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Anesthesia Pharm > Week 7 - GI System/Metabolism & PONV > Flashcards

Week 7 - GI System/Metabolism & PONV Flashcards

1
Q

What is the pathway of blood flow through the liver?

A
  • Blood flows past hepatocytes via sinusoids from branches of the portal vein and hepatic artery to a central vein
  • Central veins join to form hepatic veins, which drain into the inferior vena cava

*Only one layer of hepatocytes between sinusoids – great contact with plasma

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2
Q

Where are hepatocytes located and what do they form down the line?

A

Located adjacent to bile canaliculi – converge to form the common hepatic duct

Common hepatic duct then joins the cystic duct from the gallbladder to form the Common Bile Duct

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3
Q

What cells line the hepatic lobules? What are their function?

A

Kupffer Cells: macrophages (derived from circulating monocytes)

-Phagocytize 99% of bacteria in the portal venous blood (blood from GI tract - usually contains colon bacteria)

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4
Q

Why do the endothelial cells that line the hepatic lobules contain large pores?

A

To permit easy diffusion of certain substances, including plasma proteins, into extravascular spaces of the liver that connect with terminal lymphatics

*this extreme permeability of the lining allows large quantities of lymph to form (1/3-1/2 of all lymph is formed in the liver)

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5
Q

What are the functions of Hepatocytes?

A
  • Absorb nutrients from portal venous blood
  • Store and release carbohydrates, proteins, and lipids
  • Excrete bile salts
  • Synthesize plasma proteins, glucose, cholesterols, and fatty acids
  • Metabolize exogenous and endogenous compounds

*hepatocytes are vital to the healthy functioning liver

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6
Q

What vessels supply blood to the liver?

A

Dual Afferent Blood Supply from:

  • Portal Vein (75% of blood flow – 50-55% of hepatic oxygen supply)
  • Hepatic Artery (25% of blood flow – 45-50% of hepatic oxygen supply)
  • Hepatic artery blood flow maintains nutrition of connective tissues and walls of bile ducts (loss of this flow can be fatal)
  • Increase in hepatic O2 requirement is met by increase in O2 extraction rather than further increase in blood flow
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7
Q

How many mL per minute is the total hepatic blood flow? What percent of CO is it?

A

1450 mL per minute

20-29% CO

10-15% total blood volume

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8
Q

What is portal vein blood flow controlled by?

A

Primarily by the arterioles in the preportal splanchnic organs

-Not autoregulated

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9
Q

What determines portal venous pressure? What is a normal pressure?

A

Portal vein blood flow combined with the resistance to the flow within the liver

Normal = 7-10 mmHg

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10
Q

What is portal hypertension?

A 
Fibrotic constriction (remodeling of hepatocytes) that increases resistance to portal vein blood flow
*characteristic of hepatic cirrhosis due to chronic ETOH or Hep C

Portal venous pressures of 20 to 30 mmHg

Results in the development of shunts (varices) to allow blood flow to bypass the hepatocytes

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11
Q

What causes ascities?

A

When increased portal venous pressures cause transudation of protein-rich fluid through the outer surface of the liver capsule and GI tract into the abdominal cavity

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12
Q

What influences hepatic artery blood flow?

A

Autoregulated by arteriole tone — Sympathetic Nervous System (alpha adrenergic receptors)

*Decrease in portal vein blood flow is accompanied by an increase in hepatic artery blood flow by as much as 100% (adenosine accumulates in liver when portal vein flow decreases leading to hepatic artery vasodilation until adenosine is washed out)

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13
Q

What is the reservoir function of the liver?

A

Liver normally contains ~500mL of blood (~10% total blood volume) — Increase in CVP causes back pressure and the liver (being distendible organ) may accommodate as much as 1L extra blood

  • Acts as a storage site when blood volume is excessive (i.e CHF)
  • Supplies extra blood when hypovolemia occurs

*liver = single most important source of additional blood during strenuous exercise or acute hemorrhage

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14
Q

How do anesthetics affect hepatic blood flow?

