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Semester 2 Case Studies > Case 6 > Flashcards

Case 6 Flashcards

1
Q

what kind of measurements are recommended to confirm the diagnosis of hypertension

A

out of office BP measurements

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2
Q

how many adults had hypertension in 2000

A

1 billion

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3
Q

percentage of people in Israel with hypertension

A

23%

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4
Q

percentage of people in Poland with hypertension

A

62%

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5
Q

what BP confirm hypertension

A

> 140/90 mmHg

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6
Q

what are primary cases

A

do not have a specific cause

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7
Q

how many cases are primary

A

98%

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8
Q

how many cases are secondary

A

2%

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9
Q

what drugs cause hypertension

A

NSAIDS

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10
Q

percentage of hyperaldosteronism that is caused by adrenal adenoma

A

30%

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11
Q

percentage of primary hyperaldosteronism that is caused by adrenal hyperplasia

A

70%

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12
Q

what is main cause of primary hypertension

A

over activity of SNS and an underactive PNS

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13
Q

what happens to the heart in hypertension

A

hypertrophy of the left ventricle

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14
Q

what happens to the kidneys in hypertension

A

kidneys leak proteins, become granular and will finally fail

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15
Q

what happens in the brain

A

ruptured cerebral artery and compression of the ventricle

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16
Q

what is diabetic retinopathy

A

leading cause of blindness in working age adults

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17
Q

what is diabetic neurophathy

A

leading cause of end stage renal disease

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18
Q

what is diabetic neuropathy

A

leading cause of non truamatic lower extremity amputations

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19
Q

macrovascular complications

A

2-4 fold increase in cardiovascular mortality and stroke
heart disease
peripheral vascular disease

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20
Q

what is blood pressure

A

cardiac output x total peripheral resistance

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21
Q

endothelial cells in the artery

A

run parallel to the flow in the artery

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22
Q

vascular smooth muscle cells in artery

A

wrap around the artery and when they contract they squeeze the artery and the lumen shrinks

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23
Q

what reduces contractility in the arteries

A

when the membrane potential is lowered and the cell becomes hyper polarised because of potassium efflux. the voltage dependent calcium channels become inactivated. less calcium is able to enter the cytoplasm globally and that reduces the contractility.

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24
Q

pressure myography

A

spontaneous pressure induced constriction or time

measures the diameter of isolated, pressurized arteries to assess the functional activity of smooth muscle and endothelial cells

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25
Q

how does calcium both contract and dilate the arteries

A

influx of extracellular calcium contracts the artery the the pressure is present. however calcium is also released by vascular smooth muscle events as ‘small release events’ - calcium sparks. these are vasodilatory signals.

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26
Q

contraction mechanism

A
  1. intraluminal pressure
  2. membrane depolarisation
  3. voltage gated Ca2+ channels
  4. Ca2+
  5. pressure induced construction
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27
Q

calcium spark mechanism

A
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28
Q

both mechanism diagram

A
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29
Q

vascular ‘see-saw’ diagram

A
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30
Q

what is key regulator of vascular function

A

endothelium

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31
Q

what is the function of the endothelium

A

barrier and vasodilation

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32
Q

what regulates endothelial functions

A

intracellular Ca2+ levels, the release of nitric oxide, prostaglandins and dilating factors

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33
Q

what are the different vasodilatory pathways

A
  • release of nitric oxide
  • endothelial dependent hyperpolarisation
  • prostacyclin (cycko-oxygenase pathway)
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34
Q

small arteries regulated by membrane potential diagram

A
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35
Q

what is the metabolic rate

A

the amount of energy liberated per unit of time

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36
Q

what happens when same level of exercise is maintained

A

the rate of oxygen consumption will remain steady

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37
Q

how does lactic acid get removed

A

converted to glycogen

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38
Q

how does the PO2 level change during exercise

A

goes from 40mmHg to 25mmHg so alveolar-capillary gradient is raised

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39
Q

what is the value of oxygen entering blood during exercise

A

4000ml/min

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40
Q

what does brainstem detect

A

increases in carbon dioxide and to a lesser extent reduction in oxygen In the blood

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41
Q

what does brainstem detection lead to

A

sympathetic innervation of the heart, lungs and arteries. this increases the heart rate, breathing rate and contraction of the ateries and leads to increase of oxygen in the blood

