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
Q

What does an increase in the sympathetic NS activity in response to blood loss lead to

A

Increases heart rate
Increases ventricular contraction
Increases venosus constriction
Increases arteriole constriction

26
Q

What can increase cardiac output

A

An increased heart rate and increased stroke volume

27
Q

What is peripheral resistance

A

Resistance of the arteries to blood flow

28
Q

What does arteriole consrtiction cause

A

An increase in peripheral resistance in turn increasing mean arterial blood pressure

29
Q

How is mean arterial blood pressure increased in response to decreased blood volume

A

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
Q

How is blood volume restored

A

Shifting interstitial fluid back into blood vessels​

Decreasing fluid loss in kidney​

Increasing fluid intake

31
Q

What are the normal Starling’s forces

A

Arteriole-capillary HP (35mmHg)
Oncotic pressure - 25mmHg
Capillary-venule HP (15mmHg)

Filtration = reabsorption

32
Q

What does decreased arterial blood pressure cause

A

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
Q

What happens to Starling’s forces during haemorrhage

A

HP from constricted arteriole to capillary is only 25mmHg and 10mmHg from capillary to venule

This allows for greater reabsorption than filtration

34
Q

How is fluid loss minimised in the kidney

A

Decrease glomerular filtration
Increased reabsorption of Na+ and H20 by stimulating release of vasoconstrictors:
-Renin-angiotensin-aldosterone
-ADH

34
Q

What stimulates ADH secretion

A

Decreased plasma volume (decreased baroreceptor distension)
Increased plasma osmolarity (increased osmoreceptor activation)

35
Q

What are stimuli of thirst

A

increased plasma osmolarity; decreased ECF volume

Angiotensin II also promotes thirst

Dry mouth

36
Q

What receptors suppress drinking

A

Stretch receptors

37
Q

Where are stretch receptors found

A

Stomach

38
Q

What is erythropoiesis

A

Process of producing new RBC’s

39
Q

What long term actions does the body take to resolve significant blood loss

A

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
Q

When is erythropoietin produced

A

When oxygen delivery decreases due to a lack of RBC’s

41
Q

What is Shock

A

Inadequate blood flow to tissues

42
Q

Which type of Shock is usually fatal

A

Irreversible

43
Q

What medically would indicate shock

A

Decreased cardiac output
Decreased blood or ECF volumme

44
Q

What are the types of shock

A

Hypovolaemic shock
Low resistence (or distributive) shock
Cardiogenic shock

45
Q

What causes cardiogenic shock

A

Heart fails as a pump

46
Q

What is Low resistance shock

A

decreased peripheral resistance, due to widespread vasodilation e.g. anaphylactic shock

47
Q

What causes hypovolaemic shock

A

Decreased ECF volume, due to haemorrhage, sweating, diarrhoea, burns etc