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1. Measure of metabolic rate after laparoscopy: Objective The aim of the research was to

compare local and systemic reactions of the body to laparotomy and laparoscopy.

Design In a prospective randomized study the operative trauma and metabolic changes in

40 patients were investigated and compared in laparoscopy and laparotomy.

Main outcome measures Metabolic changes were registered by indirect calorimetry. In

order to quantify intraperitoneal trauma, short-term and medium-term pH measurements

of the peritoneal surface were made.

Results In the case of laparoscopy a severe intraoperative chemical acidosis occurred that

disappeared a short time after operation. As a result, a short-term increase of metabolic

rate was observed. Following laparotomy an increase in metabolic acidosis was registered

during the first postoperative hours and had not returned to normal after 24 h. A

prolonged catabolism lasted over 48 h.

Conclusion In patients undergoing laparotomy the intraperitoneal trauma is more marked

than in laparoscopy. Long-term metabolic intra-abdominal acidosis with resulting

catabolism may cause increased impairment of the organism.

Physiological Changes during Laparoscopic Surgery

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Laparoscopic surgeries are commonly carried out through transperitoneal or retroperitoneal

approaches with insufflation of CO2 and fewer commonly with another inert gas such as heliumor argon. The working space developed by CO2 pneumoperitoneum or pneumoretroperitoneum

would depend about the pressure of gas presentedto the patient. Typically, intra-abdominal

pressures (intra abdominal pressure) of Ten to fifteen mm Hg are sufficient for visualization anddissection. Although higher pressures are sometimes used transiently to optimize visualization,an intra abdominal pressure of 20 mm Hg or greater for any prolonged period is considered

unsafe, and pressures more than 25 mm Hg could be associated with abdominal compartmentsyndrome.

A physiologic effects seen with CO2 insufflation are transient and derive from the body'sreaction to increases in intra abdominal pressure and CO2 absorption as it tries to achieve a new

state of homeostasis. People who are otherwise healthy will tolerate laparoscopy well, whileindividuals with underlying cardiopulmonary or renal diseases may not tolerate prolonged CO2

insufflation. Additionally, patient positioning, for example steep Trendelenburg inprostatectomy, can exacerbate cardiovascular alterations in laparoscopy.

CARDIOVASCULAR RESPONSE

The cardiovascular response to increased intra abdominal pressure appears to be phasic. It begins

with an early transient phase where venous return and cardiac filling pressures increase due toupward mechanical pressure about the dintra abdominal pressurehragm. This particular, in turn,increases intrathoracic pressure as well as intra-abdominal compression about the splanchnic

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venous bed and vena cava, which increases venous return. A lot more specifically, mechanicalpressures on the venous vasculature result in increases in central venous pressure, pulmonary

capillary wedge pressure, and right- and left-side cardiac filling pressures.

Following the transient rise in venous return with the initiation of pneumoperitoneum or

pneumoretroperitoneum, a steady state of decreased blood circulation with the inferior vena cavacomes after due to the compressive effects of continued intra-abdominal cava pressure. Thecompressive effects on the arterial vasculature and capillaries increase afterload, systemic

vascular resistance (SVR), and arterial pressure, although stroke volume and cardiac outputdecrease.

Heart rate may rise transiently in response to increases in SVR and arterial blood pressure level

to maintain cardiac output, but most studies have reported no significant long-term changes inheartbeat with laparoscopy. In a tiny subset (0.5%) of otherwise healthy patients, however,

bradycardia and asystole can occur during CO2 insufflation and pneumoperitoneum. Althoughthe exact mechanism for this response and why only certain patients experience bradycardia

remain topics of continued research, it is believed that direct pressure about the vagus nerveleads to a stimulatory parasympathetic effect that leads to a decline in heart rate.

Cardiovascular changes vary with intra abdominal pressure, with higher pressures associatedwith more significant changes than lower pressures. In in any other case healthy patients

undergoing laparoscopy, the threshold intra abdominal pressure that led to hemodynamicchanges was 12 mm Hg. Those with underlying cardiac disease will likely have a lower intra

abdominal pressure threshold.

Attention to patient positioning and its impact on cardiovascular response ought not to beneglected. In cases where steep or reverse Trendelenburg positions are required, hemodynamic

changes are magnified, with drops within the cardiac index (CI) of as much as 50% in certainreports. In Trendelenburg position, venous return is improved with subsequent increases in

cardiac filling pressures. Backwards Trendelenburg position, venous pooling in the lowerextremity occurs, generating decreased venous return, ejection fraction. Due to the growing

complexity of laparoscopic urologic cases and the increased duration of pneumoperitoneumrequired, some authors have recommended invasive hemodynamic monitoring with repetitive

blood gas analysis.

RESPIRATORY RESPONSE

CO2 may be the gas of choice for laparoscopic surgeries because it is noncombustible, extremely

soluble, and readily eliminated with the lungs. Other gases for example nitrous oxide have fallenout of favor. Nitrous oxide can result in bowel distension and decreased working space and is

also combustible. Helium and argon, although inert and nonflammable, are a lesser amount ofsoluble than CO2 and therefore are hard to eliminate through ventilation. Pneumothorax caused

by helium and argon resolves much slower than CO2 pneumothorax, and gas embolisms of thoseinsoluble gases aren't well tolerated and can rapidly lead to death.

