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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
```       Obstructive shock can be caused by:       diabetes mellitus       pulmonary embolization       heart tamponade       pneumothorax ```
      pulmonary embolization       heart tamponade       pneumothorax
26
```       Clinical signs characteristic to compensated phase of hypovolemic shock:       cold, pale extremities       tachypnea       RRsys < 70 mmHg       bradycardia ```
      cold, pale extremities |       tachypnea
27
```       Clinical signs characteristic to compensated phase of hypovolemic shock:       acrocyanosis       decreased capillary filling       oliguria/anuria       tissue acidosis ```
      acrocyanosis       decreased capillary filling       tissue acidosis
28
      Changes of microcirculation in shock:       arterial/arteriolar vasoconstriction       venoconstriction       hemodilution       resistance of post capillary vessels are decreased
      arterial/arteriolar vasoconstriction |       venoconstriction
29
      Changes of microcirculation in shock:       hemoconcentration       resistance of post capillary vessels are increased       arterial/arteriolar vasoconstriction       edema
      resistance of post capillary vessels are increased |       arterial/arteriolar vasoconstriction
30
```       Cardiogenic shock can be caused by:          pneumothorax          ventricular fibrillation          rupture of the septum          embolism ```
         pneumothorax          ventricular fibrillation          rupture of the septum          embolism
31
      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
      increased serum glucose level       increased proteolysis in the muscle       increased glucose uptake by muscle cells       decreased glucose oxidation in muscle cells
32
      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
      Increased plasma alanine level       Increased pyruvate-, lactate release from muscle cells
33
      Metabolic alterations in shock:       increased ketogenesis       decreased glucose oxidation in muscle cells       decreased lipolysis in adipose tissue       decreased serum glucocorticoid level
      increased ketogenesis |       decreased glucose oxidation in muscle cells
34
      Factors enhancing the development of ARDS in shock:       over activation of the immune system       alveolar fluid accumulation       bronchoconstriction       tachypnea
      over activation of the immune system |       alveolar fluid accumulation
35
      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
      increased alveolar membrane permeability       over activation of the immune system
36
      Alterations of kidney function in shock:       decreased GFR       decreased concentrating ability       polyuria       If RR < 60 mmHg, high risk for glomerular damage
      decreased GFR       decreased concentrating ability       If RR < 60 mmHg, high risk for glomerular damage
37
      Alterations of kidney function in shock:       oliguria/anuria       If RR < 60 mmHg, high chance for tubular necrosis       decreased concentrating ability       Na+ retention
      oliguria/anuria       If RR < 60 mmHg, high chance for tubular necrosis       decreased concentrating ability       Na+ retention
38
      Alterations of bowel function in shock:       mesenteric vasoconstriction       increased permeability       bacteria invade into the blood or lymph       increased peristaltic activity
      mesenteric vasoconstriction       increased permeability       bacteria invade into the blood or lymph
39
      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
      Development of hypoxia due to centralization of circulation
40
```       Possible causes of the decompensation in the late phase of shock:       respiratory alkalosis       metabolic acidosis       tachypnea       endothelial injury ```
metabolic acidosis endothelial injury

Pathophysiology 1 MCQ (16 decks)

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