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6901 > Liver, Pancreas, Spleen > Flashcards

Liver, Pancreas, Spleen Flashcards

1
Q

Pancreas: Exocrine vs endocrine functions

A 
Exocrine
-Digestion of food
-1500-3000mL pancreatic juice daily
-98% of pancreas : Acinar cells - synthesize and secrete digestive enzymes and bicarb
Endocrine
-Regulates blood sugar
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2
Q

Arrival of chime into the duodenum/jejunum stimulates the release of ____

A

Cholecystokinin-pancreozymin (CCK-PZ) and Secretin

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3
Q

CCK effect

A

Improves digestion

  • Slows gastric emptying (increases the sensation of fullness)
  • Stimulates bile production in the liver
  • Increases release of fluid and enzymes from pancreas
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4
Q

Secretin role

A

Released in response to low pH in duodenum

-Stimulates secretion of bile from the liver, alkaline pancreatic juice, and bicarb from duodenal glands

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5
Q

Parasympathetic, alpha-adrenergic, beta-adrenergic, vagolytic drug effect on pancreas

A 
Parasympathetic
-Stimulates insulin secretion
Vagolytic
-Decreased response to secretin
Alpha-adrenergic
-Inhibits insulin secretion
Beta-adrenergic
-Inhibits insulin secretion
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6
Q

Islets of Langerhans (part of pancreas, what they are, types of cells)

A

Pancreatic islet cells, constitute 2% of pancreatic tissue
Endocrine cells-produce hormones that are secreted directly into capillary blood vessels
-Alpha cells: 35%, secrete glucagon
-Beta cells: 60-70%, secrete insulin
-Delta cells: 10%, secrete somatostatin
-Pancreatic Polypeptide cells: Inhibit exocrine pancreatic secretion

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7
Q

How many units/day of insulin does the normal person secrete

A

50 units/day

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8
Q

Somatostatin

A
  • Regulates GI function

- Distributed throughout CNS-hypothalamic inhibitor of anterior pituitary GH release

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9
Q

What stimulates lipolysis

A

Hormone-sensitive lipase

-Lipolysis=breakdown of stored triglycerides to FFA into glycerol

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10
Q

Rate of glycogenesis, lipogenesis, gluconeogenesis, glycogenolysis, and lipolysis are regulated by: ___

A

The actions of insulin

-Opposing actions of counterregulatory hormones: GH, cortisol, epinephrine, glucagon

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11
Q

How is glucose stored in skeletal muscle vs liver vs fatty tissue

A

Skeletal muscle/liver: Glycogen

Fatty tissue: Triglycerides

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12
Q

Insulin is a hormone of energy ____ vs glucagon is a hormone of energy ____

A

Insulin: Energy storage
Glucagon: Energy release

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13
Q

Diabetic patients morbidity/mortality periop, cause

A

Higher morbidity and mortality periop compared to non-diabetics of similar age

  • Ischemic heart disease=most common cause of periop mortality
  • Complications aren’t from DM itself but organ damage associated with it
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14
Q

DM: Cardiac preop considerations

A

Cardiovascular complications=most of surgical death in DM pts: HTN, CAD, Autonomic nervous system dysfunction
*Preop ECG advised for all adult DM patients (b/c of high incidence of cardiac disease)

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15
Q

DM: Respiratory preop considerations

A
  • Autonomic neuropathy: Impaired respiratory response to hypoxia, especially sensitive to respiratory depressant effects of sedative/anesthetics
  • Stiff joint syndrome: 30-40%, b/c of glycosylation of tissue proteins
  • Could indicate limited motion of atlantooccipital joint->difficult intubation
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16
Q

Common medication causes of hypoglycemia

A 
Insulin
Sulfonylureas
Beta-blockers
Ethanol
-Other medical conditions, including insulinoma: insulin-secreting tumor of the islets of Langerhans
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17
Q

Causes of post-op pancreatitis

A
  • Mobilization of abdominal viscera

- Cardiopulmonary bypass

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18
Q

Enzymes implicated as major culprits in pancreatitis are those activated by ___(3)

A

Trypsin
Enterokinase
Bile acids

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19
Q

Morphine use in pancreatitis

A

Induces spasms of the oddi sphincter - may exacerbate bile obstruction and stasis

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20
Q

What med is given during ERCP to relax sphincter of oddi

A

Glucagon

0.4-1mg IV

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21
Q

Gastrinoma (Zollinger-Ellison Syndrome)

