Liver Cirrhosis Hour 3

Front 1

What are varices?

Back 1

Dilated submucosal veins, most commonly detected in the distal esophagus or proximal stomach

Front 2

What are the classic symptoms of varices?

Back 2

upper gi hemmorrhage such as hematemsis, passage of black or bloody stools, lightheadedness, decreased urnination

Front 3

What is the gold standard to diagnosing varices?

Back 3

esophagogastroduodenoscopy (EGD)

Front 4

How are varices graded?

Back 4

small (diameter of < 5mm) or large; presence or absence of red signs (aka red wale marks)

Front 5

What are the three phases of treatment for varices?

Back 5

Prevention of first variceal hemorrhage (primary prophylaxis), control of acute hemorrhage, prevention of a 2nd hemorrhage in pt who has already bled (secondary prophylaxis)

Front 6

What is the primary prophylaxis for varices?

Back 6

nonspecific beta blocker (propanolol or nadolol)

Front 7

What is the moa of nonspecific beta blocker in primary prophylaxis for varices?

Back 7

decrease portal pressures by decreasing cardiac output (b1) and producing splanchnic vasoconstriction (b2)

Front 8

What is the goal in primary prophylaxis of varices?

Back 8

decrease WHVP (wedged hepatic venous pressure) by at least 20% or to a gradient < 12 mmHG

Front 9

What is the starting does of propranolol for prophylaxis of varices?

Back 9

20mg BID

Front 10

What is the starting dose of nadolol for prophylaxis of varices?

Back 10

40mg qd

Front 11

What are the adverse effects of nonspecific beta blockers?

Back 11

lightheadedness, fatigue, SOB, male impotence

Front 12

What are the relative contraindications for nonselective beta blockers?

Back 12

reactive airway disease, insulin-dependent diabetes, PVD (peripheral vascular disease)

Front 13

If WHVP measurement is not available, how do you dose nonspecific beta blockers in varice prophylaxis?

Back 13

titrate dose to resting HR of 55 bpm or 25% reduction from baseline

Front 14

What is EVL?

Back 14

endoscopic variceal ligation; evl works by capturing all or part of a varix resulting in occlusion from thrombosis. tissue sloughs off in days to weeks

Front 15

What is the management in acute variceal hemorrhage?

Back 15

ICU care, adequate fluid resuscitation, control bleeding, prevention of bleeding, preservation of liver function, correction of coagulopathy or thrombocytopenia, possibly Abx in Child Pugh B or C (give SBP prophylaxis)

Front 16

In the management of variceal hemorrhage, how does one correct coagulopathy?

Back 16

FFP or platelets, rFactor VIIa (needs larger RCT before being adopted)

Front 17

In the management of variceal hemorrhage, how achieve fluid resuscitation?

Back 17

usually with crystalloids (NS), may need blood and/or albumin, goal to maintain hemodynamic stability

Front 18

What Child Pugh Class has the highest risk for infection?

Back 18

Class B and C

Front 19

What is the prophylactic abx treatment during variceal hemorrhage?

Back 19

Norfloxacin 400mg po BID or Ceftriaxone 1g IVPB q24h

Front 20

What is the pharmacologic therapy in acute hemorrhage?

Back 20

Begin as soon as diagnosis is suspected, d/c beta blocker because decrease in bp will blunt the physiologic increase in HR associated with bleeding, incorporate the use of octreotide or vasopressin

Front 21

What is the trade name for octreotide?

Back 21

Sandostatin (somatostain analog)

Front 22

What are the pharmacologic effects of octreotide?

Back 22

local vasoconstrictive effect, decrease splanchinic blood flow, reduce portal/variceal pressure

Front 23

How long can octreotide be used?

Back 23

may be used for 5 days or longer

Front 24

What is the dose for octreotide?

Back 24

50 mcg bolus dose followed by 50mcg/h

Front 25

What is the stability info for octreotide?

Back 25

may dilute in d5w or NS

Front 26

What are the adverse effects of octreotide?

Back 26

sinus bradycardia, chest pain, HA, fatigue, hyperglycemia, GI, URI, dyspnea

Front 27

What are the monitoring parameters for octreotide?

Back 27

HR, BP, blood glucose, hemoglobin, hemocrit

Front 28

What is the most potent splanchnic vasoconstrictor?

Back 28

vasopressin (aka ADH or antidiuretic hormone)

Front 29

What are the side effects of vasopressin?

Back 29

cardiac and peripheral ischemia, arrhythmias, hypertension, bowel ischemia

Front 30

How can safety and efficacy be improved in vasopressin use?

Back 30

concomitant therapy with nitrates (but still has increased side effects compared to other treatments)

Front 31

How long can vasopressin be used for treatment?

Back 31

24 h because of side effect profiel

Front 32

What is the dose for vasopressin?

