hypertension 2014 update
DESCRIPTION
Hypertension lecture for medical students reflecting changes according to JNC8 report.TRANSCRIPT
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HypertensionHypertension
The Importance of Hypertension
Statistical dataStatistical data
The first killerThe first killer
Silent killerSilent killer
Masked killerMasked killer
Financial burden Financial burden
PreventablePreventable
TreatableTreatable
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Definition of Blood Definition of Blood PressurePressure
The pressure exerted by blood against the artery through which it flows
Blood pressure = ca rdiac output X systemic vascular
resistance
CO X SVR = BP
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the level of blood pressure linked with a the level of blood pressure linked with a doubled increased long-term risk for doubled increased long-term risk for adverse eventsadverse events
The level of blood pressure at which the The level of blood pressure at which the benefits of action (i.e. therapeutic benefits of action (i.e. therapeutic intervention) exceed those of inaction.”intervention) exceed those of inaction.”
Evans and Rose Brit Med Bull 1971;27:37-42Evans and Rose Brit Med Bull 1971;27:37-42
Hypertension is defined as:Hypertension is defined as:
OROR
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Definition of Hypertension
Normal <120/<80
Prehypertension 120-139/80-89
Stage 1 140-159/90-99
Stage 2 >160/>100
Chobnian JAMA 2003;289:2560
Optimal <120/<80
Normal <130/<85
High Normal 130-139/85-89
Hypertension
Grade 1 140-159/90-99
Grade 2 160-179/100-109
Grade 3 >180/>110
Isolated syst. hypertension
Grade 1 140-159/<90
Grade 2 >160/<90
Williams BMJ 2004;328;634
JNC - VII BHS
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Definitions of hypertension by officeDefinitions of hypertension by officeand out-of-office blood pressure levelsand out-of-office blood pressure levels
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Pulse Pressure
Increase in pulse pressure (PP) indicates greater stiffness in large conduit arteries, primarily the thoracic aorta.PP, therefore, is a surrogate measure of dynamic, cyclic stress during systole.PP may be a better marker of increased CV risk than either systolic BP or diastolic BP alone in older persons.
PP = SBP – DBP
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What clinical guidelines are used to categorize HTN?
The Joint Committee on Prevention, Evaluation, and Treatment of High Blood Pressure (JNC 8) guidelines provide the most current guidelines
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JNC 6 Report
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JNC 8 ReportIn patients 60 years or over, start treatment in blood pressures >150 mm Hg systolic or >90 mm Hg diastolic and treat to under those thresholds. (Strong Recommendation–Grade A)
In patients <60 years, treatment initiation and goals should be 140/90 mm Hg, the same threshold used in patients >18 years with either chronic kidney disease (CKD) or diabetes. (Expert Opinion–Grade E)
In nonblack patients with hypertension, initial treatment can be a thiazide-type diuretic, CCB, ACE inhibitor, or ARB, while in the general black population, initial therapy should be a thiazide-type diuretic or CCB. (Moderate Recommendation–Grade B)
In patients >18 years with CKD, initial or add-on therapy should be an ACE inhibitor or ARB, regardless of race or diabetes status. (Moderate Recommendation–Grade B)
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Prevalence
>65 million Americans have hypertension (HTN)Of those diagnosed with HTN < 50% have their blood pressure under controlLack of treatment leads to serious complications
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High Prevalence of Hypertension Worldwide
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3842
47 49 4955
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0
20
40
60
Italy Sweden England Spain Finland Germany
Adults aged 35–64 y (data are age- and sex-adjusted), except* (adults aged ≥ 30 y) Hypertension defined as BP 140/90 mmHg or on treatment
Wolf-Maier et al. JAMA. 2003;289:23632369;Sekikawa, Hayakawa. J Hum Hypertens. 2004; 2004;18:911–912.
USA Japan*
Pre
vale
nce
of
hype
rten
sion
(%
)
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Prevalence of HypertensionPrevalence of Hypertension
2020
Awareness, Treatment and Control of Hypertension is Rather Low Worldwide
* BP < 140/90 mmHg
Wolf-Maier et al. Hypertension. 2004;43:10–17;Sekikawa, Hayakawa. J Hum Hypertens. 2004;18:911–912.
