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liver > Apex- Liver > Flashcards

Apex- Liver Flashcards

1
Q

Which structure is responsible for eliminating bacteria from the liver?

A. Kupffer cell

B. Canaliculus

C. Sinusoid

D. Acinus

A

A. Kupffer Cell

(Acinus = Liver lobulue = functional unit of liver)

(Sinusoids are where the kuppfer cells are located)

(Bile canaliculi collect bile produced by the hepatocytes)

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2
Q

What is another name of rthe Acinus?

A

Liver lobule

*Functional unit of the liver

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3
Q

What is the functional unit of the liver

A

Liver lobule/Acinus

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4
Q

Where do lymph and proteins drain before emptying n=into the lymphatic duct?

A

space of Disse

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5
Q

What is the connective tissue covering that encapsulates the liver?

A

Glisson’s capsule

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6
Q

The liver receives SNS innervation from….

A

T3-T11

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7
Q

What % of lymph does the liver produce in the body?

A

~ 50%

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8
Q

What zone are the liver cells most susceptible to ischemic injury?

A

Zone 3 (Least oxygenated to begin with)

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9
Q

What zone has the highest concentration of CYP450 enzymes?

A

Zone 3

(also highest risk for ischemic injury)

(least oxygenated)

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10
Q

What drains blood from the intestine?

A

The portal vein

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11
Q

What produces bile and where is it stored?

A

Hepatocytes produce bile and it is stored in the GB

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12
Q

What zone is most oxygenated?

A

Zone 1

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13
Q

What cells drain bile into the bile duct?

A

Canaliculi

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14
Q

Label

A

The canniculi drain bile into the

1. Common hepatic duct

The 2. Cystic duct secretes bile and converges with the common hepatic duct to form the

3.. Common Bile duct

The 4.Pancreatic duct converges with the CBD to form the

5. Hepatopancreatic duct (Ampulla of vater)

& the 6. Sphincter of Oddi contracts to release bile into the dudodenum

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15
Q

What does the sphincter of Oddi do?

A

It controsl the flow of bile released from the common hepatic duct (CBD + pancreatic duct)

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16
Q

What is the ampulla of vater?

A

It’s where the CBD and pancreatic ducts converge

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17
Q

Another name for the apulla of vater

A

Hepatopancreatic duct

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18
Q

What do opioids do to the sphincter of oddi?

A

Contract it –> increases biliary pressure

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19
Q

What does bile even do? (3 things)

A
  1. Absorbs fat and fat soluble vitamins (DAKE)
  2. provides a pathway for excretion of bilirbuin and products of metabolism

(just think if you have a stone in your CBD, you cant drain bilirubin and thats why people get yellow)

  1. Alkalizes the duodenum
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20
Q

Cholecystokinin (CCK)

  • where is it produced
  • what increases it’s release?
  • What does it’s release do?
A

It’s produced in the duodenum ;

Eating fat and protein increases CCK release

Increased CCK release stimulates GB contraction to increase the flow of bile into the duodeum

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21
Q

Where is the space of Disse and what is it?

A

It’s located between the hapatocyte and the sinusoid

-lymph and proteins drain here before emptying into hte lymphatic duct

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22
Q

What is this structue and label it

A

The liver lobule/Ascinus (functional unit of the liver)

  1. Central Vein (Big ol’ blue thing by it’s lonesome self)
  2. Hepatocytes (Pink)
  3. Bile cannulici (Green)
  4. Branch of the portal vein (Blue between green and red)
  5. Branch of the hepatic artery
  6. sinusoid (purple)
  7. Kuppfer cell (yellow)

8.

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23
Q

T/F: Sinusoids are capillaries

A

true

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24
Q

What most accurately describes hepatic perfusion?

A. hepatic artery provides 75% of liver blood flow

B. The portal vein provides 50% of liver blood flow

C. The hepatic artery provides 75% of the liver’s oxygen content

D. The portal vein provides 50% of the livers oxygen content

A

D. The portal vein provides 50% of the livers oxygen content

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25
Q

Hepatic artery supplies ____% liver blood flow and ___% O2 content

The portal vein supplies ____% liver blood flow and ___% O2 content

A

Hepatic artery - 25% blood flow + 50% o2 content (higher concentration of o2)

Portal vein- 75% liver blood flow + 50% o2 content

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26
Q

What serves as a blood reservoir incase of acute hemorrage?

A

The liver

-Receives 30% of cardiac output

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27
Q

First 3 branches coming off the descending aorta and what do they supply?

