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Hypertension
第三組
姚佳汶、陳裔庭、吳承儒
指導藥師
陳寬軒、楊曜嘉 藥師
指導幹部
劉俐婷 科主任
Content
About Hypertension
Treatment
Special population
Case report & Discussion
2
About Hypertension
3
Definition
Hypertension is simply defined as
persistently elevated arterial blood pressure
*Hypertensive crises ≧ 180/120 mmHg as either a
hypertensive emergency or hypertensive urgency
4
Blood Pressure
I. Mean arterial pressure = (SBP × 1/3) + (DBP × 2/3)
BP = cardiac output × total peripheral resistance
*Cardiac output is a function of stroke volume,
heart rate, and venous capacitance
II. Measuring Blood Pressure
1. Sphygmomanometry- AHA Procedure
2. Self Blood Pressure Monitoring
At least 2 times/day (morning and night)
5
Pathophysiology
I. Humoral Mechanisms
1. The RAAS
2. Natriuretic Hormone
3. Insulin Resistance & Hyperinsulinemia
II. Neuronal Regulation
III. Peripheral Auto-regulatory Components
IV. Vascular Endothelial Mechanisms
V. Electrolytes & Other Chemicals
Pathophysiology (1)
Renin–Angiotensin–Aldosterone System
I. Stimulate renin secretion
1. Renal artery pressure↓ & kidney blood flow↓
2. Na and Cl delivered to the distal tubule ↓
3. Catecholamines ↑
4. Serum K+ and/ or intracellular Ca2+↓
II. The function of circulating angiotensin II:
1. Elevate BP through pressor effects:
a. Direct vasoconstriction
b. Stimulation of catecholamine release
c. Centrally mediated increases in
sympathetic nervous system activity
2. Stimulates aldosterone synthesis:
Leads to sodium and water reabsorption
→ Plasma volume↑, Total peripheral resistance↑→ BP↑
Pathophysiology (2)
Renin–Angiotensin–Aldosterone System
From pharmacotherapy 7th Chap.15 Fig.15-1
Direct
Renin
Inhibitor
ACE
inhibitors
CCBs
ARBs
CCBs &
β-blockers
Aldosterone
antagonist
Diuretics
Pathophysiology (3)
I. Natriuretic Hormone
1. ↑ Urinary excretion of Na+ and water
2. Block the active transport of sodium
→ intracellular [Na+]↑→ vascular tone and BP ↑
II. Insulin Resistance and Hyperinsulinemia
1. Renal sodium retention ↑
2. Sympathetic nervous system activity ↑
3. Growth hormone-like actions
4. Intracellular Ca2 ↑→ vascular resistance ↑
Pathophysiology (4)
Neuronal RegulationI. Presynaptic receptors (NE release)
1. α-receptors (α2) ↓
2. β-receptors ↑
II. Postsynaptic receptors1. α-receptors (α1), vasoconstriction
2. β1-receptors, ↑heart rate and contractility
3. β2-receptors, vasodilation
III. Baroreceptor reflex system1. Major negative-feedback mechanism that controls
sympathetic activity
2. May be blunted in the elderly and those with diabetes
IV. Central nervous system1. α2-adrenergic stimulation ↓ BP
2. Angiotensin II ↑ sympathetic outflow
Pathophysiology (5)
I. Peripheral Auto-regulatory Components
1. Kidney
a. Defect in sodium excretion may first develop
b. Volume-pressure adaptive mechanism
2. Local auto-regulatory
Maintain adequate tissue oxygenation
II. Vascular Endothelial Mechanisms
1. Vasodilating substances: Prostacyclin, Bradykinin
2. Vasoconstricting substances: Angiotensin II, Endothelin I
3. Nitric oxide (NO)
III. Electrolytes & Other Chemicals: Na, K, Ca
Etiology (1)
I. Essential or primary hypertension:
more than 90%
1. Unknown pathophysiologic etiology
2. Genetic factors may play an important role
in the essential hypertension
3. Cannot be cured, but it can be controlled
13
Etiology (2)
II. Secondary hypertension: fewer than 10%
1. Many secondary causes are concurrent
medical conditions or endogenously induced
2. Renal dysfunction or renovascular disease
are the very common secondary cause
3. If the cause can be identified,
hypertension has the potential to be cured
14
Secondary causes
I. Renal artery stenosis
II. Cushing’s syndrome
III. Coarctation of the aorta
IV. Pheochromocytoma
V. Primary aldosteronism
VI. Renal vascular disease
VII. Drugs
15
Epidemiology (1)
BP values increase with age,
