Liver and GI Flashcards
1
Q
in hepatic portal circulation, the vein is located between ____________
A
2 capillary beds
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
3
Q
hepatic veins return blood to
A
the inferior vena cava
4
Q
what is the largest internal organ
A
liver
5
Q
the liver is ____________ of the total body mass of adults
A
2%
6
Q
the liver receives ____________ % of CO
A
25%
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)
8
Q
Sympathetic innervation from ____________ controls resistance in the hepatic venules
A
T3 to T11
9
Q
Changes in compliance in the hepatic venous system contribute to ____________
A
the regulation of cardiac output and blood volume
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.
11
Q
“hepatic arterial buffer” response
A
the reciprocal relationship between flow in the two afferent vessels
12
Q
liver blood supply vs liver oxygen supply
A
13
Q
8 functional anatomic segments of the liver
A
14
Q
functions of the liver
A
the liver carries out essential metabolic, detoxifying, and regulatory functions to keep the body healthy
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
16
Q
liver dysfunction affects the metabolism of
A
nutrients and xenobiotics and negatively impacts nearly every other organ system
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
18
Q
what does deamination of amino acids do
A
Deamination produces ammonia, which is toxic.
19
Q
what is an additional source of ammonia
A
Intestinal bacteria are an additional source of ammonia.
20
Q
The liver removes ammonia through ____________
A
the formation of urea.
21
Q
what important nutrients does the liver store?
A
- vitamin A, D, E, K, B12, iron, and minerals
- glycogen
22
Q
____________ can be converted to glucose when the body needs energy.
A
glycogen
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
24
Q
what is detoxification
A
The liver neutralizes chemicals and drugs in the blood and readies them for excretion.
25
The liver contains ____________ which destroy bacteria and remove foreign particles from the blood.
Kupffer cells
26
the liver produces ____________ that combat infections
immune factors and proteins
27
liver blood filtration rate
The liver filters about 1.4 liters of blood per minute
28
what does the liver remove from blood
toxins, waste products, bacteria, and old red blood cells.
29
what clotting factors are and are not produced in the liver
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.**
30
vitamin K is reqiured for synthesis of ____________
prothrombin (Factor II)
31
what factors is vitamin K required for
factors VII, IX, and X.
32
most abundant plasma protein made by the liver
albumin
33
functions of albumin
It maintains oncotic pressure, transports lipids and hormones, and has antioxidant properties
34
Serum albumin levels reflect
liver function and nutritional status.
35
coagulation factors are responsible for
hemostasis and anticoagulation
36
immunoglobulins are responsible for
humoral immunity and defense
37
C-reactive protein increases dramatically during
inflammation and infection
38
CRP activates ____________ and ____________
complement and phagocytosis
39
This copper-binding glycoprotein made in the liver carries 90% of plasma copper and has ferroxidase activity.
cerloplasmin
40
what transports lipids through the circulation
lipoproteins
41
function of α-1 antitrypsin
made by the liver protects tissues from proteases like elastase.
42
low levels of α-1 antitrypsin
increase risk of emphysema.
43
clinical significance of plasma protein production
Levels indicate liver function and protein status
44
deficiencies of plasma protein production will cause...
edema, bleeding, lipid issues, infections
45
The liver produces a wide range of vital plasma proteins involved in critical physiological processes. Dysfunction impairs ____________, ____________, and ____________
transport, immunity, coagulation.
46
The liver metabolizes amino acids and converts excess amino acids to ____________
glucose or ketone bodies.
47
the liver detoxifies ammonia by converting it to ____________
urea
48
The liver takes up amino acids from the blood and regulates ____________
systemic amino acid levels.
49
In response to inflammation or injury, the liver increases production of certain plasma proteins called acute phase proteins. Examples are ____________ and ____________
C-reactive protein and serum amyloid A.
50
The liver can synthesize glucose from amino acids through ____________. This helps maintain blood glucose when glucose supply is low.
gluconeogenesis
51
The liver stores amino acids in the form of proteins like ____________
albumin
52
The liver makes carrier proteins that transport various compounds like ____________
bilirubin, hormones, metals, drugs.
53
T/F The liver synthesizes most of the coagulation factors and fibrinolytic proteins involved in blood clotting and thrombus dissolution.