A

1. Celiac artery

  • Liver (via hepatic artery) supplies 25% blood flow to liver/50% O2
  • Spleen
  • Stomach

2. Superior mesenteric artery (SMA)

  • Pancreas
  • Small intestine
  • Large intestine/Colon

3. Inferior mesenteric artery (IMA)

  • Large intestine/Colon
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28
Q

What drains blood from splanchic circulation

A

The portal vein

-supplies liver with 75% blood flow

50% o2

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29
Q

Normal portal vein pressure

A

7-10mmHg

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30
Q

Portal HTN = portal vein pressure > ____

A

20mmhg

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31
Q

Flow through the portal vein is autoregulated at what

A

Nothing, it’s not autoregulated.

So anything that increases splanchic vascular resistance, reduces portal vein flow (SNS stimulation, pain, hypoxia, hypercarbia)

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32
Q

How do varicies come about?

A

Bad liver > increase pressure through the portal vein

-portal HTN > back pressure on all the splanchic organs

>vessels become engorged in the esophagus, stomach and intestine.

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33
Q

What is acities from?

A

Portal HTN

increased pressure in the portal vein > fluid seeps out of the vasculature and into the abdominal cavity

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34
Q

What 2 major vessels supply blood to the liver?

A

Hepatic artery (

& Portal vein (drains sphlanchic circ)

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35
Q

The celiac artery provides blood flow to which 3 organs?

A
  1. Liver
  2. Spleen
  3. Stomach
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36
Q

The superior mesenteric artery supplies blood flow to what 3 organs?

A
  1. Pancreas
  2. Small intestine
  3. Large intestine/Colon
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37
Q

What organ receives blood flow from the inferior mesenteric artery?

A

The colon

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38
Q

4 things that increase splanchic vascular resistance

A
  1. hypoxia
  2. Pain
  3. SNS stimulation
  4. Propanolol
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39
Q

Hepatocytes produce: (Select 3):

  • thrombopoietin
  • alpha-1-acid glycoprotein
  • immunoglobulins
  • factor 3
  • factor 7
  • factor 8
A

thrombopoietin

Alpha-1-acid glycoprotein

factor 7

(factor 8 is produced by the sinusoids)

(factor 3 by the vascular endothelium)

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40
Q

What lab value is an early indicator of synthetic liver dysfunction and why?

A

PT

because factor 7 has the shortest half-life of all the procoagulant proteins

-whatever

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41
Q

The liver produces all the clotting factors except which 3?

A

3 (vascular endothelium)

4 (calcium from diet)

& von Willebrand (vascular endothelium)

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42
Q

T/F- the liver produces immunoglobulins

A

False- it produces all plasma proteins EXCEPT immunoglobulins

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43
Q

Vitamin K-depdent clotting factors and proteins

A

2, 7, 9, 10

C-S-Z

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44
Q

Why would someones ammonia level be high - where does ammonia come from

A

ammonia is a byproduct of protein metabolism.

-Protein gets broken down into ammonia > ammonia is cleared by liver

if liver not working, ammonia builds up > hepatic encephalopathy

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45
Q

Byproduct of protein metabolism

A

Ammonia

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46
Q

Byproduct of hemoglobin metabolism

A

Bilirubin

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47
Q

Where doe we get bilirubin

A

from the breakdown of hemoglobin

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48
Q

How is bilirubin removed from the body?

A

it’s conjugated with glucuronic acid in the liver, facilitating it’s elimination

-someone with liver failure cant do this and unconjugated bilirubin is neurotoxic (hepatic encephalopthy)

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49
Q

What coagulation protein stimulates platelet production

A

Thrombopoietin

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50
Q

Why are liver failure patients at risk for hypoglycemia?

A

Bc the liver clears insulin from systemic circulation

  • increased insulin in systemic circulation = risk of hypoglycemia
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51
Q

2 physiologic functional categories of the liver

A
  1. Synthesis of proteins (coagulation and plasma proteins)
  2. metabolism (carbs, proteins, fats)
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52
Q

The liver converts ammonia to _______; which is elminated by the kidney

A

urea

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53
Q

Why might someone with liver dysfunction have a lower BUN

A

because the liver converts ammonia to urea , so low levels of urea (BUN) may be indicative of liver disfunction

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54
Q
A
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55
Q

life cycle of a RBC

A

120 days

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56
Q

What plasma proteins are synthesized in the liver?