A
  • Regional Anesthetics: minimal effect unless hypotensive
  • Volatile Anesthetics: uniformly decrease by 20-30% (not much)
    • Halothane decreases O2 supply more than others
    • Halothane preserves hepatic blood flow (slightly)
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15
Q

What physiologic factors decrease hepatic blood flow?

A
  • Hypoxemia
  • Changes in CO2 (hypocarbia decreases hepatic artery flow – hypercarbia increases portal vein flow and overall liver blood flow while decreasing hepatic artery flow)
  • Hypovolemia
  • Hypotension
  • Sympathetic stimulation
  • Vasopressin
  • Beta blockers
  • PPV, PEEP (increased intra-abdominal pressure)
  • Greater than 1 MAC volatile
  • Surgical manipulation
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16
Q

What is Halothane Hepatitis?

A

Immunologic phenomenon initiated by halothane metabolism

  • binding of its metabolite to liver proteins to form trifluoroacetylated proteins
  • stimulate antibodies in susceptible individuals
  • re-exposure these antibodies mediate massive hepatic necrosis

Hal > Iso > Des > Sevo
*because the extent of metabolism is so much less

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17
Q

Which volatile agent is the agent of choice in cases where preservation of splanchnic blood flow is required?

A

Isoflurane

  • liver blood flow and the hepatic artery buffer response are maintained better
  • Shown to attenuate the increase in hepatic O2 consumption associated with surgery and liver manipulation
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18
Q

What is the hepatic arterial buffer system?

A

Reciprocal relationship between portal vein and hepatic artery blood flow

  • During non-fasted state Portal vein flow goes up and Hepatic artery flow goes down
  • Decrease in Portal vein flow - increase in hepatic artery flow

*liver lacks ability to directly regulate portal venous flow thus regulation of blood flow is almost exclusively by regulating hepatic arterial tone

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19
Q

What are the functions of the liver?

A
  • Metabolism of Carbohydrates, Lipids, and Proteins (**Protein metabolism is most important function)
  • Storage of vitamins and iron
  • Degradation of hormones (catecholamines/corticosteroids)
  • Degradation of many drugs (P450 system)
  • Synthesis of all coagulation factors (except VWF and factor VIIIc)
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20
Q

What is the metabolic function of the liver regarding carbohydrates?

A

Regulation of blood glucose concentration

  • During hyperglycemia: glucose is stored as glycogen in the liver
  • During hypoglycemia: glycogenolysis provides glucose
  • Gluconeogenesis: conversion of amino acids to glucose when blood glucose concentration is decreased
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21
Q

What is the metabolic function of the liver regarding proteins?

A
  • Oxidative deamination of amino acids (forms ammonia)
  • Formation of urea for removal of ammonia
  • Formation of plasma proteins and coagulation factors
  • Interconversions (transfer one amino group to another) among different amino acids
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22
Q

What is a major protein formed in the liver?

A

Albumin

  • major determinant of plasma oncotic pressure
  • T1/2 = 2-3 weeks (21 days)
  • Level <2.5 gm/dL usually chronic liver disease
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23
Q

How is bile formed and secreted?

A
  • Continually formed by hepatocytes (500mL daily), secreted into bile canaliculi, which ultimately reach the common bile duct
  • It is stored in the gallbladder
  • Most potent stimulus for secretion = fat in the duodenum (evokes the release of cholecystokinin by duodenal mucosa)
  • Cholecystokinin causes selective contraction of the gallbladder smooth muscle

*bile solubilizes fats (needed for fat absorption

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24
Q

What are the principal components of bile?

A

Bile Salts: combine with lipids in the duodenum to form water-soluble complexes that facilitate GI absorption of fats/fat soluble vitamins (once absorbed return to liver via portal vein)

Bilirubin: cell membranes of erythrocytes rupture (at ~120 days) releasing hgb which is converted to bilirubin in the reticuloendothelial cells – jaundice occurs at 3x normal plasma concentration

Cholesterol (excess causes gallstones)

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25
Q

What is the liver’s role in coagulation?

