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Principles > Physiology > Flashcards

Physiology Flashcards

1
Q

What is blood pressure?

A

The outwards (hydrostatic) pressure exerted by blood on the blood vessel walls

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2
Q

What is systolic arterial blood pressure?

A

The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart CONTRACTS

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3
Q

What is a ideal systolic pressure?

A

90-120 mm Hg

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4
Q

What is diastolic arterial blood pressure?

A

The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart RELAXES

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5
Q

What’s an ideal diastolic pressure?

A

60-90 mm Hg

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6
Q

When does hypertension occur?

A

When clinic blood pressure is 140/90 mm Hg or higher and day time average is 135/85 mm Hg or higher

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7
Q

What is pulse pressure?

A

The difference between systolic and diastolic blood pressures

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8
Q

What is a normal pulse pressure?

A

Between 30 and 50 mmHg

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9
Q

What is the mean arterial blood pressure?

A

The average arterial blood pressure during a single cardiac cycle which involves contraction and relaxation of the heart

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10
Q

How do the timings for the systolic and diastolic portions of the cycle compare?

A

The diastolic portion is around twice as long as the systolic portion

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11
Q

What are the two ways in which mean arterial blood pressure can be estimated?

A 
MAP = [(2xdiastolic) +systolic] /3
MAP = DBP + 1/3 x (difference between SBP and DBP)
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12
Q

What is the normal range that MAP should be within?

A

70-105mmHg

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13
Q

What is the minimum MAP needed to perfume the brain, heart and kidneys?

A

60mmHg

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14
Q

What happens if MAP isn’t high enough?

A

The brain, Heart, kidney and other internal organs aren’t perfused

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15
Q

What happens if MAP is too high?

A

It can damage blood vessels and put extra strain on the heart

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16
Q

Describe the negative feedback reflex in MAP

A

Deviation in MAP > triggers Baroreceptors > which informs the cardiovascular control system (medulla) > which sends instructions to the heart and blood vessels > leading to a compensatory response (varying stroke rate in the heart, stroke volume in the heart, or systemic vascular resistance in the blood vessels)
This brings the MAP back to normal and the negative feedback shuts of the system responsible for the response.

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17
Q

What are the two types of baroreceptors?

A
  • carotid receptors (carotid sinus)

- aortic baroreceptors (aorta)

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18
Q

How do signals from the aortic baroreceptors reach the medulla?

A

Aortic baroreceptors > vagus nerve > brainstem

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19
Q

How do the signals from the carotid baroreceptors reach the medulla?

A

Carotid baroreceptors > herings nerve > glossopharyngeal > brainstem

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20
Q

What happens to the firing rate in baroreceptors agreement neutrons when MAP increases?

A

It increases

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21
Q

What happens to the firing rate in baroreceptors agreement neutrons when MAP decreases?

A

It decreases

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22
Q

What happens in the brainstem when it receives baroreceptor signals?

A

> The cardiovascular control centre receives information and the nucleus tractus solitarius (NTS) is the site of the 1st synapse in the medulla.
NTS relays information to other regions of the brain
which generates a vagal (parasympathetic) outflow to the heart
regulates spinal sympathetic neurones

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23
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute

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24
Q

What is stroke volume?

A

The volume of blood pumped by each ventricle of the heart per heart beat

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25
Q

How are MAP , Cardiac output and systemic vascular resistance related?

A

MAP = CO x SVR

26
Q

How are stroke volume, cardiac output and heart rate related?

A

CO = SV x HR

27
Q

What is systemic vascular resistance?

A

The sum of the resistance of all vasculature in the systemic circulation

28
Q

How can MAP be regulated?

A

By regulating heart rate, stroke volume and systemic vascular resistance

29
Q

What is meant when the heart is described as having AUTORHYMICITY

A

The electrical signals which control the heart are generated within the heart itself and therefore require no extreme al stimuli to rhythmically beat.

30
Q

How is heart rate modified ?

A

By the autonomic (involuntary) nervous system (ANS)

31
Q

What do sympathetic neurones do?

A

Modification by the ANS which results in responses such as increased heart rate, sweating, pupil dilation etc

32
Q

What do parasympathetic neurones do?

A

Modification by the ANS to control activities when the body is at rest (salivation, urination, digestion etc)

33
Q

What happens to stroke volume when the contractile strength of the heart is increased?

A

It increases

34
Q

What regulates stroke volume?

