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Flashcards in HTN Deck (68)
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1
Q
When someone has high BP, want to prevent
A
end organ damage
(stroke, heart attack, blindness, kidney failure, heart failure)
2
Q
HTN is when BP is
A
140/90 in office multiple times
OR 135/85 at home
3
Q
AOBP is a device that allows ________
A
you to continuously/regularly check your BP at home
4
Q
Normal BP is
A
5
Q
PreHTN BP is
A
120-139 mmHg SBP or DBP 80-89 mmHg
6
Q
Stabe 1 HTN BP is
A
140 to 159 mmHg SBP or DBP 90 to 99 mmHg
7
Q
Stage 2 HTN BP is
A
> 160 mmHg SBP or > 100 mmHg DBP
8
Q
Guidelines for measuring BP
A
long table on slides 7-8
9
Q
Prevalence is highest in
A
non-hispanic blacks
10
Q
More LV hypertrophy, higher incidence of ____
A
CV events
-Reversible and treatable
11
Q
Higher BP and HTN left untreated leads to a higher incidence of
A
ESRD (end stage renal disease)
12
Q
There are cardiovascular benefits to treating
A
mild HTN (lowers risk of CVA and coronary heart disease)
13
Q
Cause of primary HTN
A
over activation of SNS and RAAS via:

-NSAIDs
-too much salt intake
-family history
-smoking
-alcohol
**Sleep apnea is a MAJOR cause of CV problems, A-Fib, HTN**
14
Q
Who should be screened for secondary HTN?
A
1. Severe or resistant HTN
(persistent HTN despite use of adequate doses of three antihypertensives from different classes)
2. Acute rise in BP in a patient with previously stable values
3. Age under 30 in non-obese, non-African American patients with negative family history
4. Malignant or accelerated HTN
5. Severe HTN and evidence of end-organ damage
6. Age of onset before puberty
15
Q
Genetic causes of secondary HTN
A
1. Liddle syndrome (psueodhyperaldosteronism)
2. hyperaldosteronism
3. HTN in pregnancy
16
Q
FMD (fiber musculodysplasia)
A
*Cause of secondary HTN
-FMD (fiber musculodysplasia) in young women (young woman with refractory HTN, reversible cause of high BP in young women; “beads on a string” sign; sign is caused by areas of relative stenoses alternating with small aneurysms; seen in renal arteries)
17
Q
95% of HTN is
A
essential (primary)
18
Q
Refractory HTN
A
*Cause of secondary HTN
-Refractory hypertension was defined as BP that remained uncontrolled after ≥3 visits to a hypertension clinic within a minimum 6-month follow-up period
19
Q
Renovascular Disease
A
*Cause of secondary HTN
-Bruits (diastolic abdominal) -PAD
-->Cr increase with ACE-I (Creat is 1.2, give ACE inhibitor, creat goes up to 2.0; suspect bilateral renal artery stenosis)
-Pulmonary edema (Flash pulmonary edema with HTN (recurrent), think renal artery stenosis)
20
Q
Other factors that can cause secondary HTN
A
oral contraceptives, NSAIDs, stimulants (cocaine, methylphenidate), calcineurin inhibitors, antidepressants,
21
Q
Pheochromocytoma
A
*Cause of secondary HTN
-paroxysmal (sudden burst) increase in BP
-Triad of pounding headache, palpitations, sweating
22
Q
Primary aldosteronism
A
*Cause of secondary HTN
-unexplained HYPOkalemia, urinary protein wasting (even thought about 1/2 of pts are normkalemic)
-Tx: Sprinolactone (aldosterone inhibitor)
23
Q
Cushing Syndrome
A
*Cause of secondary HTN
-Cushingoid facies, central obesity, proximal mm weakness, ecchymoses
-May have history of glucocorticoid use
24
Q
Sleep apnea syndrome
A
*Cause of secondary HTN
-Usually in obese men who snore loudly when sleeping
-Daytime somnolence, fatigue, morning confusion
25
Q
Coarctation of the Aorta
A
*Cause of secondary HTN
-HTN in arms with diminished femoral pulses and low/unreadable BP in legs
-Left brachial pulse is diminished and equal to the femoral pulse (if origin of L subclavian artery is distal to the coarctation)
-Bicuspid Aortic Valve is associated with coarcatiob
-Tx: stenting of the aorta to help alleviate congestion
-Bicuspid and aorta need MRI of brain, could have aneurism
26
Q
Hypothyroidism
A
*Cause of secondary HTN
-s/s of hypothyroidism
-elevated serum TSH
27
Q
Primary hyperparathyroidism
A
*Cause of secondary HTN
-elevated serum calcium
28
Q
Chronic complications of HTN
A
-Hypertensive heart disease
-Hypertensive cerebrovascular disease and dementia
-Hypertensive kidney disease
29
Q
Hypertensive emergencies
A
-Grade 3-4 HTN retinopathy
-CVA (encephalopathy, brain infarction, intracerebral or subarachnoid hemorrhage)
-Cardiac: aortic dissection, acute left vent failure, MI
-Renal: acute glomerulonephritis, renal crisis, microangiopathic hemolytic anemia
-Excessive circulating catecholamines: Pheo crisis, interactions with MAO inhibitors, cocaine/drug use, rebound HTN after stopping meds
-Eclampsia (seizures in pregnant woman with high BP and protein in urine)
-Surgical (post op)
-Body burns
-Epistaxis (nose bleeds from increased pressure)
30
Q
Most people with HTN are
A
asymptomatic
-may see headache, if severe can cause encephalopathy, N/V, confusion, vision changes
31
Q
S/S of Pheochromocytoma
A
-episodic presentation
-Anxiety, palpitations, profuse perspiration, tremor, HA
32
Q
Optho exam on pt with HTN will show
A
Cotton wool spots, AV nicking, hemorrhage, **papilledema** (optic disc swelling that is caused by increased intracranial pressure)
-->LOOK UP PIC OF HTN Retinopathy

