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Special Pop Exam 3 > Liver and GI > Flashcards

Liver and GI Flashcards

1
Q

in hepatic portal circulation, the vein is located between ____________

A

2 capillary beds

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2
Q

function of the hepatic portal vein

A

collecting blood from capillaries in visceral structures located in the abdomen and empties into the liver for distribution to the hepatic capillaries

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3
Q

hepatic veins return blood to

A

the inferior vena cava

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4
Q

what is the largest internal organ

A

liver

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5
Q

the liver is ____________ of the total body mass of adults

A

2%

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6
Q

the liver receives ____________ % of CO

A

25%

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7
Q

how does the liver receive blood

A

from two sources - oxygenated blood from the hepatic artery and nutrient-rich blood from the portal vein (each vessel provides roughly 50% of hepatic oxygen supply)

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8
Q

Sympathetic innervation from ____________ controls resistance in the hepatic venules

A

T3 to T11

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9
Q

Changes in compliance in the hepatic venous system contribute to ____________

A

the regulation of cardiac output and blood volume

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10
Q

In the presence of reduced portal venous flow, the hepatic artery can ____________

A

increase flow by as much as 100% to maintain hepatic oxygen delivery.

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11
Q

“hepatic arterial buffer” response

A

the reciprocal relationship between flow in the two afferent vessels

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12
Q

liver blood supply vs liver oxygen supply

A
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13
Q

8 functional anatomic segments of the liver

A
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14
Q

functions of the liver

A

the liver carries out essential metabolic, detoxifying, and regulatory functions to keep the body healthy

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15
Q

liver role in metabolism

A
  • The liver metabolizes carbohydrates, proteins, fats, and vitamins and regulates energy balance.
  • The liver plays a major role in the metabolism of nutrients such as glucose nitrogen and lipids and detoxifies chemicals, including lipophilic medications
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16
Q

liver dysfunction affects the metabolism of

A

nutrients and xenobiotics and negatively impacts nearly every other organ system

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17
Q

what does the liver do to amino acids

A

the liver is capable of deamination of amino acids, which is required for energy production or the conversion of amino acids to carbohydrates or fats

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18
Q

what does deamination of amino acids do

A

Deamination produces ammonia, which is toxic.

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19
Q

what is an additional source of ammonia

A

Intestinal bacteria are an additional source of ammonia.

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20
Q

The liver removes ammonia through ____________

A

the formation of urea.

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21
Q

what important nutrients does the liver store?

A
  • vitamin A, D, E, K, B12, iron, and minerals
  • glycogen
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22
Q

____________ can be converted to glucose when the body needs energy.

A

glycogen

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23
Q

T/ F In patients with altered liver function, blood glucose concentration can rise several fold higher than the postprandial levels found in patients with normal hepatic function.

A

true

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24
Q

what is detoxification

A

The liver neutralizes chemicals and drugs in the blood and readies them for excretion.

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25
Q

The liver contains ____________ which destroy bacteria and remove foreign particles from the blood.

A

Kupffer cells

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26
Q

the liver produces ____________ that combat infections

A

immune factors and proteins

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27
Q

liver blood filtration rate

A

The liver filters about 1.4 liters of blood per minute

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28
Q

what does the liver remove from blood

A

toxins, waste products, bacteria, and old red blood cells.

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29
Q

what clotting factors are and are not produced in the liver

A

The liver produces clotting factors and proteins that help the blood clot and prevent excessive bleeding.

All of the blood clotting factors, with the exception of factors III (tissue thromboplastin), IV (calcium), and VIII (von Willebrand factor), are synthesized in the liver.

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30
Q

vitamin K is reqiured for synthesis of ____________

A

prothrombin (Factor II)

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31
Q

what factors is vitamin K required for

A

factors VII, IX, and X.

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32
Q

most abundant plasma protein made by the liver

A

albumin

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33
Q

functions of albumin

A

It maintains oncotic pressure, transports lipids and hormones, and has antioxidant properties

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34
Q

Serum albumin levels reflect

A

liver function and nutritional status.

