HTN (08-04) (1) Flashcards
HTN
Primary aka essential (without identifiable cause)
Secondary – when identifiable cause exists
.
HTN Nonmodifiable?
Nonmodifiable: increasing age, male sex, black race, family history
HTN modifiable?
Modifiable: high-salt diet, alcohol, obesity, sedentary life
HTN. normotensive?
sBP <120
dBP <80
HTN. prehypertensive?
sBP 120-129
dBP <80
HTN. Stage 1 HTN?
sita yra esmine riba
sBP 130-139
dBP 80-89
HTN. Stage 2 HTN?
sBP >= 140
dBP >=90
HTN. normotensive. management?
Routine follow-up and continued promotion of a healthy lifestyle
HTN. prehypertensive. management?
Lifestyle changes:
Weight loss, exercise, dietary changes (reduced salt, alcohol in moderation, DASH diet)
HTN. Stage 1 HTN. management?
Lifestyle changes
+/- 1 antihypertensive drug
Antihypertensive drug is needed if:
Comorbid DM, CKD or ASCVD
OR
10-year risk of ASCVD > 10 proc
HTN. Stage 2 HTN. management?
Lifestyle changes
AND
1-2 antihypertensive drugs
A 2-drug combination is recommended if BP is >= 20/10 mmHg above target
HTN. kidney tests?
Serum electrolytes (Na, K, Ca)
Serum creatinine
Urinalysis (for hematuria, protein/creat. ratio)
Urine albumin/creatinine ratio (optional)
HTN. endocrine tests?
Fast glucose or HbA1c
Lipid profile (risk stratification for CAD)
TSH – Hypo –> AHD
Hyper –> sensitivity of catecholamines
HTN. cardiac tests?
ECG (evaluate CAD and LV hypertrophy)
Cardio echo (optional)
HTN other tests?
Complete blood count
Urid acid (optional)
HTN. what is DASH diet?
UW: Diet high in fruits and vegetables and
low in saturated and total fats
ESC: Increased consumption of vegetables, fresh fruits, fish, nuts, and unsaturated fatty acids (olive oil); low consumption of red meat; and consumption of low-fat dairy products
HTN. DASH diet decreases sBP?
11 mmHg
HTN. weight loss and waist target?
BMI to < 25 kg/m2
men <94 cm
female <80 cm
HTN. weight loss decreases sBP?
6 per 10 kg loss
HTN. aerobic exercises. how often?
at least 30 min of moderate dynamic exercise on 5–7 days per week
HTN. aerobic exercises. decreases sBP?
7 mmHg
HTN. dietary sodium?
UW < 1,5-2,3 g/day (response varies)
esc: < 5 g/day sodium
HTN. dietary sodium decreases sBP?
5-8 mmHg
HTN. Acohol?
UW:
=< 2 drinks/day in men,
=<1 drink/day in women
ESC:
< 14 units in men per week
<8 units in women per week
HTN. Acohol. decreases sBP?
5 mmHg
HTN. smoking?
Smoking cessation, supportive care, and referral to smoking cessation programs are recommended
Measurement: never diagnose HTN on one reading unless severe HTN or end-organ damage is present. Average measurements of >=2 readings on 2 separate occasions separated in time (days, weeks). AMBULATORY BP monitoring is the gold standard.
New onset HTN: once primary HTN is diagnosed, the next best step is to SCREEN for complications and comorbid conditions, which include HbA1c or fasting glucose, lipid panel, chemistry panel (serum Cr, BUN, K), ECG (screen for LV hypertrophy, Q waves for previous MI) and urinalysis (protein).
.
HTN. effectiveness of lifestyle interventions?
Effectiveness: Weight loss > DASH diet > exercise > restricting salt intake > alcohol limitation.
HTN. Yes >=130/80 mmHg. what evaluate then?
Evidence of end organ damage OR BP > 180/120 mmHg.
What rage is HTN in UW?
when screening:
>=130/80 mmHg
HTN. Yes >=130/80 mmHg.
Evidence of end organ damage OR BP > 180/120 mmHg. YES –>?
Hypertension.
Start treatment
HTN. Yes >=130/80 mmHg.