hypertension is very common in the elderly
USA Taiwan
In 2000,
age≧ 60 years → 65.4 %
In 2002,
age≧ 65 years → 56.6 %
Before 45 y/o : men
45-54 y/o : men slightly higher
After 55 y/o : women
Before 60 y/o : men
After 60 y/o : women
Reference: 行政院衛生署國民健康局2002年台灣地區高血壓、高血糖、高血脂盛行率調查報告。
16
Epidemiology (2)
• Hypertension in Taiwan
Male Female
Prevalence 25 % 18%
Awareness 59% 79%
On treatment 47% 64%
Controlled BP 21% 29%
Reference: 行政院衛生署國民健康局2002
年台灣地區高血壓、高血糖、高血脂盛行率調查報告。
17
Clinical Presentation of Hypertension
I. Signs: Elevated BP
II. Symptoms : Most patients are asymptomatic
III.CV risk factors:
1. Age (Men: ≥55 years / Women: ≥ 65 years)
2. Diabetes mellitus
3. Dyslipidemia
4. Microalbuminuria
5. Family history
6. Obesity (BMI ≥ 30 kg/m2)
7. Physical inactivity
8. Tobacco use
IV. Target-Organ Damage
Eyes, brain, heart, kidneys, peripheral vascular
18
Clinical Evaluation
I. Elevated BP
II. Complete medical evaluation:
1. Comprehensive medical history
2. Physical examination
3. Laboratory and/or diagnostic tests
To (a) identify secondary causes
(b) identify other CV risk factors or comorbid conditions
(c) assess hypertension-associated target-organ damage
19
Laboratory and/or diagnostic tests
I. Laboratory Tests
1. Blood urea nitrogen/serum creatinine
2. Fasting lipid panel
3. Fasting blood glucose
4. Serum electrolytes
5. Spot urine albumin-to-creatinine ratio
II. Diagnostic Tests
1. 12-lead electrocardiogram
2. Estimated glomerular filtration rate (eGFR)
3. 10-year risk of fatal coronary heart disease or
non-fatal myocardial infarction, based on Framingham scoring
20
Framingham scoring
Score: -9+4 +0 +1 +1 = -321
Therapy
I. Overall goal：
Reduce associated morbidity & mortality
II. Surrogate goal：
achieve a desired target BP value
1. Most patients--140/90 mmHg
2. DM, CAD, CKD--130/80 mmHg
3. Left ventricular dysfunction--120/80 mmHg
Avoid clinical inertia
22
Treatment
I. Nonpharmacologic therapy：
Lifestyle modification, DASH (all stage)
II. Pharmacotherapy：
Diuretics, ACE inhibitor,
Angiotensin II receptor blocker (ARB),
Calcium channel blocker
The Dietary Approaches to Stop Hypertension
23
Lifestyle Modification
24
Lifestyle modification-SABCDEI. S- Salt restriction
Salt : 6 g/day (1 g salt = 0.4 g sodium)
II. A- Alcohol limitation
Beer : M < 700 ml/day, F < 470 ml/day
Wine : M < 240 ml/day, F < 160 ml/day
III. B- Body weight reduction
BMI : 18.5-24.9
Waist : M < 90 cm (35 inches)
F < 80 cm (32 inches)
Every losing Kg can lower 1 mmHg SBP
低鈉鹽
25
Lifestyle modification-SABCDE
IV. C- Cessation of smoking
V. D- Diet adaptation
More vegetable, Less cholesterol
VI. E- Exercise adoption
30 mins / day, 5 days / week
26
Pharmacotherapy
27
28
Diuretics
Diuretics (1)
I. First-line agents for hypertension （JNC7）
II. Four subclasses
1. Thiazides
2. Loops
3. Potassium-sparing
4. Aldosterone antagonists
III. Mechanisms
1. Initial: diuresis; ↓stroke volume, cardiac output
2. Chronic: peripheral vascular resistance ↓
3. Other: mobilize sodium and water from arteriolar
walls29
Diuretics (2)
IV. Pharmacokinetic differences
different in half-life and duration of diuretic effect
has no differences in CV outcome
V. Side effects (high doses)
1. Hypokalemia, hypomagnesemia, hypercalcemia
2. Hyperuricemia (use allopurinol)
3. Hyperglycemia
4. Dyslipidemia
5. Hyperkalemia
30
Diuretics (3)
I. Thiazide
1. Thiazides are more effective antihypertensives than loop
2. Maintain potassium concentration 4.0–5.0 mEq/L to
minimize metabolic effects
3. Hydrochlorothiazide & chlorthalidone:
max effective dose: 25 mg/day
4. Chlorthalidone:
a. Twice as potent as hydrochlorothiazide
b. Additional benefits in osteoporosis
c. May require additional monitoring in patients with a
history of gout or hyperglycemia
31
藥品名稱 Hydrochlorothiazide Chlorthialidone
Potency 1 1.5~2X
Half-life (hr) 8~15 45~60
Duration (hr) 16~24 48~72
Diuretics (4)
II. Loop