Proportion of patients in the population (%)
Country Aware Treated Controlled*
Japan 16.0 – 4.1
England 35.8 24.8 10.0
Germany 36.5 26.1 7.8
Spain 38.9 26.8 5.0
Sweden 48.0 26.2 5.5
Italy 51.8 32.0 9.0
USA 69.3 52.5 28.6
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BP Control RatesTrends in awareness, treatment, and control of high
blood pressure in adults ages 18–74
National Health and Nutrition Examination Survey, Percent
II1976–80
II(Phase 1)1988–91
II(Phase 2)1991–94 1999–2000
Awareness 51 73 68 70
Treatment 31 55 54 59
Control 10 29 27 34
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Awareness, Treatment and Control of
Blood Pressure 1976-2000 (NHANES)
0
10
20
30
40
50
60
70
80
1976-1980 1988-1991 1991-1994 1999-2000
AwarenessTreatmentControl
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Benefits of Lowering BP
Average Percent Reduction
Stroke incidence 35–40%
Myocardial infarction 20–25%
Heart failure 50%
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Risk of CV Mortality Doubles With Each 20/10 mmHg BP Increase
0
2
4
6
8
10
Fol
d in
crea
se in
re
lati
ve C
V r
isk
1-fold2-fold
4-fold
8-fold
115/75 135/85 155/95 175/105SBP/DBP (mmHg)
• Meta-analysis of 61 prospective, observational studies
• 1 million adults aged 40–69 y with BP > 115/75 mmHg
• 12.7 million person-years
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2 mmHg decrease in mean SBP
10% reduction in risk of stroke mortality
7% reduction in risk of IHD and other vascular disease mortality
Each 2 mmHg Decrease in SBP Reduces CV Risk by 7–10%
Lewington et al. Lancet. 2002;360:1903–1913.
• Meta-analysis of 61 prospective, observational studies
• 1 million adults aged 40–69 y with BP > 115/75 mmHg
• 12.7 million person-years
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Preventable CHD Events from Control of Hypertension in US Adults
(Wong et al., Am Heart J 2003; 145: 888-95)
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56
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39
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0
10
20
30
40
50
60
PA
R%
/ N
NT
Men PAR% Women PAR% Men NNT Women NNT
Treatment to <140/90 mmHg Treatment to <120/80 mmHg
PAR% = population attributable risk (proportion of CHD events preventable), NNT = number needed to treat to prevent 1 CHD event ; <0.01 comparing men and women for PAR%
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CVD Risk
HTN prevalence ~ 50 million people in the United States.
The BP relationship to risk of CVD is continuous, consistent, and independent of other risk factors.
Each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range starting from 115/75 mmHg.
Prehypertension signals the need for increased education to reduce BP in order to prevent hypertension.
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Factors contribute to the development of primary HTN
1. Sympathetic nervous system hyperactivity
2. Renin-angiotensin-aldosterone system hyperactivity
3. Endothelial dysfunction
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Types of HTN?
Primary Primary • ?? ‘essential’idiopathic• Most common type
found in 90-95% of those with HTN
• Cause not well understood
• Salt sensitive• RAAS dependent
SecondarySecondary• Caused by some other
medical problem or condition:
• High-dose estrogen
• Renal artery stenosis
• Pregnancy (PET)
• Cushing’s syndrome
• pheochromocytoma
• Others?
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Renin level ??Renin level ??
ABPM ?ABPM ?
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What are the Symptoms?
