Hypertension 1 Flashcards
1
Q
How many people die per year because of cardiovascular disorders?
A
20 million
31% of all deaths
Heart attack and stroke 85%
2
Q
Influences
A
lifestyle and genetics
3
Q
Aetiological classes of hypertension
A
primary (essential, idiopathic)
secondary
3
Q
Primary
A
cause unknown but risk factors known
3
Q
Hyperlipidaemia
A
high levels of cholestrol
4
Q
Secondary
A
symptom of other identifiable condition or caused by medication
5
Q
What causes secondary hypertension?
A
diabetes
kidney disease
abnormal production of adrenal or thyroid hormones
6
Q
Renal artery stenosis
A
renal artery is blocked by atherocsclerosis which reduces blood flow to the affected kidney
the cardiovascular system tries to compensate for this by increasing the blood pressure using the renin angiotensin aldosterone system (RAAS) (heavily targetted by antihypertensive drugs)
6
Q
Pheochromocytoma
A
tumor of adrenal medulla formed from neuroendocrine chromaffin cells
many but not all pheochromocytomas synthesize adrenaline and release it into the blood stream (happens paroxysmally so in attacks)
patients will consequently have periods of over activation of their sympathetic nervous system
this increases heart rate and force of contraction leading to increased blood pressure
7
Q
Risk factors for hypertension
A
- age (increases with age and non modifiable factor)
- 30-60% genetic but no “hypertension gene” (family studies specifically twin studies show that 30-60% of risk explained by genetics)
- lifestyle (modifiable)
8
Q
Genetic risk factor protein variants (4 answers)
A
- Angiotensin converting enzyme (ACE)
- Angiotensinogen
- AT1R
- Nitric oxide synthase 3
9
Q
Angiotensin converting enzyme (ACE)
A
important target for antihypertensive drugs
10
Q
AT1R
A
receptor for angiotensin hormone
10
Q
Angiotensinogen
A
precursor to angiotensins (series of peptide hormones involved in blood pressure control)
11
Q
Nitric oxide synthase 3
A
enzyme that produces nitric acid (signals regulate blood vessels
12
Q
Lifestyle factors (7 answers)
A
- smoking
- diet
- poor sleep
- obesity
- inactivity
- smoking
- alcohol
- stress
13
Q
Obesity
A
- produces pathophysiological changes associated with hypertension
- increases insulin resistance which leads to high blood sugar levels
- causes over activation of renin angiotensin aldosterone system (regulator of blood pressure)
13
Q
Diet
A
- highly associated with hypertension
- high sodium intake and low potassium intake increases blood pressure via renal mechanisms
- large amounts of saturated, trans fats, high sugar intake, and low dietary fibre increase risk (found in highly processed foods)
14
Q
Inactivity
A
- independant risk factor through wide range of mechanisms
- results in increased sympathetic nervous system activity
- can produce indirect increases risk through weight gain
15
Q
Smoking
A
- nicotine causes release of adrenaline leading to vasoconstriction
- smoking damages lining of blood vessels leading to dysfunction
16
Q
Alcohol
A
- increases blood pressure directly by increasing activation of sympathetic nervous system and renin angiotensin outer system
- associated with weight gain and poor diet
17
Q
Stress
A
- chronic stress levels cause overproduction of cortisol which leads to increased blood pressure
- maladaptive behaviours associated with stress such as overeating, smoking, and drinking also increases blood pressure
18
Q
Sleep
A
sleep apnea (stop breathing for periods once asleep linked to increased hypertension risk)
18
Q
NICE
A
National Institute for Health and Care Excellence
19
Final guidelines
after considering professional feedback the expert community will refine the guidelines and publish them
NICE guidelines aim to produce best practice advice for doctors
19
Reviewing evidence
expert committee (healthcare professionals, researchers, patient representatives) reviews evidence on research and treatments based on:
1) effectiveness
2) safety
3) value for money
make recommendations on whether and how treatments should be used in NHS
19
Generating clinical guidelines (3 steps)
1) request to NICE
2) NICE sets scope
3) gather evidence
20
Consultation
after formulating draft guidelines, they are sent out for consultation to gain public and professional feedback
21
Other resources
to support implementation of guidelines NICE produces a variety of tools and resources for health care providers eg: step by step on which drug should be used first and what other alternatives are there
22
ASCOT trial
- prior to 2006 the main treatment for hypertension recommended by NICE was beta one adrenoceptor antagonist and thiazide diuretics (increase urine production)
- in 2006 NICE changed its guidelines significantly for patients younger than 55
23
Younger than 55
- angiotensin converting enzyme (ACE) inhibitors
- angiotensin receptor blockers (ARBs)
24
Older than 55 or of black ancestry
- calcium channel blockers (CCB)
- thiazides (diuretics)
25
Evidence used by NICE
result of Anglo Scandinavian cardiac outcome trials (ASCOT)
trial recruited 20,000 UK, Irish, and Nordic patients and treated them with either beta blockers plus thiazide if additional blood pressure control was required OR calcium channel blocker plus ACE inhibitor if additional control was needed