Higher doses may be needed for patients with
severely decreased glomerular filtration rate or
left ventricular dysfunction
III. Potassium sparing
1. Weak diuretics are used in combinations
2. Avoid in patients with severe chronic kidney
3. May cause hyperkalemia, in combination with
an ACEI, ARB, direct renin inhibitor or
potassium supplements32
Diuretics (5)
IV. Aldosterone antagonists
Avoid spironolactone in patients with chronic
kidney disease
33
ACE inhibitors and ARBs
34
ACE inhibitors & ARBs
I. ACE inhibitors - do not use in pregnancy or in
patients with a history of angioedema
1. Starting dose may be reduced 50% in patients on
a diuretic, are volume depleted, or very elderly
II. ARBs (Angiotensin receptor blockers)
Usually not cause dry cough; others as same as ACEI
35
ACE inhibitors (1)
I. Mechanism:
1. Block the ACE (bradykinase), inhibiting
conversion of angiotensin I to angiotensin II
→vasodilation and ↓ aldosterone
2. Block degradation of bradykinin→ Increased
bradykinin enhances the BP-lowering effects
3. Stimulate the synthesis of other vasodilating
substances: prostaglandin E2 & prostacyclin
36
ACE inhibitors (2)
II. Benefits:
1. Prevent or regress left ventricular hypertrophy
2. Good for atherosclerotic vascular even in the
left ventricular systolic dysfunction or heart failure
3. Reduce CV morbidity and mortality in patients
with left ventricular dysfunction
4. Decrease progression of chronic kidney disease
5. Have the potential to reduce the development of
new-onset type 2 diabetes
37
ACE inhibitors (3)III. Characteristics:
All ACEI except captopril can be dosed once daily
(Captopril is dosed 2 or 3 times daily.)
IV. Side effects:
1. Dry cough
2. Hyperkalemia→ monitor serum potassium& creatinine
3. Acute kidney failure→ prevented by slowly titrating the
dose and monitoring kidney function
4. GFR decreases: often increases serum creatinine
→ if larger increases occur, stop or reduce the dose
5. Angioedema→ Discontinue using ACEI &
requires epinephrine, corticosteroids, antihistamines
or emergent intubations 38
ACE inhibitors (4)
V. Notes:
1. ACEI can increase lithium serum conc.
2. ACEI are absolutely contraindicated in
pregnancy & with a history of angioedema
3. Start low doses of ACEI, even lower doses in
orthostatic hypotension or severe renal
dysfunction
39
Angiotensin Receptor Blockers (1)
I. Mechanism:
ARBs inhibit angiotensin II from all pathways,
directly block the angiotensin II receptor subtype 1
II. Benefits:
1. Long-term reductions in target-organ damage progression
2. Significantly reduced progression of nephropathy
in patients with type 2 diabetes and nephropathy
3. ARB + diuretic, ACE inhibitor, and β-blocker reduce risk of
CV events for patients with left ventricular dysfunction
40
Angiotensin Receptor Blockers (2)
III. Characteristics:
1. Have a fairly flat dose–response curve
2. Most ARBs have long half-life
3. Low doses of a thiazide-type diuretic + ARB
significantly increases antihypertensive effects
4. ARBs have the lowest incidence of side
effects compared to others41
Calcium Channel Blockers
42
Calcium Channel Blockers (1)I. Mechanisms:
1. CCBs inhibit influx of calcium across the cell
membrane
2. Currently available CCBs only block the
L-type channel, which leads to
coronary and peripheral vasodilation
II. Antihypertensive effect is similar
Dihydropyridine are as effective at lowering CV
events as other agent
III. All CCBs (except amlodipine and felodipine)
have negative inotropic effects
43
Calcium channel blockers (2)I. Dihydropyridines
1. Avoid short-acting
immediate-release nifedipine and nicardipine
2. Dihydropyridines are more potent peripheral
vasodilators than nondihydropyridines;
may cause more reflex sympathetic discharge
3. Benefits in Raynaud’s syndrome
4. The hepatic metabolism may be inhibited by
large quantities of grapefruit juice.