TRUE
54
____________ is a soluble plasma glycoprotein synthesized by the liver and megakaryocytes (bone marrow cells)
fibrinogen
55
During coagulation, ____________ converts fibrinogen into fibrin forming the fibrin meshwork of a blood clot
thrombin
56
10-15% is of fibrinogen is produced by ____________ which helps maintain adequate fibrinogen level even in severe liver disease
megakaryocytes
57
Cytochrome P450 enzymes metabolize drugs through chemical reactions like ____________, ____________ and ____________
oxidation, reduction, hydrolysis
58
____________ system metabolizes ~75% of all medications
P450
59
what do P450 enzymes do to drugs
makes drugs more water-soluble (polar) for easier excretion into the bile or urine
60
The liver can activate a ____________ into its active form through metabolism. It can also convert an active drug into an inactive metabolite, reducing ____________
prodrug; its pharmacological effects.
61
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.
cirrhosis
62
What do Phase I reactions do
modifies drug with functionalization actions resulting in loss of pharmacologic activity
63
what do phase II reactions do?
conjugates the metabolite with a second molecule (glucuronic acid, sulfate, glutathione, amino acid, or acetate) forming a covalent link
64
Factors like ____________ (4) affect hepatic metabolizing enzymes, altering the efficacy and side effects of medications.
age, genetics, drug interactions, and comorbidities
65
The liver helps detoxify and excrete drugs, but drug metabolites may also be ____________
more toxic than the parent drug in some cases.
66
50% of currently manufactured drugs are metabolized by ____________
a single CYP
67
Rate of metabolism can be increased or decreased with ____________
coadministration of 2 drugs metabolized by the same enzyme system
68
Enzyme induction hastens ____________ and promotes tolerance
metabolism
69
function of LFTs
Measure levels of enzymes, proteins, and bilirubin to assess liver function and identify liver injury
70
causes of hepatic dysfunction based on LFT results
71
____________ is more specific for liver injury than ____________
ALT; AST
72
____________ and ___________indicate cholestatic liver disease
ALP and GGT
73
Mechanical ventilation with positive pressure can impair ____________ and ____________
venous return and cardiac output, reducing perfusion
74
Drugs used during anesthesia like inhaled anesthetics, propofol, opioids can cause systemic vasodilation, decreasing ____________
hepatic vascular resistance and blood flow.
75
Low blood pressure reduces perfusion pressure to the liver. Causes include ____________ (3)
hypovolemia, blood loss, effects of anesthetic drugs.
76
Increase in central venous pressure is caused by factors like
mechanical ventilation, fluid overload, heart failure can increase CVP, hindering hepatic blood flow
77
Surgical manipulation during procedures like liver resection or transplant can directly ____________
occlude inflow or outflow vessels.
78
effects of anesthesia and hepatic blood flow
- ↑ in CVP
- hepatic vascular occlusion
- ↓ cardiac output
- endothelial dysfunction
- compression of IVC
79
Coexisting conditions like sepsis, ischemia-reperfusion injury can impair ____________ needed for blood flow.
vasodilation
80
Improper positioning or abdominal packing pushing on inferior vena cava can obstruct ____________
hepatic venous return.
81
effects of spinal anesthesia on the liver
82
Hypotension is common with spinal anesthesia and must be promptly treated with ... to prevent hypoperfusion
fluids or vasopressors
83
High block can impair
(2)
cardiac output and hepatic perfusion
84
T/F:
Spinal anesthesia may be preferred over general anesthesia in some liver surgeries since it better preserves hepatic blood flow.
True
85
Use caution with epi in spinal injectate bc...
can transiently reduce hepatic perfusion due to alpha-receptor mediated vasoconstriction
86
spinal anesthesia & liver fxn
(4)
* alone does not typically impair hepatic circulation
* prevent high block
* treat any resulting hypotension
* sympathetic blockade helps redirect blood to the splanchnic vessels
87
Which Volatiles reduce Hepatic Blood Flow
most to least
Halothane = greatest reduction
desfluane slightly greater than sevo and iso
88
Which volatiles are preferred for patients with liver disease?
why?
