Shock and tranfusion II Flashcards
Da-Nang lung refers to
A. ARDS
B. TRALI
C. Trauma associated cardiac overload
D. Pulmonary Embolism
ans A -
Da-nang Lung or shock lung was later identified as ARDS.
Which of the following is most sensitive to the change in intravascular volume
A. Carotid sinus pressure receptors
B. Atrial baroreceptors
C. Aortic arch baroreceptors
D. Chemoreceptors in aorta
ans B -
Baroreceptors
- Atrial baroreceptors are sensitive to change in both chamber pressure and wall stretch.
- they are activated with low volume hemorrhage or mild reductions in right atrial pressure.
Baroreceptors in aortic arch and carotid bodies respond to alterations in pressure or stretch of the arterial wall, they respond to much larger reductions in intravascular volume or pressure.
Normally - these receptors have a continuous inhibitory outflow to the sympathetic system.
When activated by decrease in intravascular volume they diminish their output and thus allow sympathetic activity to take place.
Which of the following is true regarding the chemoreceptor response -
A. Vasodilation of coronary arteries
B. Vasoconstriction of splanchnic circulation
C. Tachycardia
D. vasoconstriction of skeletal muscle circulations
ans C -
Chemoreceptors in aorta and carotid bodies are sensitive to -
- changes in Oxygen tension
- changes in H+ ion concentration
- changes in carbon dioxide levels
Stimulation of these chemoreceptors leads to
- vasodilation of the coronary arteries
- slowing down of HR
- vasoconstriction of splanchnic and skeletal muscle circulation.
Venous capacitance is increased in which of the following etiologies of shock
A. Cardiogenic
B. Septic
C. Neurogenic
D. Cardiogenic
ans B -
Hypovolemic shock - CO decreases SVR increases Venous capacitance decreases CVP decreases
Septic shock - CO increases, SVR decreases Venous capacitance increases CVP decrease/increase
Cardiogenic shock - CO decreases dramatically SVR increases dramatically no change in venous capacitance CVP raised
Neurogenic shock - CO increases SVR decreases Venous capacitance no change CVP decreased
Catecholamine levels peak after
A. within minutes
B. 6 hours from injury
C. 12 hours from injury
D. 24 hours from injury
ans D -
Catecholamine levels peak within 24 to 48 hours of injury and then return to baseline.
Persistent elevation beyond this point of time suggests ongoing injury or noxious stimulation.
Majority of the norepinephrine produced in sympathetic response to injury is derived from -
A. Adrenal medulla
B. Pituitary
C. Neuroendocrine system
D. Synapses of the sympathetic nervous system
ans D-
Epinephrine - majority from the adrenal medulla.
Norepinephrine - from the synapses of the sympathetic nervous system.
T/F
During severe hypovolemia ACTH secretion occurs independently of cortisol negative feedback inhibition.
True.
All of the following stimulate the release of ADH except -
A. Hypoglycemia
B. Pain
C. Angiotensin II
D. Epinephrine
ans A -
ADH is released in response to -
- Hypovolemia
- changes in circulating blood volume sensed by baroreceptors and left atrial stretch receptors
- increased plasma osmolality (sensed by hypothalamus)
- Epinephrine
- Angiotensin II
- Pain
- Hyperglycemia
- proinflammatory cytokines (septic shock)
- endotoxin
ADH levels usually remain elevated for ——- after injury
A. 12 hours
B. 1 day
C. 3 days
D. 1 week
ans D -
ADH levels remain elevated for about 1 week after initial insult.
All of the following are effects of vasopressin except
A. Free water absorption from collecting duct
B. Mesenteric vasoconstriction
C. Hepatic glycogenolysis
D. increased hepatic gluconeogenesis
ans C -
ADH acts on distal tubule and collecting ducts of the nephron to increase water permeability.
Potent mesenteric vasoconstrictor.
Increased hepatic gluconeogenesis and Glycolysis. (NOT Glycogenolysis)
Which of the following statements is false :
- Endotoxin induces ADH secretion independently of blood pressure, osmotic or intravascular changes.