Symptoms may or may not be present• Dizziness (unsteadiness)• Early morning headacheactivity tolerance• Malaise, fatigue• Blurring of vision• Spontaneous nosebleed• Palpitations, angina, dyspnea• Early signs/symptoms are often missed
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BP measurement
Physical assessment• Height & weight• Blood pressure
Measuring BP accurately:• No smoking or caffeine
30 minutes before• Rest for 5 minutes
prior to BP• Apply cuff to bare arm
• Proper size cuff applied 1 inch above brachial artery
• Inflate cuff to 30 mmHg above initial radial pulse check If BP elevated, wait 2 minutes, recheck
• Check BP in other arm
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BP Measurement Techniques
Method Brief Description
In-office Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm. 140/90
Ambulatory BP monitoring
Indicated for evaluation of “white-coat” HTN. Absence of 10–20% BP decrease during sleep may indicate increased CVD risk. 130/80
Self-measurement Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN. 135/85
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White Coat and Ambulatory BP monitoring ABPM White Coat and Ambulatory BP monitoring ABPM
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For persons over age 50, SBP is a more important than DBP as CVD risk factor.
Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10 mmHg throughout the BP range.
Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN.
Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be considered prehypertensive who require health-promoting lifestyle modifications to prevent CVD.
Key MessagesKey Messages
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Key Messages (Continued)
Thiazide-type diuretics should be initial drug therapy for most, either alone or combined with other drug classes.
Certain high-risk conditions are compelling indications for other drug classes.
Most patients will require two or more antihypertensive drugs to achieve goal BP.
If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic.
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Key Messages (Continued)
The most effective therapy prescribed by the careful clinician will control HTN only if patients are motivated.
Motivation improves when patients have positive experiences with, and trust in, the clinician.
Empathy builds trust and is a potent motivator.
The responsible physician’s judgment remains paramount.
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Complications of HTN
The higher the BP and the longer an individual has hypertension, the higher the risk of complications which include:• Hypertensive heart disease• Cerebrovascular disease• Peripheral vascular disease• Kidney disease • Retinal damage
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Complications of Hypertension
Heart resistance
workload left ventricular hypertrophy
• CAD, angina, MI• Heart failure
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Complications of Hypertension
Brain Brain • Atherosclerosis,
stroke
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Complications of Hypertension
Peripheral vascular Peripheral vascular diseasedisease• Aortic aneurysm
or dissectionRetinal damageRetinal damage• damage to blood
vessels of the eye
Kidney diseaseKidney disease • vessels less
elastic decreased perfusion renal failure
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Acute Complications
Hypertensive Hypertensive Crisis:Crisis:Severe and abrupt elevation of BPDiastolic over 120mm hgHigh Mortality
Sx: papilledema, progressive renal failure, encephalopathyMost common cause is untreated hypertensionGoal: slowly decrease BP
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Classifications Hypertensive Crisis
Hypertensive crisis is categorized by the degree of organ damage
Hypertensive emergency:
BP is severely elevated and there is evidence of target organ damage• Especially brain
Hypertensive urgency:
BP is elevated but there is no evidence of target organ damage
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GOAL: Reduce Complications
JNC 8 guidelines recommend a target BP of less than 140/90 Except elderly above 60 150/90
Patients with renal disease or diabetes need BP less than 140/90
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What Reduces Risk of Complications?
REDUCING MODIFIABLE RISK REDUCING MODIFIABLE RISK FACTORS IS A KEY FACTORS IS A KEY INTERVENTIONINTERVENTIONGoal = Patient teaching to reduce risk factorsDrug therapy is initiated if lifestyle changes are not effective to control BP
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Management of Hypertension
Depends on risk groupLifestyle modificationsDrug therapy is initiated if lifestyle modifications do not achieve goalAdd or change drugs if goal not achieved
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Lifestyle Modification
Lose excess weight
Cut back on salt
Exercise regularly
Cease alcohol intake
Adopt the DASH eating plan to decrease cholesterol intake
STOP smoking
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DASH Diet
http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/
Dietary Approaches to Stop Hypertension = DASH• A diet rich in fruits, vegetables and
low-fat dairy products with reduced fat content
• Limits sodium intake to 2.4 g/day
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Non-pharmacologic Management of Hypertension
Weight management• DASH
Low sodium-low fat dietSmoking cessationRestrict alcohol and caffeineRegular aerobic exerciseStress management • bio-feedback,
relaxation, yoga, Tai Chi
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Drug Therapy for HTN
Diuretics• Flush excess
water and sodium from the body
• Thiazide diuretics• Loop diuretics:
furosemide (Lasix)• Potassium
sparing: Aldactone
Beta adrenergic blockersThree classes:• Cardioselective• Non-selective• Combined alpha-
beta-blockers
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Average number of antihypertensive medications1 2 3 4
Trial (SBP achieved)
ASCOT-BPLA (137 mmHg)
ALLHAT (138 mmHg)
IDNT (138 mmHg)
RENAAL (141 mmHg)
UKPDS (144 mmHg)
ABCD (132 mmHg)
MDRD (132 mmHg)
HOT (138 mmHg)
AASK (128 mmHg)
The Majority of Hypertensive Patients Need Combination Therapy to Achieve BP Goals
Bakris et al. Am J Med. 2004;116(5A):30S–38S;Dahlöf et al. Lancet. 2005;366:895–906.