Isoflurane and sevoflurane
less disturbance in hepatic arterial blood flow
89
Anesthetic agents reduce hepatic blood flow by ___% after induction
30-50
90
Which volatile increases hepatic blood via **direct** vasodilation properties?
Isoflurane
91
# BOX 33.3
Clinicopathologic Features of Halothane Hepatitis
more common in males or females?
Female-to-male ratio
2:1
92
# BOX 33.3 Clinicopathologic Features of Halothane Hepatitis
Latent period to first symptoms
After first exposure: 6 days (11 days to jaundice)
After multiple exposures: 3 days (6 days to jaundice)
93
# BOX 33.3 Clinicopathologic Features of Halothane Hepatitis
Risk factors
* Older age
* Female
* 2+ exposures (60%–90% of cases)
* Obesity
* Familial predisposition
* Induction of CYPE1 by phenobarbital, alcohol, or isoniazid
94
These meds/substances predispose to halothane hepatitis
phenobarbital, alcohol, or isoniazid
## Footnote
Induction of CYPE1
95
# BOX 33.3 Clinicopathologic Features of Halothane Hepatitis
Clinical features
* 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
96
What can hinder hepatic flow by increasing CVP?
mechanical ventilation, fluid overload, heart failure
97
what can directly occlude inflow or outflow vessels with hepatic vascular occlusion?
Surgical manipulation during procedures like liver resection or transplant
98
can reduce cardiac output and thus, hepatic perfusion
Myocardial depression, dysrhythmias, decreased intravascular volume
99
Compression of IVC can obstruct hepatic venous return. What is an example of this?
Improper positioning or abdominal packing pushing on inferior vena cava
100
Overall list of things that can impair hepatic blood flow
* 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)
101
Spinal anesthesia induces (2)
sympathetic blockade and vasodilation
102
Spinal anesthesia Redistributes blood flow to
splanchnic vascular bed
103
A spinal will (reduce/increase) vascular resistance in hepatic arterial and portal circulation
reduce
104
Vasodilation from spinals are mediated by...
decreased vasoconstrictor hormones
105
ALL opioids have been implicated in causing a spasm of the sphincter of Oddi BUT the incidence is lower with
fentanyl
106
How to treat spasm of the Oddi sphincter
**Nalbuphine or naloxone**
Atropine, glyco, glucagon and nitro may also be effective
107
# Effects of Anesthesia on Liver Function
Reduced response to these endogenous vasoconstrictors
Angiotensin II, AVP, and norepinephrine
108
Why is there a Reduced response to endogenous vasoconstrictors?
## Footnote
Angiotensin II, AVP, and norepinephrine
release of nitric oxide, prostacyclin and other endothelial-derived factors in response to humoral and mechanical stimuli.
109
Albumin
3 major indications for treatment of cirrhotic liver disease
* After large volume paracentesis
* To prevent renal impairment (Bili >4 or Creatinine >1)
* Presence of HRS-SKI (Use with splanchnic vasoconstrictors)
110
Consider a-line for patients with
end-stage liver disease
111
# Liver Cases
Besides an A-line, these other monitors are useful
(but do a risk vs benefit assessment)
* CVP for fluid responsiveness
* PAC for pulmonary HTN and low EF
* TEE for preload, contractility, EF, regional wall abnormalities, emboli
* Avoid transgastric views
112
Liver cases
TEG is helpful for ___, but this only reflects...
PT as a predictor of bleeding risk
only reflects procoagulant factor levels
113
Diseases of the Liver
114
Cirrhosis
Histological **development of regenerative nodules surrounded by fibrous bands** in response to chronic liver injury
115
Portal HTN
abnormally high BP in the portal vein system, which carries blood from the intestines, spleen, pancreas and gallbladder to the liver.
