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Surgery 1 > Surgery 2.1 (1-3) > Flashcards

Surgery 2.1 (1-3) Flashcards

1
Q

Define “shock”

A

Inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function

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2
Q

Can shock be fatal?

A

Yes, if left untreated than shock can be fatal

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3
Q

How quickly should be treated?

A

Shock must be treated and reconised immediately or the patient may die

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4
Q

Is shock something that can be easily diagnosed by simple conditions?

A

Shock can be quite complex, for example while low blood pressure and a rapid pulse or cool palmy skin are symptoms - they are NOT the only symptoms

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5
Q

What causes shock?

A

The inadequate perfusion of of the body’s cells with oxygenated blood

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6
Q

How does the body respond to shock?

A

The insult, whether hemorrhage, injury or infection initiates both a neuroendocrine and inflammatory mediator response

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7
Q

What are the three phases of shock?

A

Compensated shock, decompensated shock and irreversible shock

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8
Q

What happens during “compensated shock”?

A

Vasconstriction, fluid shift to ECF, salt and water conservation by the kidneys

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9
Q

What happens during “decompensated shock”?

A

With tissue injury ongoing and contined hyperfusion, results cell to death.

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10
Q

Can “decompensated shock” be reversed?

A

Yes, with proper resuscitation

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11
Q

What happens during “irreversible shock?

A

Persistant hypoperfusion, fluid resuscitation and vasopressers fail to maintain adequate blood pressure

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12
Q

What are the three manisfestations of shock?

A

Tachycardia (increased heartbeat), tachypnia (rapid breathing) and pallor (pale skin)

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13
Q

What does the “initial insult” cause?

A

Whether caused by hemorrhage, injury or infection - the initial insult initiates both neuroendocrine and inflammatory responses like tachycardia, tachypnia and pallor

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14
Q

What is the psychological effect?

A

The psychological effect is proportional to the degree and length of shock

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15
Q

What causes pale skin (pallor) during shock?

A

Prompt increase in cardiac contractility and peripheral vascular tone

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16
Q

What is the hormonal responses to salt volume during shock?

A

Salt is preserved to maintain water

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17
Q

What is the hormonal responses to intravascular volume during shock?

A

Urine output will be low and increase in urine concentration

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18
Q

What local and microcirculation regions are changed during shock to regulate blood flow?

A

Skin-stomach-kidney-lungs

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19
Q

What is the goal of the neuroendocrine response during shock?

A

To maintain perfusion to the heart and brain

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20
Q

What mechanisms are employed during the neuroendocrine response to shock?

A

Automatic control of peripheral vascular tone and cardiac contractility; hormonal response to stress and volumen depletion and local microregulatory mechanisms that are organ specific and regulate regional blood flow

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21
Q

Where and how are the impulses transmitted during shock to activate the effector response?

A

The impulses are transmitted from the periphery and processed within the central nervous system

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22
Q

What is the initial inciting event for impulses?

A

Loss of circulating blood volume

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23
Q

After the initial inciting event, what other stimuli can occur to start impulses during shock?

A

Pain, hypoxemia, hypercarbia, acidosis, infection, changes in temperature, emotional arousal and hyperglycemia

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24
Q

Define “hypoxemia”

A

Low oxygen of organs and tissues in the body

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25
Q

What are “baroreceptors”?

A

Volumne receptors within atria (RA) of the heart aortic arch and carotid bodies (normally inhibit induction of ANS)

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26
Q

What happens with baroreceptors are “activated”?

A

Their outpout is diminished (disinhibiting the ANS) which leads to sympathetic activation at the vasomotor centres of the brain

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27
Q

What is the function of the “chemoreceptors”?

A

To maintain adequate pressure of fluids

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28
Q

Where are the chemoreceptors found?

A

In the aorta and carotid bodies

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29
Q

What three things are chemoreceptors sensitive to?

A

Changes in oxygen tensions, H ion concentration and CO2 levels

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30
Q

What does stimulation of the chemoreceptors result to?

A

Vasodilation of coronery arteries, slowing of the heart, vasoconstriction of the splanchnic and skeletal circulation

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31
Q

What are the four types of protein and non-protein mediators?

A

Histamine, cytokines, eicosanoids and endothelins

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32
Q

When the protein and non-protein mediators produced?

A

They aproduced at the site of injury

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33
Q

Is the production of protein and non-protein mediators part of inflammatory
respose?

A

Yes

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34
Q

What is the relationship between shock and inflammation?

A

The response of inflammation is parallel to the amount of shock. For example, an increase in severity of inflammation = an increase amount of shock

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35
Q

What is the cardiovasular response to efferent signals?