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35
Q

coagulation factors are responsible for

A

hemostasis and anticoagulation

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36
Q

immunoglobulins are responsible for

A

humoral immunity and defense

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37
Q

C-reactive protein increases dramatically during

A

inflammation and infection

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38
Q

CRP activates ____________ and ____________

A

complement and phagocytosis

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39
Q

This copper-binding glycoprotein made in the liver carries 90% of plasma copper and has ferroxidase activity.

A

cerloplasmin

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40
Q

what transports lipids through the circulation

A

lipoproteins

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41
Q

function of α-1 antitrypsin

A

made by the liver protects tissues from proteases like elastase.

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42
Q

low levels of α-1 antitrypsin

A

increase risk of emphysema.

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43
Q

clinical significance of plasma protein production

A

Levels indicate liver function and protein status

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44
Q

deficiencies of plasma protein production will cause…

A

edema, bleeding, lipid issues, infections

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45
Q

The liver produces a wide range of vital plasma proteins involved in critical physiological processes. Dysfunction impairs ____________, ____________, and ____________

A

transport, immunity, coagulation.

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46
Q

The liver metabolizes amino acids and converts excess amino acids to ____________

A

glucose or ketone bodies.

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47
Q

the liver detoxifies ammonia by converting it to ____________

A

urea

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48
Q

The liver takes up amino acids from the blood and regulates ____________

A

systemic amino acid levels.

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49
Q

In response to inflammation or injury, the liver increases production of certain plasma proteins called acute phase proteins. Examples are ____________ and ____________

A

C-reactive protein and serum amyloid A.

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50
Q

The liver can synthesize glucose from amino acids through ____________. This helps maintain blood glucose when glucose supply is low.

A

gluconeogenesis

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51
Q

The liver stores amino acids in the form of proteins like ____________

A

albumin

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52
Q

The liver makes carrier proteins that transport various compounds like ____________

A

bilirubin, hormones, metals, drugs.

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53
Q

T/F The liver synthesizes most of the coagulation factors and fibrinolytic proteins involved in blood clotting and thrombus dissolution.

A

TRUE

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54
Q

____________ is a soluble plasma glycoprotein synthesized by the liver and megakaryocytes (bone marrow cells)

A

fibrinogen

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55
Q

During coagulation, ____________ converts fibrinogen into fibrin forming the fibrin meshwork of a blood clot

A

thrombin

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56
Q

10-15% is of fibrinogen is produced by ____________ which helps maintain adequate fibrinogen level even in severe liver disease

A

megakaryocytes

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57
Q

Cytochrome P450 enzymes metabolize drugs through chemical reactions like ____________, ____________ and ____________

A

oxidation, reduction, hydrolysis

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58
Q

____________ system metabolizes ~75% of all medications

A

P450

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59
Q

what do P450 enzymes do to drugs

A

makes drugs more water-soluble (polar) for easier excretion into the bile or urine

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60
Q

The liver can activate a ____________ into its active form through metabolism. It can also convert an active drug into an inactive metabolite, reducing ____________

A

prodrug; its pharmacological effects.

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61
Q

Liver impairment or disease like ____________ can significantly impact the metabolism and clearance of many drugs. Doses may need adjustment in such patients to avoid toxicity.

A

cirrhosis

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62
Q

What do Phase I reactions do

A

modifies drug with functionalization actions resulting in loss of pharmacologic activity

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63
Q

what do phase II reactions do?

A

conjugates the metabolite with a second molecule (glucuronic acid, sulfate, glutathione, amino acid, or acetate) forming a covalent link

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64
Q

Factors like ____________ (4) affect hepatic metabolizing enzymes, altering the efficacy and side effects of medications.

A

age, genetics, drug interactions, and comorbidities

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65
Q

The liver helps detoxify and excrete drugs, but drug metabolites may also be ____________

A

more toxic than the parent drug in some cases.