116
Viral hepatitis can be caused by ...
hepatitis A (HAV), B (HBV), C (HCV), D (HDV), and E (HEV)
## Footnote
Any of these variations can lead to serious illness and death
117
Which hepatitis viruses are acute vs chronic
* A = acute symptomology
* B & **C**= significant **c**hronic sequelae
A & E rarely affect the liver chronically
118
The most common reason for liver transplantation in developing countries
Both Hep B & C
HBV and HCV
119
Hepatitis
Current treatment regimens
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
# Hepatitis
Antiviral drug choice and treatment duration are based on
* The genotype of HCV
* Stage of liver disease
* Presence of cirrhosis
* Previous response to interferon
121
Genotype 1A is the most common form in the US (70%) and is treated with
sofosbuvir/velpatasvir drug combination
## Footnote
These drugs provide a rate of infection clearance of 98% in genotype 1A and 99% in genotype 1B
122
Pregnancy-related Liver Diseases
occurrence rate
3-5% of pregnancies
123
Pregnancy-related Liver Diseases
Common causes
* hyperemesis gravidarum
* intrahepatic cholestasis of pregnancy
* preeclampsia
* HELLP syndrome
* acute fatty liver of pregnancy (AFLP)
124
3 risk factors for Hyperemesis gravidarum
(1st trimester)
* hyperthyroidism
* molar pregnancy
* multiple pregnancies
125
Hyperemesis gravidarum (1st trimester)
Will elevate which enzymes by how much?
What is NOT elevated?
up to 20-fold elevation of liver enzymes
but not bilirubin
126
most common of later pregnancy liver diseases
HELLP
127
HELLP syndrome
is comprised of...
* microangiopathic hemolytic anemia (MAHA)
* elevated liver enzymes
* low platelet count
....in the preeclamptic patient
128
How many Pre-E patients develop HELLP?
How fatal is it?
20% of severely preeclamptic patients
up to 25% maternal mortality
129
AFLP is a result of
* 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
AFLP Symptoms are similar to severe preeclampsia and HELLP BUT the patient may additionally have...
laboratory and clinical findings ***more unique to liver failure***
* hypoglycemia
* elevated ammonia
* asterixis
* encephalopathy
131
How does Cirrhosis evolve into Portal Hypertension?
1. Hepatocyte necrosis = deteriorates liver function
1. Liver parenchyma is replaced by fibrous and nodular tissue
1. Distorts, compresses, and obstructs normal portal venous blood flow
1. Portal hypertension develops
132
Cirrhosis and Portal Hypertension
by HVPG values
133
Cirrhosis and Portal Hypertension
-definition
-causes
-end result
134
3 key complications of portal hypertension include
**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
Cirrhosis & Portal HTN
Cardiac sequelae
hyperdynamic circulation due to decreased SVR causes increased CO
136
Cirrhosis & Portal HTN
Diagnosis
measuring the pressure gradient between the portal vein and IVC
typically via splenic or hepatic vein catheterization
137
Cirrhotic patients are considered to have
a **bleeding** diathesis
(vs DIC which is a *thrombotic* diasthesis)
138
Cirrhosis is a (bleeding/thrombosis) diathesis
bleeding
## Footnote
DIC = thrombotic diathesis
139
# Cirrhosis
thrombocytopenia & clotting factor deficiencies
* up to 90% of platelets may be in the spleen
* ↓ protein C & S balance the decreased levels of procoagulants
## Footnote
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
Cirrhosis is a bleeding diathesis, but they are at risk for both bleeding and thrombosis due to ...
relatively elevated
factors VIII & vWf
141
Portotopulmonary Syndrome
* Pulmonary arterial HTN + portal HTN
* with or without liver disease
* Systemic vasodilation with local pulmonary production of vasoconstrictors
142
Portotopulmonary Syndrome
Mean PAP
>25 mmHg
143
T/F:
Curative treatment of Portotopulmonary Syndrome includes 2 direct acting antiviral drugs that target specific steps within the HCV replication cycle.
False
this is hepatitis
liver transplant is the cure for Portotopulmonary Syndrome
144
Hepatopulmonary Syndrome
* **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
## Footnote
Portotopulmonary Syndrome: Pulmonary arterial HTN + portal HTN with or without liver disease
145
Hepatopulmonary Syndrome causes poor tolerance of gravitational effects on pulmonary blood flow leading to ____________
platypnea-orthodeoxia
146
Hepatopulmonary Syndrome
which position is best?
supine improves oxygenation
standing worsens hypoxemia
147
Hepatorenal Syndrome
* Acute, **reversible** kidney failure due to end-stage liver disease
* Impaired renal blood flow and intense vasoconstriction
148
Hepatorenal Syndrome
causes
* 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
Which liver syndrome/disease activates the RAAS?
