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NURS216B > Shocks II > Flashcards

Shocks II Flashcards

1
Q

What are the 2 types of shocks?

A

distributive

circulatory

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2
Q

What are the 3 subtypes of distributive shock?

A 
septic shock (pathogen)
anaphylactic shock (allergen)
neurogenic shock (injury)
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3
Q

examples of allergen

A

drugs
foods
venom
latex

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4
Q

how long after exposure will one experience s&s

A

15 minutes

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5
Q

(Drugs) _____ has the highest allergic reaction, while ____ has the lowest allergic reaction.

A

whole blood highest

albumin lowest

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6
Q

What’s the first stage of allergen-triggered inflammation?

A

vasodilation and increased capillary flow

s&s: redness due to histamine

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7
Q

what is the main mediator of allergen-triggered inflammation? (target treatment)

A

histamine

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8
Q

where does histamine bind to cause vasodilation?

A

HI receptors

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9
Q

why does too much nitric oxide lead to epithelial damage?

A

they bind with superoxide radicals produced by WBC, which then becomes toxic reactive nitrogen.

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10
Q

what happens next after vasodilation caused by histamine

A

you see an increased vascular permeability
plasma 血漿 leakage into tissues (edema)
stagnation 停待 of overall blood flow (less blood volume already) due to the low-pressure system caused by vasodilation

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11
Q

heat, redness, swelling, pain, loss of function, clotting are s&s of

A

Cardinal signs of inflammation

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12
Q

why inflammation can lead to clotting?

A

blood stasis + platelet activating factor released from mast cells

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13
Q

what is the second stage of inflammation

A

phagocyte mobilization

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14
Q

what is happening in the cellular stage

A

increased WBC in tissue for adhesion, margination, transmigration, chemotaxis

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15
Q

in chemotaxis, ______ arrives rapidly and ____ arrives slowly

A

neutrophils; monocytes

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16
Q

what are the three processes for phagocytosis

A

recognition of microbe (antigen)
endocytosis (phagosome +microbe = phagolysosome)
secretion of enzymes and oxygen radicals to eliminate

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17
Q

what are the treatments for inflammation

A
  1. antihistamines
  2. leyukotrine modifiers
  3. glucocorticoids
  4. Xolair (Omalizumab)
  5. immunotherapy
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18
Q

The function of Xolair (Omalizumab) in inflammation and route

A

reduces igE & SC

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19
Q

The function of glucocorticoid in inflammation

A

inhibit immune response and stabilize mast cell

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20
Q

state the acute progressive allergic reaction

A

allergy –> anaphylaxis –> anaphylactic shock

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21
Q

in the stage of allergy, ____ cell ____ and leads to _____

A

mast; degranulate; histamine

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22
Q

whats the primary mediator for anaphylaxis

A

igE

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23
Q

s&s of anaphylaxis

A

urticaria 尋麻疹
angioedema
laryngeal edema

24
Q

in anaphylactic shock, up to ___% of volume loss within ___ min.

A

35%; 10 min

25
Q

why is anaphylaxis life-threatening?

A

hypo-perfusion due to vasodilation & fluid shift

26
Q

s&s of anaphylactic shock

A

cyanosis

27
Q

1st s&s of allergy

A

itching, redness, swelling

28
Q

progressing s&s of allergy

A

SOB due to bronchoconstriction, tachycardia, swelling away from the site

29
Q

treatment of anaphylaxis

A
  1. adrenergic (vasoconstriction, bronchodilation, optimize CO, suppress histamine release)
  2. antihistamines
  3. glucocorticoids
  4. ABC’s
  5. stop causative agent
30
Q

which adrenergic is the 1st line treatment for anaphylaxis, route, and frequency?

A

epinephrine; IM mid-anterior lateral thigh; every 5 min x 3 dose max

31
Q

what is benadryl (diphenhydramine) and how is it given usually

A

antihistamine; IV

32
Q

what is hydrocortisone/methylprednisolone/prednisone and how is it given usually?

A

glucocorticoids; IV

*prednisone PO (continued x3 days)

33
Q

how is ABC taken care of in anaphylaxis treatment?

A 
bronchodilator
intubation
oxygen 
iv access
iv fluid resuscitation
more adrenergic (racemic epinephrine, catecholamines)
34
Q

what is ventolin (salbutamol)

when used in anaphylaxis treatment?

