Unit 10 - Liver/Gallbladder Flashcards
(227 cards)
1
Q
structure responsible for eliminating bacteria from the liver
A
Kupffer cells
2
Q
functional unit of the liver
A
acinus
otherwise known as the liver lobule
3
Q
functional unit of the liver
A
acinus
otherwise known as the liver lobule
4
Q
where do sinusoids receive blood flow
A
hepatic artery
portal vein
5
Q
where are Kupffer cells located
A
in sinusoids
6
Q
collect bile produced by hepatocytes
A
bile canaliculi
7
Q
SNS innervation of the liver
A
T3-T11
8
Q
how are hepatocytes organized in acinus
A
in zones according to proximity to portal triad & central vein
9
Q
what part of acinus are O2 and nutrient gradients the highest
A
zone 1
lowest in zone 3
10
Q
what part of acinus is most susceptible to injury
A
zone 3
11
Q
where in the acinus is the highest concentration of CYP450 enzymes
A
zone 3
12
Q
how is bile produced
A
hepatocytes
stored in gallbladder
13
Q
path of bile to duodenum
A
canniculi → bile duct → common hepatic duct → common bile duct → ampulla of Vater → duodenum
14
Q
3 Key Functions of Bile:
A
1) Absorption of fat and fat-soluble vitamins (AEDK)
2) Excretory pathway for bilirubin and products of metabolism
3) Alkalinization of duodenum
15
Q
where is Cholecystokinin produced
A
duodenum
16
Q
how is CCK production stimulated
A
Eating fat and protein increases release
17
Q
effect of CCK release
A
stimulates gallbladder contraction and ↑ flow of bile into duodenum
18
Q
function of space of Disse
A
Lymph and proteins drain into before emptying into lymphatic duct
19
Q
organ responsible for about ½ of lymph production in the body
A
liver
20
Q
how much CO does liver receive
A
~30% of CO (1500 mL/min)
21
Q
blood supply to liver
A
Dual blood supply from portal vein and hepatic artery
22
Q
liver blood flow and O2 supply from portal vein
A
75% blood flow, 50% O2 supply
23
Q
liver blood flow and O2 supply from hepatic artery
A
25% blood flow, 50% O2 supply
24
Q
how does splanchnic vascular resistance affect portal vein blood flow
A
↑ splanchnic vascular resistance = ↓ portal vein blood flow (SNS stim, pain, hypoxia, hypercarbia)
25
Portal Perfusion Pressure =
Portal Vein Pressure – Hepatic Vein Pressure
26
portal vein and sinusoid pressure in portal HTN
portal vein: > 20-30 mmHg
sinusoid: > 5 mmHg
27
normal portal vein and sinusoid pressure
portal vein: 7-10 mmHg
sinusoid: 0 mmHg
28
physiologic consequences of portal hypertension
* esophageal varices, hemorrhage
* ascites
* spider angiomas
* hemorrhoids
* encephalopathy
29
compensation for reduced portal vein flow
hepatic arterial buffer response compensates by increasing flow through **hepatic artery**
30
why are pts with severe liver disease at increased risk for inadequate hepatic blood flow
Severe liver disease abolishes the hepatic arterial buffer response
| portal vein flow is not autoregulated (and hepatic arterial flow can’t r
30
why are pts with severe liver disease at increased risk for inadequate hepatic blood flow
Severe liver disease abolishes the hepatic arterial buffer response
| portal vein flow is not autoregulated (and hepatic arterial flow can’t r
31
how does anesthesia affect liver blood flow
Both GA & neuraxial anesthesia reduce MAP and CO = dose-dependent ↓ in liver blood flow
32
how does propranolol affect liver blood flow
↓ CO and increases splanchnic vascular resistance
(**hepatic artery constriction**)
33
how do intraabd surgeries affect liver blood flow
reduce d/t retraction and release of vasoactive substances
34
what 2 major blood vessels supply blood to the liver
1. hepatic artery
2. portal vein
35
celiac artery provides blood flow to which 3 organs
1. liver
2. spleen
3. stomach
36
superior mesenteric artery provides blood flow to which 3 organs
1. pancreas
2. small intestine
