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Patho 2 > 4 - Shock/Trauma Phys > Flashcards

4 - Shock/Trauma Phys Flashcards

1
Q

How do endotoxins contribute to end stage shock?

A

Gram negative Bacteria in the intestines release endotoxin when the gut begins to die

causes increased cellular metabolism despite inadequate oxygen delivery, leading to cardiac exhaustion

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2
Q

Why is the liver particularly effected by shock?

A

Has a high metabolic rate

AND

the liver is the first-line recipient of toxins in the blood from ischemia

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3
Q

What are four cellular effects of shock?

A
  1. Sodium and Potassium transport halts. Na accumulates in the cell and K can’t get into the cell
  2. Mitochondrial activity is depressed
  3. lysosomes break open and release hydrolases
  4. glucose metabolism stops
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4
Q

What happens to adenosine once it’s stripped of all phosphates?

A

It diffuses out of the cell and is converted to uric acid

Once it’s converted, it can’t re-enter the cell, so that adenosine is permanently lost and the body has to form new adenosine

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5
Q

How difficult is it to produce more adenosine?

A

Extremely

the body can produce about 2% per hour

Depletion of high-energy phosphate is a primary killer in shock states

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6
Q

An intestinal obstruction may cause what kind of shock?

A

Hypovolemic

blocked venous flow leads to increased hydrostatic pressure in the capillaries, and fluid flows out of the vasculature into the gut

To make matters worse, a lot of that fluid is proteinaceous, so you get hypoproteinemia and hypovolemia

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7
Q

How does hemorrhagic hypovolemic shock differ from hypovolemia caused by plasma loss?

A

When just plasma is lost, the blood becomes much more viscous

exacerbates the sluggishness of blood flow

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8
Q

In anaphylaxis, where is histamine released from?

A

Basophils in the blood

mast cells in the tissues

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9
Q

What are the effects of histamine during an anaphylactic reaction?

A
  1. Venous dilation → Decreased venous return
  2. Arteriolar dilation → decreased arterial blood pressure
    1. Increased capillary permeability
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10
Q

Most cases of septic shock are caused by _____ bacteria

A

gram positive

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11
Q

What % total heat loss occurs via radiation?

A

60%

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12
Q

Convective heat loss results from:

A

air movement

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13
Q

The cooling effect of wind at low velocities is about proportional to:

A

the square root of the wind velocity

a wind of 4 miles per hour is about twice as effective for cooling as a wind of 1 mile per hour.

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14
Q

Why is being submerged in cold water so much worse than being exposed to cold air?

A

Water has a specific heat thousands of times greater than air, meaning it can absorb way more heat from the skin

Since water’s heat conductivity is so high, it’s impossible for the body to heat a thin layer of water like it does when creating an “insulator zone” in air

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15
Q

When water evaporates from the body, how much heat is lost?

A

58 kCal/1 g of water

(600-700 ml/day)

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16
Q

Why does the body sweat in high temperatures?

A

when the temperature of the surroundings are higher than body temperature, it will cause body temp to rise

the only way for the body to counteract this is to get rid of heat via evaporation

hence, sweat

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17
Q

sweat glands are innervated by ____ nerve fibers

A

cholinergic

(secrete acetylcholine but run in sympathetic nerves)

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18
Q

why is a high rate of sweating less dangerous in someone who is accustomed to heat?

A

the body learns to reabsorb higher levels of sodium as the precursor secretion moves from the gland to the pore

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19
Q

The main determinant in amount of salt loss through sweating is:

A

the rate of sweating, not the amount

at a slow rate, almost all of the sodium is reabsorbed between the gland and the pore

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20
Q

A person who is accustomed to high heat will produce more or less sweat?

A

More! Their rate of sweating will increase from 1 L/hr to 2-3 L/hr

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21
Q

In an acclimatized individual, why do they sweat more but lose less salt?

A

secretion of aldosterone causes salt retention

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22
Q

Pretty much all temperature regulating centers are located in the:

A

hypthalamus

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23
Q

deep body temperature receptors are located in: (3)

A

Spinal Cord

Abdominal Viscera

Great veins of the upper abdomen and thorax

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24
Q

both skin and deep body receptors are primarily designed to detect:

A

HYPOthermia

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25
Q

What are three important mechanisms to reduce body heat?

A
  1. Vasodilation
  2. Sweating
  3. Inhibition of shivering and chemical thermogenesis
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26
Q

Why do we get goosebumps?

A

Not helpful in humans, but in animals with fur, it allows them to entrap a thick layer of insulating air

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27
Q

If the body is cold, will thyroxine secretion be elevated or decreased?