44
Calcium channel blockers (3)
II. Nondihydropyridines
1. Extended-release and sustained-release are
preferred for hypertension treatment
2. Block slow channels in the heart
(↓ heart rate & may produce heart block)
3. Benefits in patients with atrial tachyarrhythmia
4. Drug interactions: inhibit the CYP450 3A4
45
Dihydropyridines Nondihydropyridines
1. May cause a baroreceptor
mediated reflex tachycardia
2. Do not alter conduction
through the AV node
3. Side effects:
dizziness, headache,
gingival hyperplasia,
peripheral edema,
flushing
4. Very effective in older
patients with isolated
systolic hypertension
1. Decrease heart rate and
slow AV nodal conduction
2. treat supraventricular
tachyarrhythmias (e.g. AF)
3. Side effects:
Anorexia, hypotension,
nausea & peripheral edema
Constipation.
Cardiac conduction
abnormalities)
46
β blocker
I. Mechanism
II. Pharmacodynamic
III. Pharmacokinetic
IV. Side effect
V. Abrubt cessation
47
Mechanism of β blockerI. Negative chronotropic and Inotorpic cardiac
effects-- reduce cardiac output
II. Inhibit β-adrenoceptors & renin realese
-reduce CV risk
III. β₁-receptor:
Heart (increase heart rate, contractility)
Kidney (renin release)
IV. β₂ -receptor:
Lungs, Liver, Pancreas and Arteriolar smooth
muscle (Bronchodilation and vasodilation)
48
Pharmacodynamic of β blockerI. Cardioselective ：greater affinity for β₁
1. Atenolol, metoprolol
2. Dose-dependent
3. Not likely provoke bronchospasm and
vasodilation
II. Intrinsic sympathomimetic activity (ISA)
1. Acebutolol, pindolol
2. Act as partial β-agonist
3. May increase risk post-MI or CAD
III. Mixed α & β blockers (carvedilol)
Additional α-blockade produces more orthostatic
hypotension 49
Pharmakokinectic of β blocker
I. First-pass metabolism
Propranolol and metoprolol
II. Renal excretion
Atenolol and nadolol
III. Lipophilic-penetrate CNS
1. Most-Propranolol Least-Atenolol
2. Migrane headache, essential tremor,
thyrotoxicosis
IV. Serum half-life50
Side Effect of β blocker
I. Extension of antagonize β-adrenoceptor
II. Myocardium：
Bradycardia, AV conduction abnormalities,
Acute heart failure
III. Ateriolar smooth mucsle：
Cold extremities, Raynaud’s syndrome
51
Abrupt Cessation of β blocker
I. Abrupt cessation of β-blocker therapy can
cause rebound hypertension
II. Patients with coronary disease：
Unstable angina, MI, death
III. Patients without coronoary disease ：
Tachycardia, sweating,
generalized malaise
52
From JNC753
Alternative drug treatment
I. α -blocker
II. Central α₂ agonist
III. Direct renin inhibitor
IV. Vasodilator
For patients with resistant hypertention
Only be used as add-on therapy
54
Alternative AgentsClass Drug Mechanism Note
Alpha-1
blockers
Prazosin,
terazosin,
doxazosin
Inhibit the uptake of
catecholamines in
smooth muscle
cells
“first-dose”
phenomenon
Direct renin
inhibitor
Aliskiren Block the RAAS at its
point of activation
Similar to ACEI
Containdicated in
pregnancy
Cental alpha-2
agonist
Clonidine,
guanabenz,
guanfacine,
methyldopa
Stimulate alpha-2
adrenergic receptors
in the brain
Sodium-water
retention ,depression,
anticholinergic
effect(clonidine)
Hepatitis, hemolytic
anemia(methyldopa)55
Alternative AgentsClass Drug Mechanism Note
NE depleting Reserpine Depleting