A

All of them except immunoglobulins

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57
Q

Match each lab test with its underlying pathology:

  • Transaminases:
  • Prothrombin time:
  • 5’-nucleotidase
  • Bilirubin
  • biliary obstruction, synthetic function, hepatocellular injury, hepatic clearance.
A
  • Transaminases: hepatocellular injury
  • Prothrombin time: synthetic function
  • 5’-nucleotidase: biliary obstruction
  • Bilirubin: hepatic clearance
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58
Q

What labs assess synthetic function of the liver (2)

A

PT and albumin

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59
Q

What labs assess hepatocellular injury (2)

A

AST, ALT

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60
Q

What lab assesses hepatic clearance?

A

Bilirubin

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61
Q

What 3 labs would be elevated in a biliary duct obstruction?

A
  1. Alkaline phosphatase
  2. Y-glutamyl transpeptidase
  3. 5’- nucleotidase
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62
Q

T/F - PT is very sensitive for acute hepatic injury

-why or why not

A

True

because factor 7 has a half-life of only 4-6 hours

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63
Q

Half life of albumin

A

21 days

(not sensitive for acute hepatic injury)

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64
Q

Most specific indicator of biliary duct obstruction

A

5’- Nucleotidase

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65
Q

What does marked elevation of AST and ALT suggest

A

hepatitis

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66
Q

An AST/ALT ratio > ____ suggests cirrhosis or alcoholic liver disease

A

>2

67
Q

Normal PT

A

12-14 sec

68
Q

Normal Albumin

A

3.5-5g/dL

(same as K)

69
Q

Normal AST/ALT

A

AST 10-40

ALT 10-50

(think L = love = ALT loves a wider range)

70
Q

What would indicate that a hematoma is starting to be reabsorbed? (lab)

A

increase in bilirubin

(as it’s reabsorbed, rbcs get broken down > bilirubin)

71
Q

PT is shorterend or prolonged in viatmin K deficiency

A

prolonged

72
Q

Normal bilirubin

A

0-11units/L

73
Q

Why might someone with have an elevated alk phos but normal liver function

A

it’s also in bone, placenta, and tumors

-so maybe they pregnant? maybe they have a tumor?

74
Q

Normal 5’- Nucleotidase

A

0-11

(same as bilirubin)

*indicates biliary duct obstruction

75
Q

T/F- halothane hepatitis is an autoimmune response

A

True

76
Q

What is the most common cause of chronic hepatitis?

A

Alcohol Abuse

77
Q

What is the most common form of viral hepatitis?

A

Hep A

78
Q

Which forms of hepatitis can cause cirrhosis

A

B & C

(Not A)

79
Q

What is a co-infection that happens with hepatitis B

A

Hepatitis D

80
Q

Which Hepatitis’s can be transmitted in a blood transfusion?

A

B & C

81
Q

Which hepatitis’s are transmitted by the oral-fecal route?

A

A & E

(A&E channel broadcasts fecal-oral routes)

82
Q

What is halothane metabolized into that can produce an immune-mediated response?

A

Trifluoacetic acid (TFA)

83
Q

Most common cause of liver cancer

A

hepatitis

84
Q

Drug-induced hepatitis can ber caused by what 3 drugs?

A
  • Acetaminophen
  • Halothane
  • Alcohol
85
Q

What is the antidote for acetaminophen OD?

A

Oral N-Acetylcystine

86
Q

Most common cause of drug-induced hepatitis

A

Alcohol abuse

87
Q

Whats another name of saying someone has liver inflammation

A

hepatitis

88
Q

3 causes of hepatitis

A
  1. virus’s
  2. hepatotoxins (drugs)
  3. autoimmune responses
89
Q

Most common cause of acute liver failure in the US

A

Acetaminophen OD

90
Q

Max acetaminophen dose/day

A

4g/day

91
Q

What is the toxic metabolite produced by acetaminophen? How is it elminated?

A

NAPQI

N-acetyl-p-benzoquinoneimine

it is conjugated with glutathione

92
Q

What happens with tylenol OD

A

the liver congugates the toxic metabolite NAPQI + Glutathione

-when there is no more glutathione left, the concentration of toxic NAPQI rises > hepatocellular injury

93
Q

Treatment of tylenol OD and what time frame must it be administered

A

oral N-acetylcystine within 8 hours of OD

94
Q

Which volatile agents are metabolized into TFA

A

Halothane

Desflurane

Isoflurane

*but up to 20% of halothaine is metabolized, so much higher levesl of TFA comared to the others (0.02% des and 0.2% Iso)