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66
Q

50% of currently manufactured drugs are metabolized by ____________

A

a single CYP

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67
Q

Rate of metabolism can be increased or decreased with ____________

A

coadministration of 2 drugs metabolized by the same enzyme system

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68
Q

Enzyme induction hastens ____________ and promotes tolerance

A

metabolism

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69
Q

function of LFTs

A

Measure levels of enzymes, proteins, and bilirubin to assess liver function and identify liver injury

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70
Q

causes of hepatic dysfunction based on LFT results

A
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71
Q

____________ is more specific for liver injury than ____________

A

ALT; AST

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72
Q

____________ and ___________indicate cholestatic liver disease

A

ALP and GGT

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73
Q

Mechanical ventilation with positive pressure can impair ____________ and ____________

A

venous return and cardiac output, reducing perfusion

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74
Q

Drugs used during anesthesia like inhaled anesthetics, propofol, opioids can cause systemic vasodilation, decreasing ____________

A

hepatic vascular resistance and blood flow.

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75
Q

Low blood pressure reduces perfusion pressure to the liver. Causes include ____________ (3)

A

hypovolemia, blood loss, effects of anesthetic drugs.

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76
Q

Increase in central venous pressure is caused by factors like

A

mechanical ventilation, fluid overload, heart failure can increase CVP, hindering hepatic blood flow

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77
Q

Surgical manipulation during procedures like liver resection or transplant can directly ____________

A

occlude inflow or outflow vessels.

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78
Q

effects of anesthesia and hepatic blood flow

A
  • ↑ in CVP
  • hepatic vascular occlusion
  • ↓ cardiac output
  • endothelial dysfunction
  • compression of IVC
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79
Q

Coexisting conditions like sepsis, ischemia-reperfusion injury can impair ____________ needed for blood flow.

A

vasodilation

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80
Q

Improper positioning or abdominal packing pushing on inferior vena cava can obstruct ____________

A

hepatic venous return.

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81
Q

effects of spinal anesthesia on the liver

A
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82
Q

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

A

fluids or vasopressors

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83
Q

High block can impair
(2)

A

cardiac output and hepatic perfusion

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84
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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85
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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86
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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87
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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88
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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89
Q

Anesthetic agents reduce hepatic blood flow by ___% after induction

A

30-50

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90
Q

Which volatile increases hepatic blood via direct vasodilation properties?

A

Isoflurane

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91
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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92
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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93
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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94
Q

These meds/substances predispose to halothane hepatitis

A

phenobarbital, alcohol, or isoniazid

Induction of CYPE1

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95
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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96
Q

What can hinder hepatic flow by increasing CVP?

A

mechanical ventilation, fluid overload, heart failure

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97
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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98
Q

can reduce cardiac output and thus, hepatic perfusion

A

Myocardial depression, dysrhythmias, decreased intravascular volume

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99
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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100
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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101
Q

Spinal anesthesia induces (2)

A

sympathetic blockade and vasodilation

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102
Q

Spinal anesthesia Redistributes blood flow to

A

splanchnic vascular bed

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103
Q

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

A

reduce

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104
Q

Vasodilation from spinals are mediated by…

A

decreased vasoconstrictor hormones

105
Q

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

A

fentanyl

106
Q

How to treat spasm of the Oddi sphincter

A

Nalbuphine or naloxone

Atropine, glyco, glucagon and nitro may also be effective

107
Q

Effects of Anesthesia on Liver Function

Reduced response to these endogenous vasoconstrictors

A

Angiotensin II, AVP, and norepinephrine

108
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.

109
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)
110
Q

Consider a-line for patients with

A

end-stage liver disease

111
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
112
Q

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

A

PT as a predictor of bleeding risk

only reflects procoagulant factor levels

113
Q

Diseases of the Liver

A
114
Q

Cirrhosis

A

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

115
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.