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Despite the proven effectiveness and protection of CO2 for insufflation in laparoscopy, therespiratory response to mechanical improves in intra abdominal pressure as well as hypercapnia

from absorption should be considered. With CO2 insufflation and increases in intra abdominalpressure, the dintra abdominal pressurehragm is pushed cephalad into the thoracic cavity,

constraining downward dintra abdominal pressurehragmatic excursion with respiration. All

round functional respiratory capacity, vital capacity, and pulmonary compliance drop with boostsin intra abdominal pressure, and peak airway and plateau pressures can enhance up to 50% and81%, respectively.

Despite the fact that laparoscopy is usually well tolerated, affected individuals with underlying

chronic obstructive pulmonary disease (COPD) or morbid obesity are at high risk for pulmonarydecompensation and could require positive end expiratory pressure for adequate gas exchange. In

procedures for example prostatectomy and cystectomy, where steep Trendelenburg positioningmay be required, pulmonary compliance and dintra abdominal pressurehragmatic movement are

further limited.

In addition to the mechanical consequences of pneumoperitoneum, CO2 absorption in theperitoneal cavity or retroperitoneal space will result in hypercapnia and respiratory acidosis. In

otherwise, healthy individuals without having pulmonary disease, CO2 is eliminated efficientlythrough respiration by increases in minute ventilation (increases in respiratory rate and/or tidal

volume). Similar to the phasic cardiac response, CO2 excretion rises acutely, from the typicalbaseline degree of 125 mL/min to 200 mL/min, within approximately Quarter-hour of

pneumoperitoneum then plateaus thereafter.

In patients with interstitial pulmonary disease or COPD, poor CO2 diffusion and elimination can

lead to significant and catastrophic increases of PCO2 if blood gases are not supervised. End-tidal CO2 measurements are difficult to rely on and tend to underestimate the real PCO2 on this

population due to impaired gas swap. Periodic arterial blood gas measurements ought to beobtained as well as in the big event that CO2 cannot be quickly eliminated, pneumoperitoneum

or pneumoretroperitoneum should be relieved immediately. Once PCO2 has fallen to theacceptable range, CO2 insufflation could be resumed and also the laparoscopic procedure

continuing.

RENAL RESPONSE

Oliguria is often seen otherwise expected with increases in intra abdominal pressure duringlaparoscopy and really should be described as a normal physiologic response. Effects are

transient and reversible upon desufflation. The greater concern would be to avoid over-resuscitation, fluid overload, pulmonary edema, and exacerbation of congestive heart failure.

Mechanistically, as intra abdominal pressure increases, its compressive effects on the renalvasculature, the renal parenchyma, and the IVC will reduce effective renal blood circulation(ERBF), cortical and medullary perfusion, and renal venous outflow. The renal effects are mild

to negligible once the intra abdominal pressure is under 10 mm Hg, but as intra abdominalpressure reaches and exceeds 15 mm Hg, there's a pressure-dependent decrease in the glomerular

filtration rate (GFR), ERBF, creatinine clearance, sodium excretion, and urinary output. In atypical intra abdominal pressure of 15 mm Hg, urinary output decreases by as much as 63% to

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64%, GFR by 21%, and ERBF by 26%. Despite this drop, however, there are no long-term renalsequelae, even in patients with pre-existing renal disease, and pneumoperitoneum-induced renal

failure does not occur.

Along with renal compression and decreased ERBF, a host of neurohormonal factors are freed.

Among them, renin, aldosterone, endothelin, and antidiuretic hormone are elevated, resulting insystemic vasoconstriction and fluid retention. Together with desufflation, these mediators returnto baseline levels, along with a post-desufflation diuresis is usually noted in the following hours.

Renal homeostasis is re-established within Twenty four hours after surgery with normalization ofserum and urinary creatinine and electrolytes.

The optimal fluid managing of physiologic oliguria is much more controversial in laparoscopic

live donor nephrectomy. Despite animal model data that suggest no adverse renal histologicchanges with prolonged pneumoperitoneum, optimizing ERBF during laparoscopy would seem

reasonable.

In order to preserve renal perfusion and minimize possible deleterious effects on graft function,some investigators have suggested using isotonic and hypertonic intravascular volume expansionfor transplant cases. As donors are typically healthy and at safe for cardiopulmonary

complications, volume expansion and slight fluid overload in the course of surgery might not beunreasonable as long as the surgical team understands the possible unwanted effects. An

alternative choice to volume expansion is to decrease intra abdominal pressure aroundvisualization will allow.

METABOLIC RESPONSE

Metabolic acidosis from CO2 absorption is the primary derangement with laparoscopy.

Systemic CO2 absorption and resultant metabolic consequences differ depending on thepatient's underlying respiratory status since the lung eliminates absorbed CO2 buffered by

the blood. In otherwise healthy patients, an increase in minute ventilation is enough, but

for individuals with COPD, removal of CO2 is less capable, causing them to are afflicted by

more major and extended derangements in acid-base balance. As stated earlier,

desufflation might be necessary during a long laparoscopic procedure in patients with

COPD or interstitial lung condition.