3. colon
37
1 organ that receives blood flow from inferior mesenteric artery
colon
38
4 examples of things that increase splanchnic vascular resistance
1. SNS stim
2. hypoxia
3. pain
4. propranolol
39
why is PT an early indicator of synthetic dysfunction
factor 7 has the shortest half life of all procoagulants
40
vitamin K dependent clotting factors
factors 2, 7, 9, 10
41
The absorption of vitamin K is dependent on:
bile in the gut
42
where is alpha-1 acid glycoprotein produced
liver
(hepatocytes)
43
where is von willebrand factor produced
vascular endothelial cells
44
where is factor 3 produced
vascular endothelial cells
45
where is factor 8 produced
liver sinusoidal cells and endothelial cells
46
the liver produces all plasma proteins except:
immunoglobulins
47
function of thrombopoietin
stim plt production
48
most abundant plasma protein
albumin
49
why are pts with liver failure at increased risk of hypoglycemia
Liver is an important regulator of serum glucose & clears insulin from circulation
50
body's compensation for hyperglycemia
* insulin released from pancreatic beta cells (glycogenesis)
* glucose converted to glycogen for storage
51
body's response to hypoglycemia
* release of glucagon from pancreatic alpha cells & epi from adrenal medulla (glycogenolysis & gluconeogenesis)
* glycogen from storage and non-carbohydrates (amino acids, pyruvate, lactate, glycerol) turned to glucose
52
what is amino acid deamination
allows the body to convert proteins to carbohydrates and fats.
Some of these are utilized in the Krebs cycle to produce ATP
53
how is urea eliminated from the body
* liver converts ammonia to urea
* urea is eliminated by kidneys
54
MOA of hepatic encephalopathy
Failure to clear ammonia (hepatic failure or portosystemic shunting)
55
blood reservoir for acidic drugs
albumin
56
blood reservoir for basic drugs
alpha 1 acid glycoprotein
57
erythrocyte life cycle
120 days
58
where are old RBCs broken down
by the reticuloendothelial cells in the spleen
59
byproduct of hgb metabolism
bilirubin
60
how is unconjugated bilirubin transported to liver
bound to albumin
61
how is unconjugated bilirubin excreted
* lipophilic - transported to liver bound to albumin
* liver conjugates with glucuronic acid - increases water solubility
* conjugated bilirubin excreted into bile
62
how is conjugated bilirubin metabolized & eliminated
by intestinal bacteria
eliminated in stool
63
normal PT values
12-14 seconds
64
LFT very sensitive for acute injury
PT
65
how does vitamin K deficiency affect PT
prolongs
66
normal value for albumin
3.5-5 g/dL
67
half life of albumin
21days
poor indicator of acute liver injury
| poor specificity for liver disease
68
causes of decreased albumin level
impaired synthesis or ↑ consumption
**Conditions that ↓:** infection, nephrotic syndrome, malnutrition, malignancy, burns
69
coagulation factors NOT synthesized in liver
vWF
factor 3
factor 4
70
what is glycogenesis
glucose stored as glycogen
71
what is glycogenolysis
glycogen cleaved into glucose
72
gluconeogenesis
glucose created from non-carb sources
73
what does marked elevation of both AST & ALT indicate
hepatitis
74
AST/ALT ratio > 2 suggests:
cirrhosis, alcoholic liver disease
75
normal values for AST & ALT
AST: 10-40 units/L
ALT: 10-50 units/L
76
LFTs that assess synthetic function
PT, albumin
77
LFTs that assess hepatocellular injury
AST, ALT
78
LFTs that assess hepatic clearance
bilirubin
79
LFTs that assess biliary tract obstruction
Alkaline phosphatase
Y Glutamyl transpeptidase
5’-Nucleotidase
80
most specific indicator of biliary obstruction
5’-NT
81
# normal values:
Alkaline phosphatase
Y Glutamyl transpeptidase
5’-Nucleotidase
**Alkaline phosphatase**: 45-115 units/L
**Y Glutamyl transpeptidase**: 0-30 units/L
**5’-Nucleotidase** : 0-11 units/L
82