116
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

117
Q

Which hepatitis viruses are acute vs chronic

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

A & E rarely affect the liver chronically

118
Q

The most common reason for liver transplantation in developing countries

A

Both Hep B & C

HBV and HCV

119
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

120
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
121
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

122
Q

Pregnancy-related Liver Diseases
occurrence rate

A

3-5% of pregnancies

123
Q

Pregnancy-related Liver Diseases
Common causes

A
  • hyperemesis gravidarum
  • intrahepatic cholestasis of pregnancy
  • preeclampsia
  • HELLP syndrome
  • acute fatty liver of pregnancy (AFLP)
124
Q

3 risk factors for Hyperemesis gravidarum
(1st trimester)

A
  • hyperthyroidism
  • molar pregnancy
  • multiple pregnancies
125
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

126
Q

most common of later pregnancy liver diseases

A

HELLP

127
Q

HELLP syndrome
is comprised of…

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

….in the preeclamptic patient

128
Q

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

A

20% of severely preeclamptic patients

up to 25% maternal mortality

129
Q

AFLP is a result of

A
  • rapid microvesicular fatty infiltration of the liver resulting in acute portal hypertension and encephalopathy
  • a/w abnormal enzymes involved in β-oxidation of fatty acids.
130
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
131
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
132
Q

Cirrhosis and Portal Hypertension
by HVPG values

A
133
Q

Cirrhosis and Portal Hypertension
-definition
-causes
-end result

A
134
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

135
Q

Cirrhosis & Portal HTN
Cardiac sequelae

A

hyperdynamic circulation due to decreased SVR causes increased CO

136
Q

Cirrhosis & Portal HTN
Diagnosis

A

measuring the pressure gradient between the portal vein and IVC

typically via splenic or hepatic vein catheterization

137
Q

Cirrhotic patients are considered to have

A

a bleeding diathesis

(vs DIC which is a thrombotic diasthesis)

138
Q

Cirrhosis is a (bleeding/thrombosis) diathesis

A

bleeding

DIC = thrombotic diathesis

139
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)

140
Q

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

A

relatively elevated
factors VIII & vWf

141
Q

Portotopulmonary Syndrome

A
  • Pulmonary arterial HTN + portal HTN
  • with or without liver disease
  • Systemic vasodilation with local pulmonary production of vasoconstrictors
142
Q

Portotopulmonary Syndrome
Mean PAP

A

> 25 mmHg

143
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

144
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

145
Q

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

A

platypnea-orthodeoxia

146
Q

Hepatopulmonary Syndrome
which position is best?

A

supine improves oxygenation

standing worsens hypoxemia

147
Q

Hepatorenal Syndrome

A
  • Acute, reversible kidney failure due to end-stage liver disease
  • Impaired renal blood flow and intense vasoconstriction
148
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
149
Q

Which liver syndrome/disease activates the RAAS?

A

Hepatorenal Syndrome

Intense renal vasoconstriction

150
Q

Hepatorenal Syndrome
Pathophysiology:

A
  • Reduced GFR but kidneys intact
  • Diminished natriuresis, sodium retention, ascites
151
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
152
Q

BOX 33.8 Management of Hepatorenal Syndrome (HRS)

Prevent variceal bleeding

A
  • Measures to prevent bleeding (e.g., β-receptor blocking agent, band ligation)
  • Pentoxifylline for severe alcohol-associated hepatitis
153
Q

BOX 33.8 Management of Hepatorenal Syndrome (HRS)

Prevention of hepatorenal syndrome (HRS)

A
  • Avoid volume depletion (diuretics, lactulose, GI bleeding, large-volume paracentesis without adequate volume repletion)
  • caution w/ nephrotoxins (ACEIs, ARBs, NSAIDs, antibiotics)
  • Promptly manage infections (spontaneous bacterial peritonitis [SBP], sepsis)
  • SBP prophylaxis
154
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
155
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

156
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%)
157
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

158
Q

Hepatic Encephalopathy

A
  • Neurotoxins (ammonia) accumulate and alter neurotransmission via glutamate or altered cerebral energy homeostasis
  • Mild apraxia -> behavioral changes -> decerebrate posturing -> coma
159
Q