95
Q

Most common and second most common cause of chronic hepatitis

A

most common = alcoholism

2nd most common = hep c

96
Q

6 risk factors for halothane hepatitis

A
  1. female
  2. over 40yo
  3. fat
  4. genetics
  5. more than 1 exposure
  6. CYP 2E1 induction (alchol, isoniazid, phenobarbital)
97
Q

All of the following drugs should be avoided in the patient with acute hepatitis EXCEPT:

A. amiodarone

B. tetracycline

C. acetaminophen

D. Propanolol

A

D. Propanolol

(reduces portal pressure by reducing CO (b1) and splanchic vasoconstriction (b2)

98
Q

How does propanolol reduce portal pressure (2 ways)

A
  1. Decerases cardiac output (b1) - less blood to go into portal circ
  2. Splanchic vasoconstriction (b2) - i dont understand
99
Q

Ok to proceed to surgery if someone has acute hepatitis?

A

Not if it’s elective - postpone until sx resolve and LFTs normal

100
Q

ok to proceed to elective surgery in someone with chronic hepatitis?

A

as long as the condition is stable

101
Q

How are mac levels affected in someone whos not acutely intoxicated but is a chornic alcohol user

A

INCREASED MAC

102
Q

You gotta anesthetize a drunk person; what are your first thoughts

A

Full stomach- RSI

Decreased MAC

Avoid Des (some literature says des reduces hepatic blood flow to a greater extent)

-No PEEP (increases resistance to hepatic drainage)

103
Q

How quickly do s/s alcohol withdrawl present? When do they peak?

A

6-8 hrs after BAC returns to near normal

Peak 24-36 hours

104
Q

Someone with heptitis, how is it going to affect your NMBs

A

prolong duration of sux 2nd to decreased pseudocholinesterase

-prolonged doa of roc bc of it’s biliary excretion (maybe use cist)

105
Q

What receptors does alochol work at

A

it agonizes GABA (becomes downregulated with chonric use)

& antagonizes NMDA receptors /glutamate (becomes upregulated with chronic use)

-so when you have extra nmda receptors , and not many gaba receptors and stop drinking alcohol; you have extra stimulation of the nmda recpetors and less inhibitory receptors = the increase SNS response

106
Q

vitamin B1 (thiamine) deficiency contributes to what syndrome

A

Wernike-Korsakoff syndrome

“Wernickes Aphasia” - due to loss of neurons in the cerebellum brought on by thiamine deficiency

107
Q

You see a patient on Disulfiram - what is it and what are your concerns

A

-it’s a treatment for alocholics in recovery

-it inhibits dopa-beta hydroxylase (NE synthesis) -> Hypotension

108
Q

Common physiologic changes in the patient with cirrhosis include all of the following EXCEPT:

A. Respiratory acidosis

B. Increased CO

C. Right to left shunt

D. Decreased GFR

A

A. Respiratory acidosis

P’ts with cirrhosis experience pulmonary vasodilation (lungs sense a decreased blood flow - bc its backing up in portal circulation - so they the pulm vasculature dilates to try to accept more blood)

right-to-left shunting - dont get

hypoxemia > they hyperventilate to offset the reduction in PaO2 creating a respiratory alkalosis

109
Q

What is cirrhosis?

A

It’s when liver cells die and fibrotic tissues and nodules replace healthy tissue

-decerased # of functional hepatocytes

110
Q

Most common cause of liver diseae

A

Non-alcoholic fatty liver disease

(fatty infiltration - obesity)

111
Q

What genetic enzyme deficiency leads to cirrhosis

A

Alpha-1-antitrypsin deficiency (also leads to emphysema)

112
Q

How does hemochoromatosis affect the liver?

A

Iron overload

*check coags

113
Q

What is Wilson’s disease

A

a genetic cause of cirrhosis where copper accumulates in the tissue

(WIIIILLLSSSOONNNN - put copper pipes in his liver while stranded on an island with his volleyball)

114
Q

Patient is at increased risk of perioperative morbidity and mortality if they have a child -Pugh score of ____ or a MELD score of ______.

A

Child-Pugh - C

MELD > 15

115
Q

What 3 factors does the meld score look at?

A
  1. Bilrubin
  2. INR
  3. Creat
116
Q

What does the MELD score predict?

A

90-day mortality in patients with ESLD.

117
Q

What5 factors does the modified Child-Pugh score examine?

A
  1. Albumin
  2. PT
  3. bilirubin (MELD)

4 ascities

  1. encephalopathy
118
Q

someone has splenomegaly, what do you want to check?

