Support in Trauma Flashcards

1
Q

define trauma

A

injury or wound to lining tissue caused by an extrinsic agent

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2
Q

what are the immediate vs potential later features of physical trauma

A

i - intravascular fluid loss, extravascular volume, impaired breathing
l - starvation, infection, inflammation

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3
Q

what are the three phases of mortality from trauma

A

1 - shock - 2-6hours, secret catecholamines, cytokines and cortisol - tachycardia, hypovol, peripheral vasoconstriction

2 - catabolic - 2 days after - catecholamines, glucagon, ACTH = cortisol
increased metabolic rate, o2 consumption, glycolysis, lipolysis

3 - anabolic state 3-8days after - restoration of body

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4
Q

what are the primary aims of treatment of each phase of mortality form trauma

A

1 - stop bleeding prevent infection

2 - avoid sepsis provide adequate nutrition

3 - adequate nutrition (risk of refeeding syndrome)

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5
Q

describe the inflammatory response at a trauma site

A

bacteria and pathogen enter would
platelet release clotting factors
mast cells secrete factors for vasodilation
neutrophils/macrohages = pagocytosis
macrophages - release cytokines = attract immune cells and inflammatory response

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6
Q

what is systemic capillary leak

A

injury = inflammatory mediator risk - lose water, sodium, cl, albumin and energy substrates

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7
Q

what are the 5 cardinal signs of inflammation

A
heat
redness
swelling
pain
loss of function
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8
Q

what are the endocrine effects of cytokines

A

mediate secretion of catabolic hormones eg IL-1/TNF-a and ACTH = cortisol
this increases energy release

mediate inhibition of anabolic hormones eg dec growth and insulin

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9
Q

what is the delivery of energy to the brain

A

can’t store glycogen so uses glucose
need constant glucose and o2
120g/day - will not survive longer than 2 hours without (can use ketones)

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10
Q

how are the kidneys and liver different in survival for energy from the brain

A

liver/kidney can gluconeogenesis = survive hours without blood supply

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11
Q

what are the phases of metabolic repose to trauma

A

1 - glycogenolysis - glycogen to glucose
2 - gluconeogenesis - amino acid -> glucose and lactate production
3 - lipolysis and ketogenesis - free fatty acid - acetyl CoA = acetoacetate and hydroxybutyrate (ketone bodies)

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12
Q

what is the effect on ketones of water and electrolytes

A

diuretic so loss of both

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13
Q

describe trauma protein turnover

A

new protein reduces

skeletal muscle proteolysis increases = increased FFA, ammonia and nitrogen loss

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14
Q

what is a danger with increased trauma protein turnover

A

damage to respiratory muscles = retentions of secretions = pneumonia risk

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15
Q

describe lactate production in hypoxia

A

reduced o2

pyruvate reduced to lactate - becomes toxic = tissue hypoxia

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16
Q

describe how lactate is a prognostic marker for trauma

A

failure of blood lactate to return to normal - poor prognosis
if blood lactate is higher or equal to 5mmol/L = 100% mortality

17
Q

what is the deathly cycle of high lactate

A

mito failure from hypoxia = amnerobic glycolysis positive feedback

18
Q

what is the difference between primary and secondary malnutrition

A

1 - protein calorie undernutrition (starvation)
dietary deficiency

2 - appetite suppressed, absorption and utilisation inadequate
increased demand

19
Q

what are the consequences of malnutrition

A

negative nitrogen balance - muscle wasting - cellular dysfunction

20
Q

describe refeeding syndrome

A

excessive feeding after malnourishment
shift from fat to crab metabolism - insulin secretion and hypophosphateamia, reduced electrolytes
fatigue confusion inability toi breathe, coma and death

21
Q

describe the mutation mechanism of CF

A

CFTR transmembrane cAMP Cl dependant channel mutation

stops secretion of and absorptive of epithelial cells - airways, pancreas, liver vas deferens

22
Q

what are the consequences of CF

A

lack free flowing mucus - malnutrition as no digestive enzymes, lung diseases and infection = inflammation

23
Q

how does CF affect the GIT

A

meconium - intestinal failure
hepatobiliary disease
pancreatic cyst and exocrine insufficiency (low insulin/lipase/proteases)
poor appetite low weight

24
Q

what is the treatment of CF

A

respiratory disease - physio exercise, steroids, antibiotics and mucolytics - deceased infection and inflammation

GI - creon (pancreatic enzyme replacement), nutritional supplements
maintain body weight and avoid catabolism