Hepatic Encephalopathy can result in (decerebrate/decorticate) posturing

A

decerebrate

160
Q

Hepatic Encephalopathy
differential diagnosis

A
  • Poor metabolism of gut-produced ammonia vs intracranial bleeding
  • Failure to metabolize vs failure to synthesize substances; shunting
161
Q

Hepatic Encephalopathy
treatment

A

Nonabsorbable disaccharides

162
Q

Risk Scores for Cirrhosis:
Child-Pugh Classification

A
163
Q

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

A
164
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
165
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

166
Q

How does the TIPS procedure alleviate bleeding and ascites

A

reduces the portosystemic pressure gradient

167
Q

Absolute contraindications for Transjugular Intrahepatic Portosystemic Shunt (TIPS procedure)

A
  • heart failure
  • severe tricuspid regurgitation
  • severe pulmonary hypertension
168
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

169
Q

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

A

undiagnosed cardiac dysfunction or pulmonary HTN

170
Q

TIPS Procedure
Complications

A
  • pneumothorax
  • vascular injury
  • dysrhythmias
  • hemorrhage
171
Q

TIPS Procedure
considerations

A
  • Volume resuscitation
  • Platelets and clotting factors replenished
172
Q

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

A

False
ALT = liver specific

173
Q

AST:ALT

A

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

174
Q

Which zone is affected most by hypoxia and reactive intermediates?

A

3

175
Q

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

A

pericentral hepatocytes

176
Q

Gold standard for diagnosing esophageal varices

A

EGD

177
Q

MELD scores and their mortality

A
178
Q

MELD score accounts for … (3)

A
  • Bilirubin
  • PT/INR
  • Creatinine
179
Q

MELD score ___ should not undergo elective surgery

A

> 15

180
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.

181
Q

🔷
mendelson syndrome
the gastic fluid aspirated must be…

A

0.4 ml/kg (30 ml)
pH <2.5

182
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)
183
Q

__________ is the sole definitive treatment modality for patients with acute liver failure, ESLD, and primary hepatic malignancy.

A

Liver transplantation

184
Q

___________ score is a validated system that UNOS uses for prioritizing patients on the liver transplant waiting list.

A

The Model for End-Stage Liver Disease (MELD)

185
Q

The MELD score is a validated system that uses ___________________ to mathematically rank adult patients according to their expected survival rate without transplantation.

A
  • serum total bilirubin
  • serum creatinine
  • INR values
186
Q

Three-Month Mortality According to MELD Score∗

A
187
Q

Signs and symptoms of liver failure:

A

Anorexia, weakness, nausea, vomiting, abdominal pain, hepatosplenomegaly, ascites, jaundice, metabolic encephalopathy, spider nevi.
Ascites: aspiration of fluid may see big hemodynamic shifts

188
Q

A patient with esophageal varices requires what specifics?

A

vasopressin, RSI intubation

189
Q

what is the management for pt with ascites?

A
  • need volume expanders (albumin)
  • Na restrictions and slow diuresis
190
Q

what pulmonary manifestations would you see with liver failure?

A

V/Q mismatch

191
Q

Portal hypertension typically manifests as:

A

ascites, esophageal varices; hepatic encephalopathy

192
Q

what are the CV manifestations a/w liver failure?

A
  • high cardiac output
  • high HR
  • low SVR
  • decreased RBF
  • extensive collaterals (esp lungs)
  • prolonged QT interval
193
Q

what would you see with the renal dysfxn a/w liver failure?

A

no Na or free water secretion, vasoconstricts and causes sympathetic release

194
Q

what is the anesthesia management like for liver transplants?

A

Standard monitors
A-line, large-bore IV access, CVC, PAC, cardiac output monitoring, POC ABGs, thromboelastogram (TEG), TEE, cell saver, rapid infuser, blood products (RBCs, FFPs, platelets, cryo)
PAC is gold standard in hemodynamic monitoring
Transfer to ICU on vent

195
Q

Thromboelastogram (TEG)

A
196
Q

whats included in the intraop management for a liver transplant?

