Hypertension Flashcards
1
Q
HTN increases the RR 2-4 fold for developing:
A
- CAD
- HF
- Stroke
- AF
- CKD
- PAD
- dementias (vascular/AD)
2
Q
HTN in general can shorten one’s lifespan an average of __________
A
5 years
3
Q
HTN risk factors (9)
A
1- advancing age
2- genetics: 2x as common in people w/ 1-2 first degree relatives
3- DM and dyslipidemia
4- AA (more severe and 10+ years earlier than whites)
5- CKD: higher staging—> more difficulty controlling HTN
6- etoh: >2 drinks/day on average
7- high sodium diet: >3gm/day
8- lifestyle: sedentary lifestyle and weight gain
9- personality traits (hostile, impatient, depressed)
4
Q
Minimal diastolic pressure:
A
70-80 mmHg
5
Q
Maximum systolic pressure:
A
110-120 mmHg
6
Q
Lowest risk of CV and renal complications associated with a BP of:
A
115/75
7
Q
Regulation of normal BP is dependent upon:
A
Cardiac output: sodium intake, renal fx, mineralcorticoids
Peripheral vascular resistance: dependent upon the SNS, humoral factors, and local vasculature autoregulation
8
Q
MAP calculation and goal:
A
Goal: >70 mmHg
Calculation: (DBP*2)+SBP/3
9
Q
Heart Failure Drug line tx:
A
1- ace/arb
2- beta-blocker
3- thiazide
4- aldosterone antagonist
10
Q
Post-MI drug line treatment:
A
1- Beta-blocker
2- Ace/arb
3- thiazide or CCB (this line not mandatory; one 1 and 2 required)
11
Q
High coronary disease risk drug line treatment:
A
1- Beta-blocker
2- Ace/arb
3- thiazide or CCB
12
Q
Diabetes drug line tx:
A
1- ace/arb
2- thiazide/CCB
*unless AA pt—> then put on thiazide/CCB 1st line
13
Q
CKD drug line tx:
A
1- ace/arb
2- thiazide/CCB
*AA benefit from ace/arb first line over CCB/thiazide
14
Q
Recurrent stroke prevention drug line tx:
A
1- ace/arb
2- thiazide/CCB
15
Q
Factors that affect Cardiac output
A
Renal function
Mineralcorticoids
Sodium
16
Q
Factors that affect peripheral vasculature:
A
Humoral
SNS
Local vasculature autoregulation
17
Q
One measurement of BP w/ this value—> hypertension diagnosis and requires treatment
A
SBP>180
18
Q
Blood pressure guidelines:
A
- empty bladder
- take 3 times B/L (throw out 1st one and average last 2; always take highest reading if disparity)
- no caffeine or smoking 30 minutes prior
- have pt sit for 5 minutes w/ feet flat of floor and back support
- appropriate BP cuff size
- can test orthostatic HTN in elderly adult—> rotating 1-3 mins after standing
19
Q
Preferred BP measurements taken:
A
Automated 3-6x, unattended
—> eliminated white coat effect; increased BP reproducibility and accuracy
20
Q
Normal BP
A
<120/<80
21
Q
Prehypertension
A
120-139/80-89
22
Q
Stage 1 HTN:
A
> 140-159/>90-99
23
Q
Stake 2 HTN
A
> 160/>100
24
Q
BP definitions only apply to adults:
A
- not acutely ill
- not on BP meds
25
Hypertensive urgency
>180/120 w/ no end organ damage
26
Hypertensive emergency
BP >180/120 w/ end organ damage
| —> may rq neuro, renal, opthamology, or CV teams for acute organ damage
27
Acute end organ damage in hypertensive emergency may include:(12)
```
Neuro: 4
- HTN encephalopathy
- CVA
- SAH/ICH
Cardio: 4
- aortic dissection
- acute pulmonary edema
- MI/Myocardial ischemia
- Acute left ventricular dysfunction
Renal: 1
- acute renal failure/insufficiency
Opth: 1
- HTN retinopathy
Others: 2
-preeclampsia
-microangiopathic hemolytic anemia
```
28
Screening guidelines:
- anyone >18
- preferred ambulatory monitoring prior to dx
- likely beneficial for @ home measurements
29
Increased CV risk seen in
- non-dippers
- young w/ diastolic BP
- adults and elderly w/ isolated systolic BP (normal diastolic and wider pulse pressures—> peripheral vasculature non-compliance)
30
AA patients and hypertension:
- occurs at younger age
- more severe HTN
- more responsive to: sodium, obesity, and diet
- 3-5x more likely—> end-stage kidney disease
- MC w/ strokes and hypertensive KD
31
What is resistant HTN?
HTN >140/90 while on 3 meds including thiazide and BP wont decrease
MC w/ secondary
32
What are the 6 compelling indications for treating HTN?