and blocking
transport of
norepinephri
ne
Significant
Sodium-
water
retention ,inc
reased
parasympath
etic activity
Direct Arterial
vasodilator
Hydralazine,
minoxidil
Directly relax
arteriolar
smooth
muscle
Lupus-like
syndrome(hyd
ralazine)
Hirsutism(min
oxidil)
56
Compelling Indications
I. Left ventricular dysfunction
II. Post MI
III. Coronary artery disease (CAD)
IV. Diabetes mellitus (DM)
V. Chronic kidney disease (CKD)
VI. Recurrent stroke prevention
57
Left Ventricular Dysfunction
I. BP goal：120/80 mmHg
II. ACE inhibitor (reduced CV events) +
Diuretic (edema relief)
III. Other drugs
1. Loop diuretic—for advanced disease
2. β-blocker—modify LV dysfunction
3. ARBs—alternatives for ACE inhibitor or add-on
4. Spironolactone—severe LV dysfunction
58
Post MI
I. BP goal：130/80 mmHg
II. β-blocker (without ISA) + ACE inhibitor
III. Mechanism
1. β-blockers decrease cardiac adrenergic
stimulation
2. ACE inhibitors improve cardiac remodeling,
cardiac function
3. Both can reduce CV risk
59
Coronary Artery Disease
I. BP goal：130/80 mmHg
II. Chronic stable angina
β-blocker (without ISA) + long acting CCBs
III. Acute STEMI and NonSTEMI
β-blocker (without ISA) + ACE inhibitors
60
Diabetes Mellitus
I. BP goal：130/80 mmHg
II. ACE inhibitor or ARB (nephroprotection)
III. Other drugs
1. Thiazide diuretic-- lower BP & CV risk
2. CCBs-- add-on for BP control
3. β -blocker-- CV risk reduction (may mask
hypoglycemia or induce hyperglycemia)
61
Chronic Kidney Disease
I. Strict BP goal：130/80 mmHg
II. ACE inhibitor or ARB
III. Mechanism
reduce intraglomerular pressure
62
From JNC763
Special population
64
Older people
I. Older people--Isolated systolic HTN
II. More sensitive to volume depletion
and sympathetic inhibition
III. Orthostatic hypotension
ACE inhibitors
Smaller-than-usual initial dose
65
Patients at Risk for
Orthostatic HypotensionI. Definition (from supine to standing)
1. ↓ SBP decrease 20 mmHg
2. ↓ DBP decrease 10 mmHg
II. Risks of orthostatic hypotension
1. Older patients (especially with isolated systolic hypotension)
2. Diabetes
3. Severe volume depletion
4. Baroreflex dysfunction
5. Autonomic insufficiency
6. Use of venodilators (α-blockers, mixed α/ β-blockers,
nitrates, and phosphodiesterase inhibitors)
66
Ⅰ. Definition
1. Hypertension: SBP and/or DBP that is greater than
95th percentile
2. Prehypertension: BP between 90th to 95th, or ≧
120/80 mmHg
Ⅱ. Secondary hypertension is more common
1. Family history of high BP
2. Overweight
3. Kidney disease
4. Coarctation of the aorta
Hypertension in Children and
Adolescents
Hypertension Prehypertension
67
Pregnancy (1)
I. Categorization
1. Preeclampsia (after 20 weeks gestation)
new-onset hypertension with proteinuria
2. Eclampsia
3. Gestational
new-onset hypertension (absence of
proteinuria)
4. Chronic
5. Superimposition of preeclampsia on chronic
68
Pregnancy (2)
II. Treatment
1. Restricting activity, close monitoring and salt
restriction
2. Antihypertensive agents
a. IV hydralazine or IV labetalol
b. Methyldopa, labetalol
3. Not to use: ACEIs, ARBs, Aliskiren
69
Other Concomitant Conditions (1)
I. Pulmonary Disease
1. Avoid β-blockers (especially nonselective)
2. Cardioselective β-blockers
Post-MI, coronary disease or heart failure