Hepatorenal Syndrome
Intense renal vasoconstriction
150
Hepatorenal Syndrome
Pathophysiology:
* Reduced GFR but kidneys intact
* Diminished natriuresis, sodium retention, ascites
151
BOX 33.8
Management of Hepatorenal Syndrome (HRS)
* 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
# BOX 33.8 Management of Hepatorenal Syndrome (HRS)
Prevent variceal bleeding
* Measures to prevent bleeding (e.g., β-receptor blocking agent, band ligation)
* Pentoxifylline for severe alcohol-associated hepatitis
153
# BOX 33.8 Management of Hepatorenal Syndrome (HRS)
Prevention of hepatorenal syndrome (HRS)
* 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
# BOX 33.8 Management of Hepatorenal Syndrome (HRS)
Treatment of hepatorenal syndrome
* 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
# BOX 33.8 Management of Hepatorenal Syndrome (HRS)
Vasopressor therapy
(in addition to albumin)
* 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
Hepatorenal Syndrome
Management (Box 33.8)
* Fluid restriction vs intravascular volume depletion, albumin, avoid nephrotoxins
* Vasoconstrictors, midodrine, octreotide, norepi
* Liver transplantation (without: mortality >50%)
157
T/F:
The development of Hepatopulmonary Syndrome is an ominous sign and signals the need for immediate transplantation evaluation
False
this applies to Hepatorenal Syndrome
## Footnote
Portotopulmonary Syndrome is also only cured by transplant
158
Hepatic Encephalopathy
* Neurotoxins (ammonia) accumulate and alter neurotransmission via glutamate or altered cerebral energy homeostasis
* Mild apraxia -> behavioral changes -> decerebrate posturing -> coma
159
Hepatic Encephalopathy can result in (decerebrate/decorticate) posturing
decerebrate
160
Hepatic Encephalopathy
differential diagnosis
* Poor metabolism of gut-produced ammonia vs intracranial bleeding
* Failure to metabolize vs failure to synthesize substances; shunting
161
Hepatic Encephalopathy
treatment
Nonabsorbable disaccharides
162
Risk Scores for Cirrhosis:
Child-Pugh Classification
163
Risk Scores for Cirrhosis:
Model for End-stage Liver Dx
(MELD)
164
Transjugular Intrahepatic Portosystemic Shunt
(TIPS procedure)
treats...
* refractory variceal hemorrhage and refractory ascites
* Manages portal HTN by creating a direct communication between the portal vein and the hepatic vein
165
The TIPS procedure shunts blood flow how?
Shunts portal venous flow to the systemic circulation
## Footnote
for: refractory variceal hemorrhage, refractory ascites, manages portal HTN
166
How does the TIPS procedure alleviate bleeding and ascites
reduces the portosystemic pressure gradient
167
Absolute contraindications for Transjugular Intrahepatic Portosystemic Shunt (TIPS procedure)
* heart failure
* severe tricuspid regurgitation
* severe pulmonary hypertension
168
T/F:
TIPS Procedure requires general & ETT.
False
Utilize sedation or general anesthesia
limits patient movement, controls diaphragmatic excursion, and reduces the risk of aspiration
169
TIPS increases venous return, which can unmask these 2 conditions common to chronic liver disease patients
undiagnosed cardiac dysfunction or pulmonary HTN
170
TIPS Procedure
Complications
* pneumothorax
* vascular injury
* dysrhythmias
* hemorrhage
171
TIPS Procedure
considerations
* Volume resuscitation
* Platelets and clotting factors replenished
172
T/F:
Elevations in AST are specific to liver tissue injury.
False
ALT = liver specific
173
AST:ALT
greater than 2: alcoholic liver disease
<1: fatty liver/chronic hepatitis
174
Which zone is affected most by hypoxia and reactive intermediates?
3
175
Which liver cells have the greatest quantity of cytochrome P450 enzymes and are the site of anaerobic metabolism?
pericentral hepatocytes
176
Gold standard for diagnosing esophageal varices
EGD
177
MELD scores and their mortality
178
MELD score accounts for ... (3)
* Bilirubin
* PT/INR
* Creatinine
179
MELD score ___ should not undergo elective surgery
>15
180
MELD is a scoring system that assesses
* severity of chronic liver disease
* prioritizing liver recipients
* three-month survival
## Footnote
The original MELD score was developed to determine short-term mortality in patients receiving a transjugular intrahepatic portosystemic shunt (TIPS) procedure.