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Pharmacologic Management of Hypertension
Alpha-adrenergic blockers • Suppress nerve impulses to blood vessels,
which allows blood to pass more easily so BP goes ↓
• prazosin (Minipress)
Calcium channel blockers • decrease the influx of Ca++ into muscle cells
• Act on vascular smooth muscles (primary arteries) to decrease spasm and promote vasodilation
• Amlodipine (Norvasc); felodipine (Plendil)
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Pharmacologic Management of Hypertension
Angiotensin converting enzyme (ACE) inhibitors• Decrease effect of
RAA system: Capoten, Lisinopril
• Diabetes mellitus w/proteinuria, heart failure
Angiotensin II receptor blockers (ARB)• Prevent action of
angiotensin II and produce vasodilation
• losartan (Cozaar)
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Pharmacologic Management of Hypertension
Vasodilators • Direct arterial
vasodilation• Sodium
nitroprusside (Nipride)
• Often used in hypertensive crisis
Alpha-receptor agonists• Clonidine
• Acts on central nervous system
• Lowers peripheral vascular resistance
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Why don’t some patients respond to therapy?
Non-adherence to therapy• Patients don’t take
their HTN meds → complications!!!
• Cost, inadequate teaching, side effects, inconvenient dosing
Drug related causes
Other conditions
Secondary hypertension
Volume overload
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Causes of Resistant Hypertension
Improper BP measurement Excess sodium intake Inadequate diuretic therapy Medication
• Inadequate doses• Drug actions and interactions (e.g., nonsteroidal anti-inflammatory
drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives)• Over-the-counter (OTC) drugs and herbal supplements
Excess alcohol intake Identifiable causes of HTN
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Summary Key Points
Two types of HTN: primary & secondaryInadequate BP control leads to serious complications including STROKEKey point: risk factor modificationTreatment focuses on lifestyle management and drug therapyJNC 7 provides the most current treatment guidelines for hypertension
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Identifiable Causes of Hypertension
Sleep apnea Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushing’s syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease
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Pheochromocytoma
0.01-0.1% of HTN population• Found in 0.5% of those screened
M = F3rd to 5th decades of lifeRare, investigate only if clinically suspicion:
• Signs or Symptoms• Severe HTN, HTN crisis• Refractory HTN (> 3 drugs)• HTN present @ age < 20 or > 50 ?• Adrenal lesion found on imaging (ex. Incidentaloma)
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Pheo: Signs & Symptoms
The five P’s:• Pressure (HTN) 90%• Pain (Headache) 80%• Perspiration 71%• Palpitation 64%• Pallor 42%
• Paroxysms (the sixth P!)