II. Peripheral Arterial Disease
1. BP goal: <130/80 mmHg
2. Drugs
a. ACEIs: ideal for symptomatic lower-extremity
peripheral arterial disease; decrease CV events
b. CCBs: beneficial of vasodilatory effects
c. β-blockers: problematic; stimulation of α-
receptors(vasoconstriction)70
Other Concomitant Conditions (2)
III. Dyslipidemia
1. Avoid thiazide diuretics and β-blockers without ISA
2. α-Blockers have favorable effects
IV. Metabolic Syndrome
1. Definition (more than three)
a. Abdominal obesity (＞90 cm in men; 80 cm in women)
b. Elevated triglyceride (≧150 mg/dL)
c. Lower HDL (<40 mg/dL in men;<50 mg/dL in women)
d. Elevated BP (≧130/85 mmHg)
e. Elevated fasting blood glucose (≧100mg/dL)
71
Other Concomitant Conditions (3)
2. Treatment
ACEI or ARB may be beneficial
V. Erectile Dysfunction
Erectile dysfunction in hypertension may be an
important marker for CV disease
72
Hypertensive Crisis
I. BP > 180/120 mmHg
II. Hypertensive urgency
1. Not associate with acute target-organ injury
2. Risk of rapid BP reduction
3. Management (oral; 140/90)
4. Drug: Captopril, Clonidine, Labetalol
III. Hypertensive emergency
1. Associate with acute target-organ injury
2. Management (parenteral; 25% mean artrial pressure)
3. Drug: Nitroprusside, Nitroglycerin, Fenoldopam,
Nicardipine
73
Target-organ Damage
Eyes, brain, heart, kidneys,
peripheral vascular
I. Retinopathy：
arteriolar narrowing, arterivenous crossing
change, retinal hemorrhages, disk edema
II. Cerebrovascular disease：
gross neurologic deficits
74
Target-organ Damage
III. Clincal CV events：
MI, stroke
IV. Kidney：
fibrinoid necrosis, atheroma of renal
arteries, hyaline arteriosclerosis
V. Peripheral vascular：
arterial bruits, distended veins, absent
peripheral arterial pulses
75
Combination Antihypertensive
Therapy
I. Difficult goal achievement
-BP goals <130/80 mmHg; African Americans
II. Multiple compelling indications
III. Additive antihypertensive effects
-Diuretics+(ACEI, ARB, β-blocker)
IV. Fixed-dose combination products
1. Co-Aprovel (irbesartan+hydrochlorothiazide)
2. Co-Diovan (valsartan+hydrochlorothiazide)
76
Resistant Hypertension
I. Definition
BP remains above goal in spite of concurrent
use of three antihypertensive agents of different
classes; BP is controlled with four or more
medications
II. Causes of resistant hypertension
1. Inadequate treatment regimens
2. Pseudoresistance
77
Clinical Monitoring
I. Disease progression
Signs and symptoms of progressive target-organ
disease
II. Efficacy
BP response should be evaluated 2 to 4 weeks after
initiating or making changes in therapy
III. Toxicity
With an aldosterone antagonist (3 days and 1 week)
78
病例報告
Case I Mr.W 57 yrs HTN
Case II Mrs.C 83 yrs HTN + DM
79
Case I Report (1)
Mr. W 57y/o
• Chief complaint
– 2010.12.21 BP up to 172/110 mmHg
• History of present illness
-- 2010.12.19 172/113
2010.12.20 164/108
2010.12.21 177/121
• Past medical history
– Peptic ulcer
– GERD (LA grade: B)
– Other disease of vocal cords
– Operation of larynx
(left vocal leukoplakia)
• Personal history
– Smoking 1.5ppd for 40yrs
– Alcohol 1 bolt/day (Whisky) for 40 yrs
• Family history
– HTN, DM
– Mother: HTN & stroke
• Physical examination
– Wt 74.9kg; Ht 171cm
(BMI 25.6)
• Impression
