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Special Pop Exam 3 > Liver/GI Part 2 > Flashcards

Liver/GI Part 2 Flashcards

28-53

1
Q

Hypotension is common with spinal anesthesia and must be promptly treated with … to prevent hypoperfusion

A

fluids or vasopressors

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2
Q

High block can impair
(2)

A

cardiac output and hepatic perfusion

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3
Q

T/F:
Spinal anesthesia may be preferred over general anesthesia in some liver surgeries since it better preserves hepatic blood flow.

A

True

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4
Q

Use caution with epi in spinal injectate bc…

A

can transiently reduce hepatic perfusion due to alpha-receptor mediated vasoconstriction

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5
Q

spinal anesthesia & liver fxn
(4)

A
  • alone does not typically impair hepatic circulation
  • prevent high block
  • treat any resulting hypotension
  • sympathetic blockade helps redirect blood to the splanchnic vessels
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6
Q

Which Volatiles reduce Hepatic Blood Flow
most to least

A

Halothane = greatest reduction

desfluane slightly greater than sevo and iso

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7
Q

Which volatiles are preferred for patients with liver disease?
why?

A

Isoflurane and sevoflurane

less disturbance in hepatic arterial blood flow

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8
Q

Anesthetic agents reduce hepatic blood flow by ___% after induction

A

30-50

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9
Q

Which volatile increases hepatic blood via direct vasodilation properties?

A

Isoflurane

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10
Q

BOX 33.3 

Clinicopathologic Features of Halothane Hepatitis

more common in males or females?

A

Female-to-male ratio
2:1

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11
Q

BOX 33.3 Clinicopathologic Features of Halothane Hepatitis

Latent period to first symptoms

A

After first exposure: 6 days (11 days to jaundice)

After multiple exposures: 3 days (6 days to jaundice)

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12
Q

BOX 33.3 Clinicopathologic Features of Halothane Hepatitis

Risk factors

A
  • Older age
  • Female
  • 2+ exposures (60%–90% of cases)
  • Obesity
  • Familial predisposition
  • Induction of CYPE1 by phenobarbital, alcohol, or isoniazid
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13
Q

These meds/substances predispose to halothane hepatitis

A

phenobarbital, alcohol, or isoniazid

Induction of CYPE1

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14
Q

BOX 33.3 Clinicopathologic Features of Halothane Hepatitis

Clinical features

A
  • Jaundice as presenting symptom in 25% (serum bilirubin: 3–50 mg/L)
  • Fever in 75% (precedes jaundice in 75%); chills in 30%
  • Rash in 10%
  • Myalgia in 20%
  • Ascites, renal failure, and/or gastrointestinal hemorrhage in 20%–30%
  • Eosinophilia in 20%–60%
  • Serum ALT and AST levels: 25–250 × ULN
  • Serum alkaline phosphatase level: 1–3 × ULN
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15
Q

What can hinder hepatic flow by increasing CVP?

A

mechanical ventilation, fluid overload, heart failure

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16
Q

what can directly occlude inflow or outflow vessels with hepatic vascular occlusion?

A

Surgical manipulation during procedures like liver resection or transplant

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17
Q

can reduce cardiac output and thus, hepatic perfusion

A

Myocardial depression, dysrhythmias, decreased intravascular volume

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18
Q

Compression of IVC can obstruct hepatic venous return. What is an example of this?

A

Improper positioning or abdominal packing pushing on inferior vena cava

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19
Q

Overall list of things that can impair hepatic blood flow

A
  • higher CVP (mechanical ventilation, fluid overload, heart failure)
  • Hepatic vascular occlusion - Surgical manipulation during procedures like liver resection or transplant
  • Low CO (Myo🩷 depression, dysrhythmias, decreased intravascular volume)
  • Endothelial dysfxn (sepsis, ischemia-reperfusion injury)
  • Compression of IVC (bad position, abdominal packing)
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20
Q

Spinal anesthesia induces (2)

A

sympathetic blockade and vasodilation

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21
Q

Spinal anesthesia Redistributes blood flow to

A

splanchnic vascular bed

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22
Q

A spinal will (reduce/increase) vascular resistance in hepatic arterial and portal circulation

A

reduce

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23
Q

Vasodilation from spinals are mediated by…

A

decreased vasoconstrictor hormones

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24
Q

ALL opioids have been implicated in causing a spasm of the sphincter of Oddi BUT the incidence is lower with

A

fentanyl

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25
Q

How to treat spasm of the Oddi sphincter

A

Nalbuphine or naloxone

Atropine, glyco, glucagon and nitro may also be effective

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26
Q

Effects of Anesthesia on Liver Function

Reduced response to these endogenous vasoconstrictors

A

Angiotensin II, AVP, and norepinephrine

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27
Q

Why is there a Reduced response to endogenous vasoconstrictors?

