10. shock

Question 1

shock

Answer 1

Clinical state of cardiovascular collapse (circulatory failure); due to reduced cardiac output or effective circulating blood volume

Question 2

types

Answer 2

cardiogenic
obstructive
distributive
hypovolemic

Question 3

Cardiogenic shock cause

Answer 3

Deficient emptying; Myocardial infarction, Rupture of the heart and Cardiac arrhythmias
Deficient filling; Cardiac tamponade
Obstruction to outflow; Pulmonary embolism, Ball valve thrombus and cardiac myxoma

Question 4

Anaphylactic shock

Answer 4

Systemic type I (IgE mediated) hypersensitivity reaction
Mast cells and basophils degranulation  vasodilation and increased vascular permeability
Bronchoconstriction may lead to death in a matter of minutes

Question 5

super antigens

Answer 5

activation of polyclonal T cells
Induce release of high levels of cytokines that lead to vasodilatation, hypotension and shock

Question 9

Stages of Shock

Answer 9

non progressive
progressive
irreversible

Question 9

Nonprogressive (initial, compensated and reversible) shock

Answer 9

Organs still able to maintain homeostasis without injury

Vital organ perfusion, cardiac output and blood pressure is maintained

Reflex compensatory neurohumoral mechanisms are activated
- tachycardia, peripheral vasoconstriction and renal fluid conservation

Question 9

Progressive decompensated shock

Answer 9

Organs can no longer maintain homeostasis
Organ damage begins to occur

Question 10

characteristics of progressive decompensated shock

Answer 10

tissue hypoperfusion, acidosis and ineffective vasomotor response causing peripheral pooling and vasodilatation

Question 11

Decompensated (irreversible) shock

Answer 11

rreversible organ damage has occurred

Question 12

Causes of Irreversibility

Answer 12

Persistence of widespread compensatory vasoconstriction  anoxia of tissue
Endothelial damage increased vascular permeability
Pancreas ischemia  myocardial depressant factor (MDF)decreased myocardial contractility
Cerebral ischemia  depression of vasomotor centre
Liver ischemia  no inactivation of vasodepressor material (VDM)  leading to peripheral vasodilatation
Release of TNF
Hypercoagulability of blood