A

bronchodilator

35
Q

how much oxygen is given by a non-rebreather mask to ensure ABC?

A

15L

36
Q

How much fluid is given to ensure ABC in adults/peds?

A

NS 500ml boluses (peds 20ml/kg)

37
Q

what are the subtypes of circulatory shock?

A 
hypovolemic (low blood "volume")
cardiogenic shock (low CO)
obstructive (heart cant be filled properly)
38
Q

what is circulatory shock?

A

hypoperfusion of organs leads to an insufficient supply of nutrients and O2.

39
Q

how much volume is lost in hypovolemic shock?

A

20% or more

40
Q

what are the causes of hypovolemic shock?

A

blood losses (trauma, burns, surgery) or low extracellular fluid (severe dehydration)

41
Q

how does blood loss lead to hypovolemic shock?

A

initial loss is compensated by SNS to maintain perfusion => exhaustion

42
Q

initial s&s of hypovolemic shock

A

tachycardia, thirst, cool peripheries (lead to vasoconstriction)

43
Q

progressing s&s of hypovolemic shock

A

hypotension, thready 細細的pulse, low RR, cool pale skin, oliguria (<20ml/hr), irritability, restlessness, altered LOC, edema, electrolyte imbalances, hyperglycemia

44
Q

vasoconstriction _______ hypoxia

A

accelerates

45
Q

3 treatment of hypovolemic shock and what to monitor

A

colloids (expand plasma volume)
crystalloids
blood products (whole blood, packed red blood cells)

monitor: perfusion (overload?) renal function, allergic reactions, clotting difficulties

46
Q

what are four examples of colloids drugs used to treat hypovolemic shock

A

albumin 5% or 25%

dextran and hetastarch

47
Q

What are the five main complications of shock?

A
  1. lung injury (aka. Acute Respiratory Distress Syndrome)
  2. renal injury
  3. GI injury
  4. Multiple organ dysfunction
  5. DIC
48
Q

What are the treatments for the five main complications of shock?

A
  1. lung injury: supportive, keep alveoli open via “positive end-expiratory pressure”
  2. renal injury: IV fluids, diuretics
  3. GI injury: enteral (NG tube), PPI, H2 receptor blockers
  4. Multiple organ dysfunction
  5. DIC: stage-dependent
49
Q

Describe the process of lung injury as a complication of shock.

A

An epithelial cell dysfunction/injury leads to pulmonary edema, dysfunction of surfactant, thickening of the alveolar membrane.

STILL Low gas exchange despite 02 therapy => if alveoli are not open, inflammation will be activated = more cellular damage

50
Q

Acute Respiratory Distress Syndrome can lead to _______

A

respiratory acidosis (e.g. sepsis), lung infection (direct infection), DIC

51
Q

in cardiogenic shock, low CO leads to

A

high afterload, high preload, high peripheral resistance, activation of SNS (compensation), low coronary artery perfusion, severe inflammatory response

52
Q

Examples of the causes of cardiogenic shock are _____.

A

myocardial infarction (STEMI), arrhythmias, cardiomyopathy, severe valvular malfunction, congenital heart defect, open heart surgery injury, myocardial depression due to septic shock, heart failure

53
Q

s&s of cardiogenic shock

A

hypoperfusion (cyanosis, oliguria, loc changes)

low BP with narrow PP (low CO & vasoconstriction)

high jugular venous pulse(high volume in circulation)

54
Q

treatment of cardiogenic shock

A

optimize CO (reduce pre+afterload, optimize contractility)

reduce volume (diuretics): spironolactone, furosemide)

vasodilation (caution with hypotension): Direct-acting vasodilators, ACE inhibitors, Adrenergic antagonists, Calcium channel antagonists)

improve contractility (caution with vasoconstriction): p inhibitors, catecholamines*)

55
Q

intra-aortic balloon pump inflate during ________ and deflate during _________.

A

inflate during ventricular diastole
deflate before ventricular systole

*create a suction effect in the aorta that increase blood flow

56
Q

what is obstructive shock

A

mechanical obstruction to blood flow through central circulation

57
Q

Two examples of the causes of obstructive shock are _____ & ____.

A

large embolism and cardiac tamponade (heart x stretch out fully –> hypotension)

NURS216B (6 decks)

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