albumin levels assoc. with hepatocellular injury
acute injury: no change
chronic: decreased
83
causes of prehepatic liver injury
Hemolysis
Hematoma reabsorption
84
causes of hepatocellular injury
Cirrhosis
Alcohol abuse
Drugs
Viral infection
Sepsis
Hypoxemia
85
causes of cholestatic liver injury
Biliary tract obstruction
Sepsis
86
what aspect of hepatic function is assessed by alkaline phosphatase
cholestatic
(biliary duct obstruction)
87
Most common cause of liver cancer
hepatitis
88
most common indicator for liver transplantation in adults
hepatitis
89
etiologies of hepatitis
viruses, hepatotoxins, and autoimmune responses
| also herpes simplex, CMV, Epstein-Barr
90
how does hepatitis A typically present
usually silent for 1-2 weeks after infection
then malaise, N/V, jaundice that generally last 2-12 weeks
91
transmission of hepatitis A
oral-fecal
92
serum markers of hepatitis A
early = IgM
late = IgG
93
hepatitis viruses assoc with cirrhosis and hepatocellular carcinoma
B, C
## Footnote
**B: **adults: 1-5%
children: 80-90%
**C:** up to 75%
94
transmission of hepatitis B
percutaneous
sexual contact
95
serum markers of hepatitis B
HBsAg
Anti-HBcAg
96
transmission of hepatitis C
percutaneous
97
transmission of hepatitis D
percutaneous
98
serum markers of hep C
anti-HCV (1.5-9 months)
99
hep C viruses that can be transmitted via blood
B, C
100
co-infection that occurs with hep B
hepatitis D
101
etiologies of drug-induced hepatitis
* tylenol
* halothane
* alcohol
102
most common cause of acute liver failure in US
tylenol
103
substrate for many phase 2 conjugation reactions
glutathione
104
function of glutathione in phase 2 conjugation reactions
increases a substance's water solubility so that the substance can be excreted in the bile or by the kidney
105
patho of liver toxicity with tylenol overdose
* toxic metabolite = NAPQI
* NAPQI normally conjugated with glutathione to nontoxic form
* OD consumes liver's glutathione supply
* NAPQI concentration increases, leads to hepatocellular injury
106
treatment of tylenol OD
mucomyst (N-acetylcysteine) within 8 hours of OD
107
MOA of halothane hepatitis
* liver metabolizes to TFA
* halothane up to 20% metabolism produces large amount of TFA
## Footnote
believed to be immune-mediated reaction r/t TFA
107
MOA of halothane hepatitis
* liver metabolizes to TFA
* halothane up to 20% metabolism produces large amount of TFA
## Footnote
believed to be immune-mediated reaction r/t TFA
108
MOA of halothane hepatitis
* liver metabolizes to TFA
* halothane up to 20% metabolism produces large amount of TFA
## Footnote
believed to be immune-mediated reaction r/t TFA
109
risk factors for halothane hepatitis
* Age > 40
* female gender
* > 2 exposures
* genetics
* obesity
* CYP2E1 induction (alcohol, isoniazid, phenobarbital)
110
most common cause of drug-induced hepatitis
ETOH
111
MOA of alcohol-induced hepatitis
ETOH impairs fatty acid metabolism, which causes fat accumulation in the liver and leads to hepatomegaly
112
2 most common causes of chronic hepatitis
1. alcohol
2. hep C
113
how is chronic hepatitis characterized
hepatic inflammation that exceeds 6 months
114
how is chronic hepatitis diagnosed
Increased liver enzymes and bilirubin + histologic evidence of liver inflammation
115
s/s chronic hepatitis
* jaundice
* fatigue
* thrombocytopenia
* glomerulonephritis
* neuropathy
* arthritis
* myocarditis
116
propranolol decreases portal pressure by what 2 mechanisms
1. decreased CO (beta-1)
2. splanchnic vasoconstriction (beta-2)
117
AIs for hepatitis
**maintain hepatic blood flow**
* avoid PEEP
* liberal IVF
* normocapnia
* avoid hepatotoxic drugs/CYP450 inhibitors
118
drugs to avoid in pts with hepatitis
**Hepatotoxic Drugs or those that Inhibit CYP450**
* Acetaminophen