A

platelets

119
Q

What might someones sodium look like if they have cirrhosis

A

Low

  • decreased GFR activates RAAS > sodium and water retention > dilutional hyponatremia
120
Q

What does TIPS procedure stand for?

A

Transjugular intrahepatic portosystemic shunt

121
Q

What happens with a TIPS procedure?

A

a shunt is placed to shut blood from the portal vein (inflow vessel to the liver) to the hepatic vein (hepatic outflow vessel)

  • it reduces portal pressure and backflow on splanchic organs
  • decreased likelihood of esophgeal varices bleeding
  • decreases volume of ascities

*temporary treatment for hepatorenal syndrome

122
Q

Risk of TIPS procedure

A

hemorrhage

123
Q

How are the kidneys affected with hepatorenal syndrome

A

the lack of blood flow to the liver (bc it’s diseased) - increaases cardiac output (volume going to the liver) but also leads to decreased SVR (hypotension) bc of the release of vasoactive substances

-kidneys become hypoperfused, RAAS activated, worsens issue

124
Q

Match each phase of liver transplantation with its MOST likely complication:

  • Pre-Anhapatic phase
  • Anhepatic phase
  • Neohepatic phase

-hyperkalemia, pulmonary aspiration of gastric contents, profound reduction of cardiac output

A
  • Pre-Anhapatic phase + pulmonary aspiration of gastric contents
  • Anhepatic phase + profound reduction in CO
  • Neohepatic phase+ hyperkalemia
125
Q

Most common indication for liver transplant +2 more

A

*HEP C*

  • etoh liver diseae
  • malignancy (interesting)
126
Q

What starts and ends the pre-anahepatic phase?

what’s the goal

A

start - surgical incision

end - cross clamping of portal vein, hepatic artery, and IVC

goal is to mobilize the liver and vascular structures and isolate the CBD

127
Q

What starts and ends the anhepatic phase of liver transplantation

goal

A

beings with removal of the native liver

ends with emplantation of donor liver

goal- remove and replace donor liver (allograft)

128
Q

When does the neoheptaic phase of liver transplantation begin and end

A

begins with reperfusion of the donor liver

ends with biliary anastomosis (or transport to ICU)

-goal: perfuse the donor liver, anastomosis of hepatic artery and biliary structures

129
Q

Pre-anahepatic phase goals:

hgb > ____

platelets > _____

fibrinogen > _____

MA(TEG) > ______

A

hgb > 7

platelets > 40

fibrinogen > 100

MA(TEG) > 45

130
Q

What would you expect to happen to your blood pressure during the pre-anahepatic phase of liver transplant and why?

A

hypotension

-from draining ascities, compressing vascular structures, and ongoing blood loss

131
Q

Where should your CVP be prior to clamping the IVC?

A

increase it to 10mmHg

132
Q

What 3 things can result from large volume blood product administration

A
  1. lactic acidosis
  2. hyperkalemia
  3. hypocalcemia
133
Q

why does large volume transfusion lead to hypocalemia?

A

bc of citrate toxicity

citrate binds calcium

134
Q

concerns with crystalloid resusitation

A

can cause dilutional coagulopathy and thrombocytopenia and worsen your issue

135
Q

What’s a bicaval clamp and your concerns

A

clamps are applied to IVC above and below the liver (full obstruction of IVC flow)

*significant preload reduction > hypotension, tachycardia

*aggressive fluid administration can lead to volume overload when clamps are released

136
Q

What is the piggyback technique when isolating the liver

A

the IVC is side-clamped (IVC flow is partially obstructed)

  • less preload reduction compared to bicaval clamp
  • fewer blood products required
137
Q

How is venovenous bypass used to isolate the liver for resection?

sites of cannulation

A

Site of cannulation leaving body and going to pump:

femoral vein - (systemic blood flow)

portal vein - (splanchic blood flow)

Site of cannulation leaving pump and returning to the body:

Axillary vein (blood returns to the IVC > heart)

138
Q

3 potential complications of venovenous bypass for liver transplant

A

air embolism, thromboembolism, decannulation

139
Q

Common problems with anhepatic phase of liver tranpsplant

A

worsening coagulopathy, blood loss, lactic acidosis, hypoglycemia (no glycogen storage)

*use sodium bicarb to combat acidosis

140
Q

When does warm ischemic time begin and end and what is the time limit

A

begins when donor organ is removed from ice

ends when the donor liver is reperfused

<30-60 mins

141
Q

How should you prepared for reperfusion of the donor liver

A

DECREASE POTASSIUM LEVEL beforehand bc it will rise!