Angiotensin II, AVP, and norepinephrine

A

release of nitric oxide, prostacyclin and other endothelial-derived factors in response to humoral and mechanical stimuli.

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28
Q

Albumin
3 major indications for treatment of cirrhotic liver disease

A
  • After large volume paracentesis
  • To prevent renal impairment (Bili >4 or Creatinine >1)
  • Presence of HRS-SKI (Use with splanchnic vasoconstrictors)
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29
Q

Consider a-line for patients with

A

end-stage liver disease

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30
Q

Liver Cases

Besides an A-line, these other monitors are useful
(but do a risk vs benefit assessment)

A
  • CVP for fluid responsiveness
  • PAC for pulmonary HTN and low EF
  • TEE for preload, contractility, EF, regional wall abnormalities, emboli
  • Avoid transgastric views
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31
Q

Liver cases
TEG is helpful for ___, but this only reflects…

A

PT as a predictor of bleeding risk

only reflects procoagulant factor levels

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32
Q

Diseases of the Liver

A
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33
Q

Cirrhosis

A

Histological development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury

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34
Q

Portal HTN

A

abnormally high BP in the portal vein system, which carries blood from the intestines, spleen, pancreas and gallbladder to the liver.

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35
Q

Viral hepatitis can be caused by …

A

hepatitis A (HAV), B (HBV), C (HCV), D (HDV), and E (HEV)

Any of these variations can lead to serious illness and death

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36
Q

Which hepatitis viruses are acute vs chronic

A
  • A = acute symptomology
  • B & C= significant chronic sequelae

A & E rarely affect the liver chronically

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37
Q

The most common reason for liver transplantation in developing countries

A

Both Hep B & C

HBV and HCV

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38
Q

Hepatitis
Current treatment regimens

A

2 direct acting antiviral drugs

target specific steps within the HCV replication cycle with or without interferon for a duration of 8 to 12 weeks

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39
Q

Hepatitis

Antiviral drug choice and treatment duration are based on

A
  • The genotype of HCV
  • Stage of liver disease
  • Presence of cirrhosis
  • Previous response to interferon
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40
Q

Genotype 1A is the most common form in the US (70%) and is treated with

A

sofosbuvir/velpatasvir drug combination

These drugs provide a rate of infection clearance of 98% in genotype 1A and 99% in genotype 1B

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41
Q

Pregnancy-related Liver Diseases
occurrence rate

A

3-5% of pregnancies

42
Q

Pregnancy-related Liver Diseases
Common causes

A
  • hyperemesis gravidarum
  • intrahepatic cholestasis of pregnancy
  • preeclampsia
  • HELLP syndrome
  • acute fatty liver of pregnancy (AFLP)
43
Q

3 risk factors for Hyperemesis gravidarum
(1st trimester)

A
  • hyperthyroidism
  • molar pregnancy
  • multiple pregnancies
44
Q

Hyperemesis gravidarum (1st trimester)
Will elevate which enzymes by how much?
What is NOT elevated?

A

up to 20-fold elevation of liver enzymes

but not bilirubin

45
Q

most common of later pregnancy liver diseases

A

HELLP

46
Q

HELLP syndrome
is comprised of…

A
  • microangiopathic hemolytic anemia (MAHA)
  • elevated liver enzymes
  • low platelet count

….in the preeclamptic patient

47
Q

How many Pre-E patients develop HELLP?
How fatal is it?

A

20% of severely preeclamptic patients

up to 25% maternal mortality

48
Q

AFLP is a result of

A
  • rapid microvesicular fatty infiltration of the liver resulting in acute portal hypertension and encephalopathy
  • an association between it and abnormalities in the enzymes involved in β-oxidation of fatty acids.
49
Q

AFLP Symptoms are similar to severe preeclampsia and HELLP BUT the patient may additionally have…

A

laboratory and clinical findings more unique to liver failure

  • hypoglycemia
  • elevated ammonia
  • asterixis
  • encephalopathy
50
Q

How does Cirrhosis evolve into Portal Hypertension?

A
  1. Hepatocyte necrosis = deteriorates liver function
  2. Liver parenchyma is replaced by fibrous and nodular tissue
  3. Distorts, compresses, and obstructs normal portal venous blood flow
  4. Portal hypertension develops
51
Q

Cirrhosis and Portal Hypertension
by HVPG values

A
52
Q

Cirrhosis and Portal Hypertension
-definition
-causes
-end result

A
53
Q

3 key complications of portal hypertension include

A

1. Variceal bleeding - ruptured varices are a leading cause of death

2 .Ascites - fluid accumulation in the abdominal cavity

3. Hepatic encephalopathy- confusion and altered mental state

54
Q

Cirrhosis & Portal HTN
Cardiac sequelae

A

hyperdynamic circulation due to decreased SVR causes increased CO

55
Q

Cirrhosis & Portal HTN
Diagnosis

A

measuring the pressure gradient between the portal vein and IVC

typically via splenic or hepatic vein catheterization

56
Q

Cirrhotic patients are considered to have

A

a bleeding diathesis

(vs DIC which is a thrombotic diasthesis)

