Lec 4: Hypertension Flashcards
Hypertension
Definition =
LOOK AT SLIDE 4*** FYI
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= Increased BP associated with increased risk of target organ damage
- kidney, eyes, brain, heart
- 2-3x risk of Ischemic heart disease
- 3-5x risk of stroke
- generally no symptoms
- More effects on short term regulation
- [Primary effects] on peripheral resistance through vasoconstriction
- DIRECT nerve stimulation & SMOOTH muscle (vessel) contraction
- [Secondary Effects] - volume control
- increase in ADH (released by the hypothalamus (pituitary gland)
- Renin - Angiotensin system
[Retain water & salt this leads to volume expansion & therefore increases BP
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- Renin-angiotensin-aldosterone system* - to understand not memorize
- >
-> ->
- LONGER term regulation
- Renin angiotensin system
- more effects on volume control, lesser effects on resistance
-> reduced BP (=less blood perfusion in kidney) stimulates kidneys to release Renin (stimulate conversion of angiotensin -> Angiotensin 1
-> Angiotensin 1 needs ACE enzyme to convert to Angiotension 2
-> Angiotensin 2 brings BP up & has all the effects:
[1 sympathetic activity 2 Na, Cl reabsorption, H2O retention, K excretion 3 Aldosterone secretion 4 Arteriorolar vasoconstriction 5 ADH secretion]
Epidemiology
- Most common _________
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CVD risk factor
- 1 in 4 Canadians had hypertension (2012-2015 from CHMS)
- high numbers and are not going down
- Primary HTM in 90-95% of cases
- multi factorial causes
- 5-10% secondary to another condition (damage to organ)
- renal disease - decrease blood flow to kidneys -> stimulates renin-angiotensin system
- Adrenal disorders - excess Epinephrine & Norephinephrine release
- CHF - less blood reaches the kidneys -> activates renin-angiotensin system & volume overload
Familial Risk Factors - - - - - [ ]
- Heritability from family & twin studies is about 30-50%
- Studies to date suggest few ppl have specific genetic defects that lead to high blood pressure
- Eg. defects in Na reabsorption in kidney (channels are not functioning)
- SNS hyperactive
- Abnormal renin- angiotensin system
[Blood pressure affected by many genes -> most ppl will have many variations which each affect blood pressure to a small degree]
- Simple tool to define higher risk
- Family history of HTN in first degree relative
- Male <55, Female <65 (strong risk factor) –> this is when you consider strong family history
- Ethnicity
- First nations people & people of African or asian descent at higher risk
Modifiable Risk Factors - - - -
- Low PA level
- Smoking
- Obesity
- increased blood volume, increased SNS output, increased peripheral resistance
- 1/3 obese have metabolic syndrome
- dyslipidemia - unclear if this is a causative
risk factor or associated with metabolic syndrome
- Stress & coping mechanisms for stress
Dietary Factors: SALT
- Salt sensitive =
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TABLE slide 16 - to Understand:
Possible Mechanisms of dietary salt sensitivity - - - - - - - -
- Salt Sensitive: 30-50% of those with hypertension
= Salt sensitivity (also called salt sensitivity of blood pressure) describes an increased sensitivity of someone’s blood pressure to salt consumption. Technically, a person is considered salt-sensitive when they have at least a 5 mmHg rise in blood pressure in response to a change in salt intake. - Carefully controlled dietary protocol: Gold standard method for assessing salt sensitivity
- More likely to be salt sensitive: African descent, Type 2 DM, Metabolic Syndrome, Elderly
: assess changes in ppl according to salt intakes
- Acute high Na intake - retention of fluid
- Chronic high Na intake
- decrease capacity of kidney to excrete Na2+
- possible impaired baroreflex in the SNS
- increased pressure needed to trigger response
[BAROREFLEX = is the fastest mechanism to maintain BP at nearly constant levels —- found in the vessels]
- increased pressure needed to trigger response
- Altered ion transport in vascular smooth muscle
- increase Na2+ induces increased intracellular Ca2+ –> increased contractility
- leads to increased resistance
Other Dietary Factors - - - - -
- Excessive alcohol
- Low dietary K associated with low fruits & vege * low fibre intakes
- Low dietary Ca & Mg
- Ca as a single nutrient VS Ca as a part of a healthy diet
[Ca & Mg as part of a whole diet with other nutrients (Fat, increased fruit/vege) was found to be effective in regulating BP compared to Ca as single nutrient] * Food matrix is important - High saturated fat
Role of Calcium in the constriction of blood vessels- To understand
->
Dietary Ca: Potential mechanisms of action for blood pressure regulation - to understand
*** SLIDE 20 - KNOW the ones with the orange arrows
EX:
FYI - SLIDE 22 - CHEP key messages for the management of hypertension**
-> As part of diet - Ca prevents its accumulation in blood vessels - prevents excess contraction [because it acts on other things]
Ca leads to constriction at cell level
Ca accumulation is caused by 2 sources - 1 enter @ L-type Ca channels - 2 Sarcoplasmic Reticulum releases Ca from inside cell
EX: promotes excretion of sodium
decreases intracellular calcium
Diagnosis & Management - Standardized technique: - - - [ ] - Devices: - - - - White Coat effect =
- International Classification * - SLIDE 24
Criteria for Diagnosis - - - -
FLOWCHART - Slides 26-29 ** Review
- Have patient rest for 5 min
- Use appropriate cuff size
- Usually discard 1st reading
[ Do BP measurement in triplicate & take avg of #2&3, IGNORE the 1st reading as it is usually high (outlier) ] - Mercury manometer gold standard
- Validated electronic devices now common
- Home devices
- Ambulatory measurement -> always wear machine
= effect of BP being high in the presence of Dr. or health professional in white coat
- Blood Pressure fluctuates min by mib & ‘white coat’ HT is common
- In CAN, up till 2005 - it took ~ 6 months for diagnosis of HT, unless an emergency or target organ damage was evident
- Multiple visits needed (at least 3 visits(, as recommended by hypertension CAN
- Use in context of overall CVD risk
The concept of masked hypertension
SLIDE 31 she didn’t say to know or not so REVIEW
Classes of HTN DRUGS (1) -> - - -> - ->
HOW DO BETA BLOCKERS FUNCTION?*
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** VISUAL slide 40 **
DRUGS (2) -> - - - -> - -
ROLE of Ca in the constriction of blood vessels - SLIDE 42** Review
= low BP at office YET high BP at home
- > Adrenergic antagonists
- Beta blockers - used for decades, efficacy well established, second most common after diuretics
- Alpha blockers - play a minor role in treatment (also found on surface of vessels)
-> Renin system modulators
- Angiotensin - Converting Enzyme 1 (ACE1) inhibitors - inhibits the conversion of Angiotensin 1 -> Angiotensin 2
(freq used as 1st line therapy)
-> Angiotensin 2 receptor blockers (ARBs) are receptor antagonists that block type 1 angiotensin 2 (AT1) receptors on blood vessels & other tissues such as the heart
Beta Receptors… are on the surface of cells innervated by the sympathetic nervous system
… mediate certain physiological responses to adrenaline
Beta receptor Blockers… block the activity of a beta-receptor
… decrease heart rate & force of contraction & lower high blood pressure
- > Diuretics
- have been used for decades
- most prescribed & now recommended as 1st line treatment
- some also increase K excretion {reduces pressure in the vessels} important to watch in patient as they may need a diet increased in K
- > Ca channel blockers (CCB)
- cause blood vessels to relax
- acting at vessel walls