Even though clinical implications might be minimal, immune and cytokine responses to

laparoscopic surgery have been noted. Cortisol, C-reactive protein, tumor necrosis factor-

a, interleukin (IL)-6, IL-10, granulocytic elastase, catecholamines, and leukocytes are one

of the factors released during laparoscopy that could impact your body's metabolicdemand and rest energy expenditure within the postoperative setting.

PEDIATRIC CONSIDERATIONS

Laparoscopy within the pediatric population is generally nicely tolerated. From a cardiacperspective, a similar intra abdominal pressure-dependent physiologic response could be

anticipated. When intra abdominal pressure is maintained at 10 to 12 mm Hg or less, clinically

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significant hemodynamic compromise is generally not observed; although increases in SVR(162%) and decreases in cardiac performance (67%) have been reported at pressures of 10 mm

Hg. Thus, it is advisable to minimize intra abdominal pressure if visibility allows just because alower intra abdominal pressure is associated with fewer cardiac effects. As with adults,

bradycardia and asystole may appear during gas insufflation from vagal nerve stimulation.

Children routinely have a higher resting vagal tone, and initiating pneumoperitoneum in a lowerinsufflation rate might be warranted.

In youngsters, the respiratory reaction to increased intra abdominal pressure and CO2insufflation are magnified compared with adults. From the mechanical standpoint, inhaling the

pediatric population is more determined by diphragmatic movement than on expansion from thethoracic cavity as in adults. In addition, thoracic compliance is higher in the immature chest

cavity.

With increases in intra-abdominal pressure, the diaphragm is pushed relatively more cephalad,thereby decreasing functional respiratory capacity. Equally respiratory rate and peak airway

pressures increases, and also the respiratory changes appear to be more significant withintraperitoneal than extraperitoneal insufflation. From a metabolic standpoint, CO2 absorption is

a lot more efficient in youngsters due to a relatively greater absorptive surface-to-weight ratio.To avoid hypercarbia, minute ventilation ought to be increased, with close monitoring of end-

tidal CO2 and arterial oxygenation in longer cases.

CONCLUSION

With increasing laparoscopic applications, surgeons should view the basic physiologic principles

of the cardiac, respiratory, renal, and metabolic response in laparoscopy. As the complexity ofurologic cases performed laparoscopically increases, for a longer time durations of CO2

insufflation and elevated intra abdominal pressure are required, further magnifying physiologicmodifications in patients. Thus, the laparoscopist must be mindful from the each patient's

fundamental cardiopulmonary status and anticipate the hemodynamic reaction to non-invasivesurgery. Adequacy of ventilation should be assessed by serial arterial blood unwanted gas in

affected individuals with pulmonary condition, and prevention of overhydration for physiologicoliguria is essential for patient safe practices.

1. Bacteria production most potent exotoxins = Clostridium botulinum

2. Ropivicaine vs bupivacaine: ropivicaine has least CV toxicity, similar pharmacokinetics

3.

Staging of malignant melanoma leg

TNM Classification for Malignant Melanoma

The TNM classification for malignant melanoma is provided below.[1, 2]

Table. TNM Classification for Malignant Melanoma (Open Table in a new window)

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Primary tumor (T)

TX Primary tumor cannot be assessed (ie, curettaged or severely regressed melanoma)

T0 No evidence of primary tumor

Tis Melanoma in situ

T1 Melanoma 1.0 mm in thickness

y T1a: Without ulceration and mitoses < 1/mm2

y T1b: With ulceration or mitoses 1/mm2

T2 Melanomas 1.01-2.0 mm in thickness

y T2a: Without ulcerationy T2b: With ulceration

T3 Melanomas 2.01-4.0 mm in thickness

y T3a: Without ulceration

y T3b: With ulceration

T4 Melanomas > 4.0 mm in thickness

y T4a: Without ulceration

y T4b: With ulceration

Regional lymph nodes (N)

NX Patients in whom the regional nodes cannot be assessed (ie, previously removed for anotherreason)

N0 No regional metastases detected

N1-

3

Regional metastases based upon number of metastatic nodes and presence or absence of

intralymphatic metastases (in transit or satellite metastases)

N1 1 lymph node

y N1a: Micrometastases

y N1b: Macrometastases

N2 2 or 3 lymph nodes

y N2a: Micrometastases

y N2b: Macrometastasesy N2c: In-transit met(s)/satellite(s) without metastatic lymph nodes

N3 4 metastatic lymph nodes, or matted lymph nodes, or in-transit met(s)/satellite(s) withmetastatic lymph node(s)

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Distant metastasis (M)

M0 No detectable evidence of distant metastases

M1a Metastases to skin, subcutaneous, or distant lymph nodes, normal serum lactate

dehydrogenase (LDH) level

M1b Lung metastases, normal LDH level

M1c Metastases to all other visceral sites or distant metastases to any site combined with anelevated serum LDH level

