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1. adv principles 3 exam 1 > Liver & GI > Flashcards

Liver & GI Flashcards

0
Q

(1)

  1. Where does the liver lie?
  2. how much does the liver weigh?
  3. how many lobes in the liver?
  4. what are the functional units of the liver?
A

(1)

  1. Where does the liver lie?
    - - upper right quad of the abdomen and is attached to the diaphragm
  2. how much does the liver weigh?
    - - accounts for 2% of body weight in adults and 5% in neonates
  3. how many lobes in the liver?
    - -2 lobes of the liver with 50-100,000 individual lobules
  4. what are the functional units of the liver?
    - - hepatocytes account for 50% of the liver cells and 80% of the liver volume
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1
Q

OBJECTIVES:

A
  1. ​Describe the anatomical features of the liver.
  2. ​Discuss the function of the liver as an organ.
  3. ​Outline hepatic blood flow.
  4. ​Explain the pharmacokinetics and pharmacodynamics unique to liver dysfunction.
  5. Discuss the changes in organ function related to liver disease.
    b. cardiovascular
    c. respiratory
    d. renal
    e. hepatic
  6. ​Discuss the anesthetic management for patients with liver dysfunction.
  7. Define hepatitis. List potential causes and mortality rates.
    b. List various types of hepatitis
  8. Discuss the pathophysiologic changes often associated with biliary tract disease.
  9. Describe surgical and other invasive procedures to treat portal hypertension and esophageal varices.
  10. Outline the anesthetic management of a Whipple procedure
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2
Q

(2)
what is the blood flow to the liver:
1. what forms the central vein?
2. one layer separates what from what in the liver?
3. what (in the blood) does the total area come in contact with?
4. what do the central veins become and what does this structure drain into?
5. what vein drains into the GI tract? what does it contain?

A

(2)
what is the blood flow to the liver:
1. what forms the central vein?
–blood flows past the hepatocytes from branches of the portal vein and hepatic artery to form a central vein.
2. one layer separates what from what in the liver?
–the sinusoid is separated from the hepatocytes by one layer
3. what (in the blood) does the total area come in contact with?
– plasma comes into contact with this total area
4. what do the central veins become and what does this structure drain into?
–the central veins join to form the hepatic vein which drains into the inferior vena cava
5. what vein drains into the GI tract? what does it contain?
–the portal vein drains into the GI tract and contains colon bacteria

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3
Q

(3)

  1. what type cells that permit diffusion of large substances?
  2. how does this happen?
  3. what large substances in particular are allowed to be diffused? 3b. where do they go?
A

(3)
1. what type cells that permit diffusion of large substances?

  1. endothelial cells in the hepatic lobules
  2. how does this happen?
    - it contains large pores
  3. what large substances in particular are allowed to be diffused?
    - - plasma proteins which drain into the extravascular spaces
    3b. where do they go?
    - —connect with terminal lymphatics
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4
Q

(4)

how much of the lymph is formed in the liver

A

(4)
how much of the lymph is formed in the liver
-1/3 to 1/2 of the lymph

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5
Q

(5)
III. Outline hepatic blood flow:
1. how much is the total hepatic blood flow/min and how much of the cardiac output?
2. from what vessels does the liver receive blood?
3. how much blood does the portal vein supply and how much oxygen; from where does it come from and where does it drain?
4. how much blood does the hepatic artery supply and from where does it come?
5. how much blood can be stored in the liver?

A

(5)
III. Outline hepatic blood flow:
1. how much is the total hepatic blood flow/min and how much of the cardiac output?
– total hepatic blood flow is 1450 ml/min and 20-29% of C.O.
2. from what vessels does the liver receive blood?
–the liver receives blood flow from the hepatic artery and portal vein
3. how much blood does the portal vein supply and how much oxygen
3. portal vein=75% of total blood flow, 55% of hepatic oxygen from IVC;
3b. from where does it come from and where does it drain?
–splenic branches from here drain into GI tract and contain colon bacteria
4. how much blood does the hepatic artery supply and from where does it come?
– hepatic artery=25% of total blood flow and 40-45% of hepatic oxygen from aorta
5. how much blood can be stored in the liver?
–500-1000 mL

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6
Q

(6)
what pharmacodynamic and pharmacokinetic changes does liver dysfunction cause with medications?
I. pharmacodynamics:
II. pharmacokinetics:

A

(6)
what pharmacodynamic and pharmacokinetic changes does liver dysfunction cause with medications?
I. PharmacoDynamics (what Drugs do to the body):
–1. decreased albumin causes an increased free fraction of highly protein bound medications. this causes increased sensitivity.
–2. decreased catecholamine function (d/t up-regulation) d/t liver issues
II. pharmacokinetics (what body does to drugs):
–1. cyp450 (which conjugates (metabolizes) drugs) may be decreased causing longer half life of drugs (decreased biotransformation)
–2. decreased elimination of drugs that are eliminated in bile
–3. changes in hepatic blood flow decrease hepatic function and elimination of drugs

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7
Q

(7)

Name 4 drugs that depend on hepatic blood flow?