A

Synthesis of coagulation factors (except von Willebrand factor and factor VIIIC)

-Vitamin K dependent production of factors II, VII, IX, and X

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26
Q

What are the steps involved in primary hemostasis? What coagulation factors are required for each step?

A

Formation of the Platelet Plug:

  • Adhesion of platelets to damaged vascular wall – Requires Factor VIII (VWF)
  • Activation of platelets – Requires Factor IIa (Thrombin)
  • Aggregation of platelets – Requires ADP and Thromboxane A2
  • Production of Fibrin – Requires extrinsic, intrinsic, and final common pathway
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27
Q

What is the primary function of the GI tract?

A

to provide the body with water, electrolytes, and nutrients

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28
Q

What are two major factors to maintain GI tract homeostasis?

A

Digestion and Absorption

*contents must move through the entire system at an appropriate rate

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29
Q

What are the functions of each part of the GI tract?

A

Esophagus = passage of food
Stomach = storage of food and digestion
Small Intestine = digestion of food and absorption of end products and fluids
Large Intestine = absorption of digestive end products and storage of fecal matter

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30
Q

What is the overall fluid balance in the GI tract?

A

Approximately 9L of fluid and secretions enter the GI tract daily

All but 100mL are absorbed by the small intestine and colon (Small intestine absorbs 8500mL – Colon absorbs 400mL daily)

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31
Q

What are the pH of the different GI secretions?

A 
Saliva = 6.0-7.0
Gastric Fluid = 1.0-3.5
Bile = 7.0-8.0
Pancreatic Fluid = 8.0-8.3
Small Intestine = 6.5-7.5
Colon = 7.5-8.0
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32
Q

What is the blood flow of the GI tract?

A
  • Most of the blood flow is to the gastric mucosa (supply energy needed for producing intestinal secretions/absorbing digested materials)
  • Blood flow parallels digestive activity of GI tract (Stimulation of parasympathetic increases local blood flow/increases secretions – Stimulation of sympathetic causes vasoconstriction with transient decrease in blood flow)

*80% of portal vein blood flow originates from the stomach/GI tract (remainder comes from spleen/pancreas)

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33
Q

How much blood is stored in the spleen and how is it released?

A

150-200mL of blood is stored in splenic venous sinuses

Released by sympathetic nervous system induced vasoconstriction of splenic vessels (can increase hematocrit 1-2%)

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34
Q

What is the function of the spleen?

A

To remove erythrocytes from circulation

*erythrocytes reenter the venous sinuses from the splenic pulp by passing through pores that may be smaller than the erythrocyte

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35
Q

Where does the GI tract receive innervation from?

A

ANS – Sympathetic nervous system (decreases activity) and Parasympathetic nervous system (increases activity)

Intrinsic Nervous System – Myenteric (Auerbach) Plexus and Submucous (Meissner) Plexus

*When SNS and PNS activity are absent the intrinsic systems maintain function of the GI tract

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36
Q

What part of the GI tract does the Vagus nerve innervate?

A

Parasympathetic innervation of:

  • Esophagus
  • Stomach
  • Pancreas
  • Small intestine
  • Transverse colon

*Pelvic nerves via hypogastric plexus innervates distal colon

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37
Q

What are the two mechanisms of GI motility?

A

-Mixing contractions

  • Propulsive movements (Peristalsis)
  • distension stimulates peristalsis
  • decreased by increased PNS activity and anticholinergic drugs
38
Q

What is an Ileus?

A

Lack of peristaltic movement for a period of time

Causes: trauma including surgery or pharmacologic (opioids)

  • Peristalsis generally returns in 6-8 hrs in small intestine and colonic activity can take 2-3 days
  • Can be relieved by aspiration of fluid or gas via NG tube until peristalsis returns
39
Q

What part of the brainstem houses the swallowing center?