A

Hypersecretion of gastrin -> excessive stimulation of gastric acid secretions -> severe PUD (marked potential for perf. and erosion/sever hemorrhage)
-Usually from non-beta cell pancreatic tumor

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22
Q

Electrolyte disorders common preop in pancreatic disease patients

A

Hypercalcemia
Hypomagnesemia
Hypokalemia
Hypochloremic metabolic alkalosis

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23
Q

Diabetic patients cardiac acetylcholine receptors

A

May have denervation hypersensitivity of cardiac acetylcholine receptors -> risk for severe refractory bradycardia
-Consider when anticholinesterase reversal agents are used

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24
Q

Pancreas transplant: NDMR, opioids, labs, monitoring

A

NDMRs: Minimal cardiac depressant and organ dependence on renal metabolism/clearance: Cis, vec

  • Opioids-tolerant due to pain, may be on higher end
  • q30min glucose
  • Periodic lytes, coags, ABGs
  • Monitor hemodynamics-can’t rapidly cause vascular expansion -> allograft edema -> vascular insufficiency/thrombosis -> failure
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25
Q

Airway evaluation in pancreatic transplant patients

A

Especially if they have DM

  • Worry for joint stiffness and difficult intubation
  • Evaluate head/neck joints, especially atlantooccipital axis
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26
Q

Auto Islet Cell Transplant (reason it’s done)

A

When total pancreatectomy is done (all other medical tx fail to relieve pain), islets are harvested and infused into the liver

  • Maintains insulin production and secretion
  • Pts will have to take oral pancreatic enzymes
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27
Q

Liver blood supply (mL/min, from where, % CO)

A

1500mL/min
25% from hepatic artery
75% from hepatic vein
25-30% of cardiac output

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28
Q

Liver filtering function

A
  • Blood from the gut has colonic bacilli
  • Kupffer cells (macrophages) line the hepatic sinuses and cleanse more than 99% of bacteria
  • Epithelial cells line the hepatic sinuses->diffusion of large plasma proteins to extravascular space in liver->lymph nearly equal in protein concentration to plasma
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29
Q

Splanchnic blood flow and nerves

A
  • Splanchnic blood vessels provide blood supply to liver, gallbladder, omentum, spleen, and pancreas
  • Nerves: Derived from spinal nerves T3-T11
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30
Q

Receptors in hepatic artery circulation vs portal circulation

A

Hepatic artery: Alpha and beta

Portal: Alpha only

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31
Q

Hepatic arterial flow regulation vs portal

A

Arterial flow: Autoregulated in accordance with metabolic demand or oxygen consumption
Portal: Dependent on combined venous outflow from spleen and GI tract
-Decrease in either->compensatory increase delivered by other system

32
Q

Bile (how much produced, where it’s stored, why it’s released, what it does)

A

Primary secretion of the liver

  • Produced: 1L/day
  • Stored: Gallbladder
  • Released into gallbladder in response to CCK
  • Fat and protein in duodenum->gallbladder contraction->bile through common bile duct through relaxed sphincter of oddi into duodenum
  • Assists in absorption of fat and fat-soluble vitamins (ADE&K)
33
Q

Coagulation factors synthesized by the liver

A

I, II, V, VII, IX, X, XI

-Deficiency in vitamin K=impaired production of II, VII, IX, X

34
Q

Phase I drug reactions

A

Add or expose function group: Oxidation, reduction, hydrolysis

  • Usually results in loss of pharmacologic activity (except prodrugs)
  • Important for metabolizing many anesthetic drugs: Midazolam, diazepam, codeine, phenobarbital
35
Q

Phase II drug reactions

A

Conjugation reactions

  • Phase I product conjugates with second molecule
  • Morphine, acetaminophen
36
Q

Transmission of Hep A/E vs B/C

A

A&E: Fecal oral

B&C: Body fluid contact, physical contact with disrupted cutaneous barriers

37
Q

Causes of drug induced hepatitis (toxic vs idiosyncratic vs toxic&idiosyncratic vs primary cholestatic)

A 
Toxic
-Alcohol
-Acetaminophen
Idiosyncratic
-Volatile anesthetics
-Sulfonamides
Toxic & Idiosyncratic 
-Methyldopa
-Amiodarone
Primary Cholestatis
-Chlorpromazine
-Chlorpropamide
-Oral contraceptives
-Anabolic steroids
-Erythromycin estolate
-Methimazole
38
Q

Chronic hepatitis after hep A/B/C

A
  • Doesn’t occur after hep A
  • 1-10% after hep B
  • 10-40% after hep C
39
Q