A 
(7) 
Name 4 drugs that depend on hepatic blood flow?
1. morphine
2. lidocaine
3. verapamil 
4. beta blocker
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8
Q

(8)
Cardiovascular function changes related to liver disease (cirrhosis):
1. what Decreases?
2. what Increases?

A

(8)
Cardiovascular function changes related to liver disease (cirrhosis):
1. Decreases:
-decreased PeriphVR d/t peripheral vasodilation & increased AV shunting
-decreased cardiac function (cardiomyopathy/CHF)
-decreased responsiveness to catecholamines
-decreased portal blood flow to liver
-decreased (or maintained) hepatic artery blood flow
-decreased (or maintained) renal blood flow
2. Increases:
-increased circulating blood volume (CHF)
-increased C.O.
-increased pressure of esophageal blood flow (varices)
-increased pressure on GI blood flow (hemorrhoids, periumbillical
-increased venous oxygen content (decreased difference in AV content)
-increased splanchnic (except for hepatic), pulmonary, muscle and skin blood flow

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9
Q

(9)

Respiratory function changes related to liver disease (cirrhosis):

A

(9)
Respiratory function changes related to liver disease (cirrhosis):
-V/Q abnormalities
-decreased pulmonary vasoconstriction
-hypoventilation (d/t ascites/ abdomen girth)
-decreased pulmonary diffusion capacity (d/t increased extracellular fluid)
-right shift in oxyhgb dissosociation curve (d/t increase in 2,3 DPG)
-Right to Left shunt across lungs d.t:
—-spider angiomas in lungs
—-porta-plmonary venous communications
—-humoral factors (vasodilation, glucagon, ferritin, sandostatin)

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10
Q

(10)
Renal function changes related to liver disease (cirrhosis):
1. what 2 renal conditions are caused?
2. what is the treatment for condition #2?

A

(10)
Renal function changes related to liver disease (cirrhosis):
1. what 2 renal conditions are caused?
-a. renal failure: decreased perfusion to kidneys leading to decreased kidney function
-b. hepatorenal syndrome (d/t hypoperfusion and usually following GI bleed, diuresis and/or sepsis)
—-decreased urine output (with no sodium) leading to increased ECF, edema and ascites
—-intravascular hypovolemia
—-increased bun/creat
2. what is the treatment for condition #2?
-dopamine (?renal dose)
-denver shunt (which shunts ascites to the right atrium for circulation)

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11
Q 
(11)
Hepatic and other organ function changes related to liver disease: 
1. Hepatic:
2. Brain:
3. Coagulation/ Blood:
-a. what happens with CBC?
-b. what coagulation changes occur?
-c. what factors are involved?
-d. what else increases bleeding risk?
4. Endocrine:
A

(11)
Hepatic and other organ (brain, endocrine, coagulation) function changes related to liver disease:
1. Hepatic:
-hepatic hypoxia (from hypotension and generalized hypoxia)
2. Brain:
-hepatic enchalopathy d/t inability of liver to convert ammonia to urea
-impaired citrate metabolism may lead to “citrate encephalopathy” if multiple blood transfusions are given (citrate is preservative in banked blood)
3. Coagulation/Blood:
-a. what happens with CBC?
–decreased Hct d/t increased plasma volumes and anemia
-b. what coagulation changes occur?
–prolonged PT/INR (d/t decreased factor 2)
-c. what factors are involved?
–decreased factors 2,7,9,10 (??5)
-d. what else increases bleeding risk?
–increased fibrinolysis (d/t decreased clearence of activators of fibrinolytic system)
4. Endocrine:
-increased growth hormone
-abnormal glucose utilization

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12
Q

(12)
anesthetic implications for patients with liver dysfunction:
what drugs to give:

A

(12)
anesthetic implications for patients with liver dysfunction:
what drugs to give:
1. Induction: use smaller amount of protein bound drug (d/t decrease in albumin; fentanyl, propofol, lidocaine, thiopental, etomidate are all highly protein bound). However, etomidate is the best induction drug and fentanyl is the best narcotic.
2. use paralytics that do not undergo hepatic metabolism (nimbex (cisatricurium) or tracrium (atricurium))
3. Isoflurane is probably the best VA, Des is second, sevo is last d/t flouride ion metabolites. Nitrous oxide has too many sympathomimetic side effects.

