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Flashcards in Sepsis and Shock Deck (59)
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1
Q

Largest group hospitalized for sepsis?

A

Individuals over 65 years of age, males

2
Q

Mortality rates?

A

Sepsis - 28.6 - 30%; severe sepsis - 39.4%

3
Q

Risk factors for sepsis mortality?

A

Old age, co-morbidities (diabetes, cancer, etc.), females, sepsis occurring after hospitalization

4
Q

Trend in sepsis hospitalization rates?

A

Sepsis - same, but increasing in US; severe sepsis - increasing

5
Q

What detects sepsis invaders?

A

Toll-like receptors (TLRs); TLR4 - lipopolysaccharides (endotoxins, Gm -); TLR3 - ds RNA (viral)

6
Q

Describe the TLR pathway

A
  • PAMPS (pathogen associated molecular patterns) bind TLRs
  • PAMPS may activate nuclear factor kappa B (NFκB), a transcription factor
  • Signalling cascade (from PAMPS, NFκB) results in expression of inflammatory mediators (e.g. cytokines)
  • Vasodilation, increased capillary permeability, endothelial damage, fibrin clots (via coagulation cascade)
7
Q

Criteria for SIRS diagnosis

A

At least two the following symptoms:

  • Body temperature: >38° C or 90 beats/minute (i.e. increased)
  • Respiratory rate: > 20/minute (i.e. increased) (or a PaC02 of 12,000 mm3 or < 4,000 mm3 (i.e. high or low WBCs)
  • Bands (immature WBCs): >10% (indicates body-wide inflammation)
8
Q

Severe sepsis diagnosis

A

defined as deterioration/progression of the condition such that organ systems start to fail (i.e. organ dysfunction) due to lack of perfusion

9
Q

Signs of organ dysfunction

A

Altered mentation (confusion, agitation), oliguria (i.e. decreased urine production), or increased lactate levels (insufficient oxygen delivery to cells)

10
Q

Third spacing

A

When H2O moving from extracellular space (or interstitum) and into cells (to dilute Na/Cl) causes water to flow out of the vasculature to replace it

11
Q

Cause of septic shock

A
  • Leakage of fluids into extravascular space = low BV
  • Heart compensates for low BV
  • Increased cardiac O2 demand
  • Cardiovascular dysfunction
  • Refractory hypotension
12
Q

Pathophysiology of septic shock

A
  • Refractory hypotension
  • Poor O2 tissue perfusion due to decreased systemic vascular resistance
  • Anaerobic metabolism = decreased ATP and lactic acidosis
  • Decreased ATP affects pumps/gradients; Na/Cl accumulate in cell causing swelling
  • Third spacing results in lower intravascular volume, worsening organ/tissue perfusion
13
Q

How to measure metabolic acidosis?

A

Blood lactate levels

14
Q

Most common organ system failures?

A

1 - Respiratory/pulmonary
2 - Kidneys
3 - Cardiovascular system (septic shock)
Least common - liver (highest mortality)

15
Q

Pathophysiology of pulmonary system failure

A
  • Endothelial dysfunction in capillaries/extravation of fluid = pulmonary edema/impaired gas exchange
  • Less surfactant is produced and immune cells infiltrate lung tissue causing further damage.
  • Loss of aeration leads to hypoxia and impaired perfusion in other organs, as well as the lungs causing ARDS
16
Q

ARDS?

A
  • Acute respiratory distress syndrome
  • Impaired pulmonary perfusion
  • Mechanical ventilation
17
Q

DAMPS?

A
  • Damage associated molecular patterns refer to:
    1. pathogen-associated molecular patterns from invading microorganisms or parasites
    2. molecules released by injured tissues
18
Q

Component that recognizes DAMPS?

A

Pattern recognition receptors (PRR)

19
Q

Binding to PRR results in

A
  • Over expression of pro-inflammatory mediators - Activation of the complement and coagulation systems
  • Cytokines recruit innate immune cells; release ROS and enzymes
  • Damage to endothelium causes coagulation
  • Inhibition of fibrinolysis causes disseminated intravascular coagulation (DIC)
  • Immune cell dysfunction - immunosuppression (CAIRS)
20
Q

CAIRS?

