Auer Ch 40 Post Op Care

Front 1

Complications of abdominal surgery:

Back 1

pain, ileus, adhesions, and septic peritonitis

Front 2

Butorphanol CRI dose:

Back 2

13 mg/kg/hr

Front 3

Lidocaine dose:

Back 3

loading dose of 1.3 mg/kg over 15 minutes followed by a CRI of 0.05 mg/kg/min

Front 4

Benefits of lidocaine:

Back 4

prokinetic activity, likely by reducing inflammation, stabilizing cell permeability, and reducing pain

Front 5

Side effects of lidocaine administration:

Back 5

muscle fasciculation and ataxia

Front 6

Blood concentrations of lidocaine should be:

Back 6

1-2 ug/mL

Front 7

When does POI more commonly develop?

Back 7

after small intestinal surgery, more with strangulating lesions than non-strangulating lesions

Front 8

MOA POI:

Back 8

dysregulation of motility, likely due to a variety of factors such as, altered parasympathetic and sympathetic input, disruption of the enteric nervous system & neurotransmitters, and inflammatory insult to smooth muscle cells and ICC

Front 9

Treatment of PO:

Back 9

frequent gastric decompression and therapies directed at the reduction of pain and inflammation (lidocaine, NSAIDs), prokinetic therapies can be instituted

Front 10

Classes of prokinetic drugs:

Back 10

parasympathomimetics, adrenergic antagonists, benzamides, motilin agonists, and sodium channel blockers

Front 11

NT involved in GI motility:

Back 11

ACh, 5HT, dopamine, motilin, norepinephrine

Front 12

How does ACh affect motility?

Back 12

released from ganglionic axon terminal, binds to receptors on enteric smooth muscle cells, causes excitation of the muscle cell

Front 13

How is ACh cleared from the synapse?

Back 13

degraded by acetylcholinesterase, located at the surface of the enteric smooth muscle cell

Front 14

How does serotonin (5HT) affect motility?

Back 14

can have stimulatory and inhibitory effects, based on the type of receptor it binds. 5HT1 & 5HT3 receptors have an inhibitory effect on axons, inhibiting the release of ACh from the axon terminal. 5HT4 has a stimulatory effect on axons, resulting in release of ACh from the axon terminal

Front 15

How does dopamine affect motility?

Back 15

inhibitory effect, stimulating the release of norepinephrine, which binds to alpha 1 and beta adrenergic receptors on the enteric smooth muscle cell, inhibiting muscular contraction

Front 16

How does motilin affect motility?

Back 16

binds to motilin receptors on the enteric smooth muscle cell and causes excitation of the cell

Front 17

What cells produce motilin?

Back 17

enterochromaffin cells

Front 18

Examples of parasympathomimetic drugs:

Back 18

bethanechol and neostigmine

Front 19

MOA bethanechol:

Back 19

direct acting muscarinic cholinergic agonist. It binds to the post-synaptic ACh receptors, exciting the cell

Front 20

MOA neostigmine:

Back 20

indirectly by preventing the activity of the acetylcholinesterase at the surface of the muscle cell, preventing degradation of ACh, and prolonging activity in the synapse

Front 21

Bethanechol dose:

Back 21

0.025 mg/kg SC q 3-6 hours

Front 22

Activity of bethanechol on motility:

Back 22

to increase activity in duodenum, jejunum, cecum, pelvic flexure, and in gastric and cecal emptying

Front 23

Side effects of bethanechol:

Back 23

salivation, abdominal pain, and diarrhea

Front 24

Neostigmine dose:

Back 24

0.0044 mg/kg (2mg) SC or IV, repeated q 20-60 minutes and increasing by 2mg when there is no response and no adverse effects, to a maximum of 10 mg

Front 25

Activity of neostigmine on motility:

Back 25

increase motility in the pelvic flexure, but decrease motility in the stomach and jejunum

Front 26

Neostigmine side effects:

Back 26

abdominal pain

Front 27

Examples of benzamides:

Back 27

metoclopramide, cisapride, mosapride, and tegaserod

Front 28

MOA metoclopramide:

Back 28

dopamine receptor antagonist (binds dopamine receptors preventing dopamine’s inhibition of ACh release), a 5HT3 antagonist (binds 5HT receptors preventing 5HT inhibition of ACh release), and a 5HT4 agonist (binds 5HT4 receptors and promotes release of ACh.)

Front 29

Metoclopramide dose:

Back 29

either 0.25 mg/kg diluted in saline and given over 30-60 minutes or 0.04 mg/kg/hour

Front 30

Metoclopramide activity on motility:

Back 30

increase activity in the stomach and small intestine

Front 31

Side effects of metoclopramide:

Back 31

excitement, restlessness, sweating, and abdominal pain

Front 32

MOA cisapride:

Back 32

does not have effects on dopamine receptors, but is similar to metoclopramide because it is a 5HT3 antagonist (binds 5HT3 receptors preventing 5HT inhibition of ACh release) and a 5HT4 agonist (binds 5HT4 receptors and promotes ACh release)

Front 33

Cisapride activity of motility:

Back 33

increase jejunal, large colon, and small colon activity

Front 34

Disadvantage of cisapride:

Back 34

taken off the human markets, so must be compounded for use

Front 35

MOA mosapride:

Back 35

activity as only a 5HT4 agonist (binds 5HT4 receptors enhancing release of ACh)

Front 36

Mosapride activity on motility:

Back 36

increase small intestinal and cecal motility experimentally

Front 37

MOA tegaserod:

Back 37

selective 5HT4 receptor agonist (binds 5HT4 receptors and promotes ACh release)

Front 38

Tegaserod activity on motility:

Back 38

increase activity in ileum and pelvic flexure tissue strips

Front 39

MOA erythromycin lactobionate:

Back 39

motilin receptor agonist and a 5HT3 receptor antagonist (binds 5HT3 receptors preventing inhibition of ACh release)

Front 40

Erythromycin dose:

Back 40

0.5-1 mg/kg in 1 liter saline over 60 minutes, q 6-8 hours.

