process is contained within a localize aria

self-limiting (8 to 10 days)

After the Inflammatory responses has been  stimulated what Inflammatory mediators are activated?

leukocytes, platelets, arachidonic acid, prostaglandins, leukotrienes, interleukins, tumor necrosis factor-a

What is the roll of bradykinin in the 

vascular effects of inflammation

stimulate capillary and venule endothelial cells to retract, creating spaces at junctions between cells.

"Alowing vessles to leak"

leukocytes

(also blood cells and plasma proteins)

complement, kinin-kallikrein, and coagulation systems

How is the complement cascade activated?

(three pathways)

What does it result in?

three pathways:

classic- antibodies bound to the specific antigen

lectin- same except that it is activated by bacterial        carbohydrates.

alternative- Polysaccharides from bacterial cell walls

each of these pathways results in lysis of the target cell.

stimulation of the plasma kinin cascade.

Hageman factor (factor XII)

Bradykinin has profound effects, including:

5

activated when damaged endothelial cells come into direct contact with circulating blood.

"slow path"

Activated by Tissue Factor

Fast pathway

Both Intrinsic and Extrinsic pathways lead to formation of ________

that leads to the formation of fibrin.

What are the Six Steps of Inflammation

1. Inflammatory stimulus

2. Inflammatory mediators

3. Effects on capillaries

4. Effects on phagocytes

5. Acute inflammation

6. Inflammatory repair

What are the Primary Effects of Inflammatory Mediators

Stimulate production of other inflammatory mediators

Stimulate nerve endings

Alter capillaries

Attractant and stimulate phagocytes

What type of cell Kills microbes and tumors?

What type of cell

scavenge dead cells and debris during inflammatory repair

What cell type are  Immature Macrophages

Monocytes

Monocytes

What cell type is the first line of defense

Monocytes

What cell type regulates tissue factor

Monocytes

What cell type secretes Histamine

Platelets 

How is Nitric Oxide introduces in to  the body?

Induced by bacterial products and proinflammatory cytokines (TNF)

How does Nitric Oxide affect the other cells?

Responsible for cytotoxic effects of macrophages on bacteria protozoa, and tumor cells

How does Nitric Oxide affect CARDIAC MYOCYTES

How does Nitric Oxide affect  the intestines 

Can lead to diarrhea.

How does Nitric Oxide affect smooth muscle

How does Nitric Oxide affect platlets

 Inhibits platelet aggregation

What are the key features of Prostaglandins and Leukotrienes

Produced in response to inflammatory mediators

Act as inflammatory mediators

Prostaglandins are a large family of compounds- cause pain

Leukotrienes are a complex mixture of molecules

severe infection that has spread via the bloodstream

develop either as a result of the body's own defense system or from toxic substances made by the infecting agent (such as a bacteria, virus, or fungus). "

Fever

Rapid heart rate

Rapid breathing rate

An abnormally high or low number of white blood cells

Sepsis occurs when toxins produced by the bacteria cause cells in the body to release substances that trigger inflammation.

What are the toxins called?

They can cause the blood vessels to widen (dilate), decreasing blood pressure.

They can cause blood to clot in tiny blood vessels inside organs.

Blood flow decreases to vital organs (such as the kidneys, heart, and brain).

heart- ↑ hr, weaken the heart, = organs receive even less blood

they release excess lactic acid (a waste product) into the bloodstream, making the blood more acidic.

The kidneys excrete little or no urine, and metabolic waste products (such as urea nitrogen) accumulate in the blood.

How does the worsening organ malfunction effect

 the walls of blood vessels

The walls of blood vessels may leak, allowing fluid to escape from the bloodstream into tissues and cause swelling.

How does the worsening organ malfunction effect

 the Lung function

Lung function worsens because leaking blood vessels in the lungs cause fluid to accumulate, making breathing difficult.

How does the worsening organ malfunction effect

 blood clotting

As blood clots continue to form, the proteins in blood that make up clots (clotting factors) are used up. Then, excessive bleeding may occur."