A

Increase cardiac rate and contraction
- TACHYCARDIA
- Activation of beta 1 adrenergic receptors
- Venous and arterial vasoconstriction
- Activation of alpha-adrenergic receptors

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36
Q

What effect does the catecholamine release have during shock?

A

It increase energy supply due to increase workload

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37
Q

What are the four main effects of the cardiovascular and catecholamine response during shock?

A

Hepatic glycogenolysis and gluconeogenesis
- Increase in muscle glycogenolysis
- Suppression of insulin release
- Increased glucagon release

38
Q

What are the steps of hormonal response during shock

A

Hypothalamic to pituitary to adrenal axis activation

39
Q

What is the pathway for the hormonal response during shock?

A

Shock → Hypothalamus (CRH) → Pituitary (ACTH)
→ Adrenal Cortex (Cortisol)

40
Q

Define “cortisol”

A

A steroid hormone

41
Q

What four things does cortisol do during shock?

A

Acts synergistically with epinephrine and glucagon
- Stimulates gluconeogenesis and insulin resistance
- muscle cell breakdown and lipolysis
- Causes retention of sodium and water by the nephron of
kidneys

42
Q

Define “angiotensin”

A

Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure.

43
Q

Where is aniotensin produced?

A

In the kidneys

44
Q

What is the main function of aniotensin during shock?

A

A potent vasoconstrictor of both splanchnic and peripheral
vascular beds AND stimulator of secretion of aldosterone, ACTH, and ADH

45
Q

Define “aldosterone”

A

Aldosterone, the main mineralocorticoid hormone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland.

46
Q

What function does aldosterone serve during shock

A

Acts on nephron to promote reabsorption of sodium

47
Q

What is “vasopressin”?

A

Vasopressin is a man-made form of a hormone called “anti-diuretic hormone” that is normally secreted by the pituitary gland.

48
Q

What TWO main roles does vasopressin do during shock?

A
  • Induce by epinephrine & Angiotensin 2
  • Vasoconstrictor
49
Q

What is “microcirculation”?

A

Circulation of the blood in the smallest blood vessels.

50
Q

What SEVEN things happen at a microcirculation level during shock?

A

Smaller distal arteriole dilate
- Flow at the capillary level is heterogeneous
- Endothelial swelling
- Aggregation of leukocytes producing diminished capillary perfusion in some weeks
- with transition to decompensated shock, further vasodilatation of small arterioles, with progressive loss of vasomotor tone in entire vascular bed extravascular or extracellular space into capillaries increase circulating volume
- Too much dilatation of vessels absent or lost control of fluid pressure super inflammation
- Decrease in capillary perfusion diminished capillary hydrostatic pressure promote influx of fluid from

51
Q

What is “Prolonged Hemorrhagic Shock”?

A

Shock due to massive bleeding

52
Q

What happens during prolonged hemorrhagic shock?

A

Transcapillary influx of interstitial fluid into vascular space

53
Q

What is the effect of the depolarization of cell membrane at a microcirculation level during shock?

A

Depolarization of cell membrane results in uptake of water
and sodium (cell swelling) and loss of potassium from the
cell

54
Q

What happens to oxidative phosphorylation during shock?

A

It decreases

55
Q

Does lactic acid and inorganic phosphate increase or decrease during shock

A

Increase

56
Q

Does pH increase or decrease during shock

A

Decrease

57
Q

What are four effects of the decrease in pH during shock?

A

Altered activity of cellular enzymes in cellular gene
expression
- Impaired cellular metabolic pathway
- Impeded cell membrane ion exchange
- Changes in cellular calcium metabolism and calcium-
mediated cellular signaling

58
Q

What are the first ultrastructural changes during shock?

A

Endoplasmic reticulum swelling

59
Q

What other ultrastructural changes occur?

A

Mitochondrial and cell swelling, and
- cellular membrane potential impairment

60
Q

What effect does metabolic acidosis have during shock?

A
  • Oxyhemoglobin dissociated curve is shifted to the right
  • Production of erythrocyte 2,3 DPG
61
Q

What is the result of the oxyhemoglobin dissociated curve shifting to the right?

A

RBCs cannot release O2 to the tissues)

62
Q

What is the result of the production of erythrocyte 2,3 DPG?

A

This promotes promotes O2 availability to tissues

63
Q

What is “epineprhine”?

A

Epinephrine, also known as adrenalin or adrenaline, is a hormone, neurotransmitter and medication. Epinephrine is normally produced by both the adrenal glands and certain neurons

64
Q

During shock, epinehrine do what?