A

Autonomic nervous system

35
Q

What effect do sympathetic nerves have on stroke volume?

A

They innervate the ventricular myocardium and stimulation increases the force of contraction, increasing stroke volume

36
Q

What effect does the vagus/parasympathetic nerve have on ventricular contraction ?

A

Little or no direct effect

37
Q

What is systemic vascular resistance (SVR) regulated by?

A

Vascular smooth muscles

38
Q

What is the main site of SVR?

A

Arterioles

39
Q

What happens when vascular smooth muscles CONTRACT

A

It causes vasoconstriction and increases SVR and MAP

40
Q

What happens when vascular smooth muscles RELAX

A

It causes vasodilation and decreases SVR and MAP

41
Q

How are vascular smooth muscles supplied?

A

By sympathetic nerve fibres. (The neurotransmitter is noradrenaline acting on alpha receptors.)

42
Q

What is vasomotor tone?

A

When vascular smooth muscles are partially constricted at rest

43
Q

What causes the Vasomotor tone?

A

The tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline

(Increase in sympathetic discharge = increase in vasomotor tone = increase in vasoconstriction)
(Decrease in sympathetic discharge = decrease in vasomotor tone = increase in vasodilation)

44
Q

Why can’t baroreceptors stop high blood pressure affecting somebodies wellbeing?

A

Baroreceptors only respond to acute changes in arterial blood pressure and their firing decreases if high blood pressure is sustained.

45
Q

What is Homeostatis?

A

The maintenance of steady states within our bodies by coordinated physiological mechanisms. It is essential for the survival and function of cells.

46
Q

What are intrinsic and extrinsic controls?

A 
Intrinsic = local controls that are inherent in an organ
Extrinsic = regulatory mechanisms initiated outside an organ. Accomplished by nervous and endocrine systems.
47
Q

What is feedforward?

A

A term used to describe responses made in anticipation of a change (usually in combination with negative feedback)

48
Q

What is feedback?

A

Responses made after a change has been detected. Can be positive(amplifies an initial change) or negative (opposes a initial change).

49
Q

what is the haemostasis?

A

the arrest of bleeding and the maintenance of vascular patency

50
Q

what are the requirements for haemostasis?

A
  • permanent state of readiness
  • prompt response
  • localised response
  • protection against unwanted thrombosis
51
Q

what components are essential for a normal haemostatic system?

A
  • formation of platelet plug (primary haemostasis)
  • formation of a fibrin clot (secondary haemostasis)
  • fibrinolysis
  • anticoagulant defences.
52
Q

how are platelets formed?

A

they are formed in the bone marrow by ‘budding’ from megakaryocytes.

53
Q

what does endothelial damage do?

A

exposes collagen and released Von Willebrand Factor (VWF) and other proteins to which the platelets have receptors = platelet adhesion at the site of injury.
- there is then secretion of various chemicals from the platelets which leads to aggregation of platelets and the site of injury. (platelet plug)

54
Q

what can be the causes of the failure of platelet plug formation?

A
  • vascular’-reduced no. or function of platelets

- VWF

55
Q

what are the consequences of failure of formation of the platelet plug?

A
  • spontaneous bruising and purpura
  • mucosal bleeding (epitaxes, GI, conjunctional, menorrhagia)
  • intracranial haemorrhage
  • retinal haemorrhages.
56
Q

what happens in secondary haemostasis?

A

fibrin clot formation

57
Q

what can cause failure to form a fibrin clot?

A
  • single clotting factor deficiencies (e.g. haemophilia)
  • multiple clotting factor deficiencies (usually acquired)
  • increased fibrinolysis (plasminogen to plasmin reaction, producing fibrin degradation products)
58
Q

what are consequences of failure to form a fibrin clot?

A
  • no characteristic clinical syndrome
  • may be combined primary and secondary haemostatic failure
  • pattern of bleeding depends on the abnormalities and the clotting factors involved.
59
Q

what are naturally occurring anticoagulants?

A

1 - serine protease inhibitors

2 - protein C and protein S

60
Q

Describe arterial thrombosis.

A
  • high pressure
    -atherosclerosis
  • platelet rich thrombus
    treatment = aspirin and other anti-platelet drugs
61
Q

Describe venous thrombosis.

A

-low pressure system
-platelets not activated
- activates coagulation cascade - rich in fibrin clot.
- vichows triad = stasis, vessel wall, hypercoagulability.
treatment = heparin/warfarin/ new oral anticoagulants

Principles (15 decks)

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