* Halothane
* Amiodarone
* Antibiotics: PCN, tetracycline, and sulfonamides
119
MAC considerations for EOTH
acute intoxication = decreased MAC
chronic user, not acutely intoxicated = increased MAC
120
how does alcoholism affect benzos
potentiates GABA
increased effect of benzos
121
receptors affected by ETOH
potentiates GABA
inhibits NMDA
122
early s/s alcohol withdrawal syndrome
Tremors and disordered perception (hallucinations, nightmares)
123
when do s/s alcohol withdrawal begin
6-8 hrs after the BAC returns to near normal
(peaks at 24 - 36 hours)
124
late s/s alcohol withdrawal
* Increased SNS activity (tachycardia, hypertension, dysrhythmias)
* N/V
* insomnia
* confusion
* agitation
125
treatment of alcohol withdrawal
* Alcohol
* beta-blockers
* alpha-2 agonists
126
typical onset of delirium tremens after an alcoholic stops drinking
2 - 4 days without alcohol
127
s/s Delirium tremens
* Grand mal seizures
* tachycardia
* hyper- or hypotension
* combativeness
128
delirium tremens treatment
Diazepam (or another benzo) and beta-blockers
129
what vitamin deficiency causes Wernicke-Korsakoff syndrome
B1
| thiamine
130
what is Wernicke-Korsakoff syndrome
characterized by a loss of neurons in the cerebellum brought on by thiamine deficiency
131
treatment for alcoholics in recovery
* Disulfiram
* hepatotoxic and inhibits dopamine beta-hydroxylase (NE synthesis) = hypotension
132
characteristics of cirrhosis
* cell death
* healthy hepatic tissue is replaced by nodules and fibrotic tissue
* Reduces # of functional hepatocytes & sinusoids
133
etiologies of cirrhosis
* NAFLD
* ETOH abuse
* alpha 1 antitrypsin deficiency
* biliary obstruction
* chronic hepatitis
* R heart failure
* hemochromatosis
* wilson disease
134
2 genetic causes of cirrhosis
* alpha 1 antitrypsin deficiency
* wilson disease
135
why do pts with cirrhosis develop portal HTN
* Blood can’t flow past nodules
* increased hepatic vascular resistance d/t less blood vessels passing through liver
136
what defines end stage liver disease
End-stage liver disease exists when the liver is unable to carry out its synthetic, metabolic, and clearance functions
137
MELD and Child-Pugh scores that increase risk of periop M&M
MELD > 15
Child-Pugh 10-15
138
what is the MELD score used for
* Predicts 90-day mortality in patients with ESLD
* More commonly used for patients with end-stage liver disease who require transplantation
139
what does the MELD score examine
3 factors of hepatic function: bilirubin, INR, and serum creatinine
140
**MELD Scores:**
low risk
intermediate risk
high risk
* Low risk = < 10
* Intermediate risk = 10-15
* High risk = > 15
141
what does the Child-Pugh score examine
five factors of hepatic function: albumin, PT, bilirubin, ascites, and encephalopathy
142
**Child-Pugh score:**
class A
class b
class C
* Class A (5-6 points) = 10% risk of perioperative mortality
* Class B (7-9 points) = 30% risk of perioperative mortality
* Class C (10-15 points) = 80% risk of perioperative mortality
143
child-pugh class score that should be managed medically before surgery until hepatic function improves
class C
144
circulation changes in cirrhosis
**hyperdynamic circulation**
* decreased SVR and BP
* increased CO
* increased blood volume (inc RAAS activation)
* R-L shunting
* increased SvO2
145
affects of ascites with cirrhosis
↓ Oncotic pressure
↓ Protein binding
↑ Vd
## Footnote
Drainage = hypotension
146
affects of ascites with cirrhosis
↓ Oncotic pressure
↓ Protein binding
↑ Vd
## Footnote
Drainage = hypotension
147
affects of ascites with cirrhosis
↓ Oncotic pressure
↓ Protein binding
↑ Vd
## Footnote
Drainage = hypotension
148
respiratory effects of cirrhosis
Restrictive defect
Respiratory alkalosis
Hepatopulmonary synd.
