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Pathophysiology 1 MCQ > Shock > Flashcards

Shock Flashcards

1
Q 
Compensatory mechanisms in shock
 Baroreceptor reflexes
 Chemoreceptor reflexes
 Cerebral ischemia
 Reabsorption of tissue fluid
A

Baroreceptor reflexes
Chemoreceptor reflexes
Cerebral ischemia
Reabsorption of tissue fluid

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2
Q 
 Causes of distributive shock:
 sepsis
 spinal cord injury
 allergic reaction triggered by penicillin
 pulmonary embolism
A

sepsis
spinal cord injury
allergic reaction triggered by penicillin

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3
Q 
 Cause of hypovolemic shock:
 acute pancreatitis
 diabetes insipidus
 adrenocortical-failure
 generalized exfoliative dermatitis
A

acute pancreatitis
diabetes insipidus
adrenocortical-failure
generalized exfoliative dermatitis

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4
Q

Immediate compensatory mechanisms induced by fluid depletion (BP: 90 mmHg):
activation of low pressure receptors
renin-angiotensin system
central nervous system ischemic response
activation of peripheral chemoreceptors

A

renin-angiotensin system

activation of peripheral chemoreceptors

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5
Q 
 Causes of cardiogenic shock:
 chronic heart failure
 severe systemic acidosis
 spinal cord injury
 Addison’s disease
A

chronic heart failure

severe systemic acidosis

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6
Q 
 Causes of cardiogenic shock:
 asthma cardiale
 pericardial tamponade
 valvular regurgitation or stenosis
 excessive burn
A

asthma cardiale
pericardial tamponade
valvular regurgitation or stenosis

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7
Q 
 Causes of distributive shock:
 severe systemic acidosis
 Addison’s disease
 chronic heart failure
 spinal cord injury
A

spinal cord injury

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8
Q 
 Characteristic findings in hyperdynamic stage of distributive shock:
 increased cardiac output
 decreased TPR
 normovolemia
 severe hypotension
A

increased cardiac output
decreased TPR
normovolemia

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9
Q

Causative factors of hyperdynamic stage in distributive shock:
accumulation of lactic acid
accumulation of octopamine
hypothermia
increased NO production due to nNOS

A

accumulation of lactic acid
accumulation of octopamine

increased NO production due to nNOS

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10
Q

Criteria for appropriate tissue perfusion:
appropriate cardiac function
normal volume and composition of perfusion fluid (Hb, plasma proteins, corpuscular elements etc)
structurally and functionally intact vasculature
normal lung function

A

appropriate cardiac function
normal volume and composition of perfusion fluid (Hb, plasma proteins, corpuscular elements etc)
structurally and functionally intact vasculature
normal lung function

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11
Q 
 Clinical signs indicating circulatory shock:
 respiratory rate < 7/min
 respiratory rate > 29/min
 redness, fever
 pallor
A

respiratory rate < 7/min
respiratory rate > 29/min
redness, fever
pallor

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12
Q

What is the shock index?
pulse rate (bpm) / RRsys (mmHg)
respiratory rate (1/min) / RRdias (mmHg)
respiratory rate (1/min) / mean arterial pressure (mmHg)
pulse rate (bpm) / mean arterial pressure (mmHg)

A

pulse rate (bpm) / RRsys (mmHg)

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13
Q 
 Indicative finding for shock if the shock index is: 
 ≤ 0,5
 ≤ 1
 = 0,5
 ≥ 1
A

≥ 1

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14
Q 
Type of shock in which in the early phase the pale and sweaty skin is NOT typical?
 septic
 distributive
 hypovolemic
 cardiogenic
A

septic

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15
Q 
 Type of shock in which in the early phase the pale and sweaty skin is typical?
 hypovolemic
 cardiogenic
 septic
 neurogenic
A

hypovolemic
cardiogenic

neurogenic

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16
Q 
 Typical for anaphylaxis: 
 triggered by allergic reaction
 allergen can be food
 systemic reaction of sepsis
 the consequence of vomiting or diarrhea or dehydration
A

triggered by allergic reaction

allergen can be food

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17
Q 
Indicative of irreversible phase of shock:
 weak, suppressible pulse
 gray, cyanotic skin
 comatose stage
 sweating
A

gray, cyanotic skin

comatose stage

18
Q

Mechanisms leading to the irreversible phase of hemorrhagic shock:
accumulation acidic metabolites
microembolization
contraction of precapillary sphincters
increased sympathetic tone

A

accumulation acidic metabolites
microembolization

increased sympathetic tone

19
Q

Changes of laboratory parameters observed in shock:
increased serum alanine and glutamine levels
increased blood urea nitrogen (BUN)
decreased serum lactate level
decreased serum phenylalanine and tyrosine levels

A

increased serum alanine and glutamine levels
increased blood urea nitrogen (BUN)
decreased serum lactate level
decreased serum phenylalanine and tyrosine levels

20
Q

Changes of laboratory parameters observed in shock:
increased serum glucose level
increased serum leu/tyr, leu/phe ratio
increased serum fibrinogen level
decreased levels of acute phase proteins