Anatomic stage/prognostic groups

Table. Clinical staging (Open Table in a new window)

Stage T N M

0 Tis N0 M0

IA T1a N0 M0

IB T1b N0 M0

T2a N0 M0

IIA T2b N0 M0

T3a N0 M0

IIB T3b N0 M0

T4a N0 M0

IIC T4b N0 M0

III Any T N1, N2, or N3 M0

IV Any T Any N M1

Table. Pathologic staging (Open Table in a new window)

Stage T N M

0 Tis N0 M0

IA T1a N0 M0

IB T1b N0 M0

T2a N0 M0

IIA T2b N0 M0

T3a N0 M0

IIB T3b N0 M0

T4a N0 M0

IIC T4b N0 M0

IIIA T(1-4)a N1a M0

T(1-4)a N2a M0

IIIB T(1-4)b N1a M0

T(1-4)b N2a M0

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T(1-4)a N1b M0

T(1-4)a N2b M0

T(1-4)a N2c M0

IIIC T(1-4)b N1b M0

T(1-4)b N2b M0T(1-4)b N2c M0

Any T N3 M0

IV Any T Any N M1

Stage IA:

y Lesions 1 mm in thickness with no evidence of ulceration or metastases (T1aN0M0)are associated with a 5-y survival rate of 95%

Stage IB:

y Lesions 1 mm in thickness with ulceration noted but without lymph node involvement

(T1bN0M0) or lesions 1.01-2 mm in thickness without ulceration or lymph nodeinvolvement (T2aN0M0) are associated with a 5-y survival rate of approximately 91%

Stage IIA:

y Melanomas > 1 mm but 2 mm in thickness with no evidence of metastases but withevidence of ulceration (T2bN0M0) or lesions 2.01-4.0 mm in thickness without

ulceration or lymph node involvement (T3aN0M0) are associated with an overall 5-ysurvival rate of 77-79%

Stage IIB:

y Melanomas 2.01-4 mm in thickness with ulceration but no lymph node involvement(T3bN0M0) or lesions > 4 mm in thickness without ulceration or lymph node

involvement (T4aN0M0) are associated with a 5-y survival rate of 63-67%

Stage IIC:

y Lesions > 4 mm in thickness with ulceration but no lymph node involvement (T4bN0M0)are associated with a 5-y survival rate of 45%

Stage IIIA:

y Patients with any-depth lesion, no ulceration, and 1 positive (micrometastatic) lymphnode (T1-4aN1aM0) have a 5-y survival rate of 70%

y T1-4aN2aM0 lesions (any-depth lesion, no ulceration, but 2-3 nodes positive formicrometastasis) are associated with a 5-y survival rate of 63%

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Stage IIIB:

y Patients with any-depth lesion, positive ulceration, and 1 lymph node positive formicrometastasis (T1-4bN1aM0) or 2-3 nodes positive for micrometastasis (T1-

4bN2aM0) have a 5-y survival rate of 50-53%y

Patients with any-depth lesion, no ulceration, and 1 lymph node positive formacrometastasis (T1-4a, N1b, M0) or 2-3 nodes positive for macrometastasis (T1-4aN2bM0) have a 5-y survival rate of 46-59%

Stage IIIC:

y Patients with any-depth lesion, positive ulceration, and 1 lymph node positive formacrometastasis (T1-4bN1bM0); 2-3 nodes positive for macrometastasis (T1-4bN2bM0);

or 4 metastatic lymph nodes, matted lymph nodes, or in-transit met(s)/satellite(s) have a5-y survival rate of 24-29%

Stage IV:

y Melanoma metastatic to skin, subcutaneous tissue, or lymph nodes with normal LDH

level (M1a) is associated with a 5-y survival rate of 19%y M1b disease (metastatic disease to lungs with normal LDH level) has a 5-y survival rate

of 7%y M1c disease (metastatic disease to all other visceral organs and normal LDH level or any

distant disease with elevated LDH level) is associated with a 5-y survival rate of 10%

4. Etiology of wound infection inguinal hernia

Traditionally, the operation of hernia is considered as a clean operation due to expected, low incidence

of infection, on the spot of surgical work (SSI). The incidence of SSI in hernia surgery is more frequent

then it is assumed. The important risk factors for SSI are the following: type of hernia (inguinal,

incisional), operative approach (open - laparoscopic), usage of the prosthetic material and drainage.

Comparing to inguinal hernia repair, incisional hernia repair, is more frequently followed by the

infection. The laparoscopic operations are followed with the lower incidence of SSI then in the case of

open operations. The usage of the mesh does not increase the incidence of SSI, although the

consequences of the mesh infection may be severe. A type I of the prosthesis is more resistant to the

infection then prosthesis II and III. The mesh infection (type I) never involves its body but it is present

around sutures and bended edges. The mesh infection Type II involves entire prosthesis while in the

case of Type III it is present in its peripheral part. In the case of SSI, a prosthesis Type I is possible to be

saved, while prosthesis Type II must be removed completely; and the same is for the Type III (the partial

removal is rarely suggested). The defect that remained after excision of non-resorptive prosthesis is a

long-term and very complicated surgical problem. In regard to the position of the mesh, SSI is more

common if the mesh is placed subcutaneously then in the case of sub-aponeurotic premuscular, pre-

aponeurotic retromuscular or pre-peritoneal mesh placemen. If the infection is present the nontension

