Homeostasis, Haemorrhage and shock Flashcards

1
Q

What is Shock

A

Excessive blood loss is a medical emergency​

The decreased blood volume results in a fall in blood pressure and impaired delivery of nutrients to cells​

This state is called shock

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2
Q

Why should even ‘regular patients’ be asked routinely about changes in their medical condition and medications

A

“D.B, aged 69, of North London, bled to death from having a tooth removed after failing to tell his dentist about his chemotherapy treatment for leukaemia. An inquest at Hornsey recorded a verdict of death by misadventure.”

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3
Q

What are the physiological responses to blood loss

A

Immediate:​
-Stop the bleeding​

Short term: ​
-Restore blood pressure​

Medium term:​
-Restore fluid volume​

Long term:​
-Replace blood constituents

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4
Q

What components are considered when trying to stop blood loss

A

Vascular response​

Platelet response​

Plasma response (Coagulation)

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5
Q

What components make up the vascuar response to blood loss

A

Smooth muscle​
-Spasm due to trauma​
-Myogenic response​
-Humoral factors (vasoconstrictors)​

Endothelium​
-Platelet adhesion and aggregation​
-Anticlotting and fibrinolysis

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6
Q

How do platelets respond to blood loss

A

Damage to blood vessel - turbulent blood flow - platelets come into contact with vessel wall (collagen)​

Platelets adhere; clump together (aggregate)​

Release chemicals that cause further aggregation (Positive feedback)​

Formation of platelet plug​

Effective in sealing small blood vessels

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7
Q

How does the platelet response cause vasoconstriction

A

The aggregated platelets release thromboxane and ADP which help form platelet plug while thromboxane alsoacts as a vasoconstrictor

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8
Q

How does coagulation occur

A

Various plasma proteins and tissue components combine to convert fibrinogen  fibrin to form the blood clot​

Numerous ‘clotting factors’ are involved​

Many of these are made in the liver​

The synthesis of several clotting factors requires the presence of vitamin K​

The clotting factors are activated in an enzyme cascade​

One activated factor activates the next one in the sequence

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9
Q

What proteins are needed to form insoluble fibrin

A

Prothrombin - thrombin
Fibrinogen - soluble fibrin

Factor XIIIa is used to convert soluble fibrin to insoluble fibrin

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10
Q

Why does blood clotting factor VI not exist

A

Fcator4 and 6 were the same

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11
Q

What blood clotting factors exist

A

I. Fibrinogen​
II. Prothrombin​
III. Tissue factor (‘thromboplastin’)​
IV. Calcium ions​
V. Proaccelerin​
VII. Proconvertin
VIII. Antihaemophilic globulin​
IX. Christmas factor​
X. Stuart-Prower factor ​
XI. Plasma thromboplastin antecedent​
XII. Hageman factor​
XIII. Laki-Lorand factor

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12
Q

What occurs within the extrinsic pathway to activate coagulation

A

Tissue damage,
Tissue factors (‘tissue thromboplastin’)
Factor VII

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13
Q

What are the two pathways of coagulation

A

Intrinsic and extrinsic

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14
Q

What occurs to activate the intrinsic pathway to coagulation

A

Vascular damage,
Contact activation involving Factors:
XII, XI, IX, VIII

Phospholipid and calcium ions react with Factor X to create Factor Xa

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15
Q

Why do we have an intrinsic and extrinsic pathway

A

The extrinsic pathway seems to be more important in initiating clotting after an injury ​

The intrinsic system serves to maintain the process once it has started​

However, the intrinsic system may have a role in events such as thrombosis; here, a blood clot forms inside an intact blood vessel