```
#1: HF
2- post MI
3- high CAD risk
4- DM
5- Recurrent stroke prevention
6- CKD
```
33
HF drug treatment line-up:
```
1- ace/arb
2- beta blocker
3- diuretic
4- aldosterone antagonist
*want to get all on board; preferred low dose of all
```
34
Post-MI drug treatment line-up:
1- beta blocker
2- ace/arb
*try to get both on board
35
High CAD risk drug line-up:
1- beta blocker
2- ace/arb
3- CCB or thiazide
Do not need all on board if BP therapeutic
36
Diabetes drug line-up:
1- ace/arb
| 2- CCB or thiazide
37
Stroke drug line-up:
1- ace/arb
| 2- CCB or thiazide
38
CKD drug line-up:
1- ace/arb
| 2- CCB or thiazide
39
ACE,ARB,CCB can be used in:
Gout, urinary incontinence, SSRI rx, hyponatremia
40
Thiazides, ace, arb, and CCB can be used in:
No gout, urinary incontinence, SSRI rx, hyponatremia
41
Acceptable medications in pregnancy:
- CCB, BB, or thiazides :)
| - NEVER ACE/ARB
42
Short term BP regulation:
- neural control
| - humoral control
43
Long term BP control:
- predominantly regulated by the kidney via widespread arteriole vasoconstriction and hydrostatic pressure
44
Secondary HTN etiologies: (8)
```
1- CKD (MC)
2- Polycystic kidney disease
3- Renovascular HTN (Renal artery stenosis)
4- Coarctation of the aorta
5- Thyroid dz (hypo- or hyper-)
6- Pheochromocytoma
7- Primary hyperaldosteronism
8- Meds
```
45
Renovascular HTN seen in:
- arteriosclerosis in old men w/ CAD RF's
| - women <50 w/ fibromuscular dysplasia
46
Renovascular HTN w/u:
1- renal artery ultrasound
2- CT or MR angiography of renal vessels
3- invasive angiogram
47
Consider Renovascular HTN if pt presents w/:
- abdominal bruit
- refractory HTN
- recurrent flash pulmonary edema
- AKI w/ initiation of ACE/ARB
48
CKD w/u for secondary HTN:
Renal U/s: small shrunken kidneys
49
Suspect CKD for secondary HTN if pt:
GFR >60 and proteinuria
50
Polycystic kidney disease w/u for secondary HTN:
- Renal U/S: large, cystic kidneys
51
Coarctation of the aorta w/u for secondary HTN:
1- Screen test: Chest xray
| 2- Diagnostic test: CT of the chest w/ contrast
52
Suspect Coarctation of the aorta if pt:
- abdominal bruit
- UE pulses stronger than LE pulses
- rib notching on chest xray
53
Thyroid disease w/u:
TSH to screen
54
Pheochromocytoma dx:
1- Labs: urine metanephrine and vandyllamanilic acid levels
| 2- Adrenal CT or MRI w/ contrast
55
Pheochromocytoma presents w/:
- pallor, diaphoresis, paroxysms of HTN, palpitations
56
Primary hyperaldosteronism presents w/:
metabolic alkalosis and persistent hypokalemia
| - sxs: generalized weakness
57
Primary hyperaldosteronism etiology:
adrenal adenoma or hyperplasia
58
Meds contributing to secondary HTN:
E's:
- ethanol (chronic use is a major contributor to HTN)
- eating black licorice
- ephedrine/pseudoephedrine
- exciting drugs: cocaine/meth
- estrogens
59
Natural Hx of HTN:
1- prehypertension: increased CO and BP
2- early HTN: increased PR
3- established HTN: vasculature remodeling and progressive damage
4- Complicated HTN: end organ damage
60
Pathophysiology of essential HTN: (6)
- Overactive SNS (overactive sympathetic tone leads to increased vascular tone and HTN)
- Genetics (2x more likely)
- Sodium intake (increased naturiesis)
- Reduced adult nephron mass (genetic, fetal, and postnatal factors-- hypoxia or malnutrition)
- immunologic (renal infiltration of immune cells)
- cardiac malformation (abnormal development of aortic elasticity and reduced development of the microvascular network in fetal life)
61
Contributors to essential HTN: (9)
1- obesity (increased intravascular volume, increased CO, increased RAAS activation and increased sympathetic outflow)
2- Sleep apnea (increased oxygen is good)
3- Smoking (increases nor and CV RF)
4- alcohol (increases blood catecholamines)
5- exercise (aerobic in sedentary; active- aerobic may not benefit)
6- immune system activation
7- Polycythemia (increased viscosity)
8- Sodium (increased sodium and low potassium)
9- NSAIDs (inhibit prostacyclins and increase 5 mmHG)
62
Chronic HTN leads to..
