Monday HTN lecture Flashcards

1
Q

What are 5 types of HTN?

A

1) Essential
2) Secondary hypertension
3) Resistant HTN
4) Asymptomatic severe HTN (HTN urgency)
5) HTN emergency (covered in Emergency Medicine)

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2
Q

What are 2 types of hypertensive crisis?

A

1) Hypertensive urgency
2) Hypertensive emergency

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3
Q

1) What is HTN an independent risk factor for?
2) Risk of vascular death increases from a “normal” blood pressure of < __________ mm Hg
3) What happens for every 20 mm Hg systolic or 10 mm Hg diastolic increase?

A

1) Ischemic cardiovascular events
2) 120/80
3) Risk of major cardiovascular events & stroke doubles

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4
Q

Treatment of HTN reduces what?

A

All causes of mortality and results in regression of pathologic cardiac structural changes

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5
Q

What does physiology help you do?

A

Helps you with identification of secondary causes of HTN and how the interventions work to reduce blood pressure.

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6
Q

Physiology review:
Primary role of sympathetic system is to do what? What is the resting state?

A

Regulate BP; resting state of moderate vasoconstriction

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7
Q

Physiology review:
How is vascular tone typically regulated?

A

Sympathetic stimulation = relative vasoconstriction (except?)
Decrease in sympathetic stimulation = relative vasodilation

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8
Q

Physiology review:
What converts angiotensin 1 into angiotensin II?

A

ACE in lungs + renal endothelium

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9
Q

Physiology review:
What is the effector chemical in the RAAS?

A

Angiotensin II

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10
Q

Physiology review:
What are the effects of angiotensin II?

A

1) Increase symp. activity
2) Tubular sodium + Cl reabsorption, K+ excretion, H2O retention
3) Stimulates adrenal cortex to increase aldosterone secretion
4) Arteriolar vasoconstriction (increases BP)
5) Pituitary gland’s posterior lobe to secrete ADH (increasing H2O reabsorption)

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11
Q

Give examples of modifiable and non-modifiable risk factors for HTN

A

1) Modifiable: Smoking, obesity, high-sodium diet, excessive alcohol consumption, and physical inactivity.
2) Non-modifiable: Family history, age, male sex, and ethnicity

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12
Q

Give an example of a co-morbidity related to secondary HTN

A

Chronic kidney disease

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13
Q

What are 4 questions you should be able to answer regarding HTN?

A

1) What is normal blood pressure?
2) Who should be screened for HTN?
3) How is blood pressure measured?
4) What blood pressure threshold is used to diagnose HTN?

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14
Q

True or false: Not all guidelines agree on what normal BP is

A

True

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15
Q

What are the 2 main BP guidelines?

A

ACC/AHA 2017
JNC-8 2014

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16
Q

What does the USPSTF say abt screening for HTN in kids?

A

Not enough evidence to conclude

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17
Q

What does the USPSTF say abt screening asymptomatic pregnant women for HTN?

A

Recommends screening for hypertensive disorders in pregnant women with BP measurements throughout pregnancy (B)

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18
Q

How is HTN screened and diagnosed?

A

Office visit BP measurements to screen
Out of office BP measurements to diagnose

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19
Q

Describe the diagnosis of HTN

A

-Challenging in busy practice
-Accurate diagnosis HTN is important – correct methodology of measuring BP

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20
Q

Describe screening BP in the office

A

1) Patient: Sitting quietly for 5 minutes, feet and back supported
-Avoid smoking, caffeine, and exercise for 30 minutes prior to measurement
2) Equipment: BP cuff should encircle 80% of arm, arm at heart level
-Manual or automatic
3) Initial visit: Measure in both arms (highest is documented BP)
-3 measurements 1-2 minutes apart, average used to determine BP

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21
Q

1) What is a reasonable alternative to ABPM for HTN Dx?
2) What are better predictors of CV disease than office BP?

A

1) Home BP monitoring is a reasonable alternative
2) Both ambulatory and home BP monitoring

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22
Q

1) Describe white coat HTN
2) Describe masked HTN

A

1) HTN in office, no HTN at home. Minimal/ slight increase in CVD risk, up to 35% prevalence
2) No HTN in office, but HTN at home. Similar to sustained HTN regarding CVD risk; limited data on prevalence

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23
Q

What should you do if an office BP suggests elevated BP?

A

1) Ambulatory BP measurement: GOLD STANDARD; limitations due to insurance coverage
2) Home BP measurement: initial modality to confirm for most patients
3) Out of office confirmation not practical (equipment, insurance, skill, and cost)
-Average of serial office BP measurements spaced over a period of several visits

24
Q

What are the criteria for a Dx of HTN?

A

1) Diagnosis of HTN (ICD-10 code I11.9) = serial BP measurements >130/80 mm Hg
ICD-10 code R03.0 = elevated BP w/o dx of HTN
2) At least 2 readings
3) On at least 2 different occasions
4) Out of office confirmation is recommended
-To rule out white coat HTN + capture masked HTN

25
Q

HTN crisis is quantified as what according to ACC thresholds?