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13
Q

(13)

1a. define hepatitis:
1b. s/s hepatitis:
1c. tx of hepatitis:
2. what are the 8 types of hepatitis:

A

(13)

  1. define hepatitis:
    - inflammation of liver hepatocytes; almost always viral
    1b. s/s of hepatitis:
    - dark urine, fatigue, anorexia, dehydration, low grade fever, hepatomegaly, splenomegaly, s/s of acute liver failure (confusion, edema, ascites).
    1c. tx of hepatitis:
    - symptomatic
  2. what are the types of hepatitis?
    - Hep A:
    - Hep B:
    - Hep C:
    - Hep D:
    - Hep E:
    - chronic hepatitis:
    - drug induced hepatitis
    - halothane hepatitis
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14
Q

(14)

what are potential causes of hepatitis?

A

(14)
what are potential causes of hepatitis?
-contaminated food, percutaneous, venereal, hepatotoxic drugs, halothane

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15
Q 
(15)
Hepatitis A:
1. transmission:
2. incubation:
3. mortality: 
4. treatment:
A 
(15)
Hepatitis A:
1. transmission: oral-fecal
2. incubation: 20-37 days
3. mortality: 0.2%
4. treatment: vaccinations (IgG anti-HAV)
16
Q 
(16)
Hepatitis B:
1. transmission:
2. incubation:
3. mortality: 
4. treatment:
A

(16)
Hepatitis B:
1. transmission: percutaneous or venereal
2. incubation: 60-110 days
3. mortality: 0.3- 1.5%
4. treatment: no cure; vaccinations are preventative

17
Q 
(17)
Hepatitis C:
1. transmission:
2. incubation:
3. mortality: 
4. treatment:
5. misc:
A

(17)
Hepatitis C:
1. transmission: percutaneous, most cases post transfusion hepatitis
2. incubation: 35-70 days
3. mortality: <3%
4. treatment: Interferon
5. misc: leading indication for liver transplant

18
Q

(18)
Hepatitis D:
1. transmission:
2. mortality:

A

(18)
Hepatitis D:
1. transmission: Percutaneous, requires co-infection with HBV or as a superinfection of persons with chronic HBV
2. mortality: low

19
Q

(19)
Hepatitis E:
1. transmission:

A

(19)
Hepatitis E:
1. transmission: oral-fecal (person to person is uncommon)

20
Q

(20)
Acute drug induced Hepatitis:
1. cause:

A

(20)
Acute drug induced Hepatitis:
1. cause: alcohol is most common; can be isoniazid, abx, anti htn meds, anti convulsives, tylenol, can also be idiosyncratic drug reaction

21
Q

(21)
Halothane Hepatitis:
1. cause:
2. mortality:

A

(21)
Haolthane Hepatitis:
1. cause: halothane gas metabolites (tri-fluoro-acetyl containing)
2. mortality: 50%

22
Q 
(22)
chronic hepatitis:
I. chronic active:
1. cause:
2. duration:
3. symptoms:
II. chronic lobular
III. chronic persistent
A

(22)
chronic hepatitis:
I. chronic active: most serious-progressive hepatocyte death
1. cause: hepB, hepC, autoimmune (lupus), certain drugs
2. duration: lasts longer than 6 months
3. symptoms: increased IgG levels differentiate it from viral, hepatic failure, hemorrhage from esophageal varices, multiorgan failure, encephalopathy, cirrhosis, death
II. chronic lobular:
-exacerbations of acute inflammation; progression to cirrhosis rare
III. chronic persistent hepatitis:
-non progressive, confined to portal system

31
Q 
(23)
how does blood supply and nutrients enter and leave the liver (from what vessels and from where)?
1. Venous to liver:
2. Venous from liver:
3. Arterial:
A 
(23)
how does blood supply and nutrients enter and leave the liver (from what vessels and from where)?
1. Venous to liver: 
-a) from superior mesenteric vein (draining nutrients from intestines) and from the splenic vein to the:
-b) portal vein which enters the liver
2. venous from liver:
-c) hepatic veins to:
-d) inferior vena cave
3. Arterial:
-e) from aorta to:
-f) hepatic artery
32
Q