  • hyperventillate
  • D50 + insulin
  • Bicarb
  • Albuterol
  • Furosemide
142
Q

First line tx for hyperkalemia (drugs) -2

A

calcium chloride (raide TP)

sodium bicairb

143
Q

Should your CVP be elevated or reduced after the donor graft is being reperfused

A

REDUCED - if it’s high, it will cause congestion in the graft

144
Q

How can you tell if the donor graft is taking well (3 things)

A
  • return to normothermia (fastest check)
  • stablization of glucose and acid-base balance
145
Q

What is hte most important consideration during the neohepatic phase of liver transplantation.

How do you treat it?

A

Post-Reperfusion Syndrome

systemic hypotension > 30% below baseline for at least 1 mintue

(during the first 5 mins of reperfusion)

*It’s common! 10-60%

Treat: supportive - vasopressors, lyte correction (hyperkalemia, hypocalcemia), acid-base correction

146
Q

2 signs of a poorly functioning graft (donor liver)

A
  1. contineud hemodynamic instablity
  2. lack of bile output
147
Q

T/F- epidural anestheisia is a good method of pain control for liver transplant patients

A

false- coagulopathic! epiurals are contraindicated

-PCA

148
Q

what would you anticipate your patient having once over in ICU (2 gtts)

A

PCA

Insulin (steroid-induced hyperglycemia)

149
Q

What view should be avoided when performing a TEE in a patient with esophageal varices?

A

All transgastric views

150
Q

All of the following drugs improve biliary hypertension EXCEPt:

A. Naloxone

B. Nitroglycerine

C. Glucagon

D. Octreotide

A

D. Octreotide

151
Q

Why might the doc ask for a drug to relax the sphincter of oddi during cholangiogram?

A

because if it’s contracting it can lead to a false positive result

152
Q

5 drugs you can use to relax the sphincter of Oddi and reduce biliary pressure (& Mneumonic)

A

NNAGG

Nitro

Naloxone

Atropine

Glyco

Glucagon

153
Q

What happens when someone has obstructive biliary stones?

A

Bile cant flow into the small intestine; so it backs up into the liver and pancreas resulting in inflammation

154
Q

T/F- glucagon increases risk of PONV

A

True!

155
Q

What is Murphy’s sign

A

RUQ pain that is worse with inspiration

(GB disease)

156
Q
  • Cholecystitis:
  • Cholelithiasis
  • Choledocholithiasis:

What are they are what is the surgical treatment for each?

A
  • Cholecystitis:
    • Inflammation of the GB (cholecystectomy)
  • Cholelithiasis
    • Gallstones (cholecystecomy)
  • Choledocholithiasis:
    • ​Stones in the CBD (ERCP)
157
Q

Who gets an ERCP

A

someone with stones in their CBD

158
Q

T/F- smoking is a risk factor for cholelithasis

A

False!

159
Q

Bile is produced by ________ and stored in the ________

A

hepatocytes; gallbladder

160
Q

why does the liver failure patient have hyperdynamic circulation with a low SVR and increase in CO?

A

because severe liver disease impairs the livers abilty to clear vasodilating substances from systemic ciruclation (SVR drops and CO picks up to try and compensate)

161
Q

Propanolol reduces hepatic blood flow by causing:

A. Portal vein dilation

B. Portal vein constriction

C. Hepatic artery dilation

D. Hepatic artery constriction

A

D. Hepatic artery constriction

via beta 2 receptor blockade > vasoconstriction

162
Q

When blood flow to the liver falls, what kicks in to preserve hepatic blood flow and how

A

The hepatic arterial buffer response

  • if portal vein flow comprimised, the hepatic artery dilates
  • if hepatic artery flow is compromised, the portal vein dilates
  • severe liver disease impairs this buffer response.
163
Q

What is the region most suseptible to hypoxic injury

A

Well i knew it was zone 3, but idk whats in there lol

  • ok so zone 3 is near the central vein
  • blood comes in from the terminal branches of the hepatic aretery and portal vein and enter the peipheray of the lobule (zone 1) - best oxygenated.
  • zone 3 (near the central vein) recieves the least amount of o2, making it most susceptible to hypoxic injury. (+ of course has the highest conentration of CYP450 enzymes)
164
Q

Most common form of viral hepatitis

A

A

  • makes sense bc fecal-oral transmission is easier to aquire
  • good thing hep A doesnt lead to chronic hepatitis, cirrhoisis, or cancer

liver (2 decks)

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