Back 32

0.2-0.4 unit/min (max 0.8units/min) with Nitroglycerin 40mcg/min to max 400mcg/min adjusted to maintain a SBP > 90

Front 33

What is vasopressin compatible in?

Back 33

NS or D5W 0.1-1 unit/ml

Front 34

What is the synthetic analogue of vasopressin not available in the US that has less side effects and longer duration of action?

Back 34

Terlipressin

Front 35

What is sclerotherapy?

Back 35

injecting sclerosing agent into varix which cause vein resorption; recommended in pts whom EVL is not technically feasible

Front 36

What Child Pugh Class is compensated cirrhosis?

Back 36

Class A

Front 37

What Child Pugh Class is decompensated cirrhosis?

Back 37

Child Pugh Class B or C

Front 38

What rescue therapy is available in varices hemorrhage pts when continued bleeding is present despite urgent endoscopic and/or pharmacologic therapy?

Back 38

TIPS, shunt surgery, ballon tamponade

Front 39

What Child Pugh class of patients has shunt surgery been proven to prevent bleeding?

Back 39

Class A

Front 40

Who is ballon tamponade indicated in with varice hemorrhaging?

Back 40

temporary relief for pts with a more definitive therapy is planned

Front 41

What can be done as secondary prophylaxis against varicies?

Back 41

endoscopic therapy, non-selective beta blockers, shunt surgery, TIPS

Front 42

What is hepatic encephalopathy?

Back 42

a mental or neuromotor dysfunction in a pt w/ acute or chronic liver disease; nitogenous substances direved from the gut adversely affect brain function

Front 43

What is the key factor in pathogenesis of hepatic encephalopathy?

Back 43

ammonia (crosses BBB and depresses CNS) which is derived from several tissues, from uresease acitivity of colonic bacteria, from deamidation of glutamine in small bowel

Front 44

Can ammonia level be correlated with mental state in cirrhosis?

Back 44

no

Front 45

What is the presentation of hepatic encephalopathy?

Back 45

physical findings of muscle wasting, jaundice, edema; neurologic signs of disturbance in sleep pattern, asterixis; lab abnormalities of hypokalemia, hyponatremia, and increased ammonia

Front 46

What is asterixis?

Back 46

wrist flap

Front 47

What are hepatic encephalopathy precipitating factors?

Back 47

GI bleeding (variceal or nonvariceal), infection/sepsis, electrolyte abnormalities, sedative ingestion, excessive dietary protein, constipation, renal insufficiency

Front 48

What are the two types of staging of hepatic encephalopathy?

Back 48

West Haven and Glasgow Scale

Front 49

What is the staging of West Haven based on in hepatic encephalopathy?

Back 49

based on state of consciousness, intellectual function, personality/behavior, and neuromuscular abnormalities

Front 50

Describe the Glasgow Scale

Back 50

used to evaluate level of consciousness, widely used in structural and metabolic disorders of brain dysfunction

Front 51

What is the consciousness level in stage 0 of West Haven Criteria for HE?

Back 51

Normal

Front 52

What is the intellect and behavior level in stage 0 of West Haven Criteria for HE?

Back 52

Normal

Front 53

What are the neurologic finding in Stage 0 of West Haven Criteria for HE?

Back 53

Normal exam impaired psychomotor testing

Front 54

Describe the consciousness in Stage 1 of West Haven Criteria for HE

Back 54

Mild lack of awareness

Front 55

Describe the intellect and behavior in Stage 1 of West Haven Criteria for HE

Back 55

Shortened attention span, impaired addition or subtraction

Front 56

Describe the neurologic findings in Stage 1 of West Haven Criteria for HE

Back 56

Mild asterixis or tremor

Front 57

Describe the consciousness in Stage 2 of West Haven Criteria for HE

Back 57

Lethargic

Front 58

Describe the intellect and behavior in Stage 2 of West Haven Criteria for HE

Back 58

disoriented, inappropriate behavior

Front 59

Describe the neurologic findings in Stage 2 of West Haven Criteria for HE

Back 59

obvious asterixis, slurred speech

Front 60

Describe the consciousness in Stage 3 of West Haven Criteria for HE

Back 60

somnolent but arousable

Front 61

Describe the intellect and behavior in Stage 3 of West Haven Criteria for HE

Back 61

gross disorientation, bizarre behavior

Front 62

Describe the neurologic findings in Stage 3 of West Haven Criteria for HE

Back 62

muscular rigidity and clonus hyperreflexia

Front 63

Describe the everything in Stage 4 of West Haven Criteria for HE

Back 63

coma and decrebrate posturing

Front 64

What are the goals of therapy for hepatic encephalopathy?

