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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
why is anaphylaxis life-threatening?
hypo-perfusion due to vasodilation & fluid shift
26
s&s of anaphylactic shock
cyanosis
27
1st s&s of allergy
itching, redness, swelling
28
progressing s&s of allergy
SOB due to bronchoconstriction, tachycardia, swelling away from the site
29
treatment of anaphylaxis
1. adrenergic (vasoconstriction, bronchodilation, optimize CO, suppress histamine release) 2. antihistamines 3. glucocorticoids 4. ABC's 5. stop causative agent
30
which adrenergic is the 1st line treatment for anaphylaxis, route, and frequency?
epinephrine; IM mid-anterior lateral thigh; every 5 min x 3 dose max
31
what is benadryl (diphenhydramine) and how is it given usually
antihistamine; IV
32
what is hydrocortisone/methylprednisolone/prednisone and how is it given usually?
glucocorticoids; IV *prednisone PO (continued x3 days)
33
how is ABC taken care of in anaphylaxis treatment?
``` bronchodilator intubation oxygen iv access iv fluid resuscitation more adrenergic (racemic epinephrine, catecholamines) ```
34
what is ventolin (salbutamol) | when used in anaphylaxis treatment?
bronchodilator
35
how much oxygen is given by a non-rebreather mask to ensure ABC?
15L
36
How much fluid is given to ensure ABC in adults/peds?
NS 500ml boluses (peds 20ml/kg)
37
what are the subtypes of circulatory shock?
``` hypovolemic (low blood "volume") cardiogenic shock (low CO) obstructive (heart cant be filled properly) ```
38
what is circulatory shock?
hypoperfusion of organs leads to an insufficient supply of nutrients and O2.
39
how much volume is lost in hypovolemic shock?
20% or more
40
what are the causes of hypovolemic shock?
blood losses (trauma, burns, surgery) or low extracellular fluid (severe dehydration)
41
how does blood loss lead to hypovolemic shock?
initial loss is compensated by SNS to maintain perfusion => exhaustion
42
initial s&s of hypovolemic shock
tachycardia, thirst, cool peripheries (lead to vasoconstriction)
43
progressing s&s of hypovolemic shock
hypotension, thready 細細的pulse, low RR, cool pale skin, oliguria (<20ml/hr), irritability, restlessness, altered LOC, edema, electrolyte imbalances, hyperglycemia
44
vasoconstriction _______ hypoxia
accelerates
45
3 treatment of hypovolemic shock and what to monitor
colloids (expand plasma volume) crystalloids blood products (whole blood, packed red blood cells) monitor: perfusion (overload?) renal function, allergic reactions, clotting difficulties
46
what are four examples of colloids drugs used to treat hypovolemic shock
albumin 5% or 25% | dextran and hetastarch
47
What are the five main complications of shock?
1. lung injury (aka. Acute Respiratory Distress Syndrome) 2. renal injury 3. GI injury 4. Multiple organ dysfunction 5. DIC
48
What are the treatments for the five main complications of shock?
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
Describe the process of lung injury as a complication of shock.
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
Acute Respiratory Distress Syndrome can lead to _______
respiratory acidosis (e.g. sepsis), lung infection (direct infection), DIC
51
in cardiogenic shock, low CO leads to
high afterload, high preload, high peripheral resistance, activation of SNS (compensation), low coronary artery perfusion, severe inflammatory response
52
Examples of the causes of cardiogenic shock are _____.
myocardial infarction (STEMI), arrhythmias, cardiomyopathy, severe valvular malfunction, congenital heart defect, open heart surgery injury, myocardial depression due to septic shock, heart failure
53
s&s of cardiogenic shock
hypoperfusion (cyanosis, oliguria, loc changes) low BP with narrow PP (low CO & vasoconstriction) high jugular venous pulse(high volume in circulation)
54
treatment of cardiogenic shock
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
intra-aortic balloon pump inflate during ________ and deflate during _________.
inflate during ventricular diastole deflate before ventricular systole *create a suction effect in the aorta that increase blood flow
56
what is obstructive shock
mechanical obstruction to blood flow through central circulation
57
Two examples of the causes of obstructive shock are _____ & ____.
large embolism and cardiac tamponade (heart x stretch out fully --> hypotension)

NURS216B (6 decks)

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