A

Normovolemia
Coagulopathy: hyper- or hypocoaguable
Temperature: keep warm
Limited sedation
No contraindications to induction agents
Muscle relaxants
Opioid of choice
Post-induction hypotension
Altered pharmacokinetic and pharmacodynamic response
ICP monitoring

197
Q

an autosomal recessive disease characterized by impaired copper metabolism.

A

Wilson Disease

198
Q

α1-antitrypsin deficiency

A
  • genetic disorder that results in defective production of α1-antitrypsin protein
  • this protein protects the liver and lungs from neutrophil elastase, an enzyme that can disrupt connective tissue leading to inflammation, cirrhosis, and HCC.
  • In the lungs, patients with α1-antitrypsin deficiency can develop early-onset panlobular emphysema and symptoms of chronic obstructive pulmonary disease.
199
Q

________ is a disorder associated with excess iron in the body that can lead to multiorgan dysfunction.

A

Hemochromatosis

200
Q

Inborn Errors of Metabolism

A

Wilson Disease
α1-antitrypsin deficiency
Hemochromatosis

201
Q

Most common cause of cholestasis is ________

A

obstruction of biliary tract outside of the liver

202
Q

Diseases of the Biliary Tract

A

Suppression or cessation of bile flow
Most common cause of cholestasis is obstruction of biliary tract outside of the liver
Gallstones, stricture, tumor, infection, or ischemia

203
Q

Cholecystitis: causes and S/S

A

Caused by obstruction, infection, or both
Acute cholecystitis usually related to gallstones 90-95% of the time
S/S include sudden right upper quadrant tenderness, fever and leukocytosis
Inspiratory efforts worsen pain – Murphy sign
Jaundice – complete obstruction of cystic duct
Charcot’s triad- fever/chills, jaundice, RUQ pain

204
Q

Cholecystitis Anesthesia Management

A
  • Standard induction or RSI if N/V present
  • OG to decrease stomach
    Insufflation
  • Decreased FRC, CC and increased PIP, hypotension
  • 15 mmHg routine, higher decreases CO, PreLoad
  • Increased risk of gastric reflux
    Reverse Trendelenburg
  • Decreases venous return
205
Q

Contraindications to a lap cholecystectomy

A

Coagulopathy, severe COPD, ESLD, CHF

206
Q

Achalasia

A

Impaired relaxation of LES
Chronic achalasia results in dilation of esophagus, more food and fluids retained- aspiration risk
disease of the esophagus

207
Q

GERD

A

Failure of antireflux barriers
Can manifest as ENT or pulmonary symptoms
Chronic GERD can result in abnormal epithelial cells and predisposition to developing a malignancy

208
Q

Anesthesia for Esophageal Disorders

A

Asymptomatic vs uncontrolled disease with reflux symptoms
Aspiration prophylaxis during induction and emergence
Modification of gastric acidity with preoperative medications

209
Q

Peptic Ulcer Disease

A

Gastric ulcer is loss of mucosa due to inflammation
Approx 98% of peptic ulcer occur in the stomach and duodenum
H. Pylori infection is associated with development of 90% of duodenal ulcers and roughly 75% gastric ulcers

210
Q

Peptic Ulcer Disease Common complications include:

A

Hemorrhage
Perforation
Obstruction

211
Q

Gastritis: what is it? how do you treat it? what can be life-threatening?

A

Inflammatory disorder of gastric mucosa
Stress ulceration, stress erosive gastritis, and hemorrhagic gastritis
Hemorrhagic gastritis can be life threatening
Upper GI bleed needs treatment
RSI, Fluids, Blood? Platelets? FFP?
Protein pump inhibitors, H2 receptor antagonist

212
Q

Gastric Ulcer Disease Most common complication is________

A

perforation

213
Q

Develop from degeneration of stomach’s mucosal barrier against gastric acid

A

Gastric Ulcer Disease

214
Q

Gastric Ulcer Disease

A

Develop from degeneration of stomach’s mucosal barrier against gastric acid
Pain and anorexia predispose pt to wt loss and metabolic changes
Most common complication is perforation
Most occur in anterior aspect of lesser curvature

