HTN Flashcards
1
Q
HTN is more prevalent in:
A
- Non Hispanic Black Populations
- Older Persons
2
Q
JNC7 bases BP upon:
A
-The average of two or more properly measured readings at each of two or more visits after an initial screen
3
Q
Normal BP
A
-Systolic: <80
4
Q
Pre-HTN
A
- Systolic: 120-139
- Diastolic: 80-89
5
Q
Hypertension Stage 1
A
- Systolic 140-159
- Diastolic: 90-99
6
Q
Hypertension Stage 2
A
- Systolic > or equal to 160
- Diastolic > or equal to 100
7
Q
Isolated Systolic HTN
A
When BP is > or equal to 140/<90mmHg
-Wide pulse pressure present
8
Q
Isolated Systolic HTN more common in individuals
A
Over age 60. Have diminished compliance of vasculature
9
Q
Blood pressure increases with
A
Age
10
Q
Non-reversible Risk Factors:
A
- African-American descent
- Family history of HTN
11
Q
Reversible Risk Factors
A
- Pre-HTN
- Obesity
- Sedentary Lifestyle
- High sodium diet
- Excessive alcohol intake
- Metabolic Syndrome
12
Q
HTN major risk factor for:
A
- CV disease
- Chronic Kidney Disease
- Dementia
13
Q
HTN single most important risk factor for?
A
Stroke
14
Q
MCC death in persons w/HTN is?
A
Coronary artery disease
15
Q
Left Ventricular Hypertrophy
A
Strong predictor of sudden death and MI in persons with HTN
16
Q
In HTN, microalbuminuria
A
Marker for Increased CV risk
17
Q
Diagnosis: requires SEVERAL BP measurements
A
1) Use validated sphygmomanometer
2) Correct size cuff on BARE arm
3) Resting quiet for at least 5 minutes
4) Back supported
5) Feet on ground & uncrossed
6) No talking
18
Q
Masked HTN definition:
A
Normal in office, but underlying HTN target organ injury
19
Q
PseudoHTN
A
See in older persons, falsely increased systolic & diastolic pressure by cuff due to STIFF vascular tree caused by atherosclerosis
20
Q
Ambulatory reading > office measurements
A
Classification of bp based on average of 2+ readings obtained more than 1 min. apart on 2 or more visits
21
Q
Ambulatory BP Monitoring
A
- Evaluates mean 24 hr B.P.
- Difference b/w mean daytime and mean nighttime bp
- Avg difference used to evaluate for noctural dipping.
- > 10% is dipping (good thing)
22
Q
Lack of nocturnal dipping causes
A
More strain on CV system
23
Q
Non-dipping (bad) often seen in
A
- African Americans
- Chronic Kidney Disease
- Sleep Disorders
24
Q
Lack of nocturnal dipping associated with
A
Increased CV risk
25
As we grow older our arteries become stiffer and less compliant
- Stiffening, get increased speed of reflected waves
| - Faster the pulse wave velocity, the greater the end organ damage.
26
Measurement of central aortic pressure and pulse wave velocity are better correlated with end-organ damage
> than brachial BP
27
Most anti-HTNs cannot slow pulse wave velocity
Statins do improve vasculature compliance.
28
3 questions to ask when evaluating HTN
1) BP: Essential (primary) vs. Secondary
2) CV Risk factors
3) End organ damage
29
Who is more prone to pseudo HTN?
- Elderly
- Chronically ill
- These groups are also prone to orthostatic hypotension.
30
Meds that can elevate BP:
- Oral contraceptives
- Corticosteroids
- Monoamine oxidase inhibitors
- NSAIDs
- Sympathomimetic preparations for cold or diet
- Cocaine
- Alcohol
- Serotonin
- Glycyrrhizinic acid (true licorice) in chewing tobacco
31
Physical Exam:
- Measurement of vital signs
- BMI
- Cardiopulm exam
- Auscultation of major blood vessels to identify bruits
- Fundoscopic examination
- Neuro
- Evaluate extremities for edema and circulatory abnormalities.
32
Labs:
- CBC
- Lipid and biochem profiles
- Urinalysis
- Electrocardiogram
33
Wait to measure renin and aldosterone until:
- See pt w/HYPOkalemia or resistant HTN
| - Increased plasma aldo:renin ratio: suggests dietary Na+ excess HTN.