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techniques using non-resorptive prosthetic implants are not recommended. The presence of drainage

and its duration increases the incidence of SSI. It is more common for incisional hernioplasty then for

inguinal hernia repair. If there is an indication for drainage it should be as short as possible. The cause of

SSI for elective operations are bacteria's that arrives from the skin, while in the case of opening of

various organs dominant bacteria's originate from them. The superficial infection does not lead to the

recurrence, while it is very possible in the case for deep infection. There are no prospective studies that

justify the usage of antibiotic prophylaxes in hernia surgery. The antibiotic prophylaxis is indicated for

the clean operations when placing the implants and when severe complication is expected. The

appearance of SSI increases the price of treatment and may lead to the recurrence.

5. Protein-sparing effect of glc administration

What is Protein-Sparing effect?

Protein sparing is the process by which the body derives energy from sources other than protein. Such sources can includefatty tissues, dietary fats and carbohydrates. Protein sparing conserves muscle tissue. The balance between digestibleprotein (DP) and digestible energy (DE) in the diet is a key factor. Decreasing dietary DP/DE ratio results in an increase ofprotein conservation. The amino acids are not catabolized for energy, and are conserved in the body in a greater ratio.

Leucine, a branched-chain amino acid has been recently known also to have protein-sparing effect.1.2

The amount of protein used in the body is influenced by the percentage that is digestible by the body, and the total quantityof protein fed to the body. Bodybuilding and other strength training promotes the utilization and conservation of protein'samino acids in the body. Using alternate energy sources lessens the amount of amino acids that will be metabolized forenergy. Non carbohydrate sources such as alanine, acetate, lactate, glycerol, branched-chain ketoacids are also known toexert protein-sparing effects.

In clinical nutrition, the concept of protein-sparing effect was introduced by Gamble.3

During starvation in a 70 kg man, approximately 80 g/day, or approximately 400 g for six days, of proteins was lost due tothe catabolism of body proteins. This is equivalent to approximately 2 kg of muscle. After glucose administration, the proteincatabolism was inhibited. The protein loss at a glucose dose of 100 g/day was approximately 40 g/day or approximately 200g for six days. This means, glucose administration inhibited the protein loss to approximately 50% of that during starvation. When glucose was administered at 200 g, The degree of protein catabolism was similar to that at 100 g. This indicates thatadministration of glucose, i.e., an energy source, alone cannot fully inhibit the catabolism of body proteins.

Approximately 40 g of proteins at minimum is necessary as a daily average intake to maintenance N-balances under nostress conditions. For this purpose, 100 g/day of glucose is required at minimum.

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Under stress conditions such as surgery, the energy demand is increased and protein catabolism is further enhanced. It

becomes more difficult to inhibit protein catabolism by glucose administration alone.

In this case, supplementation of not only energy sources (carbohydrates and fats) but also amino acids that are used for

protein synthesis is important to improve N-balance and protein metabolism and then inhibit the catabolism of bodyproteins.

A group of japanese investigators showed that combination of amino acids, glucose and electrolytes is more effective than

exclusive amino acids or electrolyte plus 10% glucose solution in minimizing weight loss and negative nitrogen balance

4

Intraoperative protein sparing with glucose

Schricker et al examined the hypothesis that glucose infusion inhibits amino acid oxidation during colorectal surgery 5. Theyrandomly allocated 14 patients to receive intravenous glucose at 2 mgkg1min1 (glucose group) starting with the surgicalincision or an equivalent amount of normal saline 0.9% (control group). The primary endpoint was whole body leucineoxidation; secondary endpoints were leucine rate of appearance and nonoxidative leucine disposal as determined by astable isotope tracer technique. Circulating concentrations of glucose, lactate, insulin, glucagon, and cortisol were measuredbefore and after 2 h of surgery. Leucine rate of appearance, an estimate of protein breakdown, and nonoxidative leucinedisposal, an estimate of protein synthesis, decreased in both groups during surgery (P < 0.05). Leucine oxidationintraoperatively decreased from 13 3 to 4 3 molkg1h1 in the glucose group (P < 0.05 vs. control group) whereas itremained unchanged in the control group.. The provision of small amounts of glucose was associated with a decrease inamino acid oxidation during colorectal surgery.

Parenteral nutrition and protein sparing after surgery

Although capable of inducing an anabolic state after surgery, parenteral nutrition, including glucose, leads to hyperglycemia.Even moderate increases in blood glucose are associated with poor surgical outcome. Thomas Schricker et al examined thehypothesis that amino acids, in the absence of glucose supply, spare protein while preventing hyperglycemia.6 In this

prospective study, 14 patients with colonic cancer were randomly assigned to undergo a 6-hour stable isotope infusionstudy (3 hours of fasting followed by 3-hour infusions of 10 % amino acids 10% at 0.02 mL kg1 min1, with or withoutglucose at 4 mg kg1 min1) on the second day after colorectal surgery.