A

Medulla and Lower Pons

-inhibits the medullary ventilatory center, halting breathing at any point to allow swallowing to proceed

40
Q

What is the purpose of the upper and lower esophageal sphincters?

A

To prevent air, acid, gastric contents into the esophagus

  • Lower esophageal sphincter regulates flow of food between esophagus and stomach
  • normally 4cm long and pressure = 10-30 mmHg at end expiration
  • Upper esophageal sphincter pressure prevents regurgitation into the pharynx in awake state
41
Q

What is GERD? How is it treated?

A

Transient relaxation of the lower esophageal sphincter is the major mechanism (rather than decreased LES pressure)

  • Reflux of acidic gastric fluid into the esophagus and/or oropharynx
  • Causes esophagitis (heartburn) and can cause damage to esophageal strictures
  • Treated w/ H2 receptor antagonists & proton pump inhibitors (treats the acidity to prevent scarring not the sphincter)
42
Q

What is a hiatal hernia?

A

when a portion of the stomach herniates into the chest

  • majority of patients with moderate to severe GERD have one
  • May promote GERD by trapping gastric acid in the hernia sac
43
Q

What is achalasia?

A

Degeneration of esophageal wall neurons (nitric oxide producing inhibitory neurons) that affect opening (relaxation) of LES

  • Dysphagia for both solid foods and liquids = primary symptom
  • Diagnosed with barium swallow (shows dilation of esophagus with a narrowing of esophagogastric junction)
  • Treat with nitrates and Ca+ channel blockers (relax smooth muscle of LES) – limited success
  • Pneumatic dilation therapy and Surgical myotomy of the LES may result in relief but may cause GERD
44
Q

What is the function of the stomach?

A

To store and process food for absorption

  • The ability to secrete hydrogen ions in the form of hydrochloric acid = hallmark function
  • Richly innervated by the vagus nerves and celiac plexus
45
Q

What are the gastric secretions?

A
  • Hydrochloric acid
  • Pepsinogen
  • Intrinsic factor
  • Mucus (protects gastric mucosa from mechanical/chemical destruction)

*2L daily – pH 1.0-3.5

46
Q

What are the three cell types of the stomach?

A

Parietal Cells: secrete H+ containing solution (pH 0.8) that kills bacteria, aids protein digestion, provides necessary pH for pepsin to start protein digestion, stimulates bile/pancreatic juice

Chief Cells: secrete pepsinogens that undergo cleavage to pepsins in presence of hydrochloric acid

G Cells: secrete gastrin (hormone that stimulates secretion of H+)

47
Q

What influences gastric fluid volume and emptying time?

A

Neural and humoral mechanisms:

  • PNS stimulation enhances gastric fluid secretion and motility
  • SNS stimulation decreases secretions/motility
  • elimination of liquid = exponential (emptying begins within 1 minute of ingestion)
  • elimination of solids = linear (emptying begins w/ lag time – median 49 min)
48
Q

What causes a delay in gastric emptying?

A
  • Diabetic gastroparesis (impaired neural control)
  • GERD
  • Medications (opioids, beta blockers, tryclic antidepressants, antacids, ETOH)

*Smoking slow solids emptying but accelerates liquid emptying

49
Q

What can be absorbed from the stomach?

A

Only highly lipid-soluble liquids (i.e. ethanol and some drugs such as ASA)

*It is a poor absorptive area because it lacks the villus structure characteristic of absorptive membranes

50
Q

When and how often does aspiration occur during anesthesia?

A

Adults = 1/8500
Children = 1/4400
Emergency cases = 1/400

Can occur during intubation, extubation, or during the case

  • Factors associated include - volume and acidity of aspirated gastric contents
  • Drugs aimed at increasing pH and decrease volume
51
Q

What is UIHC fasting guidelines?