-hard exudates and flame hemorrhage may also be seen
33
Q
ECG and echo will show radial-femoral delay, which is indicative of
A
Coarctation of the aorta
(both can detect end organ damage as well)

-The radial and femoral pulses are palpated simultaneously,
an appreciable delay in the femoral pulse is suggestive of coarctation of the aorta.
(HTN is highest in upper limbs and head)
34
Q
EKG shows
A
criteria for LVH
Can look at S wave of lead V3 downward portion of QRS complex

23 in a woman; 28 in a man
=HTN

S wave in lead V1 or V2 and add it to R wave in lead V5= if over 35= HTN
35
Q
Treatment should include
A
Exercise, alterations in diet (DASH diet), decrease sodium intake, limit alcohol consumption

-every 10 kg of weight loss BP can drop 10-20 mmHG
Fruits veg, Mediterranean diet can drop it 10 mmHg
36
Q
What meds to start with for African Americans?
A
CCB and thiazide
37
Q
What meds to start with for whites with isolated HTN?
A
ACE-I and BB
38
Q
However, many pts have comorbidities which should prompt targeted therapy, example:
A
AA pt with DM should receive ACE-I first
39
Q
Don't use an alpha blocker if
A
ejection fraction is low
40
Q
Use ACE inhibitor for
A
Systolic heart failure (and beta blocker), Post MI (and beta blocker), Proteinuric chronic kidney disease
41
Q
Use Beta Blocker for
A
Angina pectoris*, a fib rate control*, atrial flutter rate control*, essential tremor, hyperthyroidism, migraine

*can also use nondihydropyridine CCB
42
Q
Use Alpha Blocker for
A
benign prostatic hyperplasia
43
Q
Use Thiazide diuretic for
A
osteoporosis
44
Q
Use dihydropyridine calcium channel blocker for
A
Raynaud's syndrome
45
Q
NEVER use ACE inhibitor for ___________ (contraindication)
A
**angioedema**

KNOW FOR TEST
46
Q
Beta blockers are contraindicated for
A
bronchospastic disease

(make depression worse)
47
Q
Reserpine is contraindicated for
A
depression
48
Q
Methyldopa is contraindicated for
A
liver disease
49
Q
ACE inhibitors, ARBs and renin inhibitors are contraindicated for
A
pregnancy
50
Q
Beta blockers, nondihydropyridine CCBs
A
2nd or 3rd degree heart block
51
Q
Diuretics make _______ worse
A
gout
52
Q
Aldosterone antagonists, ACE inhibitors, ARBs and renin inhibitors make _______ worse
A
hyperkalemia
53
Q
Thiazide diuretics make _______ worse
A
hyponatremia
54
Q
Diuretics
A
-Initially lower plasma volume but decrease SVR (systemic vascular resistance)
Side effects: long-term
electrolytes, gout, ED, hyperkalemia
Thiazides, loop
55
Q
For patient in ER, don't give __________, instead give __________
A
hydrochlorothiazide

give lassie (furosemide, loop diuretic) to get rid of fluid, can give thiazides for more long term care after
56
Q
Beta blockers
A
-Decrease HR and CO, decrease renin levels
-Carvedilol decrease PVR thru alpha-blockade
-Nebivolol increases NO release
57
Q
Side effects of beta blockers
A
-Bronchospasm, bradycardia, fatigue, ED
-Do not use alone for tx of HTN from cocaine* or for pheo unless given alpha blockade
-Cocaine induced chest pain/HTN- don’t use beta blockers alone; must block alpha first, especially if they have a pheo
58
Q
Renin inhibitors
A
Lack efficacy data over ACE-I/ARB
59
Q
ACE-I
A
Inhibits RAAS, prevents degradation of bradykinin
60
Q
ARB (Angiotensin Receptor Blockers)
A
-Inhibit RAAS
-Olmesartan can be associated with sprue-like syndrome (malabsorption syndrome)
-Caution for ACE-I/ARB if Cr worsens > 25%, could be due to RAS
61
Q
Aldosterone receptor blockers side effects
A
-CHF, cirrhosis
-Can lead to gynecomastia, hyperkalemia, breast pain
62
Q
CCB side effects
A
-Peripheral vasodilation with less reflex tachy/fluid retention
-Caution in CHF
63
Q
Alpha blockers
A
-Lower PVR; useful with BPH
-First-dose hypotension, caution in CHF
64
Q
Central sympatholytic (clonidine, methyldopa)
A
-Stimulate alpha in CNS thus reducing efferent peripheral SNS outflow
-Side effects: ED, rebound HTN, dry mouth, caution in pregnancy with methyldopa
65
Q
Direct vasodilators
A
Hydralazine/minoxidil
66
Q
Peripheral Sympathetic Inhibitors
A
Reserpine (may cause depression)
67
Q
Hypertensive urgencies, treat when __________
A
when acute end-organ damage or BP > 220/125

Reduce ~ 25% in first 1-2 hrs and then target
68
Q
Treatment for HTN urgencies/emergencies
A
-Nicardipine, labetalol, nitroprusside, NTG
-Cyanide toxicity as side effect, can present as a stroke