Protein breakdown, protein oxidation, protein balance, and glucose production were assessed by stable isotope tracerkinetics using leucine and glucose isotops. Circulating concentrations of glucose, cortisol, insulin, and glucagon weredetermined. The administration of amino acids increased protein balance from 16 4 mol kg1 h1 in the fastedstate to 16 3 mol kg1 h1. Combined infusion of amino acids and glucose increased protein balance from 17 7to 7 5 mol kg1 h1. The increase in protein balance during nutrition was comparable in the 2 groups (P = .07).Combined administration of amino acids and glucose decreased endogenous glucose production (P = .001) and stimulatedinsulin secretion (P = .001) to a greater extent than the administration of amino acids alone.

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Is Protein-Sparing Effect Considered in Formulation of Maintenance Solution ?

New generation dual-chamber maintenance solutions like Aminofluid contain combination of glucose and amino acids toprevent consumption of amino acids as energy source and thus have favourable profile on nitrogen balance. In addition, the

content of electrolytes is necessary for water and electrolyte homeostasis, while microminerals and zinc facilitate cellularmetabolism.

References:

1. Shimomura Y et al. Nutraceutical Effects of Branched-Chain Amino Acids on Skeletal Muscle. American Society forNutrition J. Nutr. 136:529S-532S, February 2006

2. Mitchell JC, Evenson AR, Tawa NE: Leucine inhibits proteolysis by the mTOR kinase signaling pathway in skeletalmuscle. J Surg Res 2004, 121:311.

3. Brody T. Nutritional Biochemistry, Second Edition, p 4544. Urabe H, et al. Yakuri To Chiryo 1994;22 (Supplement):S8355. Schricker T, Lattermann R, and Carli F Intraoperative protein sparing with glucose J Appl Physiol 99: 898901,

20056. (Schricker T Parenteral nutrition and protein sparing after surgery: do we need glucose?Original Research Article

Metabolism, Volume 56, Issue 8, August 2007, Pages 1044-1050,)

6. Sensitivity vs Specificity

a. Sn = TP/TP+FNb. Sp = TN/TN+FP

7. Choice of fluid in hypovolemia: Isotonic crystalloid solutions are typically given for intravascular

repletion during shock and hypovolemia. Colloid solutions are generally not used. Patients with

dehydration and adequate circulatory volume typically have a free water deficit, and hypotonic

solutions (eg, D5 0.45% saline) are used

8. Etiology of hyperglycemia/TPN:

Stress from illness induces a hyperglycemic state,

which can be further exacerbated with TPN. Although

total parenteral nutrition (TPN) provides necessary

nutrients and calories to critically ill patients andlowers their risk of noninfectious complications, it

has been shown to contribute to hyperglycemia.

Patients (without diabetes) who received TPN and

dextrose at rates >5 mg/kg/min had a 49% chance of

developing hyperglycemia.

In contrast, the risk of hyperglycemia was substantially reduced in patients

who received infusions at lower rates

Hyperglycemia resulting from excess dextrose in TPN

solutions elevates the respiratory quotient in

ventilated patients and increases infectiouscomplications.

Higher infection rates have been

found in patients receiving TPN versus enteral

nutrition; however, the serum glucose concentrations

in the former group have been consistently higher,

emphasizing the importance of glucose control for TPN

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patients.

Avoiding hyperglycemia during TPN administration can

begin with gradual dextrose infusion, starting with

100 g to 150 g dextrose and advancing toward goal only

as glucose tolerance permits. Underfeeding will not

result in impaired nitrogen balance when there is

adequate protein in the TPN solution (>1.2 g/kg-1.5

g/kg).

Alternatively, TPN solutions can be formulated

as 3-in-1 admixtures containing lipid emulsions as a

source of calories. Incidence of hyperglycemia was

significantly reduced in patients receiving a

lipid-based admixture (80% nonprotein calories as

lipid) compared with patients receiving a

dextrose-based formulation (100% nonprotein calories

as dextrose

Insulin is very effective in managing hyperglycemia and should be

considered a part of the TPN order.

9. Etiology of shock s/p AAA repair: most commonly hemorrhagic shock

10.PA Catheter tracing see pdf

11.Process Measures SCIP

12.Rx of high-voltage electrical injury fluid resuscitation, wide debridement with longitudinal flaps

13.Dx finding sepsis see pdf

14.Etiology of lymphangitis (red streaking up extremity)

Lymphangitis is an inflammation of the lymphatic channels[1] that occurs as a result of infection at a

site distal to the channel. The most common cause of lymphangitis in humans is Streptococcus

pyogenes (Group A strep). Lymphangitis is also sometimes called "blood poisoning".