A

Before Elective Procedures:

  • 2 hr after clear fluids
  • 6 hr after non-clear fluids
  • 8 hr after meal

Children:

  • 2 hr after limited clear fluids (<5 years = 2oz, 5-13 = 4 oz, over 13 = 8 oz)
  • 4 hr after breast milk or unlimited clear fluids
  • 6 hr after formula
  • 8 hr after meal
52
Q

What is the function of the small intestine?

A

Site of most of the digestion and absorption of proteins, fats, and carbohydrates

53
Q

What are the function of the colon?

A

Absorption of water and electrolytes from the chyme and storage of feces

54
Q

What is the definition of PONV?

A

Nausea and/or vomiting occurring within 24 hours of surgery

55
Q

What are the two classifications of PONV?

A

Early PONV = within 6 hours of emergence from anesthesia

Late PONV = 6-24 hours after the procedure

56
Q

What is the leading cause of unanticipated hospital admission following outpatient surgery?

A

PONV

  • Most important complaint of patients following surgery
  • Shown to account for 12-17% of unanticipated hospital admissions
57
Q

How often does PONV occur?

A

In 30-40% of all patients who undergo general anesthesia

70-80% of high risk patients

58
Q

What are the five primary afferent pathways involved in stimulating vomiting?

A
  1. Chemoreceptor trigger zone (CTZ)
  2. Vagal mucosal pathway in the GI tract
  3. Neuronal pathways from vestibular system
  4. Reflex afferent pathways from the cerebral cortex
  5. Midbrain afferents
59
Q

What is the vomiting “center”?

A

Controls the sequence of events that occur during emesis
-Upon activation it sends efferent signals via CN V, VII, IX, X, and XII through the vagal parasympathetic fibers

Located in the medulla oblongata and consists of the tractus solitarius and parts parts of the reticular formation

60
Q

What pharmacological systems interact with the vomiting center?

A 
Dopamine
Serotonin
Substance P
Acetylcholine
Gamma-Aminobutyric acid (GABA)
Cannabinoids
61
Q

What factors cause N/V within the:

  • Stomach/Small Intestine
  • CTZ
  • Higher Cortical Centers
  • Labyrinths
A

Stomach/Small Intestine = chemo, surgery, radiotherapy

CTZ = chemo, anesthetics, opioids

Higher Cortical Centers = sensory input, memory, fear, anticipation

Labyrinths = surgery

62
Q

What is the American Society of Anesthesiologists recommendation on use of antiemetics?

A

Antiemetic agents should be used for the prevention and treatment of N/V when indicated but not routinely

*Preventing PONV is easier than treating but due to side effects the above is recommended

63
Q

What are the Patient Specific primary risk factors for PONV?

A
  • Female gender
  • Age less than 50 years old
  • Non-smoker
  • History of PONV
  • History of motion sickness

*age is mildly associated with PONV for pediatric patients (more surgery specific)

64
Q

What are the Anesthetic Related risk factors for PONV?

A
  • Use of volatile anesthetics
  • Duration of anesthesia (longer = higher risk)
  • Use of nitrous oxide
  • Postoperative opioid use
65
Q

What are the Surgery Related risk factors for PONV?

A

Type of Surgical Procedure

  • Laparotomies
  • Gynecologic surgeries
  • Laparoscopic procedures
  • ENT
  • Breast
  • Plastic surgery
  • Orthopedic
66
Q

What is the best approach for prophylaxis of PONV in high risk patients?

A

a multimodal approach

67
Q

What is the class and use of Scopolamine? How is it administered? Side Effects?

A

Anticholinergic – Prevention of Motion Induced Nausea and PONV

Admin transdermal – provides sustained therapeutic plasma concentrations (approx 5 mcg/hr) for up to 72 hours
*most effective if applied 4 hr prior

Side effects: sedation, cycloplegia, anisocoria, drying of secretions

68
Q

What is Central Anticholinergic Syndrome?

