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Pathology- fluid Hemodynamics > shock > Flashcards

shock Flashcards

1
Q

what is shock?

A

systemic hypoperfusion or ograns

  • hypoxia
  • acidosis
  • build up of toxins
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2
Q

what happens to kidneys during shock

A

tubular necrosis (acute)

  • drop in renal function
  • reduced production of urine (anuria)
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3
Q

components of ogran dysfunction

A
  • 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)
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4
Q

metabolic abnormalities

A
  1. insulin resistance and hyperglycemia

2. lactic acidosis

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5
Q

insulin resistance with shock

A
  • 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
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6
Q

key clinical feature of metabolic abnormalities

A

hyperglycemia

-poisons neutrophils

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7
Q

hypoperfusion=hypotension

A

BP= CO x PR

  • CO: heart failure (cardiogenic), hypovolemic
  • PR: inflammatory, anaphylactic
  • COxPR: neurogenic (spinal), interferes with sympathetic, decreases peripheral resistance and bradycardia
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8
Q

cardiogenic and hypovolemia

A

skin turns pale, clammy and cold

-inadequate perfusion with increased peripheral resistance

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9
Q

systemic inflammatory and anaphylactic

A

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

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10
Q

neurogenic

A

decreased vascular resistance and bradycardia

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11
Q

cardiogenic symptoms from shock

A

ventricular fibrillation
heart failure
cardiac tamponade
saddle pulmonary embolus

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12
Q

hypovolemic symptoms of shock

A

hemorrhage-> intrinsic or extrinsic
dehydration
burns

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13
Q

stage 1 of hypovolemic shock

A 
<15% volume loss (750mL)
blood pressure: normal
heart rate: normal
appearance: pallor
mental status: normal to anxious
renal output: normal
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14
Q

stage 2 of hypovolemic shock

A 
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
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15
Q

stage 3 of hypovolemic shock

A

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

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16
Q

stage 4 of hypovolemic shock

A

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

17
Q

most common cause of shock

A

staph. Aureus (G+)

18
Q

sepsis implies

A

overwhelming systemic inflammation from bacteremia

  • staph A. (toxic shock), E. coli most common
  • also Klebsiella, streptococci, pseudomonas
19
Q

in sepsis, what is the inflammatory response from?

A

production and distribution of inflammatory mediators

-“cytokine storm”

20
Q

septic shock

A

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

21
Q

innate response in septic shock

A

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

22
Q

inflammatory and counter-inflammatory responses in septic shock

A
  • 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
23
Q

endothelial cell activation and injury in septic shock

A

vasodilation, increased vascular permeability, coagulation

24
Q

counter-regulatory immunosuppressive mechanisms in septic shock

A

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

25
Q

anaphylactic shock

A

systemic release of histamine

vasodilation with increased vascular permeability-> secondary hypovolemic edema, ARDS

epinephrine-> increases vasoconstriction

26
Q

systemic release of histamine in anaphylactic shock

A

anaphylaxis-> IgE mediated

anaphylactoid-> complement factors, radiocontrast material, anesthetic gasses

27
Q

neurogenic shock

A

spinal shock

interruption of sympathetic impluses

28
Q

DIC

A
  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)
29
Q

endothelial cell activation and injury in DIC

A
  • production of pro-coagulant factors

- decreased endothelial anti-coagulant factors: TFI, thrombomodulin, protein C)

30
Q

stages of shock

A
  1. non-progressive phase
  2. progressive stage
  3. irreverisble stage
31
Q

non-progressive phase stage of shock

A

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

32
Q

progressive stage of shock

A

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
33
Q

irreversible stage of shock

A

cellular and tissue injury is irreversible

  • widespread injury
  • lysoszomal enzyme leakage
  • ischemic bowel with exposure to intestinal flora
  • anuria, renal failure
34
Q

morphology of septic shock

A
  • 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

Pathology- fluid Hemodynamics (4 decks)

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