Back 64

Provision of supportive care, identification and removal of precipitating factors, reduction of nitrogenous load from gut, assessment of need for long term therapy

Front 65

What are the recommendations of protein adjustment in the treatment of HE?

Back 65

restriction at time of acute encephalopathy, 1-1.5g/kg/d, vegetable and dairy sources preferred

Front 66

What are the recommendations of zinc in treatment of HE?

Back 66

dosed 220mg orally bid-tid in zinc deficient cirrhotic pts to improce activity of urea cycle

Front 67

What class of drug is lactulose?

Back 67

hyperosmotic laxative

Front 68

What is the moa of lactulose?

Back 68

metabolized by bacteria in the colon to acetic acid and lactic acid to decrease ph. Acidification of bowel allows ammonia to pass from the bloodstream to the colon to be excreted which leads to peripheral ammonia levels being reduced

Front 69

What is the concentration of lactulose?

Back 69

20g/30ml

Front 70

What is the HE treatment dose of lactulose?

Back 70

30 to 45 ml po q 1 h until laxative effect is achieved, then reduce to 30 to 45 ml po tid to qid. Adj q 1 to 2 d to achieve 2 to 3 soft formed stools qd

Front 71

What are the Side effects of lactulose?

Back 71

bloating, diarrhea, epigastric pain, flatulence, nv, hypokalemia, hyponatremia

Front 72

How can lactulose be give in NPO?

Back 72

lactulose retention enema

Front 73

What is the lactulose enema?

Back 73

300ml lactulose in 700ml water instilled by rectal ballon catheter for 1 h

Front 74

When are abx indicated in HE?

Back 74

for pts that are intolerant of lactulose or have continued sx despite tx (believed to reverse HE by alteration of colonic bacteria)

Front 75

What are the abx s indicated in HE?

Back 75

Metronidazole, neomycin, rifaximin

Front 76

What is the trade name for metronidazole?

Back 76

Flagyl

Front 77

What is the moa of flagyl?

Back 77

interacts with dna to cause loss of helical structure, strand breakage, and resultant inhibition of nucleic acid synthesis and cell death

Front 78

What is the dosing of flagyl for HE?

Back 78

250mg po q 8-12h

Front 79

What are the dose adj for flagyl?

Back 79

renal: decrease dose by 50% if CrCl is <10 ml/min; hepatic: decrease dose (no specific recommendations)

Front 80

What are the side effects of flagyl?

Back 80

Nausea, dizziness, HA, vaginal irritation or discharge, Stevens Johnsons syndrome, toxic epidermal necrolysis, ototoxicity, peripheral neuropathy

Front 81

What are the patient counseling point for flagyl?

Back 81

Tk with food, may discolor urin reddish brown, monitor for neuorpathy or seizures, No alcohol (concomitant use may cause disulfiramlike rxn - ab cramps, NV, HA; wait at least 1 day after stopping tx to drink ETOH)

Front 82

What class of abx is neomycin?

Back 82

aminoglycoside

Front 83

What is the moa of neomycin?

Back 83

exerts its bactericifal effect by inhibiting protein synthesis in suseptible bacterial cells

Front 84

What is the dosing for neomycin in HE?

Back 84

4 to 12g/d po divided doses for 5 to 6 d. Max 12g/d. Do not use longer than 2 wks

Front 85

What are the dosing adj in neomycin use in HE?

Back 85

renal impairment: decrease dose when CrCl < 50ml/min

Front 86

What are the side effects of neomycin?

Back 86

N/V/D; ototoxicity, nephrotoxicity, respiratory tract paralysis, concomitant anesthesia

Front 87

What is the moa of rifaximin?

Back 87

semi-sythetic, non systemic abx that inhibits bacterial RNA sythesis by binding to the beta subunit of bacterial DNA-dependent RNA polymerase

Front 88

What is the dosing in rifaximin in HE?

Back 88

400mg po tid ro 550mg BID

Front 89

What is the dosing adj for rifaximin in HE?

Back 89

no adj needed for liver or kidney failure

Front 90

What are the side effects for rifaximin?

Back 90

peripheral edema, abd pain, constipation, defication, urgency, flatulence, nausea, rectal tenesmus (feeling of retention after defication), ascites, dizziness, HA fatigue

Front 91

What is the 1st line therapy for acute and chronic HE?

Back 91

lactulose

Front 92

What is the 2nd line therapy for HE?

Back 92

abx

Front 93

What is the drug therapy for esophageal varices?

Back 93

nonselective beta blockers

Front 94

What is the drug therapy for ascites?

Back 94

diuretics

Front 95

What is the drug therapy for SBP?

Back 95

3rd gen cephalosporin or fluoroquinolone

Front 96

What is the drug therapy for variceal hemorrhage?

Back 96

octreotide

Front 97

What is the drug therapy for hepatic encephalopathy?

Back 97

lactulose