181
🔷
mendelson syndrome
the gastic fluid aspirated must be...
0.4 ml/kg (30 ml)
pH <2.5
182
Symptoms related to carcinoid syndrome
* 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
__________ is the sole definitive treatment modality for patients with acute liver failure, ESLD, and primary hepatic malignancy.
Liver transplantation
184
___________ score is a validated system that UNOS uses for prioritizing patients on the liver transplant waiting list.
The Model for End-Stage Liver Disease (MELD)
185
The MELD score is a validated system that uses ___________________ to mathematically rank adult patients according to their expected survival rate without transplantation.
- serum total bilirubin
- serum creatinine
- INR values
186
Three-Month Mortality According to MELD Score∗
187
Signs and symptoms of liver failure:
Anorexia, weakness, nausea, vomiting, abdominal pain, hepatosplenomegaly, ascites, jaundice, metabolic encephalopathy, spider nevi.
Ascites: aspiration of fluid may see big hemodynamic shifts
188
A patient with esophageal varices requires what specifics?
vasopressin, RSI intubation
189
what is the management for pt with ascites?
- need volume expanders (albumin)
- Na restrictions and slow diuresis
190
what pulmonary manifestations would you see with liver failure?
V/Q mismatch
191
Portal hypertension typically manifests as:
ascites, esophageal varices; hepatic encephalopathy
192
what are the CV manifestations a/w liver failure?
* high cardiac output
* high HR
* low SVR
* decreased RBF
* extensive collaterals (esp lungs)
* prolonged QT interval
193
what would you see with the renal dysfxn a/w liver failure?
no Na or free water secretion, vasoconstricts and causes sympathetic release
194
what is the anesthesia management like for liver transplants?
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
Thromboelastogram (TEG)
196
whats included in the intraop management for a liver transplant?
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
an autosomal recessive disease characterized by impaired copper metabolism.
Wilson Disease
198
α1-antitrypsin deficiency
* 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
________ is a disorder associated with excess iron in the body that can lead to multiorgan dysfunction.
Hemochromatosis
200
Inborn Errors of Metabolism
Wilson Disease
α1-antitrypsin deficiency
Hemochromatosis
201
Most common cause of cholestasis is ________
obstruction of biliary tract outside of the liver
202
Diseases of the Biliary Tract
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
Cholecystitis: causes and S/S
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
Cholecystitis Anesthesia Management
* 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
Contraindications to a lap cholecystectomy
Coagulopathy, severe COPD, ESLD, CHF
206
Achalasia
Impaired relaxation of LES
Chronic achalasia results in dilation of esophagus, more food and fluids retained- aspiration risk
disease of the esophagus
207
GERD
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
Anesthesia for Esophageal Disorders
Asymptomatic vs uncontrolled disease with reflux symptoms
Aspiration prophylaxis during induction and emergence
Modification of gastric acidity with preoperative medications
209
Peptic Ulcer Disease
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
Peptic Ulcer Disease Common complications include:
Hemorrhage
Perforation
Obstruction
211
Gastritis: what is it? how do you treat it? what can be life-threatening?
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
Gastric Ulcer Disease Most common complication is________
perforation
213
Develop from degeneration of stomach’s mucosal barrier against gastric acid
Gastric Ulcer Disease
214
Gastric Ulcer Disease
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
_______ cancer 2nd most common cancer worldwide, 7th most in U.S.
Gastric
216
Gastric Neoplastic Disease S/S
S/S include pain (constant, non-radiating and not relieved by food), wt loss, anorexia, fatigue, and vomiting
217
Gastric Neoplastic Disease tX
Gastrectomy or partial gastrectomy (resection of tumor) remains the primary curative treatment
218
Anesthetic Considerations for diseases of the stomach:
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
Anastamotic leakage risk factors:
anemias, co-morbidities, diabetics, vascular disease, decreased perfusion
220
Postoperative ileus risk factors:
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
Mesenteric traction syndrome s/s + tx:
tachycardia and hypotension; antihistamine and NSAIDS
222
what kind of blood flow do you see to the intestines?