Evidence of end organ damage OR BP > 180/120 mmHg. NO –>?
then evaluate office average (ambulatory for 24-48h or twice daily home BP monitoring for 1 week).
average should be >=130/80 mmHg.
HTN. Yes >=130/80 mmHg.
Evidence of end organ damage OR BP > 180/120 mmHg. NO –> ambulatory monitoring >=130/80 mmHg. What to do?
HYPERTENSION
Start treatment if >140/90. If less, consider risks
HTN. Yes >=130/80 mmHg.
Evidence of end organ damage OR BP > 180/120 mmHg. NO –> ambulatory monitoring IS NOT >=130/80 mmHg. What to do?
NO HYPERTENSION
Routine monitoring
HTN management. TARGET?
<130/80 mmHg
HTN management. Age > =60? what BP to start treatment?
> =150 sBP or > 90 dBP
target - maziau nei sitas
HTN management. Age < 60, chronic kidney disease, DM? what BP to start treatment?
> =140 sBP or > 90 dBP
target - maziau nei sitas
HTN management. for black what drugs?
Thiazide diuretic or CCB,
alone or in combination (ACEI/ARB, not first-line)
HTN management. for other ethnicities than black what drugs?
Thiazide diuretic, ACEI, ARB, CCB,
alone or in combination
HTN management: All ethnicities with chronic kidney disease?
ACEI or ARB,
alone or in combination with other drug classes.
ESC: Thresholds to initiate treatment: 18-79 y/o: 140/90 mmHg; >=80 y/o: 160/90 mmHg
.
Five major drug classes were recommended for the treatment of hypertension:
* ACE inhibitors
* ARBs
* beta-blockers
* CCBs
* diuretics (thiazides and thiazide-like diuretics such as chlortalidone and indapamide)
.
ESC. Uncomplicated HTN.
1st step: Initial dual therapy?
ACEI/ARB + CCB/diuretic
ESC. Uncomplicated HTN. in what consider monotherapy?
In low risk grade 1 (pagal ESC cia yra kai sBP 140-149) OR in very old (>80y/o) or frail patients.
ESC. Uncomplicated HTN.
2nd step: triple therapy?
ACEI/ARB + CCB + diuretic
ESC. Uncomplicated HTN.
3rd step: triple therapy + spironolactone or other durg?
It is resistant hypertension
ACEI/ARB + CCB + diuretic
+ Spironolactone (25-50 mg o.d.), alpha blocker or other BAB.
ESC. HTN + CAD.
1st step: Initial dual therapy?
ACEI/ARB + BAB/CCB
CCB + BAB/diuretic
BAB + diuretic
ESC. HTN + CAD. monotherapy indications same as in uncomplicated HTN.
.
ESC. HTN + CAD.
2nd step: triple therapy.
ACEI/ARB + BAB + CCB
diuretic + BAB + CCB
ESC. HTN + CAD. when consider to start triple therapy from sBP 130?
in very high risk patients with established cardiovascular disease
ESC. HTN + CAD.
3rd step: triple therapy + spironolactone or other drug?
It is resistant hypertension
ACEI/ARB + BAB + CCB
diuretic + BAB + CCB
+ Spironolactone (25-50 mg o.d.), alpha blocker or other BAB.
ESC. HTN
IN WHAT CASES GIVE BAB?
A beta-blocker in combination with a diuretic or any drug from the other major classes is an alternative when there is a specific indication for a beta-blocker, e.g. symptomatic angina, post-myocardial infarction, heart failure with reduced EF, or heart rate control.
HTN + chronic kidney disease.
Step 1. initial therapy?
ACEI/ARB + CCB
OR
ACEI/ARB + diuretic
HTN + chronic kidney disease.
Step 2. triple therapy?
ACEI/ARB + CCB + diuretic
ESC. HTN + chronic kidney disease.
3rd step: triple therapy + spironolactone or other durg?
ACEI/ARB + CCB + diuretic
+ Spironolactone (25-50 mg o.d.), alpha blocker or other BAB.
ESC. HTN + chronic kidney disease. what medication leads to decr. GFR and incr. in creatitine?
ACEI/ARB
ESC. In what diseases very important to give ACEI/ARB?