How does Inflammation effect  Organ Damage

1.Vasodilation: Nitric Oxide- Dilation of vessels causing maldistribution of blood and hypoperfusion to some organs

2.Increased Capillary Permeability: Leaking of fluid into tissue causes hypovolemia intravascularly. Interstitial edema can decreased perfusion and cause pain

3.Inflammatory Mediators: Prostaglandin- Pain response and activation of the sympathetic nervous system. Cortisol- Increased blood sugar and immune suppression

an exaggerated inflammatory response that becomes systemic and results in the excessive production of chemical mediators

What arw the manifestations of SIRS 

Body temperature 

Body temperature less than 36°C or greater than 38°C 

What arw the manifestations of SIRS 

Heart rate 

Heart rate greater than 90 beats per minute 

What arw the manifestations of SIRS 

respiratory rate

What arw the manifestations of SIRS 

PaCO2

What arw the manifestations of SIRS 

WBC

White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³ (12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band forms) 

SIRS can be diagnosed when _________ or more of these criteria are present

What are the S/S of a pt transitioning

from SIRS to MODS

1.failure to controle infection/inlimation

2.persistent hypoperfusion- prolonged shock- cell death

3.presences of nacrotic tissue

4.↑ cell O2 consumption (fever, shivering, agitation, pain)

What is Primary MODS

Organ failure is related to the initial injury / insult

within 5 days 

occurs quickly 

Organ failure is the result of the SIRS response to the

initial injury / insult

Occurs latent (7 -10 days) after original insult

Occurs in organs distant from the original insult

treat infection

give blood

fluid replacement

↑ O2 supply

Chronically ill + acute illness

major trauma

Sepsis

presistent infcetion

multi organ involvment

sevarity upon edmition- (delayed resusitation, malnutrition, coma, 6 U blood with in 12 h)

age > 65

immunosuppression

1. Pulmonary

2. Cardiovascular

3. Renal

4. Neurologic

5. Hepatic

6. GI

7. Hematologic

1. trans location

2. release of inflammatory mediators

3. reticoloendothelial dysfunction

4. disruption of O2 supply

What are the Neurologic effect of MODS

and early/late S/S

Neurologic - Neuroendocrine exhaustion and ischemia

EARLY Failure - Confusion, disorientation

LATE Failure - Progressive decreased LOC to coma

What are the Pulmonary effect of MODS

and early/late S/S

Pulmonary - Alveolar capillary injury

EARLY Failure - Requires  ventilator     support for 3 - 5 days

LATE Failure - Progressive ARDS (PO2/Fio2 < 200)

(PEEP > +10 and FiO2 > 50%)

What are the Cardiovascular effect of MODS

and early/late S/S

Cardiovascular - Decreased perfusion  related to MDF (myocardial depressant factor) production

EARLY Failure - Ejection fraction < 65%; capillary leak syndrome (edema/DW)

LATE Failure - Increased inflammatory mediators that depress cardiac output; hypodynamic despite inotropes- refractory to B stimulation

What are the Renal effect of MODS

and early/late S/S

Renal - Renal ischemia leads to ATN

EARLY Failure - Oliguria of < 480cc/day; Creatinine > 2-3 mg/dl; increased urine osmolality

LATE Failure - Dialysis dependent

What are the Intestinal effect of MODS

and early/late S/S

Intestinal - Bacterial translocation, Abdominal hypertension

EARLY Failure - Ileus (enteral intolerant) for > 5 days; abdominal hypertension

LATE Failure - Stress ulcer (requiring transfusion); Cholecystitis (without stones); abdominal compartment syndrome

What are the Hepatic effect of MODS

and early/late S/S

Hepatic - Reticuloendothelial system (Kupffner cells, detox blood) failure.

EARLY Failure - Bilirubin > 2 mg/dl; LFT’s  2 x normal values; decreased albumin; decreased production of clotting factors

LATE Failure - Jaundice with Bilirubin > 8-10 mg/dl; coagulopathy

What are the Hematologic effect of MODS

and early/late S/S

Hematologic - Clotting mechanisms > fibrinolytic system = procoagulant state

EARLY Failure - Pt / Ptt > 25%; Platelets < 80,000; decreased fibrinogen

LATE Failure - Evidence of DIC increased FSP/FDP & D-dimer titers are elevated 

What are the interventions for MODS that a nurse would want to insure are in place?

R/T O2

Increase Oxygen delivery- (Hgb, SaO2, PaO2)

Decrease Oxygen consumption- nuromuscular blockade 

What are the interventions for MODS that a nurse would want to insure are in place?

R/T infcection

Decrease tissue injury & infection risk-debread, protect tissue start IV antibiotics with in 1st hour

Improve nutritional status; early tube feeding (with in 72 H)

What are the interventions for MODS that a nurse would want to insure are in place?

R/T Fluid vole/blood flow

Prompt, rapid and adequate fluid resuscitation

Restoration of bowel blood supply 

What are the interventions for MODS that a nurse would want to insure are in place?

R/T  Reperfusion Injury

Use of oxygen free radical scavengers (e.g. mannitol, vitamin C and E)

What are the interventions for MODS that a nurse would want to insure are in place?

R/T burns

Extensive escharectomy during shock stage