What if the body is hot?

A

Elevated

Depressed

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28
Q

How does chemical thermogenesis release body heat?

A

norepinephrine and epinephrine are able to uncouple oxidation and phosphorylation

foodstuffs are oxidized and release heat instead of forming ATP

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29
Q

The degree of chemical thermogenesis that can occur in an animal is almost entirely dependent on:

A

the amount of brown fat

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30
Q

Why is brown fat optimal for chemical thermogenesis?

A

Contains lots of sympathetic nerve receptors, so its very sensitive to stimulation

contains large numbers of mitochondria capable of thermogenesis

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31
Q

How effective is chemical thermogenesis in adults?

In neonates?

A

10-15% increase in heat production

100% increase in heat production

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32
Q

Why are thyroid goiters more common in people living in cold climates?

A

Thyroxine production is increased by cold, leading to thyroid growth

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33
Q

What is the only really effective mechanism for preventing heat loss?

A

Behavioral control (putting on a coat, or going inside etc)

34
Q

What happens to body temperature control when the spinal cord is severed?

A

It is severely impaired

Even though there are reflexes, the are very ineffective in comparison to hypothalamic control

35
Q

Which cytokine is most important in causing fevers?

A

IL-1

36
Q

Once bacteria begin to be broken down by macrophages, how long does it take for a fever to develop?

A

Often as little as 8-10 minutes

37
Q

Why is aspirin antipyretic

A

It stops development of prostaglandin from arachidonic acid

38
Q

Why is protein metabolism elevated in shock?

A

Widespread gluconeogenesis in response to the cell’s inability to uptake glucose begins to break down cellular structures

39
Q

How does protein metabolism contribute to organ failure?

A

In anaerobic metabolism, protein breakdown liberates alanine, which is converted to pyruvate, which is is changed to lactic acid

lactic acid increases hemoglobin’s affinity for oxygen, resulting in tissue hypoxia and metabolic acidosis

40
Q

Why are serum albumin levels low in patients with shock?

A

proteins are metabolized preferentially, starting with albumin and other plasma proteins

decreases capillary osmotic pressure and contributes to third spacing

41
Q

why do patients in shock have hyperglycemia?

A

insulin resistance in the liver and muscles

adaptive response intended to ensure that glucose is available for the brain, cell nourishment and production, and wound healing

42
Q

Neurogenic shock is caused by an imbalance between:

A

parasympathetic and sympathetic

Can be parasympathetic overstimulation

OR sympathetic understimulation

43
Q

Neurogenic shock can be caused by any factor that stimulates _____ or inhibits _____

A

parasympathetic

sympathetic

44
Q

Fainting can prevent someone from going into neurogenic shock. Why?

A

It puts them in a prone position, which equalizes BP from head to toe and actually prevents progression to a shock state

45
Q

What are the six most commonly identified infections associated with sepsis in the ICU?

A

pneumonia

bloodstream

IVC

Intraabdominal

urosepsis

surgical wounds

46
Q

What is the best definition of sepsis?

A

life-threatening organ dysfunction resulting from dysregulated host responses to infection

47
Q

What are the two causes of lactic acidosis in septic shock?

A

tissue hypoxia

epinephrine-induced stimulation of aerobic glycolysis

48
Q

What are the cellular effects of prolonged shock that causes lactic acidosis?

A

Increased NO synthesis

Activated K channels in vascular smooth muscle (hyperpolarized)

depletion of ADH

49
Q

What molecules do gram-positive organisms release that trigger an inflammatory reaction?

A

Exotoxins:

Peptidoglycans

Lipoteichoic acids

Superantigens

50
Q

What molecules do gram-negative organism release to trigger an inflammatory response?

A

Endotoxins:

LPS containing toxic lipid-A moiety

51
Q

What are the three main proinflammatory cytokines that are released in response to bacterial toxins?

A

TNF- Alpha

IL1 alpha and Beta

IL6

52
Q

A release of proinflammatory cytokines results in the activation of which systems?

A

Complement

Coagulation

Kinin

Monocyte-macrophage/Neutrophil

53
Q

Name four anti-inflammatory cytokines

A

LPS binding protein

IL-1 receptor antagonist

IL10

Nitric oxide

54
Q

A p/f ratio less than _____ is consistent with respiratory failure

A

300

55
Q

What four things should be done with 3 hours of a patient presenting with sepsis-like symptoms?