A

When scopolamine and atropine enter the CNS and produce symptoms ranging from restlessness and hallucinations to somnolence and unconsciousness

*reflects blockade of muscarinic cholinergic receptors and competitive inhibition of effects of ACh in the CNS

69
Q

What is the class, use, and mechanism of action of Metoclopramide (Reglan)?

A

Benzamide/Dopamine Antagonist – Treat PONV (can be useful Post-op)

  • Stimulates the GI tract via cholinergic mechanism resulting in contraction of LES and gastric fundus, increased gastric secretions/small intestinal motility, and decreased muscle activity in the pylorus/duodenum
  • May have direct effects on CRTZ and/or vomiting center (antidopaminergic effect)
  • use in caution with Parkinson’s, restless leg syndrome or movement disorders r/t dopamine inhibition
70
Q

What is the class and use of Droperidol? What dose is used?

A

Butyrophenones – Prophylaxis and rescue therapy for PONV

  1. 625-1.25 mg IV = effective/safe for prevention/treatment of PONV
    * Black box warning due to association with prolonged QT syndromes – results with higher doses than necessary for treatment of PONV
71
Q

What are Extrapyramidal Symptoms?

A

Dyskinesias

  • Repetitive, involuntary, and purposeless body or facial movements
  • Tongue movements
  • Lip smacking
  • Finger movements
  • Eye blinking
  • Movements of arms/legs

*Risk of all antidopaminergic agents

72
Q

How is Dexamethasone useful in managing PONV? What dose?

A

Corticosteroid – mechanism not fully known

  • proposed to centrally inhibit prostaglandin synthesis and control endorphin release
  • in combo w/ 5-HT3 receptor antagonists it may reduce levels of serotonin, release of serotonin in the gut, and sensitize 5-HT3 receptor to other antiemetics

4mg = effective antiemetic
*synergistic effect with zofran

73
Q

How do 5-HT3 Receptor Antagonists treat N/V?

A
  • 5-HT3 receptors are extensively distributed on enteric neurons in the GI tract and brain
  • Serotonin is released from the enterochromaffin cells of the small intestine, stimulates the vagal afferents through the 5-HT3 receptor and initiates the vomiting reflex
  • Antagonism of these receptors results in the antiemetic effect
74
Q

What is Ondansetron and its properties?

A

Specific 5-HT3 receptor antagonist – used for prevention and treatment of PONV

  • Free of neurologic side effects common to droperidol and metoclopramide
  • Most common side effect is headache and diarrhea

Dose: 4mg IV or 8mg PO (Don’t exceed 16mg – risk of QT prolongation)
T1/2: 4 hours (works better toward the end)
Metabolized in the liver and excreted in the urine

75
Q

What are the 5-HT3 receptor antagonists used for PONV?

A

Ondansetron (Zofran) – 4mg IV 8mg PO
Granisetron – 1mg
Palonosetron – 0.075mg, 0.25mg (newest, greatest affinity for receptor, works for 72 hours, no QT prolongation)

*Palonosetron reduced the incidence of late on-set vomiting significantly better than Ondansetron

76
Q

What are the pros and cons of 5-HT3 receptor antagonists as use in PONV?

A

Pros:

  • non-sedating and relatively few side effects
  • effective prophylactic especially in combination with dexamethasone

Cons:

  • headache
  • can effect QT (except for palonsetron)
77
Q

What anti-histamines are used for PONV?

A
  • Promethazine (Phenergan)
  • Diphenhydramine (Benadryl) – 1mg/kg IV
  • Dimenhydrinate (Dramamine)
78
Q

What are the pros and cons of anti-histamine use in PONV?

A

Pros:

  • Rescue medication
  • Motion sickness (high number of histamine receptors in vestibular center)

Cons:

  • Sedating
  • Drying
  • IV infiltration of Promethazine is bad
79
Q

What is Aprepitant?