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16
Q

What is fibrinolysis

A

When the blood clot has served its purpose it is dissolved

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17
Q

What enzyme is involved in fibrinolysis

A

Plasmin

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18
Q

How is Plasmin produced

A

Plasminogen reacts with plasminogen activator to form plasmin

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19
Q

What does plasmin react with to breakdown the blood clot

A

Breaksdown Fibrin into soluble fibrin fragments

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20
Q

What happens to blood pressure in the short term in response to blood loss

A

Fall in blood pressure​

Compensatory mechanisms triggered by the arterial baroreceptors​

These mechanisms aim to restore the blood pressure

21
Q

What hormones are involved in the mediation of the baroreceptor reflexes

A

Adrenaline
Angiotensin II
Vasopressin (ADH)

22
Q

What nerves mediate baroreceptor reflexes

A

Sympathetic nerves

23
Q

What effect does a decrease in blood volume have on the CVS centres

A

They increase the sympathetic NS activity

24
Q

What does an increase in both ventricular contraction and vein constriction cause

A

An increase in stroke volume

25
What does an increase in the sympathetic NS activity in response to blood loss lead to
Increases heart rate Increases ventricular contraction Increases venosus constriction Increases arteriole constriction
26
What can increase cardiac output
An increased heart rate and increased stroke volume
27
What is peripheral resistance
Resistance of the arteries to blood flow
28
What does arteriole consrtiction cause
An increase in peripheral resistance in turn increasing mean arterial blood pressure
29
How is mean arterial blood pressure increased in response to decreased blood volume
Decreased bloo pressure Decreased baroreceptor firing activates CVS centres in brainstem Increased sympathetic NS activity Increased heart rate, vent contraction, venosus constriction and arteriole constriction In turn increasing cardiac output, stroke volume and peripheral resistance Subsequently leading to an overall increase in the mean arterial blood pressure
30
How is blood volume restored
Shifting interstitial fluid back into blood vessels​ Decreasing fluid loss in kidney​ Increasing fluid intake
31
What are the normal Starling's forces
Arteriole-capillary HP (35mmHg) Oncotic pressure - 25mmHg Capillary-venule HP (15mmHg) Filtration = reabsorption
32
What does decreased arterial blood pressure cause
Vasoconstriction of arterioles -Increased Total Peripheral Resistance -Decreased capillary blood pressure This decreases the hydrostatic pressure pushing fluid out of the capillary More fluid is drawn back into the capillaries by the oncotic pressure
33
What happens to Starling's forces during haemorrhage
HP from constricted arteriole to capillary is only 25mmHg and 10mmHg from capillary to venule This allows for greater reabsorption than filtration
34
How is fluid loss minimised in the kidney
Decrease glomerular filtration Increased reabsorption of Na+ and H20 by stimulating release of vasoconstrictors: -Renin-angiotensin-aldosterone -ADH
34
What stimulates ADH secretion
Decreased plasma volume (decreased baroreceptor distension) Increased plasma osmolarity (increased osmoreceptor activation)
35
What are stimuli of thirst
increased plasma osmolarity; decreased ECF volume Angiotensin II also promotes thirst Dry mouth
36
What receptors suppress drinking
Stretch receptors
37
Where are stretch receptors found
Stomach
38
What is erythropoiesis
Process of producing new RBC's
39
What long term actions does the body take to resolve significant blood loss
Restore plasma proteins -Released from liver (3-4 days) Replace blood cells, esp. RBCs Erythropoiesis -Regulated by erythropoeitin (EPO) -EPO released from kidney -Stimulates RBC production in bone marrow -Return to normal in 2-3 months
40
When is erythropoietin produced
When oxygen delivery decreases due to a lack of RBC's
41
What is Shock
Inadequate blood flow to tissues
42
Which type of Shock is usually fatal
Irreversible
43
What medically would indicate shock
Decreased cardiac output Decreased blood or ECF volumme
44
What are the types of shock
Hypovolaemic shock Low resistence (or distributive) shock Cardiogenic shock
45
What causes cardiogenic shock
Heart fails as a pump
46
What is Low resistance shock
decreased peripheral resistance, due to widespread vasodilation e.g. anaphylactic shock
47
What causes hypovolaemic shock
Decreased ECF volume, due to haemorrhage, sweating, diarrhoea, burns etc