Splanchnic blood flow
223
Zollinger-Ellison syndrome
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
Abdominal Compartment Syndrome
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
Carcinoid Tumors
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
Carcinoid Syndrome systemic effects:
Flushing, bronchoconstriction, hypotension, hypertension, diarrhea; life-threatening perioperative hemodynamic instability
227
Carcinoid heart disease S/S:
Right sided cardiac involvement
Tricuspid and pulmonary valves
Tumors along valves
Bronchoconstriction
Metastasized by the lungs
228
Carcinoid Syndrome Tx:
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
Carcinoid crisis:
can necrose and release massive amounts of substances into circulations
Stress reduction can help prevent
230
Alpha-adrenergic sympathetic stimulation inhibits _______
insulin secretion
231
Exocrine digestive enzyme and endocrine hormonal capacity
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
Insulin suppression results from:
Arterial hypoxemia
Hypothermia
Traumatic stress
Surgical stress
233
_____ and ______ also inhibit insulin secretion
Beta-adrenergic sympathetic and Cholinergic blockade
234
Insulin secretion is enhanced by:
Parasympathetic vagal stimulation
Beta adrenergic sympathetic activation
Cholinergic drub administration
235
Acute Pancreatitis causes include:
alcohol abuse, trauma, ulcerative penetration, infection, vascular, metabolic disorders, autoimmune
80% of pancreatic disorder from alcohol and gallstones
236
Acute Pancreatitis S/S include:
Abdominal distention
N/V
Pain
Hypotension
Hypovolemia
237
Severe Acute Pancreatitis (SAP): what is it a/w? what is the main COD?
SAP associated with organ failure, local complications, prolonged ICU and 25% mortality rate
Multiple Organ dysfunction is main cause of death
238
Describe the pain a/w pancreatitis and managing it.
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
Anesthetic Considerations for Pancreatic Disease:
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
Chronic Pancreatitis most common etiology is _____
alcohol-70% of cases
241
Chronic Pancreatitis S/S:
Abdominal pain
Wt loss
Malnutrition
Hepatic disease
Predisposed to pericardial and pleural effusions
Hypoalbuminemia
Hypomagnesemia
242
Chronic Pancreatitis: WHAT IS IT?
Permanent and irreversible damage to the pancreas
Chronic inflammation, fibrosis, destruction of exocrine and endocrine tissue
243
Pancreatic Tumors s/s
Painless jaundice
Dull aching midepigastric or back pain
Anorexia
Fatigue
New-onset DM is occasionally the 1st symptom
244
Pancreatic Tumors
Pancreatic cancer 80-90% ductal adenocarcinomas
Can grow extensively before they produce symptoms
Generally resected by pancreaticoduodenectomy (Whipple)
245
________ most common functioning tumor of the pancreas
Insulinoma
246
Insulinoma s/s
Hypoglycemia
Seizures
Coma (symptoms of catecholamine release)
247
Diagnostic Hallmark- Whipple triad S/S
Hypoglycemia (catecholamine release)
Low blood glucose (40-50 mg/do)
Relief after IV administration of glucose
248
Whipple Procedure
249
describe Splenic blood flow.
300mL/min and arises from splenic artery
250
spleen function include:
blood filtering, maintenance of normal erythrocytes and immune processing of blood-borne foreign antigens
251
Abnormal blood cells from disease such as sickle cell disease, thalassemia and spherocytosis removed by_________.
macrophages
252
Splenic Disease can lead to ______
worsening anemia and symptomatic splenomegaly
253
Pt undergoing splenectomy are at greater risk for post-op________
infection
254
T/F the spleen is esstential for life
FALSE
Spleen not essential for life
255
What is the most frequently injured abdominal organ?
Spleen is the most frequently injured abd organ
25-60% of adults intraabd trauma
256
Injury to splenic artery can produce _______
lethal hemoperitoneum
257
why is damage to the spleen important?
most vascular body organ, receiving 5% of the CO
258
how can the spleen be removed if the pt is stable? Unstable?
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
what are the considerations for the spleen removal?
Labs, fluid resuscitation, blood products available