3 different syndromes of chronic hepatitis based on biopsy

A 
Chronic persistent
-Benign, confined to portal areas
Chronic lobular
-Recurrent exacerbations of acute inflammation
-Progression to cirrhosis is rare
Chronic active
-Most serious, progressive
-Results from hepatocyte destruction, cirrhosis, hepatic failure
40
Q

Anesthetic considerations for acute alcohol intoxication

A

Less anesthesia needed (alcohol is an anesthetic)

  • Aspiration precautions
  • Surgical bleeding may be increased - interfered platelet aggregation
  • Brain is less tolerant of hypoxia
  • Increased level of circulating catecholamine - labile vital signs, exaggerated response to drugs and stimuli (decreased neurotransmitter uptake)
41
Q

Anesthetic considerations in patients going through alcohol withdrawal

A

High mortality rate (50%)

42
Q

Anesthetic considerations in acute hepatitis

A

Surgery/anesthesia greatly increases the risk for further hepatic decompensation

  • Risk is confounded by development of renal failure, encephalopathy, and other organ system decompensations
  • Best to postpone elective surgery until liver function is normalized/optimized
  • Indicated by improvement in LFTs and adequate platelet counts
43
Q

Child classification system “CTP score”

A

Used by surgeons to assess the severity of cirrhosis -> anesthetic risk

  • Add points for encephalopathy, ascites, bilirubin, PSC, albumin, PT
  • A (mild) = 5-6
  • B (moderate) = 7-9
  • C (severe) = 10-15
44
Q

Meld score

A

Model for end stage liver disease

-Consider dialysis and lab values: INR, bilirubin, creatinine

45
Q

3 major complications from cirrhosis

A 
Variceal hemorrhage
-Portal hypertension
Intractable fluid retention
-Ascites, hepatorenal syndrome
Hepatic encephalopathy/coma
46
Q

Anesthetic management in cirrhosis

A

Preserve hepatic blood flow
-Avoid halothane (reduces hepatic blood flow by as much as 25%)
-Sevo is best
Consider regional if possible based on coags
-Normocapnia
-Avoid PEEP
-General volume maintenance

47
Q

Medications with situational potential hepatotoxicity

A 
Acetaminophen
Sulfonamides
Tetracycline
Penicillin
Amiodarone
48
Q

Anesthetic Hemodynamic management in cirrhosis patients

A
  • Anticipate hypovolemia
  • Assess for high CO and low Peripheral VR/SVR
  • Increased endogenous vasodilators -> hyperdynamic circulatory state (also decreased blood viscosity)
  • Suspect portal HTN and variceal bleeding even without history
  • Anticipate depressed response to inotropes and pressors
  • AV shunting because of extensive systemic collateral vessel development (because of back pressure)
49
Q

Pharmacokinetics and pharmacodynamics in cirrhosis patients

A

Altered volume of distribution
-Decreased albumin, intravascular volume is unpredictable
Portosystemic shunted blood bypasses liver
-Drugs highly extracted by liver are especially affected

50
Q

4 mechanics responsible for ascites

A

Portal hypertension
Hypoalbuminemia
Seepage of protein-rich lymphatic fluid
Avid renal sodium retention

51
Q

Positive pressure ventilation in liver disease patients

A

Can worsen an already poor venous return -> decreased CO

52
Q

Liver disease drug metabolism

A 
Induce enzymatic pathways
-Metabolized quickly-more drug
Inhibit enzymatic pathways
-Metabolize slower-less drug
Highly bound protein drugs
-Decreased protein binding, medications will have greater effect
Larger volume of distribution
-NDMRs may need to increase dose
Deficient plasma cholinesterase
-May prolong succs, esmolol, enhance toxic effects of LA
53
Q

Preop ECG, EBG, PFTs

A
  • ECG absolutely warranted
  • Consider ABG pre procedure or immediately after induction
  • PFTs might be indicated if the patient has suspected respiratory impairment
54
Q

Liver labs following surgical procedures

A

Mild elevations are common regardless of the anesthetic used

  • Alk Phos
  • ALT
  • Bilirubin
55
Q

Acceptable hematocrit and platelet counts for cirrhosis patients

A

Hct: 30%
Plt: 100,000

56
Q

Liver blood flow is dependent on ___ in cirrhosis

A

Hepatic arterial perfusion

-Portal venous blood flow is reduced in cirrhosis patients

57
Q

GABA levels in cirrhosis patients

A

GABA levels are increased

58
Q

Hepatic arterial vasoconstriction intraoperatively for liver pts

A

Caused by increased sympathetic nervous system outflow

  • Hypotension
  • Hypovolemia
  • Hypoxia
  • Hypercarbia
  • Light anesthesia
  • Most profound etiologic factor that causes this is abdominal surgery, especially if the liver is involved
59
Q

