pathology 9 - shock

Question 0

what are the sequence of events leading to shock?

Answer 0

haemorrhage, sepsis etc - reduced circulating blood volume and reduced CO - systemic hypotension and hypoperfusion - tissue hypoxia - cell death.

Question 1

what is shock? caused by?

Answer 1

another word for cardiovascular collapse. Low circulating blood volume. it is the final stage of a number of threatening conditions. eg. sever haemorrhage, burns, blood loss, sepsis.

Question 2

3 types of shock?

Answer 2

1. cardiogenic
2. hypovolaemic
3. blood maldistribution.

Question 3

explain cardiogenic shock?

Answer 3

failure of the heart to adequately pump blood. eg. myocardial infarct, arrythmias, obstruction of blood (pulmonary embolism)SV and CO cant compensate - stangant blood and tissue hypoxia. eg. RAV valve (tricuspid) if displaced then blood cant leave heart and so leads to concentric hypertrpophy due to increased after load. cardiomegaly.

Question 4

explain hypovolaemic shock? how much of body% is blood?

Answer 4

shock due to reduced circulting volume. -blood loss due to haemorrhage or fluid loss eg. diarrhoea/burns/vomit. hypotension (low bp) and hypoperfusion leading to hypoxia and infarct. initally there is compensation for heart, kidneys and brain, lungs. 10% can recover from
35-45% - fatal.
blood = 7% of body. if cat loses 150mls an weighs 5kg. then normal blood is 350mls - has lost 42% of blood = fatal.

Question 5

blood maldistribution?

Answer 5

decreased peripheral resistance - blood pools in periphery and so doesnt reach vital organs. vascular space increased s effective circulting volume is decreased. stagnation and hypoxia occur.

Question 6

3 main types of blood maldistribution?

Answer 6

1. neurogenic
2. anaphylactic
3. septic shock

Question 7

explain neurogenic blood maldistribution?

Answer 7

trauma to CNS. usually spinal cord. loss of signals to SM in blood vessel walls and so vasodilation! blood pools in veins. eg. electrocution.

Question 8

explain anaphylactic blood redistribution?

Answer 8

generalised type 1 hypersensitivity. (anaphylaxis allergic reaction)eg. insect bite/allergens. substance interacts with igE bound t mast cells. mast cells degranulate - histamine released, systemic vasodilation to allow leukocytes into btissue from blood. increased permeability - hypotension and hypoperfusion.

Question 9

explain septic shock blood maldistribution? most commonly due to what? what are the effects of LPS? what is LPS?

Answer 9

most common. mediated by vascular and infmallatory mediators. resonse to bacterial/fungal infection. most commonly endotoxaemia. - in the cell wall of gram negative bacteria are lipopolysaccarides (LPS). these are pattern associated molecular patterns (PAMPS) they bind to CD14 AND TLR4 - membrane molecules which allow range of microbes to activate cells. (ENDOTOXIN) ACTIVATE macrophages, ednothelial cells and complement. raised il-1 and TNF. (fever) cause vasodilation, hypotension, reduced myocardial contractility, hypoperfusion, BV injury, leads to DIC.

Question 10

3 THINGS that lead to vasodilation?

Answer 10

1. LPS - endotoxin in the cell wall of gram negative bacteria.
2. histamine - from mast cells
3. fewer autonomic signals - loss of signal to the SM in vasculature.

Question 11

3 stages of shock?

Answer 11

1. non-progressive (compensated)
2. progressive stage - prolonged and severe
3. irreversible shock.

Question 12

explain non-progressive (compensated) shock? GFR? RAAS? ADH?

Answer 12

increased sympathetic output (ADRENALINE) to cause vasoconstriction and larger force of contraction of heart, rate etc. higher CO. this raises blood and tissue O2. PLUS - CONTROL WATER BALANCE.

• GFR - drops - CONSTRICT THE EFFERENT ARTERIOLE. (macula densa)
• RAAS - kidney relases renin - acts on liver to release angiotensinogen - angiotensin1 - angiotensin II. this acts on adrenal cortex to release ALDOSTERONE. - promotes na and water reabsorbtion in kidneys to increase blood volume.
• ADH - controls plasma osmolarity. hypothalamus - released when osmoreceptors are stimulated by high solutes in blood. (low water) controls permeability of collecting ducts to water (low urine volume)

Question 13

explain progressive stage of shock?

Answer 13

prolonged/severe. hypovolaemia - no compensation. blood pooling and tissue hypoperfusion. cells then have anaerobic respiration - cell damage - lysosomal enzymes are released and so leads to necrosis.

Question 14

explain irreversible shock?

Answer 14

mechanisms for vasoconstriction are overcome - widespread vasodilation. multiorgan failure!!!!.

Question 15

clinical features of shock?

Answer 15

hypotension (low bp)
weak pulse and tachcardia
hyperventilation
low urine production (trying to retain water)
hypothermia (peripheral vasoconstriction)

Question 16

what kinds of lesions would you see with shock?

Answer 16

congestion and pooling of blood
oedema (increased vascular permeability)
haemorrhage - petechial and ecchymotic
thrombosis due to stasis of blood
cellular necrosis (cells die)