetamol)

Answer 85

diabetes & cardiomyopathy

Answer 86

Neuropsych involvement may impair their ability to give informed consent surg may aggravate neurologic symptoms D-penicillamine (a copper chelator used in Rx) may impair wound healing so decrease dose prior to surg & for 1-2 wks postop

Answer 87

can trial vit K if suspect vit K deficiency. Don't give cryoprecipitate or plasma to correct if asymptomatic as lack evidence & may cause volume overload could try short course of thrombopoietin receptor agonist for severe thrombocytopenia (<50) but risk thrombotic events & require 10 days to raise plt count

Answer 88

Yes- due to risk of wound dehiscence & abdo wall herniation- also it increases mortality risk independent of MELD score. Use diuretics if also have peripheral oedema If no peripheral oedema or no time for diuretics, drain during laparotomy

Answer 89

Urea & creatinine may be lower due to reduced synthesis so renal function may be overestimated

Answer 90

No- unless they're bleeding

Answer 91

Limited data- thought to be safe if plt >50x10^9/L

Answer 92

if multiple blood transfusions, periop bleeding, haemodynamic instability, systemic infection

Answer 93

reduces bacterial translocation & haemodynamic disturbances with vasoactive endotoxins- reduces risk of SBP, ascites & variceal bleeding

Answer 94

Abdo surgery, cardiac surgery & hepatic resection

Answer 95

No. But if done & found to be abnormal, if <2x the ULN, reasonable to repeat them. If >2x ULN or increasing, postpone surgery & evaluate further.

Answer 96

hypoxia, hypovolemia, alkalemia, hypoglycaemia, hypokalaemia, hyponatremia

Answer 97

No (aside from TEG guidance, which results in less transfusion of blood products & no increase in bleeding complications). Administer vit K for pts w suspected deficiency (eg. poor nutrition, cholestatic disease, antibiotic use). Transfuse platelets to achieve >=50 & cryo to maintain fibrinogen >2g/L. NOT routinely FFP to correct INR unless closed cavity surgery (it's a useful marker of liver function & Rx asymptomatically may cause vol overload)

Answer 98

NASH, NAFLD & hep C

Answer 99

MPAP >50mmHg in presence of portal HTN. | liver transplant

Answer 100

Theoretically as they do undergo hepatic metabolism to trifluoroacetyl chloride BUT they undergo this hepatic metabolism 0.02% & 0.2% (vs 20% w halothane) so low if any risk. Sevo doesn't undergo metabolism to trifluoroacetyl chloride so hasn't bee associated with immune-mediated hepatic injury.

Answer 101

Not known to- it may reduce HBF via SNS stimulation, may inhibit methionine synthase so in pts w vit B deficiency (eg. some cirrhotic pts), there may be incr risk neurotoxicity w exposure to N2O

Answer 102

Drugs w high HER (eg. propofol, lignocaine) are impacted by liver blood flow, those with low HER (eg. midaz) are affected by PB & hepatocellular dysfunction

Answer 103

- Clearance of standard doses of propofol, STP or ketamine not impacted BUT pt more sensitive to pharmacodynamic effects & clinical recovery times may be prolonged after infusions - BZD low HER- both elimination half-life & free drug are increased so there'll be prolonged DOA- dose reduce midaz - dexmed metabolised primarily by liver, Cl is decreased & half life prolonged & Brady may limit dosing - care ++ w opioids which may precipitate HE - fentanyl- a better option (less histamine release, inactive nontoxic metabolites), especially useful if concomitant renal failure. no dose adjustment for a single dose but reduce dose & freq by 25-50% w repeated dosing - oxycodone metabolised to active metabolites- may have delayed onset, variable efficacy & risk accumulation - increased bioavailability by up to 100% due to diminished first-pass extraction, wide variability of efficacy & prolonged half life or accumulation of metabolites w complex effects (eg. resp depression, neurotox) in pts w cirrhosis & renal failure- reduce dose approx 50%, titrate dose, AVOID if cirrhosis & renal failure! - half dose in mild liver disease, contraindicated in advanced CLD or cirrhosis - hepatic metabolism to active metabolite, has variable onset & analgesic efficacy & risks accumulation in cirrhosis, avoid in decompensated cirrhosis or pts @ risk for seizures - titrate roc & veg w TOF (doa, Cl & elimination prolonged in advanced liver disease) BUT may get resistance to initial dose due to increased gamma globulins & VD

Answer 104

Pts w cirrhosis or malnutrition have limited glutathione which is needed to block metabolism formation of paracetamol's toxic metabolite NAPQI Available glutathione further reduced by active ETOH consumption Paracetamol t1/2 may be prolonged up to 2x cf healthy individuals in pts w cirrhosis who DON'T use ETOH, max 2g paracetamol/day Avoid if advanced CLD or cirrhosis and active ETOH consumption/malnourishment or taking potent hepatic enzyme inducers warn pts re: OTC products w paracetamol

Answer 105

No- they're hepatically metabolised & highly protein bound so risk accumulation/prolonged action/toxicity They risk GI ulceration/mucosal & variceal bleeding, risk renal injury & diuretic-resistant ascites Also avoid COX-2 inhibitors due to lack of data & incr CV events in pts without cirrhosis

Answer 106

>100 x10^9/L

Answer 107

less volume

Answer 108

right, since this is 2/3 of the liver mass

Answer 109

consider head up, restricting fluids +/- diuretics +/- vasodilators- to reduce hepatic & portal venous pressures hence operative bleeding sites. Low CVP risks VAE (especially in head-up position, furthermore head-up doesn't reduce the hepatic vein pressure!).

Answer 110

intermittent clamping of hepatic artery & PV for 15-20mins to interrupt vascular inflow during resection to prevent or control bleeding Reduces CO by 30%, increases afterload

Answer 111

It may take several hours to access the PV. PTs may be unable to tolerate supine, may have aspiration risk as likely to have massive ascites (TIPSS is performed for pts w severe liver disease)