A

Produce more glucose and ATP

65
Q

What is “glycogenolysis”?

A

Glycogenolysis, process by which glycogen, the primary carbohydrate stored in the liver and muscle cells of animals, is broken down into glucose to provide immediate energy and to maintain blood glucose levels during fasting.

66
Q

What is the effect of epineprhine during shock?

A

Starts the process of Hepatic glycogenolysis
- Starts the process of glucogenesis
- Starts the process of ketogenesis
- Helps skeletal muscle protein breakdown
- Starts the process of adipose tissue lipolysis
- Induces further release of glucagon (epinephrine)

67
Q

List five things the release of glucagon does during shock

A

Inhibits pancreatic B cell insulin release
- Forces glucose mobilization
- Helps with lipolysis (the breakdown of lipids)
- Helps with protein breakdown
- Negative nitrogen

68
Q

Define “catabolic state of injury”

A

The early state of injury

69
Q

Define “anabolic state of injury”

A

The recovery stage of injury (like in a week)

70
Q

List five cytokines released during shock

A

TNF-alpha; Interleukin-IB; Interleukin-2; Interleukin-6; and Interleukin-10

71
Q

What is one of the earliest cytokines released?

A

TNF-alpha

72
Q

When is the peak level for TNF-alpha release?

A

About 90 minutes from stimulation

73
Q

What is TNF-alpha produced by?

A

Monocyte
- Macrophages
- T cells

74
Q

What is TNF-alpha induced by?

A

Bacteria
- Endotoxin
- Hemorrhage
- Ischemia

75
Q

What are five effects of TNF-alpha release during shock?

A

Peripheral vasodilation
- Stimulate a wide array of cellular metabolic Changes
- Activate release of other cytokines
- Induce procoagulant activity
- muscle protein breakdown and cachexia

76
Q

There is a cytokine released with similar results as TNF-alpha, what is it?

A

Interleukin-IB

77
Q

What is the lifespan of Interleukin-B?

A

Very short (6 minutes)

78
Q

What are the effects of the release of Interleukin-B during shock?

A
  • Febrile response to injury by activating prostaglandins
    (hypothalamus)
  • Anorexia by activating satiety center
  • Augments secretion of ACTH, glucocorticoids and beta- endorphins
  • Stimulate other cytokines such as IL-2, IL-4, IL-6, IK-8, GM CSF and IFN-y
79
Q

How long does it take for the peak level of Interleukin-2?

A

90 minutes from stimulation (and return to baseline
within 4 hours)

80
Q

What is Interleukin-2 produced by?

A

Activated T-cells
- NK cells
- other lymphocytes subpopulation

81
Q

What are the effects of Interleukin-2?

A

Promotes shock induced tissue injury and development
of shock
- Depression of immune function after Hemorrhage

82
Q

What is Interleukin-6 induced by?

A

Hemorrhage; shock; major operative procedure; and trauma

83
Q

What are the effects of Interleukin-6?

A
  • Contribute to lung, liver and gut injury after hemorrhage
    shock
  • Role in development of alveolar damage and ARDS
  • Mediators of hepatic acute phase response to injury
  • Enhance expression and activity of complement, C-
    reactive protein, fibrinogen, amyloid A, a-antitrypsin
  • Promote neutrophil activation
84
Q

Why is Interleukin-10 unique as a cytokine?

A

It is the most important anti-inflammatory cytokine

85
Q

What is Interleukin-10 induced by?

A

Shock and trauma

86
Q

What is Interleukin-10 secreted by?

A

Monocyte
- Macrophages
- T cells

87
Q

What does Interleukin-10 inhibit?

A

Pro-inflammatory cytokines secretion
- Oxygen radical Production
- Adhesion molecule expression
- Lymphocyte Activation

88
Q

What is the main effect of Interleukin-10?

A

Immunosuppressive properties

89
Q

How is the “Compliment Cascade” activated?

A

injury
- shock
- Severe infection

90
Q

What is the effect of the compliment cascade?

A
  • Contributes to host defense and proinflammatory
    activation and joins epinephrine, proinflammatory substances
  • Contribution in development of organ dysfunction ARDS and MODS
  • Potent mediators: C3a, C4a and C5a = ↑ Vascular
    permeability
  • Smooth muscle contraction
  • Histamine and arachidonic acid by product release
  • Adherence of neutrophils to vascular endothelium
91
Q

What are “neutrophils”?

A

Neutrophilic white blood cells

92
Q

Why are they signficant?

A

Neutrophils are the first cell to be recruited to site of injury

Surgery 1 (7 decks)

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