What to avoid intraop for liver pts

A

Hypotension
Excessive SNS activation
High airway pressures during controlled ventilation
*All known to reduce hepatic blood flow

60
Q

Sphincter of oddi spasms related to anesthesia

A

Can be narcotic induced
-Morphine > meperidine > butorphanol > nalbuphine
-Synthetic narcotics (fentanyl) are preferred
May be from surgical manipulation, cold irrigation, contrast dye
-Increases biliary pressure

61
Q

Inhalation agents in cirrhosis patients

A

Avoid halothane
Sevo should perhaps be avoided (Fl ion)
*Iso is agent of choice: Least effect on heart, hepatic blood flow

62
Q

Portal hypertension pharmacologic management

A 
Vasopressin
-Splanchnic vasoconstrictor
-0.1-0.4 units/min
-Consider NTG with it to prevent HTN
Octreotide (somatostatin analog)
-Inhibits GI peptide hormone activity -> decreased gut motility and venous return to portal circulation
-50mcg/hr
63
Q

TIPS anesthesia considerations

A

Same as for liver disease

  • Avoid N2O
  • Keep PaCO2 >40mmHg to maintain portal blood flow if an advanced airway is present
  • Use large amounts of albumin
  • NS/LR controversial: Na retention with NS, LR can exacerbate liver failure (breakdown of bicarb)
  • Use mannitol to maintain UOP 50mL/hr (avoid Lasix)
64
Q

Anesthesia considerations for liver transplant

A

Completely patient and anesthesia provider independent

-No single anesthesia technique is indicated

65
Q

Complications to the donor for living donor hepatic transplant

A
  • Biliary complications (stricture/leak)
  • Infection
  • Blood-product transfusion
  • Major risks-not a recommended procedure
66
Q

Antifibrinolytics to use in hepatic surgery

A

Amicar

Aprotinin

67
Q

Vascular vs avascular attachments to the spleen

A

All vascular except gastro-splenic ligament

-Colon, kidney/adrenal gland, diaphragm

68
Q

3 zones of the spleen

A 
Red pulp
-Splenic sinusoids
-Large thin-walled vessels
White pulp
-End arterial branches of central arteries
-Contains lymphocytes, macrophages, plasma cells
Marginal zone
-Ill-defined vascular space
-Contains red and white pulp
69
Q

Blood flow to spleen (mL/min)

A

300 mL/minute

70
Q

Splenectomy is often a necessary part of therapy in these 3 disorders

A

Sickle cell anemia
Thalassemia
Primary or secondary hypersplenism

71
Q

Carcinoid tumors

A

Slow growing malignancies composed to enterochromaffin cells

  • Usually found in GI tract (75%) - metabolic products are released to the portal circulation and destroyed by the liver before causing systemic issues
  • May also develop in lungs, pancreas, thymus, and liver
72
Q

Substances released from carcinoid enterochromaffin tumors

A 
Serotonin
Bradykinin
Tachykinins
Prostaglandins
ACTH
Histamine
-Can directly affect hemostasis
-Direct stimulation of tumor and beta adrenergic stimulation can enhance the release of these hormones
73
Q

Anesthetic gas use in carcinoid syndrome

A

Consider des or sevo

-Patients with high serotonin levels may have prolonged recovery time

74
Q

Preop labs/tests for carcinoid syndrome patients

A

CBC, lytes, LFTs, glucose
Urine 5-HIAA levels
EKG/Echo

75
Q

Anesthetic considerations for carcinoid syndrome patients

A
  • Keep deep
  • Minimize effects of histamine: H1/H2 blockers
  • Avoid histamine releasing meds: Morphine, thiopental, atracurium
  • Avoid sympathomimetic agents: Ketamine, ephedrine, epinephrine
  • Tx hypotension with phenyl
  • Monitor glucose (prone to hyperglycemia) - insulin
  • Aprotinin - inhibits kalikreins - reverses carcinoid-induced bronchospasm/hypotension
  • Normothermia - avoid catecholamine-induced vasoactive mediator release
76
Q

Preop meds for carcinoid syndrome

A 
Octreotide
-Nonselective somatostatin analog 
-Continue postop
Somatostatin
-Inhibitory peptide - antagonizes and suppresses release of tumor products
-Binds to tumor cell receptors 
-Short half life: 2-3 mins

6901 (9 decks)

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