A

> 180 systolic or 120 diastolic

26
Q

ACC/AHA guidelines; list them for:
1) Clinical CVD or 10yr ASCVD risk >/=10%, diabetes, HTN, CKD, CHF, CAD, PAD
2) Secondary stroke prevention

A

1) >/=130/80 threshold for Tx; goal of <130/80
2) >/= 140/90 threshold for Tx; goal of <130/80

27
Q

ACC/AHA guidelines; list them for:
1) No clinical CVD and 10yr ASCVD risk <10%
2) Older persons (>/=65 years; noninstitutionalized, ambulatory, community-living adults)

A

1) >/= 140/90 to Tx, goal of <130/80
2) >/= 130/80 to Tx, goal of <130 (SBP)

28
Q

Diagnostic evaluation of HTN should focus on several major areas, including what? (4 things)

A

1) Possible secondary HTN
2) S/Sx of coexistent illness
3) HTN mediated organ damage – brain (and retina), heart, PVD, kidneys
-Acute or chronic
4) Assessment of overall cardiovascular risk

29
Q

Describe primary HTN

A

Common
Onset is gradual
Usually over 40 y/o
Symptoms remote from onset
+ Family history
Idiopathic
Life long

30
Q

Describe secondary HTN
(important)

A

Less common
Onset acute
Younger/elderly onset
Symptomatic at onset
Family Hx +/-
May resolve with treating underlying etiology

31
Q

List the ACC BP thresholds (4 categories)

A

1) Normal: <120 and <80
2) Elevated: 120-129 and <80
3) HTN stage 1: 130-130 or 80-89
4) HTN stage 2: >/= 140 or >/= 90

32
Q

List 2 common causes of secondary HTN not emphasized on the slides (but that he mentioned)

A

Thyroid issues (esp. hyper), hyperaldosteronism (Addison’s disease)

33
Q

Secondary HTN causes:
1) How common is OSA?
2) Main Sx?
3) How is it screened for?
4) How is it diagnosed?
5) How is that scored? How is it treated?

A

1) Very common condition
2) Snoring
3) STOP-BANG
4) Sleep study
5) AHI 5-15 is mild
15 – 30 is moderate
> 30 is severe
-CPAP device

34
Q

Secondary HTN causes:
1) What is chronic kidney disease?
2) What are 2 types of renovascular disease?

A

1) Renal parenchymal diseases
2) Atherosclerosis
Fibromuscular dysplasia

35
Q

Secondary HTN causes:
1) What are 2 types of renal parenchymal disease?
2) What are a couple clues?
3) The first-line imaging test is what?
4) Do you need to refer these pts?

A

1) Glomerulonephritis and polycystic kidney disease
2) Early-onset and resistant HTN
-Frequent urinary tract infections, hematuria, nocturia, family history of polycystic kidney disease, and/or elevated serum creatinine level
3) Renal ultrasonography, to assess for the presence of underlying disease
4) Referred to a nephrologist for further evaluation, including possible kidney biopsy

36
Q

1) Renovascular disease has a prevalence of up to _______ of patients with secondary HTN.
2) Who is it suspected in?
3) Renal artery stenosis also should be considered if there is more than a _____% decrease in eGFR after management with an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB)

A

1) 1/3
2) Patients with resistant/difficult-to-control HTN
3) 30%

37
Q

1) What are some clues for renal artery stenosis?
2) What may it present with?

A

1) Younger than < 30 y/o, most common due to fibromuscular disease
Older than 30 y/o, most common atherosclerotic disease
2) Accelerated or resistant HTN, renal disfunction, flash pulmonary edema
-ACEi/ARBs may worsen renal function and/or hyperkalemia

38
Q

Clinical findings suggestive of renovascular disease in a hypertensive patient include what 2 things?

A

1) Bruits (abdominal/renal): systemic effects of atherosclerotic vascular disease
2) Significant increase in serum creatinine after starting Rx for HTN

39
Q

Renovascular disease in HTN pts:
1) What is the initial diagnostic imaging?
2) What is as effective as renal artery revascularization (angioplasty or stenting) in managing atherosclerotic RAS?

A

1) Renal magnetic resonance angiography (MRA)
2) Medical therapy

40
Q

Recommended medical approach to renal artery stenosis includes what? (4 things)

A

1) Improved glycemic control for patients with diabetes,
2) Rx: initiation of a renin-angiotensin system (RAS) antagonist – e.g., spironolactone
3) Rx: antiplatelet and statin therapy (for atherosclerosis – a systemic process)
4) Lifestyle - smoking cessation

41
Q

Secondary causes of HTN:

Renovascular disease: Who should you Tx with revascularization?