Front 41

MOA Alpha adrenergic antagonists:

Back 41

bind alpha adrenergic receptors preventing the inhibitory effects of alpha agonists (norepinephrine, xylazine, detomidine) alpha agonist prevent the release of ACh from the ganglionic axon terminal

Front 42

Examples of alpha adrenergic antogonists:

Back 42

acepromazine, yohimbine, tolazoline, and atipamezole

Front 43

Disadvantages of acepromazine:

Back 43

non-selective antagonist and will bind alpha 1 and alpha 2 receptors. Alpha 1 antagonism caused hypotension

Front 44

When is adhesion formation initiated?

Back 44

disruption to the mesothelial layer by traumatic handling, ischemia, distension, and drying

Front 45

What factors are implicated in increasing risk of adhesions?

Back 45

hemorrhage, foreign material and bacterial contamination

Front 46

MOA of adhesion formation:

Back 46

Disruption of the mesothelial layer resulting in exposure of submesothelial tissue and activation of the intrinsic and extrinisic coagulation cascase, resulting in the formation of fibrin at the site of disruption. Pathologic fibrous adhesion subsequently develop because of reduce fibrinolysis due to decreased tissue plasminogen activator and increased plasminogen activator inhibitor and well as increased fibrin production

Front 47

When does conversion of fibrinous adhesion to fibrous adhesions begin?

Back 47

about 4 days after formation of the fibrinous adhesion

Front 48

How are adhesion prevented?

Back 48

gentle surgical handling, perioperative NSAIDs and antibiotics, intra- and post-operative lidocaine administration, heparin administration, intra-operative sodium carbocymethylcellulose application, sodium hyaluronate, intra-operative peritoneal crystalloid infusion, and post-operative peritoneal lavages

Front 49

What type of molecule is heparin, where produced?

Back 49

GAG, is produced by connective tissue mast cells

Front 50

Why type of molecule is antithromin, where produced?

Back 50

glycoprotein, which is produced in the liver and endothelium

Front 51

Effects of heparin:

Back 51

facilitates AT inactivation of clotting factors IX, X, XI, XII, and thrombin. it also suppressed thrombin mediated coagulation amplification and thrombin mediated conversion of fibrin to fibrinogen

Front 52

What limits efficacy of heparin?

Back 52

AT is limited

Front 53

Side effects of heparin:

Back 53

anemia due to erythrocyte agglutination

Front 54

Advantages of LMW heparin:

Back 54

does not cause erythrocyte agglutination, constant anti-coagulent activity (anti-factor X) , greater bioavailability, and longer half-life

Front 55

MOA Sodium CMC:

Back 55

lubricating barrier that minimizes tissue trauma and prevents the establishment of fibrin tags between 2 surfaces

Front 56

Dose of CMC:

Back 56

1% solution administered in the peritoneum at the time of tissue handling or at the time of abdominal closure at a dose of 7 mL/kg body weight

Front 57

Disadvantages of HA:

Back 57

local application to regions that are unlikely to be involved in adhesion formation (i.e. adhesions form far from anastomosis)

Front 58

Peritoneal lavage benefits:

Back 58

removing fibrin, inflammatory mediators, and bacteria thus decreasing risk of adhesion formation

Front 59

Disadvantages of peritoneal fluid lavage:

Back 59

drain obstruction, leakage around the drain, and SQ fluid accumulation

Front 60

What are the possible effects of small intestinal resection?

Back 60

Malabsorption, diarrhea, and weight loss may be noted with removal of 60% or greater of small intestine, however, with removal of 70% of the small intestine and institution of a frequent, pelleted diet post-operatively, no malabsorptive complications were noted

Front 61

What effect does bacteria contamination have on the peritoneal cavity?

Back 61

increased peritoneal fluid volumes occur due to vascular permeability changes. Fluid contains fibrin, inflammatory mediators, and clotting factors which exacerbate the inflammatory response and cellular infiltration

Front 62

How is peritoneal fluid removed from the peritoneal cavity?

Back 62

through diaphragmatic stomata that communicate with lymphatics

Front 63

Parameters used for differentiating septic from non-septic peritonitis:

Back 63

presence of intra- or extraceullular bacteria in the peritoneal fluid, a serum-peritoneal fluid glucose difference of greater than 50 mg/dL, peritoneal fluid pH less than 7.2, and a peritoneal glucose less than 30 mg/dL

Front 64

Common peritoneal bacteria:

Back 64

e.coli, staph, steph, rhodococcus, bacteroides, clostridium, and fusobacterium

Front 65

Incisional complications:

Back 65

infection, dehiscence, suture sinus formation, and herniation

Front 66

When are incisional complications increased?

Back 66

with repeat celiotomy, increased duration of surgery, NFFN pattern, use of chromic gut, leukopenia, incisional edema, postoperative pain, and weight greater than 300 kg. Incisional infection has also been associated with the use of staples for skin closure and closure by a less experienced surgeon in 1 study

Front 67

When should antibiotic therapy be used in incision infection?

Back 67

If fever or significant tissue reaction occur at the incision

Front 68

Erythromycin effects on motility:

Back 68

phase 3 of the MMC

Front 69

Disadvantages of erythromycin:

Back 69

colitis, especially c. difficle