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42
Q

what happens to curve when you reduce pH

A

curve shifts to the right and there is increased oxygen delivery to the muscles

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43
Q

what shifts the curve to the right and what is the name of this effect

A
  • temperatures, 2,3-BPG, carbon dioxide and protons
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44
Q

how is BPG produced

A

by red blood cells during glycolysis

45
Q

when is the curve shifted to the left

A

as the blood temperature is reduced compared to the muscles

46
Q

what do reductions in temperature and increase in blood pH do

A

will increase the affinity of haemoglobin for oxygen

47
Q

what does increase in DPG and CO2 in the muscles during exercise do

A

encourage haemoglobin to release oxygen

48
Q

what does activation of the SNS cause

A

arterial vasoconstriction

49
Q

what does active hyperaemia do

A

dilation of skeletal muscle arterioles leads to a reduction in total peripheral resistance which reduces the mean arterial blood pressure

50
Q

where do the baroreceptors send electrical impulses

A

the medulla oblongata

51
Q

starlings law explantation

A

as venous return causes an increase in the load on muscle fibres this increases the stretch on the heart muscle which in turn increases the contractility
At rest and diastolic volume of the ventricle does not cause optimal overlap of actin and myosin
As the venous return increases, the ventricular wall is stretched more and there comes a point where there’s a more optimal degree of overlap between the action and myosin and the stretching of the muscle increases the affinity of troponin C calcium which causes a greater number of cross bridges to form
So an increase in sympathetic tone means the increased noradrenaline increases intracellular calcium and this results in a faster cross bridge formation which causes an increase in conrtactility
This means there’s an increases in stroke volume despite the reduced filling time because the heart rate has increased

52
Q

what does aerobic exercise training cause

A

eccentric left ventricular hypertrophy

53
Q

what does Fick equation state

A

that oxygen available to muscles increases by increase CO or muscles ability to extract oxygen from arterial blood

54
Q

haemoconcentration

A

we get an increase in the hydrostatic pressure across the capillary wall
Means that more blood is squeezed out of the capillaries into the interstitial space surrounding the muscles
Increase in oncotic pressure across the capillary wall and this is because metabolites leak out of the muscle and into the interstitial space and this increase in oncotic pressure also helps to drive fluid out of the muscle cell capillaries
And because of this loss of fluid there is effectively an increase in the concentration of red blood cells and that increases concentration gradient of oxygen from the capillaries to the muscles and this therefore speeds up diffusion
Muscles are more efficient at extracting oxygen from capillaries

55
Q

diagram for haemoconcentration

A
56
Q

when does greatest contractile force occur

A

when there is less overlap between actin and myosin. as cardiac muscle stretches the degree of overlap between actin and myosin is reduced

57
Q

average VO2 max in men and women

A

men is 40-50 and women is 30-40

58
Q

UK physical guidelines advice (LEARN)

A
59
Q

what is blood pressure

A

cardiac output x total peripheral resistance

60
Q

what is the cardiac output

A

stroke volume x heart rate

61
Q

what is the stroke volume explanation

A

volume of blood ejected per beat. it is equal to the end diastolic volume. this is the volume of blood in the ventricles at the end of diastole.

62
Q

other way to work out stroke volume

A

end diastolic volume - end systolic volume

63
Q

what is the preload

A

the tension in the cardiac myocytes before they contract.

64
Q

contractility

A

contraction force of the myocardium for a given preload

65
Q

what is the after load

A

the blood pressure in the aorta and pulmonary trunk

66
Q

what decreases the heart Tate

A

acetylcholine
cold temp
intense visceral pain

67
Q

what is the total peripheral resistance effected by

A
  • viscosity of the blood - stable
  • vessel length - unchanged
  • vessel radius - easily changed
68
Q

how are blood vessels maintained

A

in a state of partial vasoconstriction

69
Q

where is vessel radius controlled

A

controlled by the vasomotor centre in the medulla oblongata

70
Q

what are the sensors of blood pressure control;

A
  • baroreceptors
  • volume receptors
  • chemoreceptors
  • osmoreceotpors
71
Q

neural control of the BP

A
  • automomic nervous system
  • directly influence heart and blood vessels
  • short term mechanism
72
Q

humeral control of BP

A
  • circulating hormones
  • directly influence heart and blood vessels or alter blood volume
  • intermediate and long term mechanisms
73
Q

where are baroreceptors found

A

carotid and aortic senses

74
Q

what nerve is connected to the carotid sinus

A

glossopharyngeal nerve

75
Q

what nerve is connected to the aortic sinus

A

the vagus nerve

76
Q

where is afferent information take to

A

the nucleus solitarius in the brain stem. it modulates the activity of the CV centres and sensitivity of the receptors can be altered

77
Q

accelerator centres in the brain

A

vasomotor centre and cardiac accelerator are groups of sympathetic neurones in the medulla

78
Q

inhibitor centre

A

dorsal motor nucleus of the vagus and the nucleus ambiguous. tonally active - vagal tine

79
Q

what does vagal tone do

A

slows heart rate

80
Q

what happens if BP goes up

A

increases firing rate to cardiac and vasomotor centres.

  • stimulates cardio inhibitory centre, increase in PNS activity to the SA node and therefore decrease in heart rate -
  • inhibits cardioacceleratoe and vasomotor centres, decrease in SNS activity snd therefore decreased heart rate and vasoconstriction
81
Q

what happens f BP falls

A

there is a decrease in firing rate to cardiac and vasomotor centres

  • stimulates the cardioaccelerator and vasomotor centres, then increase in SNS activity to SA node and increase in heart rate which increases the force of contraction and vasoconstriction
  • inhibits cardio inhibitory centre therefore decreased PSN activity to SA node and therefore increased heart Tate
82
Q

what happens if blood volume is not replaced?

A
  • venous return continues to fall therefore decreased EDV
  • the heart rate increase therefore less filling time and EDV decreased
  • decreased EDV therefore decreases force of contraction (starlings Law of the heaert0
83
Q

valsalva manoeuvre

A
84
Q

humoral control systems

A
  • catecholamines - epinephrine and norepinephrine
  • RAAS
  • ANP (atrial natriuretic peptide)
  • ADH
85
Q

where are catecholamines released

A

from the adrenal medulla

86
Q

alpha 1 vascular smooth muscle cells

A

vasoconstrictor

87
Q

alpha 2 presynaptic membrane

A

negative feedback

88
Q

beta 1 SA node and cardiac muscle

A

increased heart rate and contraction force

89
Q

beta 2 vascular smooth muscle in heart

A

vasodilator, bronchodilator

90
Q

beta 3 adipocytes

A

lypolysis

91
Q

RAAS system.

A
92
Q

atrial natriuretic peptide ANP

A
93
Q

ADH production

A

produced by the hypothalamus, secreted in the pituatary and released by the posterior pituariry

94
Q

ADH

A
95
Q

how would the carotid sinus baroreceptors respond to occlusion of both common carotid arteries and what would be the cardiovascular responses?

A
96
Q

physiological response to haemorrhage

A
97
Q

are blood vessels innervated?

A

yes by synthetic fibres only

98
Q

what is normal LDL:HDL ratio in males

A

100mg/dl LDL but > 40 mg/dl HDL

99
Q

In the Stages of Change Model, in which stage do people begin ‘weighing’ up the pros and cons

A

Contemplation

100
Q

Approximately what percentage of women aged over 75 have hypertension

A

65%

101
Q

By what mechanism do dihydropyridines decrease blood pressure

A

Increasing natriuresis

102
Q

What is the main social predic

tor of smoking initiation

A

Having parents that smoke

103
Q

what is nitric oxide released in response to

A

parasympathetic nervous stystem stimulation

104
Q

direct pathway of NO

A

the PNS uses NO as a neurotransmitter and has a direct effect on the smooth muscle cells. The drug GTN, once converted into NO, acts directly on the smooth muscle cells

105
Q

the indirect pathway of NO

A

the PNS uses acetyl choline as a neurotransmitter and stimulates the endothelial cells to produce NO, which then act on the smooth muscle cells.

106
Q

how is nitric oxide stimulated in endothelial cells

A

Nitric oxide synthase (NOS) enzymes in endothelial cells synthesize NO from arginine and oxygen and by reduction of inorganic nitrate.

107
Q

what does nitric xide activate

A

Activates guanylate cyclase (G-cyclase).
This increases formation of cGMP, which activates protein kinase G.
This leads to the dephosphorylation of myosin light chains and sequestration of intracellular Ca2+, with consequent relaxation.

108
Q

what vasocontrictors can stimulate NO

A

angiotensin II

109
Q

Endothelin

A

Endothelin is present in the endothelial cells of all blood vessels.
It greatly increases when the vessels are injured.
After severe blood vessel damage, release of local endothelin and subsequent vasoconstriction helps to prevent extensive bleeding from arteries.

Semester 2 Case Studies (11 decks)

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