Both ACE inhibitors and ARBs reduce albuminuria more than other BP-lowering drugs and are effective at delaying the progression of diabetic and non-diabetic CKD.
ESC. HTN + chronic kidney disease.
In what eGFR thiazides/thiazides-like are less effective and in what eGFR not effective?
less effective in eGFR <45 mL/min) and
become ineffective when the eGFR is <30 mL/min.
ESC. HTN + chronic kidney disease. what give when low eGFR and cannot give thiazides/thiazides-like?
In such circumstances, loop diuretics such as furosemide (or torasemide) should
replace thiazides and thiazide-like diuretics to achieve an antihypertensive effect.
ESC. HTN + HFrEF. what is frequent complication?
hypertension
ESC. HTN + HFrEF.
Step1 initial therapy?
ACEI/ARB + diuretic + BAB
ESC. HTN + HFrEF.
Step 2 therapy?
ACEI/ARB + diuretic + BAB + MRA (spironolactone or eplerenone)
ESC. HTN + HFrEF. what drug DONT GIVE?
CCBs are less effective at preventing HfrEF (HF GUIDELINES DO NOT RECOMMEND TO USE CCB IN HFrEF).
ESC. HTN + AFib.
1st step Initial therapy?
ACEI/ARB + BAB/non DPH CCB (verapamil/diltiazem)
Or
BAB + CCB
ESC. HTN + AFib.
2nd step triple therapy?
ACEI/ARB + BAB + DHP CCB or diuretic
OR
BAB + DHP CCB + diuretic
ESC. HTN + AFib.
why combination BAB + non DHP CCB cannot be combinated?
due to potential marked reduction in HR
resistant HTN.
Recommended treatment of resistant hypertension is:
* Reinforcement of lifestyle measures, especially sodium restriction.
* Addition of low-dose spironolactone to existing treatment;
* Or the addition of further diuretic therapy if intolerant to spironolactone, with either eplerenone, amiloride, a higher dose thiazide/thiazide-like diuretic, or a loop diuretic;
* Or the addition of bisoprolol or doxazosin.
.
Resistant HTN. When spironolactone is not tolerated??? what to do
When spironolactone is not tolerated, replace with amiloride or eplerenone.
Resistant HTN.
Amiloride or eplerenone. what two measurement need to check prior use?
The use of these drugs should be restricted to patients with an estimated glomerular filtration rate >=45 mL/min and a plasma potassium concentration of <= 4.5 mmol/L, because of the risk of hyperkalemia.
Resistant HTN.
when A loop diuretic should replace thiazides/thiazide-like diuretics ? gfr
A loop diuretic should replace thiazides/thiazide-like diuretics if the estimated glomerular filtration rate is <30 mL/min
Resistant HTN.
spironolactone gfr and K
Use of spironolactone for resistant hypertension should usually be restricted to patients with an eGFR >=45 mL/min and a plasma potassium concentration of concentration of <= 4.5 mmol/L.
Hypertensive complications.
What is Hypertensive URGENCY?
Severe hypertension (usually >=180/120 mm Hg) with no urgency symptoms or acute end-organ damage
Hypertensive complications.
What is Hypertensive EMERGENCY?
Severe hypertension (usually >=180/120 mm Hg)
+
Acute, life-threatening, end-organ complications
Hypertensive complications.
What is malignant hypertension?
It is a hypertensive emergency seen in patients with long-standing and uncontrolled hypertension.
Hypertensive complications.
Malignant hypertension features?
Retinal hemorrhages, Exudates, Papilledema, malignant nephrosclerosis (Acute renal failure, Hematuria, Proteinuria)
Hypertensive complications.
in emergency tactic of BP reduction?
In hypertensive emergencies, MAP should be lowered by 10%-20% in the 1st hour and by another 5%-15% over the next 24 hours
!!! An excessive drop in blood pressure can lead to cerebral ischemia
Hypertensive complications.
excessive drop in BP can cause what?
!!! An excessive drop in blood pressure can lead to cerebral ischemia
Resistant hypertension UW. What definition?
It is defined as persistent hypertension despite using >= 3 antihypertensive medications of different classes.