(35)
Billiary tract disease
Name them:

A 
(35)
Billiary tract disease
Name them:
1. Cholestasis
2. Pancreatitis
3. Pancreatic tumors
33
Q

(36)
Cholestasis:
1. What is it?
2. 3 Common causes:

A 
(36)
Cholestasis:
1. What is it? Reduction of the hepatic secretion of bile, uaually d/t extrahepatic obstruction to billiary tract
2. Common causes:
-gall stones
-stricture
-tumor
34
Q

(37)

  1. Procedures to releive cholestasis:
  2. What is involved with this procedure?
A

(37)

  1. Procedures to releive cholestasis-
    - -ERCP:
  2. What is involved with this procedure?
    - sphincterotomy: a wire on the end of the endoscope is used to make an incision in sphincter to open duct and remove stone
    - gallstone removal
    - stent placement
    - balloon dilation
35
Q 
(24)
pathophysiological changes caused by billiary tract disease:
1. cardiovascular
2. coagulation
3. renal
A

(24)
pathophysiological changes caused by billiary tract disease:
1. cardiovascular: increased bilirubin levels decrease catecholamine response
2. coagulation: vitamin K defeciencies cause decreases in vitamin k related coagulation factors (2,7,9,10)
3. renal: obstruction of biliary tree causes a reversible decrease in GFR (when obstruction is resolved)

36
Q

(25)
anesthesis induction for hepatic patient:
-what should you be mindful of?

A

(25)
anesthesis induction for hepatic patient:
-what should you be mindful of?
1. may be full stomach –RSI
2. if alcoholic cirrhosis; is patient intoxicated–RSI
3. consicer CV and respiratory implications (ascites, distended abdomen, pleural effucisons (from ascites), fluid overload.
4. may have decreased pseudocholinesterase so Sux may have prolonged effect
5. decrease dosages of all meds.
6. patient may have autonomic neuropathy (fixed tachycardia with orthostatic hypotension)

37
Q 
(26) 
monitoring of hepatic patient under anesthesia:
1. what should be monitored?
1b. why?
1c. what type of lines should they have?
2. what should be avoided?
A 
(26) 
monitoring of hepatic patient under anesthesia:
1. what should be monitored? 
-urine output
-arterial blood pressure
-CVP (if cardiac issues)
1b. why?
-loss of peritoneal fluid leads to intravascular depletion and protein loss; and if the patient has cardiac issues- should be monitored closely
1c. what type of lines should they have?
-probably should have art line
-possibly have central line
-large bore IV access
2. what should be avoided?
-unnecessary esophageal insturmentation (no esophageal sthesoscope)- may have varices
38
Q

(27)
maintainance of anesthesia for hepatic patient:
1. If regional anesthesia is chosen, what should you be aware of?
2. what effect will VAs have on this patient?
3. what drugs should have doses reduced?
4. what VAs are the best?

A

(27)
maintainance of anesthesia for hepatic patient:
1. If regional anesthesia is chosen, what should you be aware of?
-coags (remember decreased vitamin K decreases factors 2,7,9,10)
2. what effect will VAs have on this patient?
-VAs impair hepatic artery vasodilation and decrease hepatic blood flow
3. what drugs should have doses reduced?
-highly protein bound drugs (opioids, benzos)
4. what VAs are the best?
-Iso or Des

39
Q

(28)

  1. What fluids may need to be given for hepatic patients undergoing surgery?
  2. what happens when ascites (peritoneal fluid) is drained?
  3. what is the max amount of peritoneal that fluid should be drained in 1 day?
  4. what should be given for each 1L of peritoneal fluid that is drained?
    4b. why?
  5. what is a good diuretic to use for fluid overload (d/t ascites) in a hepatic patient?
A

(28)

  1. What fluids may need to be given for hepatic patients undergoing surgery?
    - blood
    - FFP, cryo
    - colloids (for intravascular depletion)
  2. what happens when ascites (peritoneal fluid) is drained?
    - causes intravascular depletion
  3. what is the max amount of peritoneal that fluid should be drained in 1 day?
    - 1 liter
  4. what should be given for each 1L of peritoneal fluid that is drained?
    - 50 mL of 25% albumin
    4b. why?
    - each 1 liter of peritoneal fluid contains 10 g or protein
  5. what is a good diuretic to use for fluid overload (d/t ascites) in a hepatic patient?
    - aldactone (aldosterone agonist)
40
Q

(29)

what are severely jaundiced hepatic surgical patients more likely to develop post op?