A

increased serum glucose level
increased serum leu/tyr, leu/phe ratio
increased serum fibrinogen level

21
Q

Factors involved in the mechanism of reperfusion injury:
tissue hypoxia
endothelial cell damage
activation of the renin-angiotensin-aldosteron system (RAAS)
increased sympathetic tone

A

tissue hypoxia

endothelial cell damage

22
Q 
 Compensatory mechanisms in shock EXCEPT:
 immune system activation
 baroreceptor reflex
 chemoreceptor reflex
 cerebral ischemic reflex
A

immune system activation

23
Q 
Hypovolemic shock can be caused by:
 diabetes mellitus
 acute pancreatitis
 pulmonary embolism
 pneumothorax
A

diabetes mellitus

acute pancreatitis

24
Q 
 Obstructive shock can be caused by:
 acute pancreatitis
 pulmonary embolization
 ventricular fibrillation
 pneumothorax
A

pulmonary embolization

pneumothorax

25
Q 
 Obstructive shock can be caused by:
 diabetes mellitus
 pulmonary embolization
 heart tamponade
 pneumothorax
A

pulmonary embolization
heart tamponade
pneumothorax

26
Q 
 Clinical signs characteristic to compensated phase of hypovolemic shock:
 cold, pale extremities
 tachypnea
 RRsys < 70 mmHg
 bradycardia
A

cold, pale extremities

tachypnea

27
Q 
 Clinical signs characteristic to compensated phase of hypovolemic shock:
 acrocyanosis
 decreased capillary filling
 oliguria/anuria
 tissue acidosis
A

acrocyanosis
decreased capillary filling

tissue acidosis

28
Q

Changes of microcirculation in shock:
arterial/arteriolar vasoconstriction
venoconstriction
hemodilution
resistance of post capillary vessels are decreased

A

arterial/arteriolar vasoconstriction

venoconstriction

29
Q

Changes of microcirculation in shock:
hemoconcentration
resistance of post capillary vessels are increased
arterial/arteriolar vasoconstriction
edema

A

resistance of post capillary vessels are increased

arterial/arteriolar vasoconstriction

30
Q 
 Cardiogenic shock can be caused by:
 pneumothorax
 ventricular fibrillation
 rupture of the septum
 embolism
A

pneumothorax
ventricular fibrillation
rupture of the septum
embolism

31
Q

Characteristic metabolic alterations in shock:
increased serum glucose level
increased proteolysis in the muscle
increased glucose uptake by muscle cells
decreased glucose oxidation in muscle cells

A

increased serum glucose level
increased proteolysis in the muscle
increased glucose uptake by muscle cells
decreased glucose oxidation in muscle cells

32
Q

Metabolic alterations in shock:
Increased plasma alanine level
Increased glucose oxidation in muscle cells
Increased pyruvate-, lactate release from muscle cells
Decreased glucose uptake in muscle cells

A

Increased plasma alanine level

Increased pyruvate-, lactate release from muscle cells

33
Q

Metabolic alterations in shock:
increased ketogenesis
decreased glucose oxidation in muscle cells
decreased lipolysis in adipose tissue
decreased serum glucocorticoid level

A

increased ketogenesis

decreased glucose oxidation in muscle cells

34
Q

Factors enhancing the development of ARDS in shock:
over activation of the immune system
alveolar fluid accumulation
bronchoconstriction
tachypnea

A

over activation of the immune system

alveolar fluid accumulation

35
Q

Factors enhancing the development of ARDS in shock:
alveolar membrane injury
increased alveolar membrane permeability
opening of AV-shunts
over activation of the immune system

A

increased alveolar membrane permeability

over activation of the immune system

36
Q

Alterations of kidney function in shock:
decreased GFR
decreased concentrating ability
polyuria
If RR < 60 mmHg, high risk for glomerular damage

A

decreased GFR
decreased concentrating ability

If RR < 60 mmHg, high risk for glomerular damage

37
Q

Alterations of kidney function in shock:
oliguria/anuria
If RR < 60 mmHg, high chance for tubular necrosis
decreased concentrating ability
Na+ retention

A

oliguria/anuria
If RR < 60 mmHg, high chance for tubular necrosis
decreased concentrating ability
Na+ retention

38
Q

Alterations of bowel function in shock:
mesenteric vasoconstriction
increased permeability
bacteria invade into the blood or lymph
increased peristaltic activity

A

mesenteric vasoconstriction
increased permeability
bacteria invade into the blood or lymph

39
Q

Pathological changes of adipose tissue in shock:
Increased lipolysis
Development of hypoxia due to centralization of circulation
Increased formation of ketone bodies in adipose tissue
Increased glucose uptake

A

Development of hypoxia due to centralization of circulation

40
Q 
 Possible causes of the decompensation in the late phase of shock:
 respiratory alkalosis
 metabolic acidosis
 tachypnea
 endothelial injury
A

metabolic acidosis

endothelial injury

Pathophysiology 1 MCQ (16 decks)

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