1- increased arterial wall stiffness
2- increased SBP's
3- widened pulse pressures
63
the vasculature remodeling associated w/ chronic HTN leads to:
- decreased coronary perfusion pressures
- increased myocardial oxygen consumption
- LVH of myocytes
64
Cardiac Pathophysiology of HTN:
- myocardium structural changes (in response to increased afterloads)
- hypertrophied cardiac myocytes
1- diastolic dysfx: impaired passive relaxation of left ventricle secondary to hypertrophy
2- leads to increased LV end-diastolic pressures
3- leads to increased left atrial pressures
4- systolic dysfx w/ LVH impinging on the heart cavity and limiting diastolic filling and SV
65
Cardiac involvement in HTN manifests as: (6)
- LVH/diastolic HF
- systolic HF
- left atrial enlargement
- aortic root dilation and valve incompetance
- atrial and ventricular arrhythmias
- ischemic HD and cardiomyopathy
66
LVH is associated w/:
increased risk of premature death and morbidity
67
Patho of HTN in the CNS: w/ chronic HTN
- cerebral autoregulation: to maintain constant cerebral blood flow
- CNS adapts to elevated perfusion pressures via increased cerebral vascular resistance
- decreases in blood flow induce cerebral ischemia
- very dangerous to drop blood pressure rapidly, requires slow taper over weeks
68
Patho of HTN in the CNS: w/ acute rise in BP
- leads to hyperperfusion and increased cerebral blood flow
| - causes increased ICP and cerebral edema (end organ damage)
69
Patho of HTN in the Kidney:
- chronic HTN damages small BV of kidney (endothelial cell dysfunction and impaired vasodilation)
- impaired autoregulation of blood flow to glomerulus
- intraglomerular pressure changes w/ SBP
- volume expansion is the MAIN CAUSE of HTN in pts w/ glomerular dz
- overactivation of the RAAS is the MAIN CAUSE of HTN in pts w/ vascular damage
- Both are MAIN CAUSES of HTN in pts w/ chronic renal failure
70
Renovascular HTN resultant of:
- complete or partial occlusion of the renal artery
| - + RAAS; hyper-reninemia; severe vasoconstriction and aldosterone release
71
Renovascular HTN w/ one healthy kidney:
can handle sodium and water retention so volume does not contribute to HTN
72
Renovascular HTN w/ significant CKD or one solitary, ischemic kidney:
volume contributes to HTN
73
Screening for HTN rqs. asking about these events: hx and (6)
Hx: CAD/ACS, MI, revascularization
- HF
- PAD
- sleep apnea
- CKD
- stroke/TIA
- DM
74
Screening for HTN rqs. end organ damage assessment:
- eye: Retinopathy
- Vasculature: PAD
- CKD
- brain: cerebral atrophy, dementia
- heart: LVH, diastolic/systolic dysfx, wall motion abnormalities
75
Assessment of pt's CV risk status: (9)
- tobacco use
- LDL/HDL levels
- DM
- obesity
- exercise?
- age: >55 men/>65 for women
- estimated GFR <60 (CKD stage 3)
- microalbuminuria: spot urine ACR
- Fam hx of premature CAD (>55 men/>65 for women)
76
Secondary causes of HTN: (6)
- OTC meds, OCs, etoh or illicit drugs
- CKD
- Pheochromocytoma
- thyroid
- sleep apnea
- hyperaldosteronism
77
Diagnostic w/u in HTN: (6)
```
1- urinalysis
2- CBC
3- A1c or fasting blood glucose
4- Fasting Lipid panel
5- electrolytes
6- Baseline EKG
```
78
Causes of drug-induced HTN: (12)
```
Prescription drugs: (5)
- high dose OC's
- NSAIDs
- Pseudoephedrine
- migraine meds
- psych meds: SSNRIS, TCAs)
Situations w/ RX: (1)
- beta-blocker w/o an alpha-blocker first in tx: pheochromocytoma or cocaine-induced HTN
Foods: (2)
- ethanol
- sodium
Street drugs: (4)
- cocaine
- cocaine withdrawal
- St. John's wort
- narcotic withdrawal
```
79
Screen for Secondary HTN:
- new onset HTN <30 y.o.
| - resistant HTN
80
Screening for Secondary HTN rqs. and typical lab features include:
- clinical suspicion
| - hypokalemia, epigastric bruits, episodic HTN/flushing/palpitations, different BP in b/l arms
81
Recommended BP goal in DM and CKD:
<130/80
82
Recommended BP goal w/ age >80:
<150/90
83
Recommended BP goal in general population:
<140/90
84
In diagnosing HTN: Visit #1
BP>180/110=HTN
BP<140/90= pt is fine!
BP= 140-180/90-110; requires out of office assessment
85
Out of office assessment for HTN f/u prefers:
1- Ambulatory BP monitoring
2- home BP monitoring
3- 3 f/u visits over 1 month
86
Describe BP monitoring over 3 f/u visits over 1 month:
*only if ABPM and HBPM not available
Visit A: SBP>140 or DBP>90 then go to..
Visit B: SBP>160 or DBP>100--> dx HTN; if <160/100 then go to..
Visit C: SBP>140 or DBP>90--> dx HTN; if <140/90, no HTN!
87
In diagnosing HTN: Visit #2
- daytime ABPM or HBPM: >135/85 or ABPM (night) >130/80
| - also if HTN 3 f/u visits w/ average BP>140/90