observed rate of developing serious cardiovascular disorders, results indicated that a significantly lower rate of stroke and heart attack in patients taking calcium blockers + ACE
rate of type 2 diabetes, known side effect of beta blockers, lower in people with calcium channel blockers +ACE
26
Step 1: Diagnosis + Classification
1 of 3 bands:
under 140/90 mmHg (BP) or under 135/85 mmHg (ABPM)
stage 1 (140/90-179/119 and 135/85-149/94)
stage 2 (180/120 or more and 150/95 or more)
27
Under 140/90 mmHg (BP) or under 135/85 mmHg (ABPM)
drug treatments not considered and person is offered lifestyle advice
28
Stage 1 hypertension
lifestyle advice offered but next step depends on how old they are
29
Stage 2 hypertension
lifestyle advice offered but next step depends on how old they are
30
Hypertension under 40
rare and may be indication of serious illness so evaluated by specialist
31
Hypertension over 40
treatments options discussed and doctor will encourage if other risk factors involved or if they have stage 2 hypertension
32
Stage 3
assessed immediately for damage to target organs such as kidney or eye then drug treatments offered
33
Treatment option
- stepped approach care
- hypertension care has 4 steps
34
Patient characteristics
treatment depends on age, diabetic status, and family origin
angiotensin receptor blockers (ARBs) are favored over angiotensin converting enzyme inhibitors (ACE) for Africa/Caribbean patients
34
Stepped approach care (2 types)
1) first line therapy: based on individual characteristics
2) second line therapy: combination of treatments
35
Step 1
divide patients into those with diabetes and those without
diabetic patients should be given either ACE inhibitor or ARB
non-diabetic patients subdivided according to age and family origin
patients under 55 years old and not of African origin are given ACE OR ARB
patients over 55 and of African origin given calcium channel blockers
35
Step 2
combination of drugs offered
people will diabetes or people under 55 not African given angiotensin converting enzyme inhibitor or angiotensin receptor blocking drug +calcium blocker or thiazide diuretic
people over 55 or African offered calcium channel blockers +angiotensin converting enzyme inhibitor, angiotensin receptor blocker, thiazide, or thiazide like diuretic
36
Step 3
angiotensin converting enzyme inhibitor or angiotensin receptor blocking drug + thiazide diuretic + calcium channel blocker
37
Step 4
resistant hypertension and patients may need more drugs which included adrenoceptor antagonist drug or spironolactone
38
Polypharmacy consequences
- drug interactions
- lots of side effects
- drugs to treat side effects
38
Polypharmacy stats
- 60% of people with hypertension taking 2+ drugs
- 25% of adults in UK take 3+ drugs
- 33% of people over 75: 6+ drugs
38
Polypharmacy
5+ more drugs used
39
AHA/ACC guidlines
in US thiazide, CCB, ACE inhibitors, and ARBs are first line treatment
thiazide + CCBs for older patients and African
ACE inhibitors + ARBs for diabetic patients
39
Evidence base of AHA/ACC
ALL HAT antihypertensive and lipid lowering treatment to prevent heart attack
thiazides vs calcium channel blockers/ ACE inhibitors
thiazide superior especially in African people (35% of participants)
40
AHA/ACC vs NICE
start drugs at stage 1 in AHA/ACC (130-139mmHg)
combinations start at stage 2
40
Renin Angiotensin Aldosterone System (RASS)
minute to hour timescale
activated by decreased blood flow to kidney
kidney detects low levels of sodium by SNS
renin angiotensin aldosterone hormone cascade causes vasoconstriction by direct effects on blood vessels
increases production of aldosterone and antidiuretic hormone which promotes salt and water retention by the kidney increasing blood volume
both effects increase blood pressure
41
Generation of angiotensin hormones
RASS system is a peptide signaling pathway that regulates blood pressure
renin, a protease, cleaves inactive angiotensinogen into angiotensin I, which is then converted by ACE into the active angiotensin II
angiotensin II acts mainly on AT1 receptors causing vasoconstriction and stimulating aldosterone release—key in hypertension
can also be further processed into angiotensin III and IV, which have limited activity at AT1 receptors and interact with other receptors
42
Where is renin secreted?
Renin is secreted into the circulation from a distinct set of cells in a part of the kidney called the juxtaglomerular apparatus
By contrast, angiotensin converting enzyme (ACE) and the two aminopeptidases (AP-A, AP-N) are produced locally in the tissues where angiotensin II is made. This means that while renin acts as a kind of global control for RAAS, ACE and AP-A and AP-N can bring about local fine-tuning of the system
43
How is renin release stimulated?
Renin release is stimulated by factors like noradrenaline and adrenaline via β1 adrenoceptors, certain hormones, prostacyclins, low kidney blood pressure, and reduced sodium in the distal tubule
44
Where is angiotensinogen produced?
angiotensinogen which is a serum globulin is produced in the liver and secreted into the circulation
45
Where are ACE and AP-A and AP-N produced?
by contrast (ACE) and the two aminopeptidases (AP-A, AP-N) are produced locally in the tissues where angiotensin II is made
this means that while renin acts as a kind of global control for RAAS, ACE and AP-A and AP-N can bring about local fine-tuning of the system
