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Year 2 Medicine @ Lancaster Uni > 1.12 - Hypertension and Blood Pressure 💉 > Flashcards

1.12 - Hypertension and Blood Pressure 💉 Flashcards

1
Q

What is the accepted value for hypotension?

A

Less than 90/60

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2
Q

What is classed as a normal blood pressure?

A

Between 90/60 - 120/80

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3
Q

What is classed as hypertension?

A

Greater than 120/80 (140/90)

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4
Q

What are the different grades of hypertension and the values related to them?

A

Grade 1 - 140/90 - 159/99
Grade 2 - 160/100 - 179/109
Grade 3 - >180/110

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5
Q

What is the definition of primary/essential hypertension?

A
  • Unknown, probably multifactorial aetiology
  • Genetic susceptibilty
  • RAAS abnormalities
  • Na+/K+ transport issues
  • Excessive sympathetic activity
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6
Q

What is the definition of secondary hypertension?

A
  • Caused by lack of exercise
  • Caused by renal, endocrine, respiratory, drugs etc.
  • Coarction of aorta (Congenital narrowing)
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7
Q

What are the three different mechanisms that can help to control blood pressure?

A
  1. Autonomic nervous system
  2. RAAS system
  3. Hormonal control (Kidneys and adrenals)
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8
Q

How is mean arterial pressure calculated?

A

(2 x diastolic) + systolic / 3

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9
Q

How does the autonomic nervous system control blood pressure?

A

Utilises baroreceptors in carotid and aortic bodies to detect changes in blood pressure.
Aortic has a higher threshold
Utilises vagus nerve

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10
Q

Where do baroreceptors send impulses?

A

Send afferent impulses to the medulla in a negative feedback loop

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11
Q

What happens with increased MAP?

A
  • Increased stimulation
  • Decreased sympathetic outflow
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12
Q

What happens with decreased MAP?

A
  • Decreased stimulation
  • Increased sympathetic outflow
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13
Q

What are the three main components of the RAAS system?

A
  • Renin
  • Angiotensin II
  • Aldosterone
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14
Q

How does reduced perfusion trigger the RAAS system?

A

-Reduced perfusion pressure detected in the juxtaglomerular apparatus
-This causes the conversion of pro-renin into renin

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15
Q

What is the action of renin in the RAAS system?

A
  • Converts angiotensinogen into angiotensin I
  • Which is then converted into angiotensin II by ACE
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16
Q

What is the action of angiotensin II?

A
  • Acts on the adrenal cortex to release aldosterone
  • This increases Na+/H2O retention
  • Restoration of blood pressure
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17
Q

What are the different hormones that help to control of blood pressure?

A
  • Aldosterone
  • ADH
  • Adrenaline/Noradrenaline
  • Atrial Natriuretic Peptide (NAP)
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18
Q

What is the action of aldosterone?

A

Increased H2O/Na+ retention which leads to restoration of blood pressure

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19
Q

What is the action of ADH? (Anti-Diuretic Hormone)

A

When it is increased there is less water lost in urine therefore blood pressure is maintained.
When it is increased, more water excreted in urine therefore blood pressure can drop

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20
Q

What is the role of adrenaline/noradrenaline in the control of BP?

A
  • Secreted from adrenal medulla in response to sympathetic stimulation
  • Leads to increased cardiac output and vasocontriction and therefore increased blood pressure
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21
Q

What is the role of atrial natriuretic peptide in the control of blood pressure?

A
  • Secreted from atria vasodilator
  • Reduces renin production and is a natriuretic and diuretic
  • Counters increase in blood pressure and volume caused by RAAS
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22
Q

What percentage of cases of hypertension are classified as primary/essential?

A

Approximately 95%

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23
Q

What percentage of cases of hypertension are classified as secondary?

A

Approximately 95%

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24
Q

What is the definition of stage 1 HTN?

A

BP = 140/90 +
ABPM = 135/80 +

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25
Q

What is the definition of stage 2 HTN?

A

BP = 160/100 +
ABPM = 150/95 +

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26
Q

What is the defintion of severe HTN?

A

Systolic = 180 +
Diastolic = 110 +

27
Q

What is the epidemiology of HTN?

A
  • One of the most prevalent conditions globally
  • Increased risk with age and being a male
  • Is a global health concern
28
Q

What are the clinical features that HTN presents with?

A
  • Headache
  • Fatigue
  • Confusion
  • Retinopathy
  • Angina
  • Dyspnoea
  • Irregular pulse
  • Heamaturia
29
Q

What are the modifiable risk factors relating to HTN?

A
  • Smoking
  • Drinking
  • Exercise
  • Obesity
30
Q

What are the non-modifiable risk factors relating to HTN?

A
  • Genetics
  • Age
  • Sex
  • Family history
  • Other factors (Coagualtion issues)
31
Q

What is the first line management of HTN?

A

ACEi or ARIIA (ARB)

32
Q

How does an ACEi work?

A

Works by inhibiting the RAAS system by reducing/preventing the conversion of angiotensin I into angiotensin II

33
Q

How do angiotensin-II receptor antagonists (ARB) work?

A

They prevent the detection of angiotensin-II by the adrenal cortex which prevents the release of aldosterone

34
Q

When would you give a CCB as a first line medication?

A

In those who are over 55 and/or black/caribbean

35
Q

What is the second line treatment for HTN?