34
Clinical marker for LVH:
- S4 gallop
- Apical lift ECG
- ECHO
35
Clinical marker for angina, prior MI, prior revascularization
History
36
Clinical marker for heart failure:
-History, lung RALES, S3 gallop, Chest x-ray, Echo
37
Marker for Stroke, TIA, Leukoariosis (white matter changes on imaging)
History and brain imaging
38
Marker Chronic Kidney Disease
eGFR, Creatinine, U/A, microalbumin
39
Marker Peripheral Artery Disease
-Claudication, bruits, diminished pulses
40
Marker Retinopathy
-Fundoscopic evaluation, general and focal narrowing, AV nicking, Copper wiring, cottom wool spots, microaneurysms, Frame and blot hemorrhages
41
Essential HTN
90% of patients with htn evaluated in the primary care setting
42
Classic Features of Essential HTN
- Onset in fourth or fifth decade of life
- A positive family hx for HTN
- Initial BP low categorized as stage 1 HTN
- And easily controlled with 1 or 2 medications
- No target organ damage
- Normal results of routine lab studies
- BP that does not increase from an established level of control over a short period of time
43
Things that make you think secondary forms of HTN:
- Age of onset, before 30, over 50
- BP >180/110 mmHg at diagnosis, significant target organ damage
- Poor response to an appropriate 3 drug regimen
44
Lifestyle modifications are appropriate to lower bp in patients with
Pre-HTN
45
Lifestyle modifications + drug treatment
Stage 1 or greater HTN
46
Weight Reduction, maintaining normal body weight
5-20 mmHg reduction/10 kg weight loss
47
Adapting DASH eating plan
8-14 mmHg reduction
48
Dietary sodium reduction, no more than 1500 mg/day
2-8 mmHg
49
Physical Activity, 30 minutes/day
4-9 mmHg
50
Moderation of alcohol consumption
2-4 mmHg
51
Goal of treatment of HTN:
Reduce CV mortality and morbidity by lowering BP
52
Goal in general population of anti-HTN treatment
Lower BP below 140/90 mmHg
53
Linear, progressive increase risk of ischemic heart disease and stroke in patients with bp higher than
115/75 mmHg
54
Most anti-HTN agents reduce blood pressure by 10-15% and ALL classes of anti-HTN drugs
Reduce CV morbidity and mortality vs. placebo
55
Treatment of systolic heart failure and proteinuria in kidney disease
ACE Inhibitors and ARBs
56
Salt sensitive HTN
Diuretics, may be good in:
- Elderly
- Low GFR
57
Coronary artery disease and migraine headaches
Beta-blockers
58
Clinical trials have shown that achieving appropriate blood pressure targets is MORE important in reducing morbidity and mortality than
The choice of Anti-HTN therapy
59
Use these drugs to help lower BP in patients who are likely to be sodium sensitive:
- Older patients
- Black
- Lower pre-txt plasma renin activity
Calcium channel blockers
| Diuretics
60
Use for younger, white, and higher pre-txt plasma renin activity
ACE-Inhibitors or
| Beta-blockers
61
Lifestyle modification and drug treatment are indicated for all patients with
Stage I HTN or greater
62
Patient with stage II HTN often require treatment with
more than one agent
63
Resistant HTN
Patients whose BP remains above goal on maximum doses of 3 meds one of which is a diuretic.
64
10% cases HTN due to secondary htn
Consider in pts who have clinical features inconsistent with essential HTN.
Common secondary causes: drugs, increasing obesity, obstructive sleep apnea
65
Renal vascular htn
1-3% general HTN population
10% patients with resistant htn
30% pts in htn crisis
66
Renal artery stenosis does NOT make a diagnosis of
Renal vascular htn
67
70% or more luminal narrowing
Increases renin production from ischemic kidney
68
Not all abdominal bruits are from renal artery
Diastolic component to bruit= renal artery lesion
69
Unilateral disease
-nonischemic kidney increased perfusion, higher Na+ excretion and suppression of renin release
70
Bilateral disease
-Increases in renin cause ECV expansion and volume dependent htn.
71
Pulse pressure is a good assessment of
End organ damage
72
Fibromuscular dysplasia
Most common cause of renovascular htn in younger women, esp childbearing age. Medial subtype most common. "String of beads" on angiography.
* Balloon angioplasty is the treatment of choice
- Stents reserve only if angioplasty fails
73
Renal revascularization only improves htn in patients with
Anatomic lesion that is hemodynamically significant to activate the renin-angiotensin system.
74
BOLD MRI
Bilateral renal artery stenosis present, ACE inhibitors and ARBS can make acute renal failure worse.
75
Gold standard for identifying renal artery stenosis
-Renal angiography
76
Top causes of secondary HTN
```
#1: Primary hyperaldosteronism
#2: Renal parenchymal disease
```
77
HTN is the 2nd most common cause of
End stage renal disease.
78
3 mechanisms involved in HTN of renal disease
1) volume expansion b/c can't get rid of salt and water
2) over secretion renin
3) Decreased production renal vasodilators
79
Primary aldosteronism
- Overproduction of aldosterone by adrenal glands
- HTN, hypokalemia with renal wasting of potassium and metabolic ALKALOSIS.