- Chronic therapy with ACE inhibitors increased the risk of developing hypotension and vasodilatory shock with open heart surgery.
- Most alterations in cardiac output in the normal heart are related to changes in preload
- Sympathetic tone produces a greater decrease in skeletal muscle blood volume compared to the splanchnic blood volume
Ans 4.
Increases in sympathetic tone have a minor effect on skeletal muscle beds but produce a dramatic reduction in splanchnic blood volume, which normally holds 20% of blood volume.
All of the following are acute responses to intravascular volume changes except -
A. Change in venous tone
B. Systemic vascular resistance
C. ADH release
D. Change in intrathoracic pressure
ans C-
Acute responses in intravascular volume include changes in venous tone, systemic vascular resistance and intrathoracic pressure, with the slower hormonal changes less important in early response to volume loss.
Majority of the afterload is contributed by the -
A. Arterioles
B. Precapillary smooth muscle sphincters
C. systemic arteries
D. Capillaries
ans B -
Arterial pressure is the major component of afterload. This vascular resistance is determined by pre-capillary smooth muscle sphincters.
Dysoxia is defined as -
A. Increased alveolar-arterial oxygen gradient.
B. Decreased Oxygen carrying capacity of Hb
C. Failure to sustain oxidative phosphorylation
D. Any of the above
ans C -
Complete oxidation produces _______ mol of ATP from 1 mol of glucose
A. 2 mol
B. 30 mol
C. 36 mol
D. 38 mol
ans D -
Failure of oxidative phosphorylation, leads to shift to anerobic metabolism and glycolysis to generate ATP.
Glycolysis is a RAPID process but inefficient. Producing only 2 mol of ATP from 1 mol of glucose, compared to complete oxidation of 1mol of glucose that produces 38 mol of ATP.
expression of all of the following genes are increased by shock except -
A. Heat shock proteins
B. VEGF
C. eNOS
D. Heme-oxygenase-1
ans C -
Expression of gene products such as heat shock proteins, VEGF, iNOS, Heme-oxygenase-1 and cytokines is increased by shock.
All of the following are DAMPs except
A. Mitochondrial DNA B. Hyaluronan oligomers C. Heparan sulfate D. Extra domain A of fibronectin E. Interleukin 1-alpha F. LPS
ans F -
Endogenous DAMPs
- mitochondrial DNA
- Hyaluronan oligomers
- Heparan sulfate
- Extra domain A of fibronectin
- HSP 60,70
- gp 96
- surfactant protein A
- Beta-defensin 2
- Fibrinogen
- Biglycan
- HMGB-1
- Uric acid
- Interleukin 1alpha
- S-100
- Nucleolin
DAMPs are intracellular molecules released by broken cells that can have paracrine and endocrine like effects on distant tissues to activate inflammatory and immune responses. This is called Danger signalling.
They are recognized by Pattern Recognition Receptors or PRRs which include Toll Like Receptors and Receptor for advanced glycation end products or RAGE.
LPS is a Pathogen-associated molecular pattern or PAMP.
which of the following cells function as sentinel responders -
A. Macrophages
B. Neutrophils
C.Lymphocytes
D. Monocytes
ans A -
Before the recruitment of leukocytes to the site of injury, tissue based macrophages or mast cells act as sentinel responders releasing histamines, eicosanoids, tryptases and cytokines.
TNF-alpha levels peak within
A. 30 min
B. 1 hour
C. 1.5 hour
D. 2 hours
ans C-
TNF-alpha is one of the earliest cytokines released in response to injurious stimuli. Monocytes, macrophages and T cells release this potent inflammatory cytokine.
TNF-alpha levels peak within 90 minutes of stimulation and return frequently to baseline levels within 4 hours.
TNF-alpha all are true except -
A. Released by monocytes, macrophages and T cells.
B. Released in response to endotoxins, hemorrhage and ischemia.
C. Increase in TNF-alpha in trauma patients is much higher than that seen in septic patients.
D. Causes peripheral vasodilation, procoagulant activity and cachexia
ans C -
TNF alpha is released by monocytes, macrophages and T cells.
Released in response to Bacterial endotoxin in septic shock as well as hemorrhage and ischemia.
The increase in serum TNF-alpha levels reported in trauma patients is far less than that seen in septic patients.
Effects -
- Peripheral vasodilation
- release of other cytokines
- Procoagulant activity
- muscle protein breakdown
- cachexia
IL-1 all are true except -
A.Half life is 6 minutes.
B. induces febrile response to injury
C. induces anorexia
D. supresses the release of Beta endorphins
ans D -
IL-1 has actions similar to TNF-alpha.
Half life : 6 min.
Primarily paracrine action - local cellular responses.
Systemic action -
- induces febrile response by stimulating PG production in anterior hypothalamus.
- anorexia by activating satiety centre.
- augments secretion of ACTH, Glucocorticoids and Beta-endorphins.
- stimulates release of other cytokines - IL-2, IL-4, IL-6, IL-8, GMCSF, IFN-gamma.
Diffuse alveolar damage and ARDS in shock is mediated largely by -
A. TNF-alpha
B. IL-6
C. IL-1
D. IL-2
ans B -
IL6
elevated in - hemorrhagic shock, major surgery and trauma.
Levels correlate with shock
Contributes to Lung, Liver and Gut injury after hemorrhagic shock.
May play a role in development of diffuse alveolar damage and ARDS.
IFN-gamma - also promotes ARDS.
All of the following hepatic acute phase proteins except -
A. C-reactive protein B. Fibrinogen C. Albumin D. Haptoglobin E. Alpha-1 Anti-trypsin
ans C -
IL-6 and IL-1 are mediators of the hepatic acute phase response and they enhance the expression of -
- Complement
- CRP
- Fibrinogen
- Haptoglobin
- Amyloid A
- Alpha-1 antitrypsin
which of the following is correctly matched.
A. IL-1 - induces febrile response by activating prostaglandin in posterior hypothalamus
B. IL-2 Promotes gut barrier integrity
C. IL-4 Increases the production of IL-1, IL-6 and IL-8
D. IL-8 Chemoattractant to monocytes.
ans B -
IL-1: Induces fevers through PG activity in anterior hypothalamus, promotes Beta-endorphin release from pituitary and half life <6min.
IL-2 - promotes lymphocyte proliferation, immunoglobulin production, gut barrier integrity
IL-4 - induces B-lymphocyte production of IgG4 and IgE, mediators of Allergic and anti-helminthic response.
Downregulates TNF, IL-1, IL-6 and IL-8
IL-5 - promotes eosinophil proliferation and airway inflammation.
IL-6 - Elicited by virtually all immunogenic cells. Long half life. Prolongs survival of activated neutrophils.
IL-8 - chemoattractant for Neutrophils, basophils, eosinophils, lymphocytes.
which of the following are anti-inflammatory cytokines
A. IL-10
B. IL-15
C. IL-13
D. Both A and B
ans D -
IL-10 - Prominent anti-inflammatory cytokine, reduces mortality in animal sepsis and ARDS models.
Inhibits proinflammatory cytokine production, O2 radical production by phagocytes, adhesion molecule expression, lymphocyte activation.
IL-12 - Promotes Th1 differentiation, synergistic action with IL-2.
IL-13 - Promotes B lymphocyte function and structurally similar to IL-4. Inhibits Nitric oxide and endothelial activation.
IL-15 - anti-inflammatory cytokline. Promotes lymphocytic activation, promotes neutrophil phagocytosis in fungal infection.
IL-18 - Similar to IL-12 in function. Levels are increwased in Sepsis, especially Gram positive infections and high levels found in cardiac death.
IL that is found in high levels in cardiac death -
A. IL-13
B. IL-15
C. IL-18
D. IL-17
ans C
IL-18 -
produced by macrophages, Kupffer cells, Keratinocytes, adrenal cortical cells and Osteoblasts.
Similar to IL-12 in function, and levels are increased in sepsis, especially in gram positive infections.
High levels of IL-18 are found in cardiac death.
which IL has structural similarity to IL-4
A. IL-5
B. IL-13
C. IL-10
D. IL-12
ans B -
IL-13 is structurally similar to IL-4 and it also promotes B lymphocyte function.
Inhibits Nitric oxide and endothelial activation.
All of the following are key mediators in ARDS except -
A. HMGB1
B. IL-6
C. IFN-gamma
D. TGF-Beta
ans D -
HMGB1 - high mobility group box chromosomal protein. It is a DNA transcription factor. Late mediator of inflammation leading to ARDS, Gut barrier disruption. Induces “Sickness behavior”
IFN-gamma - Mediates the IL-12 and IL-18 functions. Promotes ARDS. It is usually found in wounds 5-7 days after injury.
Which of the following interleukins is preferentially secreted by Th2 cells -
A. IL-18
B. IL-21
C. IL-13
D. IL-15
ans B -
IL-21 is preferentially secreted by Th2 cells. Structurally similar to IL-2 and IL-15. Activates NK cells, B cells and T cells. Influences adaptive immunity.
C3a, C4a and C5a induce all of the following except -
A. Increased adherence of neutrophils to vascular ednothelium.
B. Vascular permeability increased.
C. Smooth muscle cell contraction.
D. Histamine release.
E. All of the above
ans E -
Significant complement consumption after hemorrhagic shock.
Trauma pts - degree of complement activation is proportional to the magnitude of injury and may serve as a marker for severity of injury.
First cells to be recruited to the site of injury are -
A. Neutrophils
B. Monocytes
C. Macrophages
D. Lymphocytes
Ans A -
Neutrophil activation - early event. First cells to be recruited to the site of injury.
All of the following are true regarding PMNs
A. produce reactive oxygen species that induce lipid peroxidation.
B. Tocopherol and Glutathione are used up reactive oxygen species.
C. Elastase and cathepsin G are proteolytic enzymes released by neutrophils.
D. Ischemia - reperfusion injury also activates PMNs
E. All of the following
Ans E -
Activated PMNs generate reactive oxygen species (Superoxide anion, hydrogen peroxide, hydroxyl radical) which cause lipid peroxidation.
Proteolytic enzymes such as elastase and Cathepsin G are released as well as vasoactive mediators - eicosanoids, leukotrienes, platelet activating factor.
Oxygen free radicals also consume glutathione and tocopherol.
Ischemia reperfusion activates PMNs and causes PMN induced organ injury.
In animal models - activation of PMN correlates with irreversibility of shock.
In humans, activation of neutrophils has a role in MODS. Plasma markers of PMN activation - Elastase - correlates with severity of injury.
Which of the following is the plasma marker of neutrophil injury -
A. Elastase
B. Collagenase
C. Neuron Specific Enolase
D. S100
ans A -
Elastase is the plasma marker of neutrophil activation.
True regarding - TLR4 mediated cell signalling
A. MyD88 dependent mechanism activates NF-kB.
B. MyD88 independent pathway induces IRF3
C. Both A and B
D. Neither A nor B
ans C -
Most common cause of shock in surgical patients?
A. Hypovolemic shock
B. Hypothermic shock
C. Septicemic shock
D. Neurogenic shock
ans A -
Average amount of blood loss in class III hemorrhagic shock -
A. <750 mL
B. 750-1500 mL
C. 1500-2000mL
D. >2000 mL
ans C -
Blood loss
Class I : <15% or <750mL, HR<100.
Class II : 15-30% or 750-1500 mL. HR > 100.
Class III : 30-40% or 1500-2000 mL, HR > 120.
Class IV : >40% or >2L, HR >140.
Orthostatic hypotension is seen in which stage of hemorrhagic shock
A. Class I
B. Class II
C. Class III
D. Class IV
ans B -
Orthostatic hypotension is seen in which stage of hemorrhagic shock
A. Class I
B. Class II
C. Class III
D. Class IV
ans B -