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Pathology -- Cardiology > Shock > Flashcards

Shock Flashcards

1
Q

Definition of shock?

A

Acute generalized failure of the circulatory system resulting from blood volume that is too low to fill the vascular system or insufficient cardiac output

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2
Q

General characterization of shock?

A

Hypotension + Hypoperfusion –> Impaired perfusion+Hypoxia

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3
Q

BP =

A

CO X Peripheral Resisitance (PR)

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4
Q

Three causes of shock?

A

Decreased Cardiac Fxn
Decreased Blood Volume
Decreased Peripheral resistance

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5
Q

Causes of decreased peripheral resistance

A

Systemic inflammation (Septic Shock)
Systemic mast cell activation (Anaphylaxis)
Systemic loss of vascular tone (Neurogenic shock)

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6
Q

End result of shock

A

Cellular Hypoxia
Failure to transport CO2, Toxic substances away from cells
Cell Death/Tissue Dysfunction

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7
Q

Five types of shock

A 
Cardiogenic
Hypovolemic/Hemorrhagic
Spetic
Anaphylactic
Neurogenic
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8
Q

Causes of cardiogenic shock

A

Myocardial infarction
Ventricular arrythmias
Cardiac tamponade
Saddle Embolism

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9
Q

Causes of hypovolemic shock?

A

Hemorrhage, Burns, Dehydration

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10
Q

What is septic shock?

A

Systemic inflammatory reaction from bacteremia with an organism expressing LPS or LOS

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11
Q

What is Systemic Inflammatory Response Syndrome (SIRS)?

A

LPS activation of macrophages, endothelial cells. Overproduction of inflammatory cytokines and mediators. Decreased PR, BV loss throughout the peripheral.

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12
Q

Most common cause of mortality in ICU

A

Septic Shock

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13
Q

Central feature of Septic Shock

A

LPS activation of inflammation

Activated endothelial cells, monocytes, macrophages, and compliment

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14
Q

What do activated endothelial cells in septic shock do? (Molecular)

A

Decrease production of tissue factor pathway inhibitor (TFPI) and thrombomodulin

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15
Q

How does LPS activate Monocytes/Macrophages?

A

LPS/LPS BP complex binds CD14 on cell surface.
Signalling mediated thru TLR4, NFkB transcription
Cytokine storm
Triggers NO release and systemic inflammatory effects

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16
Q

Effects of Endothelial cell activation?

A

Increased vascular permeability, adhesion molecule expression. Inhibition of anti-coagulation properties. Switch to pro-coagulation phenotype.

17
Q

Describe initial stages of sepsis.

A

Widespread systemic inflammatory response
systemic vasodilation, diminished contractility.
Widespread adhesion + capillary damage.
Coagulation and DIC

18
Q

Describe the later stages of sepsis.

A

Burned out inflammatory and immune responses.

Immune hypo-reactiveness and immune paralysis

19
Q

What happens in the non-progressive stage of shock?

A

Compensatory mechanisms maintain cardiac output and blood pressure, perfusion of vital organs.

20
Q

Examples of compensatory mechanisms that play a role in the non-progressive stage of shock

A 
Baroreflexes
Sympathetic NS, Catecholamine release
Renin-Angiotensin Axis
ADH
Tachy, Peripheral Vasoconstriction, Pallor
H2O Conservation
21
Q

What happens in the progressive phase

A

Anerobic Glycolysis –> Metabolic Acidosis –> low pH retards vasomotor response –> arterial dilation –> blood pooling in microvasculature –> decreased CO

22
Q

What happens in the irreversible phase of sepsis?

A

Survival not possible
Lysosomal Enzyme release
NO synthesis causes low myocardial contractility
Ischemic bowel and release of gut bacteria into bloodstream

23
Q

Most commonly seen symptoms of hypovolemic and cardiogenic shock

A

Hypotension
Weak, Rapid Pulse
Tachypnea
Cool, Clammy, Cyanotic Skin

24
Q

Most commonly seen symptoms of septic shock

A

Warm, Flush skin from peripheral vasodilation

25
Q

Most commonly seen symptoms of anaphylaxis

A

Bronchoconstriction and Edema

Urticaria

26
Q

Which two kinds of shock are most reversible?

A

Hypovolemic and Anaphylactic

27
Q

Which is least reversible?

A

Cardiogenic

28
Q

What is DIC?

A

Sudden or insidious development of numerous fibrin thrombi within the microvasculature. Consumption of clotting components later leads to widespread hemorrhaging.

29
Q

Mechanism of DIC

A

Rapid consumption of platelets, prothrombinen, f, actors V, VIII, X, platelets and fibrin.
Fibrin –> Anoxia/Hypoxia –> Coagulation Necrosis
No platelets –> Hemorrhage

30
Q

Synonym for DIC

A

Consumption Coagulopathy

31
Q

Pathologic findings of DIC

A

Widespread Fibrin Thrombi
Diffuse Circulatory Insufficiency
Brain, Lungs, heart, Kidneys
Inc. D Dimer and Hemorrhage

32
Q

Difference between Septic Shock vs. DIC

A
  • Degree of Activation of Endothelial Cells
  • Degree of activation of coagulation cascade
  • Severe septic shock –> DIC
33
Q

Clinical Settings to look for Shock in.

A

Sepsis, Trauma, Malignancy, Obstetric calamities, vascular abnormalities, hepatic failure, severe toxic or immunologic reactions

34
Q

Severe toxic or immunologic reactions associated with shock

A

Snake Bites
Transfusion reactions
Recreational drugs

Pathology -- Cardiology (13 decks)

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