- Suppressed plasma renin activity
- Increased aldosterone levels
80
When to suspect primary aldosteronism:
Person with spontaneous hypokalemia, marked hypokalemia precipitated by usual dose of diuretics, resistant HTN, hypertension and adrenal mass, or hypokalemia despite use of ACE inhibitors or ARBs.
81
Almost half of patients with primary aldosteronism have
Normal potassium levels
82
Plasma aldosterone: renin ratio
Screening test for primary aldosteronism
urine aldosterone excretion 12 mcg/24 hours (33.2nmol/day) or higher after correction of hypokalemia and adherence to HIGH sodium diet for 3 days.
83
Adrenal imaging
- Aldosterone producing adenoma (Conn syndrome)
| - Primary unilateral adrenal hyperplasia
84
Can use spironolactone for treatment of
Primary aldosteronism
85
Sometimes obese pts or with resistant htn can see dramatic decrease in bp when started on
Aldosterone antagonist
86
Pheochromocytoma
Tumors of chromaffin cells, derived from neural crest.
- Cause paroxysmal or sustained htn
- excess production of catecholamines
- Diaphoresis, headache, and anxiety frequently associated symtpoms
87
Complications of pheochromocytoma
- MI, stroke, cardiovascular collapse
| - Can have germ-line mutations
88
Familial pheochromocytoma occurs in
- multiple endocrine neoplasia type II
- von Hippel-Lindau disease
- Neurofibromatosis
- Familial paraganglioma
89
Diagnosis pheo
- Confirm excess catecholamine production supported by imaging studies
- Fractionated catecholamines and metanephrines can be measured in the serum or via a 24-hour urine collection
- MRI
- CT scanning can localize
90
Treatment of choice for pheochromocytoma
Surgical resection
| -10-14 days before surgery give alpha blocker phenoxybenzamine , then beta-blockers started
91
**Do NOT use Beta blockers without alpha blockage b/c
-Can lead to unopposed alpha stimulation and an increase in BP
92
Catecholamines can induce vasoconstriction and pressure naturesis can cause decrease in plasma volume
-We can institute high sodium diet and avoid diuretics.
93
HTN patient with impaired fasting glucose
Cushing syndrome
94
Hypothyroidism
- associated with diastolic htn
- state of decreased cardiac output and contractility
- Tissue perfusion maintained by increase in peripheral vasc. resistance mediated by increased activity of the sympathetic nervous system
95
Hyperthyroidism
- Associated with systolic HTN
| - Wide pulse pressure due to increased CO and decreased peripheral vasc. resistance
96
Hyperparathyroidism
-Hypercalcemia may increase BP directly by increasing peripheral vascular resistance and indirectly by increasing vascular sensitivity to catecholamines
97
Acromegaly
-Can develop HTN due to Na+ retaining effects of GH.
98
Coarctation of aorta
- Constriction of vessel, detected in childhood
- More common males
- Assoc. with bicuspid aortic valve
- Classic feature: increased BP in upper extremities and low BP in lower extremitie
99
Symptoms of coarctation of aorta
Headache, cold feet, and claudication (pain by too little blood flow during exercise)
-Clinical signs: elevated bp in arms, murmurs in front and back of chest and delay in femoral pulse when radial and femoral pulses palpated.
100
**NOTCHED ribs
Coarctation! Do surgical repair or balloon angioplasty
101
Obstructive Sleep apnea
- Upper body obesity
- Overweight pts that snore loudly
- Complains: morning headaches, daytime sleepiness
- Sleep study**
- Increased sympathetic nervous system
- Treatment: continuous POSITIVE pressure, lower BP 3-5 mmHg.
- Encourage to lose weight
102
HTN emergency:
- Need to hospitalize
- Parenteral therapy!!!
- HTN encephalopathy, aortic dissection, unstable angina, MI, eclampsia, pulmonary edema, and acute renal failure
- Fibrinoid necrosis vascular lesion of malignant HTN
103
HTN urgency
- Severe HTN without evidence acute organ injury but occurring in setting in which it is important to decrease bp.
- Oral therapy
104
Common causes HTN urgency
- Neglected essential HTN
- Discontinuation of anti-htn therapy
- Renovascular disease
- Scleroderma
- Stroke
105
Sodium nitroprusside
- DOC htn emergency
- Don't use in pts with kidney disease
- Raises intracranial pressure in animals
- Nitroprusside: worry about cyanide and thiocynate toxicity
106
Labetalol
A combo of alpha and beta blocker
| can use orally & IV
107
Nicardipine and clevidipine
Ca2+ channel blockers
108
Fenoldapam
IV dopamine agonist
| Preserves renal perfusion and is good for patients with Increased creatinines
109
Nitroglycerin
Good for pts w/acute congestive heart failure or coronary ischemia
110
Esmolol
DOC for Aortic dissection!