A

Neurokinin-1 Antagonist – Antiemetic

-Competitively binds to the NK1 receptor, which blocks the binding of substance P and prevents the emetic signal being transmitted

Pros: lasts up to 48 hours and is as effective as Zofran as a single antiemetic
Cons: must be taken pre-op (best if 3 hours before anesthesia), not a rescue medication

80
Q

What dose of Propofol is shown to have antiemetic effects?

A

Sub-hypnotic doses (20 mcg/kg/min, 1mg/kg/hr)

  • treatment in post-op care phase (short duration with bolus)
  • Efficacy in tonsils and lap chole for reduction in PONV

*also helps decrease amount of volatile anesthetic agents (lowering the anesthetic risk factor of PONV)

81
Q

How do alpha2 agonists have an antiemetic effect?

A

Clonidine and Dexmedetomidine showed a weak short lived antiemetic effect

*Thought to be more of an opioid sparing effect rather than a direct effect?

82
Q

What dose of Gabapentin is used for PONV?

A

600-800mg given 2 hours pre-op

*Opioid sparing effect?

83
Q

What are the classes of GI motility drugs?

A
  • Oral antacids (neutralize or decrease secretion of HCL)
  • Histamine Antagonists
  • Proton Pump Inhibitors
  • GI Prokinetics
    • Dopamine blockers
    • Macrolides
    • 5-HT4 Agonists
84
Q

Sodium Bicarb

A

Oral Antacid

  • Results in prompt and rapid antacid action
  • Increases pH but if pH becomes >5 = no digestion of food occurs since acidic pH is needed
  • Neutralization increases gastric motility via gastrin and increase in LES tone

*can cause acid rebound

85
Q

Magnesium Hydroxide (Milk of Magnesia)

A

Oral Antacid

  • produces prompt neutralization of gastric acid
  • NOT associated with significant acid rebound
  • Prominent laxative effect is characteristic
  • Systemic absorption of Mg+ can lead to neurologic, neuromuscular, and cardiac effects
86
Q

Calcium Carbonate

A

Oral Antacid

  • produces neutralization but can have acid rebound
  • increases calcium levels in plasma transiently
  • can cause hypophoshatemia
87
Q

Aluminum Hydroxide

A

Oral Antacid

  • aluminum compound causes slowing of gastric emptying and marked constipation
  • minimal systemic absorption
88
Q

Sodium Citrate

A

Oral Antacid

  • Nonparticulate (clear) antacid
  • Less likely to cause foreign body reaction if aspirated
  • Mixing with gastric fluid is more complete than particulate antacids
89
Q

What are the first generation H1 antagonists?

A
  • Chlorpheniramine
  • Diphenhydramine
  • Hydroxyzine
  • Highly selective for H1 receptors w/ very little effect on H2, H3, H4
  • Produces sedation
  • Also activate muscarinic, cholinergic, serotonin, & alpha adrenergic receptors
90
Q

What are the second generation H1 antagonists?

A
  • Loratadine
  • Acrivastine
  • Azelastine
  • Highly selective for H1 – don’t act on other receptors either
  • Decreased CNS toxicity
  • DON’T cause sedation
91
Q

What are H2 antagonists?

A

-Cause selective and reversible inhibition of H2 receptor mediated secretion of H+ from parietal cells

  • Cimetidine, Ranitidine, Famotidine, and Nizatidine
  • May be used to prevent aspiration in at risk individuals but not recommended for routine use

*Numerous drug-drug interactions (Mainly Cimetidine)

92
Q

What are Proton Pump Inhibitors and why are they used in anesthesia?

A
  • Block movement of H+ ions via the proton pump decreasing the secretion of hydrochloric acid by gastric parietal cells
  • Used as a pre-op medication to increase gastric fluid pH and decrease gastric fluid volume
  • crosses BBB, may cause headache, agitation, and confusion
  • can cause bacterial overgrowth in small intestine due to acid suppression

Anesthesia Pharm (18 decks)

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