Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > week 13: multiple interacting systems > Flashcards

week 13: multiple interacting systems Flashcards

1
Q

shock

A

condition during which the cardiovascular system fails to perfuse the tissues adequately; causes general and widespread impairment of cellular metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

common pathways in all types of shock

A

Impairment of cellular metabolism as a result of decreased delivery of oxygen and nutrients
Frequently coupled with an increased demand and consumption of oxygen and nutrients
Decreased removal of cellular waste products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

classes of shock

A

cardiogenic, neurogenic or vasogenic, anaphylactic, septic, hypovolemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

shock cm

A

Weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath, and generally “feeling sick”
Decreased blood pressure, cardiac output, and urinary output
Increased respiratory rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

shock tx

A

Oxygenation: Absolute necessity in all shock states
Correct or remove underlying cause
Provide supportive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cardiogenic shock causes

A

myocardial ischemia, myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cardiogenic shock

A

Inability of the heart to pump adequate blood to tissues and end organs from any cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

as cardiac output decreases compensatory adaptive responses are activated:

A

Renin-angiotensin, neurohormonal, and sympathetic nervous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cardiogenic shock cm

A

Chest pain, dyspnea, and faintness, along with feelings of impending doom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cardiogenic shock hallmarks

A

Tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cardiogenic shock tx

A

Intraaortic balloon counterpulsation (IABP) or percutaneous or ventricular assist devices (VADS)
Fibrinolytic therapies: To disintegrate coronary thrombus
Percutaneous interventions: Balloon angioplasty, stent placement, and thrombectomies
Surgery: Coronary artery bypass, ventriculoplasty, or heart transplantation
Cardiosupportive drug and fluid regimens
Continuous hemodynamic monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hypovolemic shock

A

insufficient intravascular fluid volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

causes of hypovolemic shock include

A

hemorrhage, burns, emesis, diuresis, diaphoresis, diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what compensates hypovolemic shock

A

compensatory vasoconstriction, increased systemic vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypovolemic shock clinical manifestations

A

poor skin turgor, thirst, oliguria
low systemic and pulmonary pressure
rapid heart rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hypovolemic shock tx

A

prompt control of hemorrhage

fluid replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

neurogenic shock

A

Widespread vasodilation occurs from an imbalance between parasympathetic and sympathetic stimulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

neurogenic shock causes persistent

A

vasodilation, and creates relative hypovolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

causes of neurogenic shock

A

trauma, severe pain and stress, anesthesia, and depressant drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

neurogenic shock clinical manifestations

A

very low SVR, bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

neurogenic shock tx

A

decrease pain level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

anaphylactic shock

A

outcome of widespread hypersensitivity to an allergen that triggers a reaction known as anaphylaxis

23
Q

widespread hypersensitivity rxn leads to

A

vasodilation, peripheral pooling, relative hypovolemia

24
Q

anaphylactic shock cm

A

Anxiety, difficulty breathing, gastrointestinal (GI) cramps, edema, hives (urticaria), sensations of burning or itching of the skin, fever, and hemolysis.

25
Q

anaphylactic shock tx

A

Begins with the removal of the antigen, if possible.
Epinephrine: Decreases mast cell and basophil degranulation, causing vasoconstriction; reverses airway constriction.
Intravenous (IV) volume expanders (lactated Ringer solution): Reverses relative hypovolemia.
Antihistamines and steroids: Stops inflammatory reaction.

26
Q

septic shock most common infection sites

A

lungs, bloodstream, intravascular catheter, intraabdominal, urinary tract, and surgical wound.

27
Q

septic shock progression

A

systemic inflammatory response syndrome
sepsis
severe sepsis
septic shock

28
Q

septic shock cm

A

Persistent low arterial pressure, low tissue perfusion, low SVR from vasodilation, and an alteration in oxygen extraction by all cells.

29
Q

septic shock tx

A

Check lactate level; obtain blood cultures; start antibiotic and vasopressor medications; implement fluid challenge; and achieve goals for blood pressure, central venous pressure, and central venous oxygen saturation.

30
Q

macule

A

flat circumscribed area that is a change in the colour of the skin less than 1cm diameter

31
Q

patch

A

flat, nonpalpable irregular shaped molecule more than 1cm diameter

32
Q

papule

A

an elevated, firm, circumscribed area less than 1cm

33
Q

plaque

A

elevated, firm, and rough lesion with flat top surface area greater than 1cm

34
Q

benign skin tumours

A

seborrheic keratosis
actinic keratosis
nevi

35
Q

malignant skin tumours

A

basal cell cercinoma
squamous cell carcinoma
malignant melanoma

36
Q

first degree burns

A

A.K.A. partial (superficial) thickness injury involving only epidermis
Skin maintains water vapor and bacterial barrier functions

37
Q

first degree burns s&s

A

Local pain and erythema, no blisters for ~24hrs

Extensive burn may cause chills, headache, localized edema and N &

38
Q

superficial partial sickeness second degree burns

A

fluid-filled blisters appear immediately, pain due to exposures of nerve endings to air if blisters break open
heal in 3-4 weeks if well nourished and no complications
usually no scar (depends on skin type)

39
Q

deep partial thickness second degree burns

A

usually involves entire dermis (hair follicles are preserved)
looks waxy white surrounded by superficial partial-thickness injury
usually can’t distinguish between this burn and 3rd degree until day 7 when skin buds appear
take weeks to heal
tx. autograft
lots of scarring
potential for infection

40
Q

third degree burns

A

A.K.A. full thickness burns
Destruction of entire epidermis, dermis & often underlying tissues (subcutaneous, muscle, bone)
Elasticity of dermis is destroyed (dry, leathery appearance)
Edema - distal circulation may be affected in areas of circumferential burns so…
Escharotomies to relieve pressure - painless d/t destroyed nerve endings

41
Q

severity of burns is affected by

A

age, medical hx, extent and depth of injury, involved body area

42
Q

within several hours, capillar integrity is lost due to the release of

A

histamin and prostaglandin

43
Q

burns exceeding 20% TBSA are considered

A

major

44
Q

three main areas of burn patho

A 
cardiovascular and systemic response
cellular response
- metabolic
- immunologic
evaporative water loss
45
Q

fluid passes from intravascular system to

A

interstitial system

46
Q

hallmark of burn shock

A

inadequate perfusion

47
Q

basal fluid replacements per day

A

1500ml/day/m2 body surface area =

24 hour requirement

48
Q

evaporated water loss

A

(25 + % total body surface area burn)

X (2 m2 body surface area) = ml/hr

49
Q

total hourly maintenance fluids

A

basal fluid requirements per day / 24 hours + evaporated water loss per hour = ml/hr

50
Q

end point of burn shock

A

ndividual has adequate urine output for 2 hours + (30 ml/hr)

51
Q

cellular effects of burns

A

altered cell membrane permeability, loss of normal electrolyte homeostasis - contributes to shock
Transmembrane changes also occur in undamaged cells

52
Q

immunologic response to burns

A

result is immunosuppression with inc. susceptibility to potentially fatal systemic burn wound sepsis
Cytokines are identified in immed. postburn period which contribute to the immune response as well as healing
Cortisol is released as a stress response which can increase risk for infection

53
Q

three elements of burns survival

A

meticulous wound management
adequate fluids and nutrition
earlier surgical excision and grafting

54
Q

burns dx and tx

A 
Rule of Nines
BUN, creatinine clearance
urine output
CBC, electrolytes
Narcotics for pain relief
Remove rings and jewelry ASAP
O2 administration
Hydration

Pathophysiology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions