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PHSL 232 > L26 > Flashcards

L26 Flashcards

1
Q

what are they 2 types of hypertension and what % of people with hypertension have each type

A

primary hypertension = 95% of people

secondary = 5%

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2
Q

what causes primary hypertension

A

the cause is unknown = idiopathic essential

it happens with stiffer arteries with ageing

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3
Q

what causes secondary hypertension

A

this has specific causes

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4
Q

the 2 main causes of primary hypertension are an increase in arterial blood volume and a decrease in arterial compliance

which is the most important factor

A

we don’t know between these 2

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5
Q

Salt retention in kidney = increase in blood volume

autoregulation result in arteriolar vasoconstriction

arterial compliance decrease = increase in total peripheral resistance (TPR)

how do these processes relate to each other

A

Sympathetic activation of the arterioles (hypothalamus-medulla oblongata) = arteriolar vasoconstriction -> arterial compliance decrease -> increase TPR

this causes less blood flow to kidney = release of vasoactive substances and salt retention which increase blood volume

These are not mutual inclusive or inclusive

This indicates the important of the kidney and arterial compliance and sympathetic activation pathway in hypertension. therefore they are both as important as each other

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6
Q

Sympathetic is being activated during moderate exercise

what does this cause

A

In the vessels we have vasodilation is some vascular beds to that the tissues get more O2 but constriction in other vascular beds

As a consequences of sympathetic activation and excerise means that TPR decreases. This means that during moderate exercise arterial pressure is kept constant. It increases slightly during intense exercise

The increase in overall sympathetic activity then HR goes up SV goes up and MAP goes up

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7
Q

BP is very similar in all mammals

what is an example where this is not the case

A

a giraffe

their MAP is 172-200mmHg

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8
Q

giraffes are not born hypertensive (they are born normotensive)

why do they develop high blood pressures

A

because of their neck

As giraffe grows, blood flow to cardiovascular brainstem reduces, due to effects of gravity

Sympathetic nerve outflow increases to cause nerve-mediated hypertrophy of vessel wall (G-suit)
Increase in TPR, and thereby MAP, to preserve cerebrovascular flow

tibbia artery will have massive wall and small luman

carotid artery will have huge luman

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9
Q

giraffes have to put thei heads down to drink

how do they overcome this problem

A

Minimise blood flowing back into head:
Upper neck - rete mirabile
Jugular veins - seven valves

Lower legs - great pressures
Very tight sheath of thick skin over lower limbs
maintain high extravascular pressure

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10
Q

what are some consequences of hypertension

A
  • Kidney disease
  • Development of Atherosclerosis – Stroke
  • Atrial Fibrillation
  • Myocardial Infarction / Coronary artery disease
  • Cardiac Remodelling (Hypertrophy - Heart Failure)
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11
Q

why do you get cardiac remodelling of the heart in hypertrophy

A

Increases workload (afterload) of the heart because of the stiffer tube (aorta) to eject blood into causing a faster returning reflected pulse wave

it is also because of higher resistance to the output

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12
Q

what ae the 2 ways of cardiac remodelling

A

there is remodelling at the cellular level

OR

remodelling at the organ level

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13
Q

what is cellular remodelling of the heat

A

hypertrophy of the cardiac myocytes

or hypertrophy because of fibrosis (this passably could be organ remodelling)

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14
Q

describe hypertrophy of the cardiac myocytes

A

Increase in number of sarcomeres in the cardiomyocytes (size)
NOT in number of cardiomyocytes or the size of the sarcomeres (might even be less cardio myocytes because of apoptosis)

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15
Q

what causes fibrosis in the heart

A

If the hearts is under increased load there are tiggers to make more fibrosis

This is because you are the making the cells bigger but you also need to make the scaffolding bigger to support them

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16
Q

hypertrophy cased by fibrosis causes an increase in the extracellular matrix

what does this contain

A 
Collagen type I + III
Elastin
Proteoglycans
Laminin
Fibronectin
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17
Q

what collagen type increases first in fibrosis

A

type 3 and then type 1

i think type 3 is the stiff one

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18
Q

what is the difference between concentric and eccentric remodelling

A

concentric = wall thicker

eccentric = luman bigger

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19
Q

does pressure overload cause concentric or eccentric remodelling

A

concentric

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20
Q

does volume overload cause concentric or eccentric remodelling

21
Q

what does pressure overload cause

A

thickening of the LV and no dealation in early stages of disease

22
Q

what does volume overload cause

A

thinning of the LV and significant dilation

this is usually because there is something wrong with the valve

23
Q

what is hypertrophic cardiomyopathy caused by

A

predominantly genetic mutations

24
Q

what does hypertrophic cardiomyopathy cause

A

gross thickening of the LV walls with no dilation/decrease in LV chamber size

25
Q

cardiac dilation in heart failure is because of

A

increase in myocyte length&raquo_space; and width

leads to…..

extensive fibrosis

myocyte death

advanced cardiac disfunction

26
Q

pathological hypertrophy in heart failure is because of

A

increase in myocyte length &laquo_space;and width

fibrosis

maybe some cardiac dysfunction

27
Q

hypertrophy in cardiac failure leads to

A

you have an increase in MAP which leads to..

increase wall thickness to
normalise wall stress. this further increase in MAP
(vicious circle)

You get a increase in wall thickness and MAP to normalise the stress within the wall. You need this increase in pressure because you need to increase the afterload. If you didn’t change the wall thickness then the stress in th cardiomyocytes would be very increased

This then goes into a deadly cycle and eventually leads to thinned ventical

28
Q

what % of cardiac failure is because of either concentric or eccentric hypertrophy

A

concentric = 50-60%

eccentric = 40-50%

29
Q

describe concentric heart failure

A 
Heart failure with preserved
ejection fraction (HFpEF)

this is also known as diastolic heart failure

30
Q

describe eccentric heart failure

A 
Heart failure with reduced
ejection fraction (HFrEF)

also known as systolic HF

31
Q

what are the 2 types of heart failure

A

concentric/diastolic HF

eccentric/systolic HF

32
Q

what kind of heart failure are males and females more likely to get

A

male = eccentric/systolic

female = concentric/diastolic

33
Q

factors influencing form of remoderling/transition

these show that the heart can respond in many ways to hypertension

A

Blood pressure (Hypertension) = Concentric

Old age = Concentric

Coronary Artery Disease = Concentric

Valve leaks = Eccentric
Obesity = Eccentric / concentric (predominantly eccentric)

Diabetes = Concentric / eccentric (predominantly concentric)

Familiar Dilated Cardiomyopathy = Eccentric

34
Q

in systemic hypertension what is the effect on the right ventricle

A

ealt stage = mo effect

late stage = hypertrophy of RV

35
Q

what causes right ventricular hypertrophy

A

Increase LV filling pressure translates into pulmonary circulation

Hypertrophied LV interacts
with the RV

the above means that When the septum gets really thick (because of left ventricular hypertrophy) it will push into the right ventricle which will then cause the right vertical to get bigger to compensate

36
Q

In the early stages of hypertension the right ventricle does not remodel

BECAUSE

the development of atherosclerosis in the aorta increases afterload.

A

both statments are correct but not causally related

37
Q

what are some risk factors for developing hypertension

A
  • Age
  • Ethnicity
  • Family History
  • Smoking
  • Lack of activity/exercise
  • Diet (Lipids, salt, alcohol)
  • Overweight/obesity
  • Diabetes
  • Stress
  • Medications
38
Q

what are the 2 main types of treatments for hypertension

A

change in life sytel and pharmacological

39
Q

what are some lifestyle changes that can decrease hypertension

A
  • Change Diet (less salt & lipids, more fish, fruit & vegetables)
  • Reduce Alcohol consumption
  • Stop Smoking
  • Perform Physical activity - Exercise training
  • Loose Weight
40
Q

what is the role of diuretics on hypertension

A

Thiazides, decrease blood volume

therefore decrease hypertension

41
Q

what is an example of and what do β-adrenergic receptor blockers do

A

carvedilol, decreases CO and baroreceptor sensitivity

therefore decreasing hypertension

(it effects the heart)

42
Q

what do Calcium channel blockers, Angiotensin II receptor blockers and Angiotensin converting enzyme (ace) inhibitors all have in common

A

they also decrease TPR

43
Q

what are Calcium channel blockers, Angiotensin II receptor blockers and Angiotensin converting enzyme (ace) inhibitors often used along side of

A

diuretics (decrease in blood volume)

together these would decrease TPR and blood volume = dramatic effect

44
Q

why is renal denervation an alternative treatment for hypertension

A

The kidney has sympathetic nerves that are innovated and signals are send from the brain to the kidney altering its function

The kidney also has afferent nerves to send signals back to the brain about how the kidney is functioning

This system usually works but when it doesn’t it is because the sympathetic drive from the brain to the kidney and from the kidney back to the brain is increase

Therefore one of the suggested treatment to to stop this communication

45
Q

what does renal denervation involve

A

Radiofrequency ablation of efferent and afferent nerves

46
Q

how does renal denervation use Radiofrequency ablation of efferent and afferent nerves

A

The tip is brought up the aorta into the renal arteriy and then by radial oblation they oblate (cut) both the afferent and efferent nerves

In animals this works really well

47
Q

What do you need to be human and qualify to have a renal denervation

A

Hypertensive patients (160-180 mmHg) taking >2 antihypertensive drugs

48
Q

Nerves can potentially grow back. what test can we do to see if they have

A

they measured muscle sympathetic nerve activity to skeletal muscles. The graph shows an overall activation of skeletal muscle (sympathetic activation)

After 12 months of renal deprivation then you can see that also the sympathetic drive is decreases as well to the muscle showing a over body decrease in sympathetic activation

you can look at the muscles to see if they have less sympathetic nerve activity, if they do then the nerves haven’t grown back

PHSL 232 (30 decks)

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