shock

Question 1

what is shock?

Answer 1

systemic hypoperfusion or ograns

• hypoxia
• acidosis
• build up of toxins

Question 2

what happens to kidneys during shock

Answer 2

tubular necrosis (acute)

• drop in renal function
• reduced production of urine (anuria)

Question 3

components of ogran dysfunction

Answer 3

• cell and tissue hypoxia
• cytokines and secondary mediators diminish myocardial contractility and cardiac output (sepsis)
• decrease renal perfusion
• acute respiratory distress syndrome (from inflammatory mediators)
• brain hypoxia
• adrenal dysfunction (W-F syndrome)

Question 4

metabolic abnormalities

Answer 4

1. insulin resistance and hyperglycemia

2. lactic acidosis

Question 5

insulin resistance with shock

Answer 5

• TNF, IL-1, stress induced hormones (glucagon, glucocorticoids)
• gluconeogenesis
• impaired surface expression of GLUT-4 glucose transporter
• initial surge of glucocorticoids followed by adrenal insufficiency and functional glucocorticoids deficits

Question 6

key clinical feature of metabolic abnormalities

Answer 6

hyperglycemia

-poisons neutrophils

Question 7

hypoperfusion=hypotension

Answer 7

BP= CO x PR

• CO: heart failure (cardiogenic), hypovolemic
• PR: inflammatory, anaphylactic
• COxPR: neurogenic (spinal), interferes with sympathetic, decreases peripheral resistance and bradycardia

Question 8

cardiogenic and hypovolemia

Answer 8

skin turns pale, clammy and cold

-inadequate perfusion with increased peripheral resistance

Question 9

systemic inflammatory and anaphylactic

Answer 9

inadequate pressure due to to decreased peripheral resistance
-skin is red and hot

Question 10

neurogenic

Answer 10

decreased vascular resistance and bradycardia

Question 11

cardiogenic symptoms from shock

Answer 11

ventricular fibrillation
heart failure
cardiac tamponade
saddle pulmonary embolus

Question 12

hypovolemic symptoms of shock

Answer 12

hemorrhage-> intrinsic or extrinsic
dehydration
burns

Question 13

stage 1 of hypovolemic shock

Answer 13

<15% volume loss (750mL)
blood pressure: normal
heart rate: normal
appearance: pallor
mental status: normal to anxious
renal output: normal

Question 14

stage 2 of hypovolemic shock

Answer 14

volume loss: 15-30% (750-1500ml)
BP: systolic normal, diastolic high, narrow pulse pressure
HR: >100bpm
Appearance: pale, cold, clammy skin
mental status: mildly anxious, restless
renal output: 20-30 ml/hr

Question 15

stage 3 of hypovolemic shock

Answer 15

volume loss: 30-40% (1500-2000ml)
BP: systolic 120bpm (increased RR as well, hyperventilating)
appearance: sweating, with cool, pale skin
mental status: confusion, anxiety, agitation
renal output: 20ml/hr

Question 16

stage 4 of hypovolemic shock

Answer 16

volume loss: >40% (>2000ml)
BP: systolic 140 bpm (also hyperventilating)
appearance: skin is sweaty, cold, and extremely pale
mental status: decreased consciousness, lethargy, coma
renal output: negligible

Question 17

most common cause of shock

Answer 17

staph. Aureus (G+)

Question 18

sepsis implies

Answer 18

overwhelming systemic inflammation from bacteremia

• staph A. (toxic shock), E. coli most common
• also Klebsiella, streptococci, pseudomonas

Question 19

in sepsis, what is the inflammatory response from?

Answer 19

production and distribution of inflammatory mediators

-“cytokine storm”

Question 20

septic shock

Answer 20

presence of microbial organism cause systemic activation of endothelial and inflammatory cells

Question 21

innate response in septic shock

Answer 21

recognition of microbial factors
-endotoxin-> LPS
-toxic shock-> superantigen (polyclonal T cell activation)
Complement activation
TLR
activation of coagulation factors (hageman factor)
release of inflammatory mediators

Question 22

inflammatory and counter-inflammatory responses in septic shock

Answer 22

• TLR’s, PAMP’s, G-protein couple receptors, NOD1, NOD2
• TNF, IL-1, IL-6, IFN-gamma, IL-12, IL-18
• ROS, lipid mediators (PG, LT)
• complement cascade

Question 23

endothelial cell activation and injury in septic shock

Answer 23

vasodilation, increased vascular permeability, coagulation

Question 24

counter-regulatory immunosuppressive mechanisms in septic shock

Answer 24

shift from Th1 to Th2
anti-inflammatory mediators (soluble receptor blockers)
apoptosis of lymphocytes
hyperglycemia deactivation of neutrophils

Question 25

anaphylactic shock

Answer 25

systemic release of histamine vasodilation with increased vascular permeability-> secondary hypovolemic edema, ARDS epinephrine-> increases vasoconstriction

Question 26

systemic release of histamine in anaphylactic shock

Answer 26

anaphylaxis-> IgE mediated | anaphylactoid-> complement factors, radiocontrast material, anesthetic gasses

Question 27

neurogenic shock

Answer 27

spinal shock | interruption of sympathetic impluses

Question 28

DIC

Answer 28

1. endothelial cell activation and injury 2. vascular stasis in small vessels 3. fibrin-rich thrombi in small vessels 4. consumption of coagulation factors with disastrous results: fibrinolytic peptides, d-dimer 5. waterhouse-friderichsen syndrome (bleeding into adrenal glands)

Question 29

endothelial cell activation and injury in DIC

Answer 29

- production of pro-coagulant factors | - decreased endothelial anti-coagulant factors: TFI, thrombomodulin, protein C)

Question 30

stages of shock

Answer 30

1. non-progressive phase 2. progressive stage 3. irreverisble stage

Question 31

non-progressive phase stage of shock

Answer 31

compensatory mechanism activated and perfusion is maintained -neurohormonal response to shock -activation of baroreceptors with catecholamine release -activation of R-A -ADH release -generalized sympathetic stimulation NET EFFECT: tachycardia, peripheral vasoconstriction, renal conservation of fluid

Question 32

progressive stage of shock

Answer 32

tissue hypoxia with worsening circulatory and metabolic imbalances - widespread tissue hypoxia - intracellular aerobic respiration replaced by anaerobic glycolysis - excessive production of lactic acid - decreased tissue pH with dilation of arterioles - peripheral pooling of blood - anoxic injury to endothelium - vital organs begin to fail

Question 33

irreversible stage of shock

Answer 33

cellular and tissue injury is irreversible - widespread injury - lysoszomal enzyme leakage - ischemic bowel with exposure to intestinal flora - anuria, renal failure

Question 34

morphology of septic shock

Answer 34

- widespread hypoxia cell and tissue injury - adrenals-> cortical cell depletion (stress) - kidneys-> acute tubular necrosis - lungs-> resistance to hypoxic injury from hypovolemic shock, trauma or sepsis results in diffuse alveolar damage (chock lung) - DIC with widespread deposition of fibrin-rich microthrombi: consumption of platelets and coagulation factors results in petechial hemorrhages on serosal surfaces and skin