Portopulmonary HTN
149
what causes restrictive defect in cirrhosis
Ascites & pulmonary effusion = ↓ compliance & atelectasis
150
why do pts with cirrhosis have resp alkalosis
hyperventilation to compensate for hypoxemia
151
what is hepatopulmonary syndrome
complication of cirrhosis
Pulmonary vasodilation = R-L shunt = hypoxemia
152
what defines portopulmonary HTN in cirrhosis
PAP > 25 mmHg in setting of portal HTN
153
how is increased ammonia treated
lactulose, abx, ↓ protein intake
154
MOA of hepatic encephalopathy in cirrhosis
↓ hepatic clearance = ↑ ammonia = cerebral edema = ↑ ICP
Bleeding = reabsorption = ↑ nitrogen load = ↑ ammonia
155
mechanism of thrombocytopenia in cirrhosis
* splenomegaly = increased platelet consumption
* decreased thrombopoietin and bone marrow suppression
156
renal effects of cirrhosis
**decreased GFR**
* renal hypoperfusion
* dilutional hyponatremia
* renal failure
157
definitive treatment of hepatorenal syndrome
liver tx
158
why do pts with cirrhosis have decreased CaO2
hemorrhage, folic acid deficiency, hemolysis, bone marrow suppression
159
what is the TIPS procedure
Bypasses a portion of the hepatic circulation by shunting blood from the portal vein (hepatic inflow vessel) to the hepatic vein (hepatic outflow vessel)
160
effects of TIPS procedure
reduces portal pressure and minimizes back pressure on the splanchnic organs
## Footnote
reduces the likelihood of bleeding from esophageal varices and reduces the volume of ascites
161
effects of TIPS procedure
reduces portal pressure and minimizes back pressure on the splanchnic organs
## Footnote
reduces the likelihood of bleeding from esophageal varices and reduces the volume of ascites
162
effects of TIPS procedure
reduces portal pressure and minimizes back pressure on the splanchnic organs
## Footnote
reduces the likelihood of bleeding from esophageal **varices** and reduces the volume of ascites
163
significant risk during the TIPS procedure
hemorrhage
164
temporary treatment. of hepatorenal syndrome
TIPS procedure
165
indications for liver transplant
hep C (most common)
alcoholic liver disease, malignancy
166
can TEE be used during liver transplant
reasonably safe so long as transgastric views are avoided
167
when does pre-anhepatic stage begin and end
* **Begins** with surgical incision
* **ends** with cross clamping of portal vein, hepatic artery, and IVC/hepatic vein
168
lab used to guide replacement therapy in liver transplant
TEG or ROTEM
169
lab goals in pre-anhepatic stage of liver tx
* Hgb > 7 g/dL
* platelets > 40,000
* fibrinogen > 100 mg/dL
* and MA (TEG) >45
170
causes of CV instability in pre-anhepatic stage of liver tx
* drainage of ascites
* compression of vascular structures
* ongoing blood loss
171
how can biliary obstruction contribute to cirrhosis
inflammation & tissue destruction
172
how can chronic hepatitis contribute to cirrhosis
inflammation & tissue destruction
173
how can right sided heart failure contribute to cirrhosis
increased hepatic vascular resistance
174
which stage of liver tx is assoc with regurgitation and aspiration
pre-anhepatic stage
175
stage of liver tx assoc with hyperkalemia
neohepatic stage
176
stage of liver tx assoc. with profound decrease in CO
anhepatic stage
177
stage of liver tx with no liver function
anhepatic
178
when does the anhepatic stage of liver tx begin and end
**Begins** with removal of native liver & **ends** with implantation of donor liver
179
technique used during anhepatic stage of liver tx assoc with reduced operating and warm ischemic time
piggyback technique
180
technique used in anhepatic stage assoc with significantly reduced preload
bicaval clamp
181
where is the bicaval clamp placed when used in liver tx
to IVC above/below liver
| full obstruction of IVC flow
182
where is the bicaval clamp placed when used in liver tx
to IVC above/below liver
| full obstruction of IVC flow
183
option if patient doesn't tolerate piggyback technique during liver tx
VV bypass
184
liver tx:
outflow cannulas (towards pump)
femoral vein = systemic blood flow
portal vein = splanchnic blood flow
185
liver tx with VV bypass:
cannula with return to body
axillary vein (blood returns to IVC - heart)
186
benefits of piggyback technique over bicaval clamp in liver tx
* Reduced operating and warm ischemic time
* Fewer blood products required
* less preload reduction vs. bicaval clamp
187
complications assoc with VV bypass in liver tx
air embolism, thromboembolism, decannulation
188