A
  • Compensatory anti-inflammatory response system
  • Reduced expression of pro inflammatory cytokines
  • Increased level of anti inflammatory cytokines and cytokine inhibitors
  • High rate of apoptosis of lymphocytes, dendritic cells and epithelial cells
  • Late stage sepsis - immune paralysis - opportunistic infections
21
Q

Most effective way to treat sepsis

A
  • Early recognition, early treatment
22
Q

The golden hours?

A

The period when recognition of sepsis and intervention with fluids and antibiotics can save the life of a patient

23
Q

Early goal directed therapy?

A
  • Treatment for severe sepsis within 6 hours of recognition
  • Fluids, antibiotics, and culture within an hours
  • Crystalloid/colloids to increase CVP
  • Vasoactive agents to increase MAP
  • Inotropes to increase SvO2
24
Q

Approved pharmacological treatment for sepsis?

A
  • Recombinant Human Activated Protein C (rhAPC, also known as Drotecogin alpha and Xigris)
  • Natural inhibitor of Factors 5a and 8a of coagulation cascade
  • Inhibits antifibrinolytic effects, cytokines, selectins
  • Anti-inflammatory, anti-apotitic
  • IV over 96 hours
25
Q

rhAPC reduction in mortality?

A

6%

26
Q

Disadvantages of rhAPC?

A
  • $10, 000 per dose

- Increased bleeding

27
Q

What other pathologies lead to the development of shock?

A
  • Cardiogenic
  • Hypovolemic
  • Neurogenic → distributive shock (no fluid loss; rather there is a redistribution of fluid that impairs tissue perfusion)
  • Anaphylaxis → distributive shock
28
Q

Symptoms of all types of shock?

A
  • Low blood pressure
  • Decreased urine production
  • Poor perfusion leading to acidosis
  • Body temperature and heart rate vary depending on type of shock
29
Q

Body temperature effects for each type of shock

A
  • Most = low body temperature
  • Neurogenic = high body temperature
  • Early septic shock = high body temperature
30
Q

Heart rate effects for each type of shock

A
  • Most - increased HR

- Neurogenic - decreased HR

31
Q

Symptoms of anaphylactic shock

A
  • Apprehension
  • Abdominal cramping
  • Coughing
  • Wheezing
  • Hives
32
Q

Pathophysiology of cardiogenic shock

A
  • RAAS: fluid retention and vasoconstriction
  • ADH: increased BV
  • Catecholamines: increased HR and vasoconstriction
  • Pulmonary/peripheral edema
  • Increased myocardial O2 demand
  • Decreased BP
  • Insufficient O2 = cardiac/organ system dysfunction
33
Q

Causes of cardiogenic shock

A
  • Consequence of MI
  • Severe myocardial ischemia
  • Late stage result of coronary artery disease
34
Q

Causes of hypovolemic shock

A
  • Hemorrhage
  • Plasma loss (e.g. burns)
  • Shift in fluid from the vascular compartment to the extra-vascular space to replace lost fluids (e.g. vomiting or diuresis)
35
Q

Amount of blood loss affecting CO

A
  • 10%: CO and perfusion

- 35-45%: CO and MAP

36
Q

Pathophysiology of hypovolemic shock

A
  • RAAS/ADH: fluid retention
  • Increased HR
  • Increased contractility, vasoconstriction
  • Hepatic blood released into circulation
  • Hypothalamus stimulates thirst
37
Q

Causes of neurogenic shock

A
  • Imbalance between PNS and SNS
  • Trauma to spinal cord or brain
  • Depressant drugs, anesthetics, insufficient delivery of glucose to the brain (e.g. excess insulin)
38
Q

Pathophysiology of neurogenic shock

A
  • Loss of vascular tone
  • Prolonged vasodilation
  • Drop in BP
  • SNS suppressed: HR slows, increased temp.
39
Q

Rarest form of shock?