Resistant hypertension UW. What to evaluate?
All patients with resistant hypertension should be evaluated for a secondary cause
UW. Isolated ambulatory HTN. what definition?
- It is also called masked hypertension
- It is characterized by incr. average hypertension throughout day and night but normal blood pressure during clinic visits
UW. Isolated ambulatory HTN. Presentation?
- Presentation: Hypertensive end-organ damage (eg, retinal arteriovenous nicking consistent with hypertensive retinopathy, incr. QRS-complex voltage consistent with left ventricular hypertrophy)
UW. Isolated ambulatory HTN.
What is diagnostic criteria?
Ambulatory blood pressure monitoring: an average blood pressure >= 135/85 mm Hg is considered diagnostic of hypertension.
UW. Hypertensive encephalopathy. Mechanism?
It is associated with cerebral edema due to breakthrough vasodilation from failure of autoregulation due to severe hypertension
UW. Hypertensive encephalopathy. Presentation?
Headache, Nausea, Vomiting, Neurologic symptoms (Restlessness, confusion, seizures, coma), subarachnoid or intracerebral hemorrhage.
UW. HYPERTENSIVE RETINOPATHY
4 features
Arteriovenous nicking
Cotton-wool spots
Hard exudates
Arteriolar narrowing
UW. HYPERTENSION SCREENING
Screening should be focused on assessment of two points?
a. Complications or comorbid conditions of hypertension
b. Atherosclerotic risk factors
Do basic tests for HTN.
Further investigation should be performed in patients with a possibility of secondary hypertension.
Signs of suspected secondary hypertension are? 4
a. Age of onset < 30 y/o without family history of HTN
b. Severe or malignant HTN
c. Resistant HTN
d. Sudden BP rise in a patient with previously controlled BP.
Chronic mild to moderate smokers have lower blood pressure than nonsmokers, possibly because:
1. Smokers generally have lower BMI
2. Cotinine (a nicotine metabolite) has a vasodilatory effect
.
Inadequate response to antihypertensive therapy. causes? 3
a. Non-adherence to lifestyle changes and diet
b. Medication noncompliance
c. Use of medications that can raise blood pressure or reduce the response of antihypertensive agents: NSAIDs, Decongestants, Glucocorticoids
CARDIOVASCULAR EFFECTS OF PRIMARY HYPERPARATHYROIDISM.
What is major cause?
Majority of cases are due to parathyroid adenoma
CARDIOVASCULAR EFFECTS OF PRIMARY HYPERPARATHYROIDISM.
Cardiac features? 4
Cardiovascular effects: Hypertension, ventricular hypertrophy, arrhythmias, vascular and valvular calcification
CARDIOVASCULAR EFFECTS OF PRIMARY HYPERPARATHYROIDISM.
What need to evaluate in these patients? (for what pathology)
Evaluate for MEN syndrome in these patients
RENOVASCULAR HYPERTENSION.
It is the most common cause of secondary hypertension. In what cases need to evaluate it as a possible cause of HTN?
a. Onset of severe hypertension after age 55
b. Elevation in serum creatinine >30% from baseline after starting ACEI/ARBs
c. Presence of abdominal bruit
d. Severe hypertension in patients with recurrent flash pulmonary edema
e. Severe hypertension in patients with diffuse atherosclerosis
f. Hypertension in a patient with asymmetric kidney size or a small atrophic unilateral kidney
RENOVASCULAR HYPERTENSION. UW table.
HTN related symptoms? 5
Resistant HTN (uncontrolled despite 3-drug regimen)
Malignant HTN (with end-organ damage)
Onset of severe HTN (>180/120 mm Hg) after age 55
Severe HTN with diffuse atherosclerosis
Recurrent flash pulmonary edema with severe HTN
RENOVASCULAR HYPERTENSION.
supportive evidence. physical evaluation? 2
Physical examination
* Asymmetric renal size (>1.5 cm)
* Abdominal bruit
RENOVASCULAR HYPERTENSION. supportive evidence. lab evaluation? 2
Laboratory results
* Unexplained rise in serum creatinine (>30%) after starting ACE inhibitors or ARBs Imaging results
* Unexplained atrophic kidney