A
  1. Measure lactate level
  2. Blood cultures
  3. Broad-spectrum antibiotics
  4. Fluid challenge of 30ml/kg crystalloid for hypotension OR lactate > 4
56
Q

When should IV steroids be considered in a septic patient?

A

If BP is unresponsive to fluid resuscitation

57
Q

In an intubated septic patient, plateau pressures should be less than

A

30 cmH20

58
Q

When are CRP and PCT levels useful?

A

In trending the degree of inflammation, especially in infections that are occult (like osteomyelitis)

A drop in either can also be an indication that antibiotics are no longer needed

59
Q

Which is only present in bacterial inflammation: CRP or PCT?

A

PCT

CRP is produced in the liver in response to IL-6 inflammation of any type

60
Q

What’s the difference between primary and secondary MODS?

A

Primary MODS is organ failure as a direct result of a shock state

Secondary MODS happens when the body is recovering from a shock state and the primed inflammatory system receives a second postinjury insult, dramatically overreacting and leading to a SIRS state

61
Q

Which two mediators are primarily responsible for secondary MODS?

A

IL-1 and TNF

62
Q

Why do release of TNF and IL1 cause endothelial damage?

A

When stimulated by TNF or IL1, endothelial cells change to a pro-inflammatory state and express adhesion molecules, attracting and adhering neutrophils

The injured endothelium also produced NO, leading to a loss of tone

The endothelium loses its ability to express thrombomodulin, leading to clotting

it also becomes more permeable

63
Q

What effect does kinin activation have on SVR?

A

Produces bradykinin, which reduces SVR

64
Q

What is the respiratory burst?

A

When neutrophils adhere to the endothelium, they undergo a respiratory burst, releasing large amounts of ROS

These ROS are extremely damaging to the endothelium and the tissue cells, attacking DNA and leading to tissue necrosis

65
Q

What are the three arachidonic acid metabolites?

A

Prostaglandins

Thromboxanes

Leukotrienes

66
Q

What effect does TXA2 have on vasculature?

PGI2?

A

Powerful vasoconstrictor

Powerful vasodilator

67
Q

Overall, the inflammatory processes at work in MODS cause ____ and _____

A

maldistribution of blood flow

hypermetabolism

68
Q

In septic shock/MODS, why is oxygen uptake so low, despite adequate oxygen delivery?

A
  1. Autoregulation is lost in the capillary beds, because TXA2 causes selective vasoconstriction

Also, injured endothelial cells lose the ability to respond to normal vasodilators

  1. interstitial edema from increased permeability increases the distance between cells and capillaries
  2. Capillaries get clogged d/t thrombi and WBC clumps
69
Q

What causes the hypermetabolism associated with sepsis?

A

Stress response from catecholamines and cortisol

TNG and IL-1

70
Q

What is supply-dependent oxygen consumption

A

The combined decrease in oxygen delivery and increase in oxygen consumption cause an imbalance

Normally oxygen consumption is dependent on cellular needs, since more oxygen is delivered than is needed

In MODS, the amount of oxygen consumed is completely dependent on the amount the circulation is able to deliver

71
Q

What causes reperfusion injury?

A

during ischemic episodes, xanthine dehydrogenase (an enzyme that combines xanthine and NAD to form NADH) is converted to xanthine oxidase (an enzyme that combines xanthine and O2 to form superoxide ROS)

During reperfusion of ischemic tissue, XOD is released en masse into the blood stream and attacks vulnerable tissues

72
Q

What is capillary seal?

A

the term use to indicate that burn shock from increased permeability has ended

73
Q

In addition to loss of the skin layer, why are burn victims so prone to infection?

A

WBCs are altered

Decreased opsonization and phagocytosis

74
Q

What is endotoxemia?

A

translocation of bacteria from the gut into the bloodstream d/t altered gut perfusion

75
Q

What is the minimum acceptable urine output in an infant?

A Child?

An Adolescent?

A

2 ml/kg/hr

1ml/kg/hr

0.5ml/kg/hr

76
Q

What is the most common type of shock in children?

A

Hypovolemic

77
Q

What usually causes hypovolemic shock in children?

A

Dehydration and trauma

78
Q

What is the most common terminal cardiac rhythm in children?

A

Bradycardia

Signals impending collapse

79
Q

When do children with shock become hypotensive?

A

Only when the shock is very, very severe

80
Q

What is the most sensitive indicator of inadequate systemic perfusion in children?

A

lactate

81
Q

Why are children < 2 at increased risk for dehydration?

A

They lack the ability to concentrate urine AND have a larger body surface area in relation to weight

Patho 2 (24 decks)

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