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
2
Q
Arrival of chime into the duodenum/jejunum stimulates the release of ____
A
Cholecystokinin-pancreozymin (CCK-PZ) and Secretin
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
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
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
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
7
Q
How many units/day of insulin does the normal person secrete
A
50 units/day
8
Q
Somatostatin
A
- Regulates GI function
- Distributed throughout CNS-hypothalamic inhibitor of anterior pituitary GH release
9
Q
What stimulates lipolysis
A
Hormone-sensitive lipase
-Lipolysis=breakdown of stored triglycerides to FFA into glycerol
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
11
Q
How is glucose stored in skeletal muscle vs liver vs fatty tissue
A
Skeletal muscle/liver: Glycogen
Fatty tissue: Triglycerides
12
Q
Insulin is a hormone of energy ____ vs glucagon is a hormone of energy ____
A
Insulin: Energy storage
Glucagon: Energy release
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
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)
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
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
17
Q
Causes of post-op pancreatitis
A
- Mobilization of abdominal viscera
- Cardiopulmonary bypass
18
Q
Enzymes implicated as major culprits in pancreatitis are those activated by ___(3)
A
Trypsin
Enterokinase
Bile acids
19
Q
Morphine use in pancreatitis
A
Induces spasms of the oddi sphincter - may exacerbate bile obstruction and stasis
20
Q
What med is given during ERCP to relax sphincter of oddi
A
Glucagon
0.4-1mg IV
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
22
Q
Electrolyte disorders common preop in pancreatic disease patients
A
Hypercalcemia
Hypomagnesemia
Hypokalemia
Hypochloremic metabolic alkalosis
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
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
25
Airway evaluation in pancreatic transplant patients
Especially if they have DM
- Worry for joint stiffness and difficult intubation
- Evaluate head/neck joints, especially atlantooccipital axis
26
Auto Islet Cell Transplant (reason it's done)
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
27
Liver blood supply (mL/min, from where, % CO)
1500mL/min
25% from hepatic artery
75% from hepatic vein
25-30% of cardiac output
28
Liver filtering function
- 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
29
Splanchnic blood flow and nerves
- Splanchnic blood vessels provide blood supply to liver, gallbladder, omentum, spleen, and pancreas
- Nerves: Derived from spinal nerves T3-T11
30
Receptors in hepatic artery circulation vs portal circulation
Hepatic artery: Alpha and beta
| Portal: Alpha only
31
Hepatic arterial flow regulation vs portal
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
Bile (how much produced, where it's stored, why it's released, what it does)
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
Coagulation factors synthesized by the liver
I, II, V, VII, IX, X, XI
| -Deficiency in vitamin K=impaired production of II, VII, IX, X
34
Phase I drug reactions
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
Phase II drug reactions
Conjugation reactions
- Phase I product conjugates with second molecule
- Morphine, acetaminophen
36
Transmission of Hep A/E vs B/C
A&E: Fecal oral
| B&C: Body fluid contact, physical contact with disrupted cutaneous barriers
37
Causes of drug induced hepatitis (toxic vs idiosyncratic vs toxic&idiosyncratic vs primary cholestatic)
```
Toxic
-Alcohol
-Acetaminophen
Idiosyncratic
-Volatile anesthetics
-Sulfonamides
Toxic & Idiosyncratic
-Methyldopa
-Amiodarone
Primary Cholestatis
-Chlorpromazine
-Chlorpropamide
-Oral contraceptives
-Anabolic steroids
-Erythromycin estolate
-Methimazole
```
38
Chronic hepatitis after hep A/B/C
- Doesn't occur after hep A
- 1-10% after hep B
- 10-40% after hep C
39
3 different syndromes of chronic hepatitis based on biopsy
```
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
Anesthetic considerations for acute alcohol intoxication
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
Anesthetic considerations in patients going through alcohol withdrawal
High mortality rate (50%)
42
Anesthetic considerations in acute hepatitis
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
Child classification system "CTP score"
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
Meld score
Model for end stage liver disease
| -Consider dialysis and lab values: INR, bilirubin, creatinine
45
3 major complications from cirrhosis
```
Variceal hemorrhage
-Portal hypertension
Intractable fluid retention
-Ascites, hepatorenal syndrome
Hepatic encephalopathy/coma
```
46
Anesthetic management in cirrhosis
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
Medications with situational potential hepatotoxicity
```
Acetaminophen
Sulfonamides
Tetracycline
Penicillin
Amiodarone
```
48
Anesthetic Hemodynamic management in cirrhosis patients
- 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
Pharmacokinetics and pharmacodynamics in cirrhosis patients
Altered volume of distribution
-Decreased albumin, intravascular volume is unpredictable
Portosystemic shunted blood bypasses liver
-Drugs highly extracted by liver are especially affected
50
4 mechanics responsible for ascites
Portal hypertension
Hypoalbuminemia
Seepage of protein-rich lymphatic fluid
Avid renal sodium retention
51
Positive pressure ventilation in liver disease patients
Can worsen an already poor venous return -> decreased CO
52
Liver disease drug metabolism
```
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
Preop ECG, EBG, PFTs
- ECG absolutely warranted
- Consider ABG pre procedure or immediately after induction
- PFTs might be indicated if the patient has suspected respiratory impairment
54
Liver labs following surgical procedures
Mild elevations are common regardless of the anesthetic used
- Alk Phos
- ALT
- Bilirubin
55
Acceptable hematocrit and platelet counts for cirrhosis patients
Hct: 30%
Plt: 100,000
56
Liver blood flow is dependent on ___ in cirrhosis
Hepatic arterial perfusion
| -Portal venous blood flow is reduced in cirrhosis patients
57
GABA levels in cirrhosis patients
GABA levels are increased
58
Hepatic arterial vasoconstriction intraoperatively for liver pts
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
What to avoid intraop for liver pts
Hypotension
Excessive SNS activation
High airway pressures during controlled ventilation
*All known to reduce hepatic blood flow
60
Sphincter of oddi spasms related to anesthesia
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
Inhalation agents in cirrhosis patients
Avoid halothane
Sevo should perhaps be avoided (Fl ion)
*Iso is agent of choice: Least effect on heart, hepatic blood flow
62
Portal hypertension pharmacologic management
```
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
TIPS anesthesia considerations
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
Anesthesia considerations for liver transplant
Completely patient and anesthesia provider independent
| -No single anesthesia technique is indicated
65
Complications to the donor for living donor hepatic transplant
- Biliary complications (stricture/leak)
- Infection
- Blood-product transfusion
- Major risks-not a recommended procedure
66
Antifibrinolytics to use in hepatic surgery
Amicar
| Aprotinin
67
Vascular vs avascular attachments to the spleen
All vascular except gastro-splenic ligament
| -Colon, kidney/adrenal gland, diaphragm
68
3 zones of the spleen
```
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
Blood flow to spleen (mL/min)
300 mL/minute
70
Splenectomy is often a necessary part of therapy in these 3 disorders
Sickle cell anemia
Thalassemia
Primary or secondary hypersplenism
71
Carcinoid tumors
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
Substances released from carcinoid enterochromaffin tumors
```
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
Anesthetic gas use in carcinoid syndrome
Consider des or sevo
| -Patients with high serotonin levels may have prolonged recovery time
74
Preop labs/tests for carcinoid syndrome patients
CBC, lytes, LFTs, glucose
Urine 5-HIAA levels
EKG/Echo
75
Anesthetic considerations for carcinoid syndrome patients
* 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
Preop meds for carcinoid syndrome
```
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
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