common problems during anhepatic stage of liver tx
* worsening coagulopathy
* ongoing blood loss
* lactic acidosis
* hypoglycemia
189
how often should labs be checked during anhepatic stage of liver tx
q 15-30 min
190
when does warm ischemic time begin in liver tx
begins when donor liver is removed from ice and ends when reperfused
191
max warm ischemic time in liver tx
should not exceed 30-60 minutes
192
6 methods to treat increased K+ with reperfusion after liver tx
* hyperventilation
* D50 + insulin
* bicarb
* albuterol
* Lasix
* CVVHD
193
when does the neohepatic stage of liver tx begin and end
**Begins** with reperfusion of donor liver & **ends** with biliary anastomosis (or transport to ICU)
194
objectives of neohepatic stage of liver tx
* reperfusion of donor liver
* anastomosis of hepatic artery
* anastomosis of biliary structures
195
key complications of neohepatic stage of liver tx
* hyperkalemia
* hypocalcemia
* cytokine release
* lactic acidosis
* embolic debris
* hypovolemia
* systemic hypotension (decreased SVR)
* pulmonary hypertension (increased PVR)
* hypothermia
* cardiac arrest
196
CVP goal in neohepatic stage of liver tx
Avoid an elevated CVP, as this will cause congestion in the graft
197
findings that suggest good graft function in neohepatic stage of liver tx
* stabilization of serum glucose and acid-base status
* prompt return to normothermia
198
how is post-reperfusion syndrome defined
systemic hypotension > 30% below baseline for at least 1 minute during the first 5 minutes of reperfusion of donor liver
199
incidence of post reperfusion syndrome after liver tx
common (incidence 10-60%)
200
treatment of post-reperfusion syndrome in liver tx
vasopressors, correct hyperkalemia/hypocalcemia, correct acid-base
201
consequences of crystalloid resuscitation in neohepatic stage of liver tx
dilutional coagulopathy
thrombocytopenia
202
consequences of large blood volume admin in neohepatic stage of liver tx
* lactic acidosis
* hyperkalemia
* hypocalcemia
| r/t citrate toxicity
203
s/s poorly functioning graft after liver tx
continued HD instability and lack of bile output
204
can epidural analgesia be used in liver tx
contraindicated because of the patient's coagulation status
205
most common gallbladder diseases are caused by:
obstruction or inflammation
206
s/s biliary stone obstruction in cystic duct
* gallbladder distension
* edema
* risk of perforation
* jaundice
207
s/s biliary stone obstruction in common bile duct
* cholecystitis
* jaundice
* pancreatitis
* peritonitis
208
factors that increase incidence of biliary stones
* obesity
* aging
* rapid weight loss
* pregnancy
* women > men
209
s/s biliary stones
* Leukocytosis
* fever
* RUQ pain
* Murphy’s sign (pain worse with inspiration)
210
biliary pathology of biliary stones
(LFTs)
* ↑alkaline phosphatase
* ↑ conjugated bilirubin
* ↑ amylase
* ↑ Y glutamyl transpeptidase
* ↑ 5'-nucleotidase
211
why does prolonged NPO time increase likelihood of gallstones
lack of CCK release contributes to biliary stasis
212
treatment for cholecystitis
cholecystectomy
| (Cholecystitis = gallbladder inflammation)
213
treatment for cholelithiases
cholecystectomy
| (cholelithiases = gallstones)
214
treatment of Choledocholithiasis
ERCP
| (Choledocholithiasis = stones in common bile duct)
215
drugs that relax the sphincter of Oddi and decrease biliary pressure
* glucagon
* glyco
* atropine
* naloxone
* nitroglycerin
## Footnote
some debate that octreotide can cause
216
consequences of sphincter of Oddi spasm
**increased biliary pressure
**
can cause biliary colic and false positive of intraop cholangiogram
217
patho of biliary stones
obstructive defect that impedes flow of bile & pancreatic enzymes
218
what 2 hepatic structures converge at ampulla of Vater
* pancreatic duct
* common bile duct
219
location of portal vein
between splanchnic circulation and liver
220
why does blood that arrives to the liver via portal vein have a lower O2 content
this blood has already oxygenated the splanchnic organs
(spleen, intestine, stomach, gallbladder, pancreas)
221
receptors that line the hepatic artery
alpha 1
beta 2
222
receptors that line portal vein
alpha 1
223
which types of hepatitis are most likely to be contracted during blood transfusion
A, C
224
management of esophageal varices
* decrease hepatic venous pressure to < 10 mmHg
* TIPS procedure
* propranolol
* moderate fluid resuscitation
* balloon tamponade
225
drugs that relax the sphincter of Oddi
* glucagon
* glycopyrrolate
* atropine
* narcan
* nitro