Signs and symptoms include a deep reddening of the skin, warmth, lymphadenitis, and a raised

border around the affected area. The person may also have chills and a high fever along with

moderate pain and swelling. A person with lymphangitis should be hospitalized and closely

monitored by medical professionals.[2]

Lymphangitis is the inflammation of the lymphatic vessels and channels. This is characterized by

certain inflammatory conditions of the skin caused by bacterial infections. Thin red lines may be

observed running along the course of the lymphatic vessels in the affected area, accompanied by

painful enlargement of the nearby lymph nodes

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15.FENa calculation

Fractional Excretion of Sodium (FENa) = (PCr* UNa

) / (PNa x UCr) %

Prerenal Intrinsic Renal Postrenal

UNa (mmol/L) 40 >40

FENa 1% >4%

Prerenal: Anything that causes decreased

effective renal perfusion: Hypovolemia, CHF,

Renal Artery Stenosis, Sepsis, etc. Remember,

contrast-induced nephropathy will often look pre-

renal.

Intrinsic Renal: ATN, AIN, Glomerulonephritides,etc

Postrenal: Obstruction (BPH, bladder stone,

bilateral ureter obstruction)

16.Monitoring LMWH Rx - activated factor X assay

LMWH therapy is monitored by the anti-factor Xa assay, measuring anti-factor Xa activity. The

methodology of an anti-factor Xa assay is that patient plasma is added to a known amount of excess

factor Xa and excess antithrombin. If heparin or LMWH is present in the patient plasma, it will bind to

antithrombin and form a complex with factor Xa, inhibiting it.

[5]

The amount of residual factor Xa isinversely proportional to the amount of heparin/LMWH in the plasma. The amount of residual factor Xa

is detected by adding a chromogenic substrate that mimics the natural substrate of factor Xa, making

residual factor Xa cleave it, releasing a colored compound that can be detected by a

spectrophotometer.[5]

Antithrombin deficiencies in the patient do not affect the assay, because excess

amounts of antithrombin is provided in the reaction.[5]

Results are given in anticoagulant concentration

in units/mL of antifactor Xa, such that high values indicate high levels of anticoagulation and low values

indicate low levels of anticoagulation

17.Rx for diffuse bleeding resuscitation and identification of bleeding source

18.Arterial supply of head of pancreas

. Vessels supplying head of pancreas

a. Superior & inferior pancreaticoduodenal arteries

b. Both divide into two parallel vessels

c. one anterior and one posterior to head

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19.GI hormone enhance appetite ghrelin (decreased s/p RYGB)

20.Decreased Chloride levels with increase in pancreatic exocrine secretion

21. Initiation of intestinal protein digestion: There are three mechanisms for gastric acid secretion. The

first is the cephalic phase. During this phase, chewing and swallowing stimulate the vagus nerve, which in

turn signals cells in the stomach to release acid. The second phase is the gastric phase. Distension of the

stomach as food enters sends a signal to the local nerves, which in turn stimulate the acid-producing cells in

the stomach to release acid. The last phase is the intestinal phase. As protein digestion occurs in the

intestine, signals are sent via molecules to the stomach to produce more acid. Once the acid is secreted, it

activates pepsin, which initiates protein digestion.

22.Crohns disease associated with granulomas and aphthous ulcers

Table 2. Endoscopic Features of Crohn's Disease vs Ulcerative Colitis

Crohn's disease Ulcerative colitis

Rectum often spared Rectum involved

"Skip" areas Continuous uniform involvement

Aphthous ulcers Loss of vascular markings

Cobblestoning from submucosal edema Diffuse erythema

Linear or serpiginous ulcers Mucosal granularity ("wet sandpaper")

Fistulas Fistulas not seen

Ulceration of the terminal ileum Normal-appearing terminal ileum

23.Primary pigment of human bile

PRIMARY PIGMENT OF HUMAN BILE

Bile: Bile is made up of bile salts, bile pigments, and other substances dissolved in an alkaline

electrolyte

solution that resembles pancreatic juice. About 500ml of bile is secreted per day. Some of the

components of

bile are reabsorbed in the intestine and then excreted again by the liver (enterohepatic circulation).

Bile Salts: These are sodium and potassium salts of the bile acids (primary bile acids cholic and

chenodeoxycholic acid and secondary bile acids deoxycholic and lithocholic acid), which are

conjugated to

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either glycine or taurine and secreted into intestines. They serve many important functions that aid

in fat

emulsification, digestion, and absorption.

Bile Pigments: The glucoronides of the bile pigments, bilirubin and biliverdin, are responsible for the

goldenyellow

color of bile. Bilirubin, the primary pigment of human bile, is the end-product of the metabolic

degradation of heme, the prosthetic group of hemoglobin, myoglobin, the cytochrome P450s, and

various other

hemoproteins. 70-90% of bilirubin is derived from the degradation of hemoglobin of senescent or

injured

circulating red blood cells.

The conversion of heme to bilirubin first entails the oxidative opening of the heme molecule by the

microsomal

enzyme heme oxygenase, resulting in the formation of the green tetrapyrrole biliverdin. Biliverdin is

then

reduced by a second enzyme, biliverdin reductase, to bilirubin. Bilirubin produced in the

extrahepatic

reticuloendothelial system (e.g. spleen) is transported to the liver within the plasma where it is

tightly bound to

albumin.