A

ACEi or ARIIA (ARB) with a CCB

36
Q

When are thazide diuretics used as a second line treatment for HTN?

A

If the CCB can not be tolerated by the patient

37
Q

What is the third line treatment for HTN?

A

ACEi or ARIIA (ARB) + CCB or Thiazide Diuretic

38
Q

When can HTN be classified as resistant?

A

When third line interventions have little to no effect on the blood pressure of the patient.

39
Q

What is the recommendation for resistant hypertension?

A
  • Refer on to a specialist
  • Add low-does spironolactone (Potassium sparing diuretic)
40
Q

What is an example of an ACEi and what is its suffix?

A

-pril
Eg. Ramipril, Lisinopril

41
Q

What is an example of an ARIIA and what is its suffix?

A

-sartan
Eg. Losartan

42
Q

What is an example of a CCB and what is its suffix?

A

-dipine
Eg. Amlodopine

43
Q

What is an example of a beta blocker and what is its suffix?

A

-olol
Eg. Propranolol

44
Q

What is an example of a diuretic and what is its suffix?

A

-ide
Eg. Furosemide

45
Q

What are some different factors that contribute to the development of HTN?

A
  • Cardiac problems
  • RAAS problems
  • ANS Overstimulation
  • Hormones
  • Blood vessels
  • Co-morbs
46
Q

What investigations can be done to monitor blood pressure?

A
  • ABPM or HBPM
  • Allows pattern of BP to be established
47
Q

What none-BP investigations can be done for HTN?

A
  • ECG
  • FBC
  • Ultrasound
  • Angiogram
  • Urinanalysis
48
Q

What is the genetic contribution to the development of HTN?

A
  • Most likely a combination of genes
  • More likely when both parents have HTN
  • Ethnic component
  • Genetic abnormalities that cause other conditions
49
Q

How does HTN effect blood vessels?

A
  • Causes acceleration of atherosclerosis formation
  • Caused by increased flow of normal protein through vessels
50
Q

How does HTN effect the heart?

A
  • Major risk factor for the development of IHD/CHD
  • Can lead to LVHT
  • Decreased prevalance due to use of antihypertensives
51
Q

How does HTN effect the eyes?

A
  • Blurred vision due to papillodema and retinal haemorrhages
  • Gradual degradation of blood vessels in the eye
  • Can lead to hypertensive retinopathy (Pressure on vessels in the back of the eye)
52
Q

What are the features of hypertensive retinopathy?

A
  • Narrowing of arterioles
  • AV nipping
  • Cotton wool spots
  • Haemorrhages
  • Papilloedema
53
Q

How does HTN effect the nervous system?

A
  • A frequent cause of intracerebral haemorrhage
  • AF can complicate hypertension and can lead to embolic stroke
54
Q

How does HTN effect the kidneys?

A
  • Can be the cause/result of renal disease
  • Renal vessels can be thickened due to athersclerosis
  • Can lead to proteinuria
  • Can lead to bilateral RAS (Renal artery stenosis)
55
Q

What is the drug profile of an ACEi?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Relaxes veins/arteries to reduce BP
  • Cough, Hyperkalaemia
  • CI = Bilateral RAS, Angio-oedema
  • Example = Ramipril - 2.5mg - 10mg
56
Q

What is the drug profile of an ARB?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Antagonises the effects of angiotensin-II
  • Hyperkalaemia
  • CI = Bilateral RAS
  • Example = Losartan - 25mg - 100mg
57
Q

What is the drug profile of a dihydropyridine CCB (DHP CCB)?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Peripheral vasodilation (Vascular selective)
  • Constipation, headaches
  • Indications = Specified in pregnancy
  • Example = Amlodopine - 5mg - 10mg
58
Q

What is the drug profile of a non-dihydropyrdine CCB (Non-DHP CCB)?

A
  • Peripheral vasodilation (Cardiac selective)
  • Constipation, Bradycardia
  • CI = Bradycardia, Heart block
  • Example = Verapamil - 120mg - 480mg
59
Q

What is the drug profile of thiazide diuretic?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Vasodilation, H2O loss
  • Electrolyte imbalances
  • Indications = Heart failure
  • CI = Gout
  • Example = Indapamide - 1.5mg - 2.5mg
60
Q

What is the drug profile of a K+ sparing diuretic?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Salt/H2O loss
  • Ion imbalances
  • Indicated = Resistant hypertension
  • CI = Hyperkalaemia, Addison’s
61
Q

What is the drug profile of a beta-blocker?

A
  • Vasodilation, reduced contractility (Block effects of adrenaline)
  • Bradycardia, Sleep issues
  • Indications = IHD, Heart failure
  • CI = Asthma
  • Example = Bisoprolol - 2.5mg - 10mg
62
Q

What is the drug profile of an alpha-blocker?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Venodilation
  • Postural hypotension
  • CI = Heart failure
  • Example = Doxazosin - 1mg - 8mg x2
63
Q

What is the drug profile of central acting drug agents?

Mechanism, SE, Indications, Contra-indications, Example

A
  • Sympatholysis
  • Depression, Drowsiness
  • Indications = Methyldopa in pregnancy
  • CI = Mood disorders
  • Example = Methyldopa 250mg - 300mg x3

Year 2 Medicine @ Lancaster Uni (15 decks)

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