57
Q

Cirrhosis is a (bleeding/thrombosis) diathesis

A

bleeding

DIC = thrombotic diathesis

58
Q

Cirrhosis

thrombocytopenia & clotting factor deficiencies

A
  • up to 90% of platelets may be in the spleen
  • ↓ protein C & S balance the decreased levels of procoagulants

Thus they are at risk for both bleeding as well as thrombosis (due to relatively elevated levels of factors VIII and von Willebrand factor)

59
Q

Cirrhosis is a bleeding diathesis, but they are at risk for both bleeding and thrombosis due to …

A

relatively elevated
factors VIII & vWf

60
Q

Portotopulmonary Syndrome

A
  • Pulmonary arterial HTN + portal HTN
  • with or without liver disease
  • Systemic vasodilation with local pulmonary production of vasoconstrictors
61
Q

Portotopulmonary Syndrome
Mean PAP

A

> 25 mmHg

62
Q

T/F:
Curative treatment of Portotopulmonary Syndrome includes 2 direct acting antiviral drugs that target specific steps within the HCV replication cycle.

A

False
this is hepatitis

liver transplant is the cure for Portotopulmonary Syndrome

63
Q

Hepatopulmonary Syndrome

A

* Triad of portal HTN, hypoxemia, and pulmonary vascular dilatations
* Arteria hypoxemia caused by intrapulmonary vascular dilatations
* PaO2 <80 mmHg
* or A:a gradient >15mm Hg

Portotopulmonary Syndrome: Pulmonary arterial HTN + portal HTN with or without liver disease

64
Q

Hepatopulmonary Syndrome causes poor tolerance of gravitational effects on pulmonary blood flow leading to ____________

A

platypnea-orthodeoxia

65
Q

Hepatopulmonary Syndrome
which position is best?

A

supine improves oxygenation

standing worsens hypoxemia

66
Q

Hepatorenal Syndrome

A
  • Acute, reversible kidney failure due to end-stage liver disease
  • Impaired renal blood flow and intense vasoconstriction
67
Q

Hepatorenal Syndrome
causes

A
  • Splanchnic vasodilation and reduced systemic resistance in liver failure
  • Decreased effective arterial blood volume
  • Activation of renin-angiotensin and sympathetic nervous systems
  • Intense renal vasoconstriction
68
Q

Which liver syndrome/disease activates the RAAS?

A

Hepatorenal Syndrome

Intense renal vasoconstriction

69
Q

Hepatorenal Syndrome
Pathophysiology:

A
  • Reduced GFR but kidneys intact
  • Diminished natriuresis, sodium retention, ascites
70
Q

BOX 33.8 
Management of Hepatorenal Syndrome (HRS)

A
  • Prevent variceal bleeding
  • Prevention of hepatorenal syndrome (HRS)
  • Treatment of hepatorenal syndrome
  • Vasopressor therapy (in addition to albumin)
  • Evaluation of patient for liver transplant
71
Q

BOX 33.8 Management of Hepatorenal Syndrome (HRS)

Prevent variceal bleeding

A
  • Measures to prevent variceal bleeding (e.g., β-receptor blocking agent, band ligation)
  • Pentoxifylline for severe alcohol-associated hepatitis
72
Q

BOX 33.8 Management of Hepatorenal Syndrome (HRS)

Prevention of hepatorenal syndrome (HRS)

A
  • Avoidance of intravascular volume depletion (diuretics, lactulose, GI bleeding, large-volume paracentesis without adequate volume repletion)
  • Judicious management of nephrotoxins (ACEIs, ARBs, NSAIDs, antibiotics)
  • Prompt diagnosis and treatment of infections (spontaneous bacterial peritonitis [SBP], sepsis)
  • SBP prophylaxis
73
Q

BOX 33.8 Management of Hepatorenal Syndrome (HRS)

Treatment of hepatorenal syndrome

A
  • No nephrotoxic agents (ACEIs, ARBs, NSAIDs, diuretics)
  • Antibiotics for infections
  • IV albumin—bolus of 1 g/kg/day on presentation (maximum dose, 100 g daily). Continue at a dose of 20–60 g daily as required to maintain the central venous pressure between 10 and 15 cm H2O
74
Q

BOX 33.8 Management of Hepatorenal Syndrome (HRS)

Vasopressor therapy
(in addition to albumin)

A
  • Midodrine and octreotide (MAP increase 15+ mm Hg)