-- Primary hypertension
80
Case I Report (2)
• Laboratory and diagnostic tests (10/12/19)– BUN: 12 mg/dl 7~20 mg/dl
– Na: 139 mg/l 135~145 meq/l
– K: 3.9 meq/l 3.4~4.5 meq/l
– GLU: 90 mg/dl 60~110 mg/dl
– CREAT: 0.94 mg/dl 0.7~1.5 mg/dl
– ALT: 30 U/l 0~35 U/l
– AST: 32 U/l 8~40 U/l
– HDL: 60 mg/dl 40~60 mg/dl
– TG: 81 mg/dl 20~200 mg/dl
– TC: 235 mg/dl 125~240 mg/dl
– eGFR: 85.2 ml/min/1.73m2 > 60 ml/min/1.73m2
81
Case I Report (3)
• Plan to do:
10/12/21
– Salt restriction
– Give Norvasc 5mg, po, qd
11/01/04
– Salt restriction
– Add Micardis 80mg, po, qd
11/03/03
– Salt restriction
– Smoke cessation
– Bring home BP device next time
82
Case I Report (4)
• Patient drug profile– Norvasc 5mg, po, qn (10/12/21 OPD)
– Micardis 80mg, po,qd (11/01/04 OPD)
– Nexium 40mg, po, qdac
– Gascon 40mg, po, tidpc
– Mosapride 5mg, po, tid
– Alpraline 0.5mg, po, qn
83
• Discussion病人評估治療目標非藥物治療辦法藥物治療選擇
• 治療目標
– BP < 140/90 mmHg
• 非藥物治療辦法
– 戒菸戒酒
– 減重(運動)
– 飲食(限鹽,低脂,
少糖,高纖維)
• 病人評估
– Risk factor
• Age
• Family history
• Tobacco
– Framingham score
• 8+3+3-1+2=15 (20%)
– Target-organ harm
• Nil
Case I Report (5)
84
85
JNC 7 guideline
86
NICE guideline
87
Case I Report (6)
11/01/04
Add on
Micardis (Telmisartan)
10/12/21
Norvasc
(Amlodipine)
88
50
70
90
110
130
150
170
190
2010/12/13 2010/12/23 2011/1/2 2011/1/12 2011/1/22 2011/2/1
SBP
DBP
Case II Report
89
Case II Report (1)
Mrs. C 83 y/o
• Chief complaint
Regular Meta OPD follow up for DM & HTN control
• History of present illness
Type 2 DM more than 10 yrs
HTN more than 2 years
• Past medical history
Iron deficiency anemia. 2007.09 Colon cancer.
• Personal history
Smoking (-), Alcohol (-),
Drug & Food Allergy: No known allergy90
• Family history: nil
• Lab data
100/1/21 GLU: 180 mg/dl ; HbA1c: 8.2 %
• Impression
DM & Primary HTN
• Plan to do
Case II Report (2)
Drugs
Norvasc 5 mg 1 tab PO qd
Cozaar 50 mg 1 tab PO qd
Amaryl 2 mg 4 tab PO qdac
Januvia 100 mg 1 tab PO qd
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Case II Report (3)• Patient drug profile
• Laboratory and diagnostic test
Norvasc 5 mg 1.5 tab qd 2008/07/03 - 2009/02/24
Norvasc 5 mg 1 tab qd 2009/02/24 - 2011/02
Add Cozaar 50 mg 1 tab qd 2009/12/08 – 2011/02
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II. 高血壓治療目標
BP < 130/80 mmHg
III.非藥物治療辦法
– 運動
– 飲食(限鹽,低脂,
少糖,高纖維)
• Disccusion:
I.病人評估
- Risk factor
• Age
• DM
- Framingham score
• Not needed
• Coronary artery disease
risk equivalent
- Target-organ harm
• Nil
Case II Report (4)
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Case II Report (5)
IV.藥物治療選擇
Norvasc (Amlodipine) - CCB, dihydropyridine Cozaar (Losartan) – ARB
★ UK guidelines ★JNC7
For DM patients:First-line: ACEI or ARBAdd on: thiazide orCCB-nondihydropyridine
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Evaluation-PROCEED
P- Previous experience of patient
R- Risk factors
O- Organ damage
C- Contraindicaton
E- Expert or doctor judgment
E- Expense or cost
D- Delivery and compliance
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References
• Pharmacotherapy 7th Chap.15
• JNC7
• 2006.UK NICE guideline
• J. Formos Med. Assoc.
2010;109(10):740-733
• 2002年行政院衛生署國民健康局,台灣地區高血壓、高血糖、高血脂盛行率調查報告
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