A

(29)
what are severely jaundiced hepatic surgical patients more likely to develop post op?
-sepsis
-acute renal failure

41
Q

(30)
how would you do the anesthesia on a whipple procedure:
1. what type of case is it similar to?
2. what type of lines?
3. pain control?
4. what labs will you monitor?
5. what will the patient need post op (he/she will be going to the AICU)

A

(30)
how would you do the anesthesia on a whipple procedure:
1. what type of case is it similar to?
- large abdominal case
2. what type of lines?
-central line
-arterial line
-larg bore IVs
-epidural
3. pain control?
-epidural with frequent boluses throughout case or infusion
-to PCA post op
4. what labs will you monitor?
-glucose (may have hypo or hyperglycemia)
-electrolytes
-cbc (prone to anemia)
5. what will the patient need post op (he/she will be going to the AICU)
-post op ventilation (patient may be on vent x 24 hours or to next am).

42
Q

(31)
1. Surgical/invasive treatment for portal HTN (with varices):
2. what are the potential side effects of these procedures?

A

(31)
1. Surgical/invasive treatment for portal HTN:
- Portal/caval shunt: a shunt is placed from the portal vein to the superior vena cava
- warren shunt (spelo-renal shunt) or DSRS (distal spleno-renal shunt): the blood vessels are re-routed so that the left renal vein is anastamosed with the splenic vein and blood is shunted from the stomach and spleen. Also, the left gastric vein is cut to decrease pressure in the varices and preserves portal vein blood flow.
2. what are the potential side effects of these procedures?
- encephalopathy
- hepatic failure

43
Q 
(32)
what is the medical treatment for Esophageal Varices:
1. what medications?
2. what procedures?
3. what devices?
A

(32)
what is the medical treatment for Esophageal Varices:
1. what medications?
-beta blockers: to decrease portal venous pressure
-vasopressin: 0.1-0.4 units/min (used co-comitantly with nitro gtt to avoid peripheral vasoconstriction and ischemia)
-octreotide (sandostatin): 50 mcg/hr gtt as a gastric vasoconstrictor (s/e=decreased insulin and glucagon)
-terlipressin: 0.5 mg q 4 hours (less s/e than vasopressin)
2. what procedures?
-Sclerotherapy: sclerosing substance is injected into varices (s/e: GI>esophageal ulcerations, strictures;
resp>can also cause pleural effusion and respiratory distress)
-TIPS: Trans Intra-hepatic Portal system Shunting- creates a stent between the portal and hepatic venous system within the liver which may have become stenosed or occluded (causing the portal HTN) It is good for bleeding not controlled by sclerosing but can lead to encephalopathy
3. what devices?
-Blakemore- placed in esophagus and tamponades the varices

44
Q

(33)

  1. what is a normal ammonia level?
  2. at what point does a patient experience encephalopathy?
A 
(33)
1. what is a normal ammonia level?
- 50
2. at what point does a patient experience encephalopathy?
-
45
Q

(34)

How do you treat hepatic encephalopathy (4 ways)?

A

(34)
How do you treat hepatic encephalopathy?
1. stop bleeding (less blood breakdown decreases ammonia levels)
2. decrease protein intake
3. decrease bacteria that produce ammonia in GI tract (neomycin 500 mg q6 hrs)
4. lactulose oral/ enema -converts ammonia to ammonium which is deficated out

46
Q

types of cirrhosis:

A

a. alcoholic (laennec’s)
-b. post necrotic
-c. wilson’s disease: d/t copper accumulation in hepatocytes
s/s: Kayser-Fleisher ring (pigmented cresent around cornea)
-d. Hemochromatosis: hereditary-causes iron deposits in hepatocytes
s/s: hepato-splenomegaly causing liver cancer in 15-20%
dx:liver bx
-e. Alpha-1-antitrypsin globulin defeciency (this globulin protects the lungs)
s/s: may be accompanied by emphysema; may have hep B or C
-f. Jejunoileal bypass (gastric bypass)
s/s: increased fat accumulation
tx: reanastamosis of the bowel
-g: chronic billiary inflammation or obstruction
-h: primary billiary cirrhosis:
cause: ??autoimmune; women 90%cases; not alcohol related; slowly progressive
-i: non alcohol fatty liver disease:
cause: obesity, hyperlipid, poor control of DM, rapid weight loss

1. adv principles 3 exam 1 (3 decks)

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