OR

  • Norepi drip (0.1–0.7 mcg/kg/min; Increase by 0.05 mcg/kg/min Q4 hr; MAP increase 10+)

pressors for max 2 wks until HRS reverses or liver transplant

75
Q

Hepatorenal Syndrome
Management (Box 33.8)

A
  • Fluid restriction vs intravascular volume depletion, albumin, avoid nephrotoxins
  • Vasoconstrictors, midodrine, octreotide, norepi
  • Liver transplantation (without: mortality >50%)
76
Q

T/F:
The development of Hepatopulmonary Syndrome is an ominous sign and signals the need for immediate transplantation evaluation

A

False
this applies to Hepatorenal Syndrome

Portotopulmonary Syndrome is also only cured by transplant

77
Q

Hepatic Encephalopathy

A
  • Neurotoxins (ammonia) accumulate and alter neurotransmission via glutamate or altered cerebral energy homeostasis
  • Mild apraxia -> behavioral changes -> decerebrate posturing -> coma
78
Q

Hepatic Encephalopathy can result in (decerebrate/decorticate) posturing

A

decerebrate

79
Q

Hepatic Encephalopathy
differential diagnosis

A
  • Poor metabolism of gut-produced ammonia vs intracranial bleeding
  • Failure to metabolize vs failure to synthesize substances; shunting
80
Q

Hepatic Encephalopathy
treatment

A

Nonabsorbable disaccharides

81
Q

Risk Scores for Cirrhosis:
Child-Pugh Classification

A
82
Q

Risk Scores for Cirrhosis:
Model for End-stage Liver Dx
(MELD)

A
83
Q

Transjugular Intrahepatic Portosystemic Shunt
(TIPS procedure)
treats…

A
  • refractory variceal hemorrhage and refractory ascites
  • Manages portal HTN by creating a direct communication between the portal vein and the hepatic vein
84
Q

The TIPS procedure shunts blood flow how?

A

Shunts portal venous flow to the systemic circulation

for: refractory variceal hemorrhage, refractory ascites, manages portal HTN

85
Q

How does the TIPS procedure alleviate bleeding and ascites

A

reduces the portosystemic pressure gradient

86
Q

Absolute contraindications for Transjugular Intrahepatic Portosystemic Shunt (TIPS procedure)

A
  • heart failure
  • severe tricuspid regurgitation
  • severe pulmonary hypertension
87
Q

T/F:
TIPS Procedure requires general & ETT.

A

False
Utilize sedation or general anesthesia

limits patient movement, controls diaphragmatic excursion, and reduces the risk of aspiration

88
Q

TIPS increases venous return, which can unmask these 2 conditions common to chronic liver disease patients

A

undiagnosed cardiac dysfunction or pulmonary HTN

89
Q

TIPS Procedure
Complications

A
  • pneumothorax
  • vascular injury
  • dysrhythmias
  • hemorrhage
90
Q

TIPS Procedure
considerations

A
  • Volume resuscitation
  • Platelets and clotting factors replenished
91
Q

T/F:
Elevations in AST are specific to liver tissue injury.

A

False
ALT = liver specific

92
Q

AST:ALT

A

greater than 2: alcoholic liver disease
<1: fatty liver/chronic hepatitis

93
Q

Which zone is affected most by hypoxia and reactive intermediates?

A

3

94
Q

Which liver cells have the greatest quantity of cytochrome P450 enzymes and are the site of anaerobic metabolism?

A

pericentral hepatocytes

95
Q

Gold standard for diagnosing esophageal varices

A

EGD

96
Q

MELD scores and their mortality

A
97
Q

MELD score accounts for … (3)

A
  • Bilirubin
  • PT/INR
  • Creatinine
98
Q

MELD score ___ should not undergo elective surgery

A

> 15

99
Q

MELD is a scoring system that assesses

A
  • severity of chronic liver disease
  • prioritizing liver recipients
  • three-month survival

The original MELD score was developed to determine short-term mortality in patients receiving a transjugular intrahepatic portosystemic shunt (TIPS) procedure.

100
Q

🔷
mendelson syndrome
the gastic fluid aspirated must be…

A

0.4 ml/kg (30 ml)
pH <2.5

101
Q

Symptoms related to carcinoid syndrome

A
  • episodic flushing (kinins, histamine)
  • diarrhea (serotonin, prostaglandins E and F)
  • heart disease, tricuspid regurgitation,
  • pulmonic stenosis,
  • supraventricular tachydysrhythmias (serotonin)
  • bronchoconstriction (serotonin, bradykinin, substance P)
  • hypotension (kinins, histamine)
  • hypertension (serotonin)
  • abdominal pain (SBO)
  • hepatomegaly (metastases),
  • hyperglycemia
  • hypoalbuminemia (pellagra-like skin lesions resulting from niacin deficiency)

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