In the liver hepatocytes, the free (unconjugated) bilirubin is conjugated to glucoronic acid in a

reaction catalyzed

by glucoronyl transferase. This bilirubin diglucoronide (conjugated bilirubin) is much more water-

soluble than

free (unconjugated) bilirubin. Most of the conjugated bilirubin is secreted into the bile and into the

intestine;

however, a small amount of conjugated bilirubin can escape into the blood and is fi ltered and

excreted in the

urine, unlike the free (unconjugated) bilirubin that is never excreted in the urine regardless of how

high the

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concentration gets because it is tightly bound by albumin and not filtered across the glomeruli.

Normally, the gut

does not see unconjugated (free) bilirubin because all of it would have been conjugated before it

was excreted.

Following secretion into bile, conjugated bilirubin reaches the duodenum and passes down the

gastrointestinal

tract without reabsorption by intestinal mucosa. Although some reaches the feces unaltered, an

appreciable

fraction is converted to urobilinogen (a colorless compound), urobilin and stercobilin by bacterial

metabolism

within the ileum and colon. Urobilinogen is reabsorbed from these sites, reaches the liver via the

portal

circulation, and re-excreted into bile. Urobilinogen not taken up by the liver reaches the systemic

circulation

from which it is cleared by the kidneys. Urobilin and stercobilin are excreted in the feces with the

stool and are

primarily responsible for the brownish pigmentation of stool.

24.Site of protein absorption

50% of the ingested protein is absorbed between the stomach and thejejunum and 90% is absorbedby the time the digested food reaches the ileum

25.Advantage of pressure-control ventilation

Patients can breath spontaneously on pressure control as long a the inspiratory time has not

be unduly prolonged. The trigger mechanism is the same as in volume control. The key

advantage of pressure targeted ventilation is unlimited flow in inspiration to satisfy the

patients demands. The harder the patient draws in, the greater the pressure gradient, and

the higher the flow

26

.Pathophysiology of pulse loss in claudication vasodilation and stealing of blood from areasdistal to occlusion

27.Pathophysiology of atherosclerosis plaques,

28.Physiology of PEEP

Positive end-expiratory pressure (PEEP) refers topressure in the airway at the end of

passiveexpiration that exceeds atmospheric pressure. Gas exchange1. Redistributes fluid within the

alveoli and reducesintrapulmonary shunting2. Improves arterial oxygenation (PaO2)3. Reduces FIO2

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requirements and risk of oxygen toxicity Lung mechanics1. Helps prevent alveolar collapse2.

Stabilizes and recruits lung units3. Increases functional residual capacity4. Improves lung

compliance5. Shifts tidal deflections to the right along theinspiratory pressure-volume curve

minimizing potentialfor ventilator-induced lung injury by preventingrepetitive collapse of lung units

at end-expirationfollowed by re-openingduring inspiration6. May decrease the inspiratory work of

breathing dueto auto-PEEP in patients with obstructive airway diseaseHemodynamic effects of

PEEP-induced increases inintrathoracic pressure1. Increases intraluminal central venous pressure2.

Decreases venous return3. Decreases left and right ventricular preload(end-diastolic volume)4.

Increases right ventricular afterload5. Decreases cardiac output, as a result of theabove effectsa.

Hypotension and organ hypoperfusion canoccur.b. Reduction of both cardiac output and

bloodpressure is particularly likely in the presenceof hypovolemia.6. Decreases left ventricular

afterload7. Decreases ventricular compliance8. Increases intracranial pressure, by increasing CVP

29. Indication for surgical tx of asymptomatic aneurysms see table

30.Nerve injury associated with flexor carpi radialis weakness median nerve

31.Role of vitamin C in collagen synthesis vit C cofactor for prolyl hydroxylase and lysylhydroxylase

32.Treatment of extraperitoneal bladder rupture foley drainage, repair later (immediate OR for

intraperitoneal bladder rupture)

33.Characteristic of medullary cancer in MEN-2a - major clinical symptom of metastatic medullary

thyroid carcinoma is diarrhea; occasionally a patient will have flushing episodes. Both occur

particularly with livermetastasis. Occasionally, diarrhea or flushing will be the initial presenting

complaint. The flushing that occurs in medullary thyroid carcinoma is indistinguishable from that

associated with carcinoid syndrome. The presumed cause of flushing and diarrhea is the

excessive production ofcalcitonin gene products (calcitonin or calcitonin gene-related peptide)

and differs from the causation of flushing and diarrhea in carcinoid syndrome. Sites of spread ofmedullary thyroid carcinoma include local lymph nodes in the neck, lymph nodes in the central

portion of the chest (mediastinum), liver, lung, and bone. Spread to other sites such as skin or

brain occurs but is uncommon

34.Etiology for decline of breast ca - decrease in breast-cancer incidence began in mid-2002 and

occurred shortly after the highly publicized series of reports from the randomized trial of the

Women's Health Initiative, which reported a significant increase in the risks of coronary heart

disease and breast cancer associated with the use of estrogenprogestin combination therapy.3

By the end of 2002, the use of hormone-replacement therapy had decreased by 38% in the

United States, with approximately 20 million fewer prescriptions written in 2003 than in 2002.

35.Dx of sickle cell dz -

36.Mechanism of inheritance of MEN syndromes = autosomal dominant