The Classical Triad:• Pain (Headache), Perspiration, Palpitations• Lack of all 3 virtually excluded diagnosis of pheo in a series of
> 21,0000 patients
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Pheo: Paroxysms, ‘Spells’
10-60 min durationFrequency: daily to monthlySpontaneousPrecipitated:
• Diagnostic procedures, I.A. Contrast (I.V. is OK)• Drugs (opiods, unopposed -blockade, anesthesia induction,
histamine, ACTH, glucagon, metoclopramide)• Strenuous exercise, movement that increases intra-abdo
pressure (lifting, straining)• Micturition (bladder paraganlgioma)
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Pheo: ‘Rule of 10’
10% extra-adrenal (closer to 15%)
10% occur in children
10% familial (closer to 20%)
10% bilateral or multiple (more if familial)
10% recur (more if extra-adrenal)
10% malignant
10% discovered incidentally
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Plasma Metanephrines
Not postural dependent: can draw normally
Secreted continuously by pheo
SEN 99% SPEC 89%
False Positive: acetaminophen
Assay not widely available yet
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Localization: Imaging
CT abdomen• Adrenal pheo SEN 93-100%
• Extra-adrenal pheo SEN 90%
MRI• > SEN than CT for extra-adrenal pheo
MIBG Scan• SEN 77-90% SPEC 95-100%
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Renovascular HypertensionRenovascular Hypertension
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Endocrine Hypertension
Catecholamine producing tumours
Mineralocorticoid hypertension
Renin-dependent hypertension
Hyperthyroidism and hypothyroidism
Acromegaly
Hyperparathyroidism
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Typical clinical scenarios
Difficult hypertension with hypokalaemia, on polypharmacy- referred to endocrinologist for exclusion of 2ary hypertensionCoincidentaloma of adrenal with hypertension, on polypharmacyWhich drugs are permissible, and after how much delay should there be before investigation?
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Mineralocorticoid hypertension- in whom should it be suspected?
Diagnosis should be suspected in patient with hypertension, spontaneous hypokalaemia (<3.5mmol/l), and alkalosis.Severe hypokalaemia (<3.0) on diureticsInvestigate patient hypertension refractory to conventional therapy, or adrenal coincidentaloma Recent onset of hypertensionNormokalaemia present in >35% patients on low salt diet
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Clinical features of hyperaldosteronism
Mild to severe hypertensionSodium retention + intravascular vol exp mineralocorticoid escapeResetting of osmostat (thirst provoked at higher [Na+])K+ loss (kaliuresis) +/- low serum K+ (unprovoked: rule out diuretics, laxatives, vomiting, herbal supplements)Suppression of renin generation (rule out drugs,excessive dietary sodium intake)Polyuria, nocturia,fatigue,cramps, Mg++↓Exclude liquorice abuse / carbenoxolone therapyNB minor mineralocorticoids DOC, compound B
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Imaging in 1ary hyperaldosteronism
High resolution CT scanning with thin (2-3mm) slicesBilateral adrenal venous catheter (measure cortisol, adrenaline + aldosterone) remains gold standard – operator dependent: right adrenal notoriously difficult to cannulate. Give iv ACTH (2μg/min) during sampling to magnify difference between tumour and non-tumorous sideNon-tumorous side PAC = peripheral value because of suppressed PRA
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Glucocorticoid remediable hyperaldosteronism GRA (FH1)
Due to aberrant expression of chimeric gene formed by unequal recombination of promoter and initial parts of CYP11B1 and section of CYP11B2 with aldosterone synthase activityAldosterone under ACTH controlAutosomal dominant: FH of early onset BP↑ with CVA ,K+↓High levels of 18-hydroxy and 18-oxocortisolRx : chronic administration of low dose GC, spironolactone, or amiloride
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Liddle syndrome
Familial BP↑, unprovoked K+↓, PRA↓, and undetectable PAC
Autosomal dominant, caused by constitutive activation of distal renal epithelial sodium channel (β,γ C-terminal subunit mutations prevent trafficking of channel)
Treated by amiloride
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Liddle's – low renin, low aldoLicorice and SAME -- low renin, low aldoRenal artery stenosis and renin-secreting tumors -- high renin, high aldoAdrenal hyperfunction -- low renin, high aldo
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Renin Aldo
Liddle low low
Licorice low low
RAS high high
Conn’s low high
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Renin-Angiotesnin-Aldosterone System
A drop in BP or blood volume causes kidneys to secrete reninrenin, a precursor to
angiotensin I
Angiotensin-converting enzyme turns angiotensin I into angiotensin I into angiotensin II,angiotensin II, a potent vasoconstrictor
Stimulates adrenal glands to release aldosteronealdosterone
This prompts the kidneys to retain sodium and water
The increased volume and vasoconstriction raise BP
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