215
Q

_______ cancer 2nd most common cancer worldwide, 7th most in U.S.

A

Gastric

216
Q

Gastric Neoplastic Disease S/S

A

S/S include pain (constant, non-radiating and not relieved by food), wt loss, anorexia, fatigue, and vomiting

217
Q

Gastric Neoplastic Disease tX

A

Gastrectomy or partial gastrectomy (resection of tumor) remains the primary curative treatment

218
Q

Anesthetic Considerations for diseases of the stomach:

A

Many procedures are laparoscopic
Pts are usually acutely ill
Consider volume, albumin, usually anemic
Lab
Large IVs
T/C, have products available
Consider epidural for post-op pain management

219
Q

Anastamotic leakage risk factors:

A

anemias, co-morbidities, diabetics, vascular disease, decreased perfusion

220
Q

Postoperative ileus risk factors:

A

pain, anesthesia, manipulation of bowel contents, unbalanced electrolytes, immobility, intestinal wall swelling from IV fluids; prevention: start PO feeds as early as possible, early ambulation, minimize bowel manipulation

221
Q

Mesenteric traction syndrome s/s + tx:

A

tachycardia and hypotension; antihistamine and NSAIDS

222
Q

what kind of blood flow do you see to the intestines?

A

Splanchnic blood flow

223
Q

Zollinger-Ellison syndrome

A

Gastroduodenal and intestinal ulceration together with gastrin hypersecretion and a non-β islet cell tumor of the pancreas (gastrinoma)
Gastrin stimulates acid secretion through gastrin receptors on parietal cells and via histamine release; also excerts a trophic effect on gastric epithelial cells
Gastrinomas can develop in the presence of multiple endocrine neoplasia (MEN) type I, a disorder involving primarily three organ sites: the parathyroid glands, pancreas, and pituitary gland

224
Q

Abdominal Compartment Syndrome

A

Greater than 20mm HG intraabdominal pressure; normal pressure is less than 10mm HG
Measured with a bladder manometer
Organ dysfunction develops if longer than six hours; can lead to death
abdominal trauma, hemoperitoneum, mesenteric arterial thrombosis, acute pancreatitis, intestinal obstruction, visceral edema, and massive fluid volume replacement
Resuscitative efforts & exposure of the abdomen induce mesenteric edema formation and bowel dilation; delay closure until tension is resolved

225
Q

Carcinoid Tumors

A

Benign, slow growing
Symptoms related to space occupying
Usually originates in the GI tract
Usually asymptomatic
Can be metastatic
Hormones released are metabolized by the liver
Serotonin, histamine, kinin peptides

226
Q

Carcinoid Syndrome systemic effects:

A

Flushing, bronchoconstriction, hypotension, hypertension, diarrhea; life-threatening perioperative hemodynamic instability

227
Q

Carcinoid heart disease S/S:

A

Right sided cardiac involvement
Tricuspid and pulmonary valves
Tumors along valves
Bronchoconstriction
Metastasized by the lungs

228
Q

Carcinoid Syndrome Tx:

A

Octreotide: can be given IV; samatostatin
surgical excision, no chemo
Stress reduction: Carcinoid crisis
Avoid medications that increase release of hormones and mediators from tumor cells
Avoid meds that will release histamine

229
Q

Carcinoid crisis:

A

can necrose and release massive amounts of substances into circulations
Stress reduction can help prevent

230
Q

Alpha-adrenergic sympathetic stimulation inhibits _______

A

insulin secretion

231
Q

Exocrine digestive enzyme and endocrine hormonal capacity

A

Continuous secretion of 2.5 L of color, colorless, bicarbonate rich pancreatic juices (pH 8.3); main function duodenal alkalinization
Endocrine functional cells reside in the islets of Langerhans
Alpha cells secrete glucgon; Beta cells secrete insulin

232
Q

Insulin suppression results from:

A

Arterial hypoxemia
Hypothermia
Traumatic stress
Surgical stress

233
Q

_____ and ______ also inhibit insulin secretion

A

Beta-adrenergic sympathetic and Cholinergic blockade

234
Q

Insulin secretion is enhanced by:

A

Parasympathetic vagal stimulation
Beta adrenergic sympathetic activation
Cholinergic drub administration

235
Q

Acute Pancreatitis causes include:

A

alcohol abuse, trauma, ulcerative penetration, infection, vascular, metabolic disorders, autoimmune
80% of pancreatic disorder from alcohol and gallstones

236
Q

Acute Pancreatitis S/S include:

A

Abdominal distention
N/V
Pain
Hypotension
Hypovolemia

237
Q

Severe Acute Pancreatitis (SAP): what is it a/w? what is the main COD?

A

SAP associated with organ failure, local complications, prolonged ICU and 25% mortality rate
Multiple Organ dysfunction is main cause of death

238
Q

Describe the pain a/w pancreatitis and managing it.

A

Difficult to control pain from pancreatitis
will need narcotics, Morphine?, epidural analgesia
Pain radiates from midepigastric to periumbilical, can be worse in supine position

239
Q

Anesthetic Considerations for Pancreatic Disease:

A

Fluids and electrolytes resuscitation is imperative
Monitor labs
C-reactive Protein (CRP) > 150mg/L correlates with severity
ASA standard monitors, large IVs, consider CVP and A-line
Caution with medications that undergo hepatic biotransformation

240
Q

Chronic Pancreatitis most common etiology is _____

A

alcohol-70% of cases

241
Q

Chronic Pancreatitis S/S:

A

Abdominal pain
Wt loss
Malnutrition
Hepatic disease
Predisposed to pericardial and pleural effusions
Hypoalbuminemia
Hypomagnesemia

242
Q

Chronic Pancreatitis: WHAT IS IT?

A

Permanent and irreversible damage to the pancreas
Chronic inflammation, fibrosis, destruction of exocrine and endocrine tissue

243
Q

Pancreatic Tumors s/s

A

Painless jaundice
Dull aching midepigastric or back pain
Anorexia
Fatigue
New-onset DM is occasionally the 1st symptom

244
Q

Pancreatic Tumors

A

Pancreatic cancer 80-90% ductal adenocarcinomas
Can grow extensively before they produce symptoms
Generally resected by pancreaticoduodenectomy (Whipple)

245
Q

________ most common functioning tumor of the pancreas

A

Insulinoma

246
Q

Insulinoma s/s

A

Hypoglycemia
Seizures
Coma (symptoms of catecholamine release)

247
Q

Diagnostic Hallmark- Whipple triad S/S

A

Hypoglycemia (catecholamine release)
Low blood glucose (40-50 mg/do)
Relief after IV administration of glucose

248
Q

Whipple Procedure

A
249
Q

describe Splenic blood flow.

A

300mL/min and arises from splenic artery

250
Q

spleen function include:

A

blood filtering, maintenance of normal erythrocytes and immune processing of blood-borne foreign antigens

251
Q

Abnormal blood cells from disease such as sickle cell disease, thalassemia and spherocytosis removed by_________.

A

macrophages

252
Q

Splenic Disease can lead to ______

A

worsening anemia and symptomatic splenomegaly

253
Q

Pt undergoing splenectomy are at greater risk for post-op________

A

infection

254
Q

T/F the spleen is esstential for life

A

FALSE
Spleen not essential for life

255
Q

What is the most frequently injured abdominal organ?

A

Spleen is the most frequently injured abd organ
25-60% of adults intraabd trauma

256
Q

Injury to splenic artery can produce _______

A

lethal hemoperitoneum

257
Q

why is damage to the spleen important?

A

most vascular body organ, receiving 5% of the CO

258
Q

how can the spleen be removed if the pt is stable? Unstable?

A

Unstable/emergency laparotomy in a trauma to examine all abd organs
If stable, can be done laparoscopic, in lateral decubitus position
Caution with respiratory function, possible rib fractures for injury

259
Q

what are the considerations for the spleen removal?

A

Labs, fluid resuscitation, blood products available

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