33

Systemic metabolic response to injures

Embed Size (px)

Citation preview

Page 1: Systemic metabolic response to injures
Page 2: Systemic metabolic response to injures

جمهوری اسالمی افغانستان

وزارت صحت عامه

ریاست شفاخانه استقالل

دیپارتمنت جراحی عمومی

Page 3: Systemic metabolic response to injures

ترینی سال اول(احدی)داکتر صالح الدین -:ترتیب کننده

جراحی عمومی

ترینر (سادات)استاد سید حمیدهللا رداکت-:استاد رهنما

متخصص جراحی عمومی

هه شمسی1393سال

موضوع کنفرانسSystemic Metabolic Response to

Injury

Page 4: Systemic metabolic response to injures

Definitions

سیستم معافیتی به منظور جواب به میکرواورگانیزمهای

خنثی کردن اثرات آنهاوهماهنگی باترمیم نسجی -پتالوژیک

یاالتهاب شامل به اسیب جواب التهابی . شکل گرفته است

-. مراحل ذیل است

های حجرویپیام cell signaling -1- cell migrationمهاجرت حجروی 2

مدیاتورهاازادسازی mediator release -3

Page 5: Systemic metabolic response to injures
Page 6: Systemic metabolic response to injures

The Systemic Inflammatory Response Syndrome (SIRS)

Page 7: Systemic metabolic response to injures

CNS regulation of inflammation

Integral role in inflammatory response that is mostly involuntary

Autonomic system regulates HR, BP, RR, GI motility and temp

Page 8: Systemic metabolic response to injures

CNS Regulation of Inflammation

Page 9: Systemic metabolic response to injures

Hormonal Response to Injury

Includes:

Cytokines

Glucagon

Insulin

Epinephrine

Serotonin

Histamine

Glucocorticoids

Prostaglandins

leukotrienes

Page 10: Systemic metabolic response to injures

ACTH

A. Its synthesized in the anterior lube of pituitary gland.

B. Its increased by pain, anxiety and injury

C. Continues to be released in a circadian pattern in injured patients

D. Causes the release of mineralocorticoids from the adrenal in a circadian pattern

Page 11: Systemic metabolic response to injures

ACTH

Page 12: Systemic metabolic response to injures

Cortisol Essential for survival during physiologic

stress

Potentiates the effects of glucagon and epinephrine manifesting as hyperglycemia

In liver, stimulate gluconeogenesis

Induces insulin resistance in skeletal muscle and adipose tissue

In skeletal muscle induces protein breakdown and release of lactate

Immunosuppressive agent

Page 13: Systemic metabolic response to injures

A primary action of aldosterone is

to:

A. Convert angiotensinogen to angiotensin

B. Decrease Cl reabsorption in the renal tubule

C. Decrease K secretion in the renal tubule

D. Increase Na reabsorption in the renal tubule

E. Increase renin release by the juxtaglomerular apparatus

Page 14: Systemic metabolic response to injures

Catecholamine elevation after

injury

A. Its limited to epinephrine only

B. Its limited to norepinephrine only

C. Increases by 3- to 4-fold after injury

D. Its sustained 24-48 hours before decreasing

Page 15: Systemic metabolic response to injures

C-reactive proteinA. Its increased or decreased plasma

concentration in response to inflammatory stimuli such as traumatic injury and infection.

B. Specifically, CRP has been studied as a marker of proinflammatory response in many clinical settings, including appendicitis, vasculitis, and ulcerative colitis.

C. Does not increase in response to stress in patients with liver failure

D. Its less sensitive than ESR as a marker of inflammation

Page 16: Systemic metabolic response to injures

Mediators of Inflammation

Cytokines

Heat shock proteins

Reactive oxygen metabolites

Eicosanoids Includes prostaglandins, leukotrienes,

thromboxane

Fatty Acid metabolites

Kallikrien-Kinen system

Serotonin

histamine

Page 17: Systemic metabolic response to injures

Cytokine Response to Injury

Lots of cytokines

Most potent mediators of inflammatory response

Pro- and anti-inflammatory

Page 18: Systemic metabolic response to injures

Cytokines….

TNF one of the earliest and most potent mediators of

host response Primary source: monocytes/macrophages and T

cells Half life of 20 min but potent

IL-1 Primarily released by macrophages and endothelial

cells Half life less than 6 mins. Classic febrile response to injury

IL-6 Linked to hepatic acute phase proteins production

Page 19: Systemic metabolic response to injures

Impt Eicosanoids

Prostacyclin (PGI2)

From endothelium

Decreases platelet aggregation

Promotes vasodilation

Thromboxane (TXA2)

From platelets

Increases platelet aggregation

Promotes vasoconstriction

Page 20: Systemic metabolic response to injures
Page 21: Systemic metabolic response to injures

Nitric Oxide

A. Its primarily made in hepatocytes

B. Has a half-life of 20-30 minutes

C. Its formed from oxidation of L-arginine

D. Can increase thrombosis in small vessels

Page 22: Systemic metabolic response to injures

Surgical Metabolism

Basic metabolic needs = 25 kcal/kg/day

Page 23: Systemic metabolic response to injures

Where do we get our caloric needs?

Fat 9 kcal/g

Protein 4 kcal/g

Oral carbs 4 kcal/g

Dextrose (in IV fluids) 3.4 kcal/g

Page 24: Systemic metabolic response to injures

Surgical Metabolism during fasting

Starvation: fat is the main source of energy in trauma and starvation

Carbohydrates are stored in the form of glycogen (2/3 skeletal muscle, 1/3 liver)

Due to deficiency in glucose-6-phosphatase, skeletal muscle not available for systemic use and therefore, liver stores are used quickly

Page 25: Systemic metabolic response to injures

Gluconeogenesis

Occurs in the liver

Precursors include:

Amino acids

(alanine)

Lactate

Pyruvate

Glycerol

Cori cycle

In late starvation gluconeogenesis occurs in kidney

Page 26: Systemic metabolic response to injures

Metabolism following Injury

Page 27: Systemic metabolic response to injures

Fat digestion

Broken down into micelles and FFAs

Micelles enter enterocytes

Chylomicrons are formed which enter thoracic duct

Medium and short chain amino acids enter portal system with amino acids and carbs

Page 28: Systemic metabolic response to injures
Page 29: Systemic metabolic response to injures

Protein Metabolism

6 g protein = 1 g N

Provides substrates for gluconeogenesis and acute phase proteins

1g protein=4kcal

Page 30: Systemic metabolic response to injures

Protein metabolism

Page 31: Systemic metabolic response to injures

Healthy patients undergoing uncomplicated surgery

can remain NPO (with IVF) for how many days

before significant protein catabolism occurs?

2 days

4 days

7 days

10 days

Healthy patients without malnutrition undergoing uncomplicated surgery can tolerate 10 days of partial starvation before any significant protein catabolism occurs

Page 32: Systemic metabolic response to injures

Schwartz's Principles of Surgery, Ninth Edition

REFRENCE ;

Page 33: Systemic metabolic response to injures

تشکر از توجه شما