A

Patients who do not benefit from medical management and for those with Takayasu arteritis (large vessel arteritis/fibrosis) or fibromuscular dysplasia

42
Q

Describe primary hyperaldosteronism (incl. who it’s found in, what supports Dx, what is on BMP, etc)

A

1) Present in 5-10% of HTN patients and 7-20% of those with resistant HTN
2) Unprovoked hypokalemia further supports this diagnosis although is not present on the majority of cases
3) Low K+ noted in BMP
4) Diagnosis is based on aldosterone:renin ratio

43
Q

What are some other secondary causes of HTN? Incl. in children.

A

1) Pheochromocytoma
2) Hypercortisolism
3) Hyperthyroidism
4) Excessive alcohol
5) Meds: NSAIDS, corticosteroids, some antidepressants, sympathomimetics
6) In children: coarctation of aorta, renal parenchymal disease

44
Q

Give the OLDCARTS for HTN

A

CC: none – found with screening BP or may have CC consistent with end organ damage
Onset, duration, timing – chronic, insidious (may be acute if secondary)
Location: cardiovascular (may be more widespread if secondary)
Character: asymptomatic (may have end organ damage if secondary)
Alleviating: none (treat underlying cause is secondary)
Aggravating: OTC and Rx medications, anxiety, lifestyle
Risk factors:
Modifiable – smoking, obesity, excessive salt intake and alcohol consumption, physical inactivity
Non-modifiable – family history, age, sex, ethnicity
Associated Symptoms: primary HTN – none, secondary HTN varies

45
Q

When looking for signs of end organ damage on PE:
1) What should you look for regarding general appearance?
2) What abt in VS?

A

1) Distribution of body fat, skin lesions, muscle strength, alertness/orientation (brain, aldosterone, Cushing’s)
2) BMI, BP both arms (Subclavian Steele syndrome) and one leg (aortic coarctation)

46
Q

When looking for signs of end organ damage on PE, what may fundoscopy show for hypertensive retinopathy?

A

-Ischemia causes optic nerve edema, cotton wool spots
-While leakage causes hemorrhage and disc edema
-Elevated retinal artery BP causes A-V nicking, copper wire arterioles

47
Q

When looking for signs of end organ damage on PE, what should you look for for each of the following?:
1) Neck
2) Lungs
3) Abdomen
4) Extremities

A

1) Palpation and auscultation of carotids and thyroid gland
2) CTA
3) Renal masses, bruits over abdominal aorta and renal arteries, femoral pulses
4) Peripheral pulses, edema

48
Q

When looking for signs of end organ damage on PE, what should you look for for each of the following?:
1) Skin
2) Neurologic

A

1) Stigmata of Cushing’s
2) MS changes (confusion), visual disturbance, focal weakness

49
Q

When looking for signs of end organ damage on PE, what should you look for on a cardiovascular exam?

A

1) Cardiac PMI displacement (enlarged LV), S4 gallop (stiff LV)
2) Palpate peripheral pulses and listen for bruits; especially renal

50
Q

Subclavian Steel Syndrome:
1) What is it?
2) What does it cause?

A

1) Right subclavian stenosis
2) Blood flows from left vertebral artery to basilar to right subclavian artery to right arm resulting in potential posterior CNS ischemia

51
Q

Coarctation of the aorta:
1) What is it?
2) What does it result in?

A

1) Stenosis of the aortic arch
2) Blockage of blood flow to the descending aorta and distribution
-Overload and elevated BP of head and UE

52
Q

Hard exudates, inflamed macula, flame hemorrhage, and cotton wool spots may indicate what?

A

HTN damage

53
Q

What lab testing should you do for HTN?

A

1) CBC (CKD with microcytic anemia)
2) Renal panel – electrolytes (K+) and serum creatinine to calculate eGFR (CKD)
-look for hyperaldosteronism
3) Urinalysis – proteinuria + …. Prompt urinary albumin to creatinine ratio
4) Fasting glucose or A1C
5) TSH
6) Lipid profile (additional) CV risk

54
Q

1) Why should you do an ECG for HTN?
2) What should you calculate if appropriate?

A

1) ECG for LVH, LAE
Echo if LVH seen on ECG
2) 10-year ASCVD risk

55
Q

What additional testing should be done & for who with HTN?

A

1) Urinary microalbumin to creatinine ratio in all patients with CKD or DM
2) Microalbumin : creatinine ratio is recommended annually in all DM

56
Q

Describe Targeted approach of evaluation for secondary HTN in patients with unusual presentation

A

1) New onset in young or old age
2) Presentation with severe HTN
3) Abrupt onset in previous normotensive patient
4) Significant recent elevation in BP in a patient with previously well controlled HTN (compliant patient)

57
Q

1) What is drug resistant HTN a sign of?
2) Give examples of clinical clues for a specific cause of HTN

A

1) Drug resistant HTN (3 or more drugs and still not well controlled BP) concerning for secondary HTN
2) Abdominal bruit (RAS), low serum K+ (primary aldosteronism)