A

Neurogenic

40
Q

Causes of anaphylactic shock

A

Systemic allergic response due to exposure to an antigen (e.g. shellfish, bee stings, nuts, drugs)

41
Q

Pathophysiology of anaphylactic shock

A
  • Vasodilatory substances (e.g. histamine) are released = vasodilation, increased capillary permeability
  • Drop in BP = reduced tissues perfusion, altered mentation
  • Constriction of extravascular SM (e.g. broncoconstriction, laryngospasm, GI cramps)
  • Death within minutes
42
Q

Treatment of anaphylactic shock

A
  • EpiPen (IV, IM)
  • Vasoconstriction, reverse SM constriction, minimizes release of histamine
  • Short half life; may require multiple doses
43
Q

Effect of pH on O2

A
  • Drop in pH reduces hemoglobin’s affinity for O2
44
Q

Effects of shock on glucose?

A
  • Hypoperfusion reduces glucose delivery
  • Uptake reduced (via hormones, vasoactive substances, and steroids)
  • lipolysis, gluconeogenesis, and glycogenolysis
45
Q

Effects of lypolysis

A
  • Increased FFAs and TGs
  • Cytotoxicity (esp. pancreatic B cells)
  • Cell death
46
Q

Effects of gluconeogenesis

A
  • Uses protein
  • Increases urea and toxic ammonia
  • Low protein = fluid movement from vasculature
  • Alanine generation, converted to pyruvate = lactic acidosis
  • Muscle wasting, impaired immune function, organ failure
47
Q

Initial treatment for neurogenic shock?

A
  • Stabilization of the spine
48
Q

How is BV increased?

A
  • Colloids (albumin) and crystalloids (5% dextrose) - Whole blood
49
Q

Causes of pancreatitis?

A
  • Gallstones
  • Alcohol abuse (75%)
  • Endoscopic Retrograde Cholangiopancreatography (ERCP)
  • Drug reactions
  • Abdominal trauma
  • Hypertriglycridemia
  • Idiopathic
50
Q

Roles of pancreas?

A
  • Endocrine: insulin, glucagon
  • Exocrine: acinar cells produce digestive enzymes (e.g. proteolytic enzymes, amylase, lipases, trypsin inhibitors) deliver to duodenum
51
Q

Pathophysiology of pancreatitis?

A
  • Acinar cell injury
  • Activation of trypsin
  • Premature activation of other enzymes
  • Auto-digestion of the pancreatic tissues
52
Q

Role of trypsin (pancreas)?

A
  • Activates proteolytic enzymes, amylase, lipases in SI

- Enzymes are released from acinar cells with trypsin inhibitors to prevent premature activation

53
Q

Consequences of pancreatitis?

A
  • Inflammation with release of pro-inflammatory cytokines
  • Complement system activation
  • Systemic inflammation
  • SIRS
  • Organ dysfunction (such as ARDS or ATN)
  • Possible fluid accumulation in abdomen = reduced BV and hypoperfusion
  • Gut lining dysfunction = intestinal bacteria enter blood stream causing sepsis
54
Q

Symptoms of pancreatitis?

A
  • Severe epigastric or mid-abdominal pain (radiation to back)
55
Q

Indicators of pancreatitis?

A
  • Elevated serum lipase level (best indicator)
  • Serum amylase
  • C-reactive protein (CRP) (inflammation; indicates severity)
56
Q

Pain relief for pancreatitis?

A
  • Meperidine hydrochloride (Demerol)
  • Prescribe over morphine due to reduced incidence of spasm in the pancreatic ducts’ sphincter
  • Also fentanyl for mild cases (less damaging to kidneys)
57
Q

Pancreas rest?

A
  • No food or fluids by mouth
  • Nasogastric tube to remove gastric fluids
  • Somatostatin (IV/SC) to limit secretions
58
Q

Other precautions for pancreatitis

A
  • IV fluids
  • Ultrasound: gallstones
  • CT scan: fluid accumulation, necrosis
  • Cholecystectomy (gall bladder removal) for necrosis, gall stones
  • Nutritional support
59
Q

Nutrition for pancreatitis

A
  • Mild pancreatitis: soft-food, low-fat diet once as pain has subsided
  • NPO for first 7 days
  • Enteral feeding after 7 days
  • TPN if enteral feeding is not tolerated