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PAEP Renal > Hypertension + antihypertensive meds > Flashcards

Hypertension + antihypertensive meds Flashcards

1
Q

what mean office BP is a direct HTN dx?

A

> =180/110

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2
Q

what does AOBP stand for?

A

automated office BP

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3
Q

what is white coat HTN?

A

untreated condition in which BP is elevated in the office but is normal when measured
by ambulatory blood pressure monitoring (ABPM), home blood pressure measurement (HBPM), or both.

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4
Q

what is masked HTN?

A

untreated patients in whom the BP is normal in the office but is elevated when measured by
HBPM or ABPM

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5
Q

what is HBPM?

A

home blood pressure measurement

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6
Q

what is ABPM?

A

ambulatory blood pressure monitoring

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7
Q

How would we diagnose a non-diabetic pt with HTN if they had a mean office BP < 180/110?

A
  1. Do an AOBP or an OBPM (>=135/85 or >=140/90)
  2. Do an out-of-office measurement to rule out white-coat HTN
  3. ABPM (preferred) ➔ daytime mean of >=135/85 or 24hr mean >=130/80
  4. could also do a HBPM series where a mean >=135/85
  5. confirmed HTN
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8
Q

what is OBPM?

A

office blood pressure measurement

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9
Q

why are there different thresholds for diabetic pts to dx htn?

A

because being diabetic makes the vessels more stiff over time ➔ less flexible to changes in BP ➔ increases systemic vascular resistance ➔ more prone to developing HTN at lower levels of BP

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10
Q

what is primary/essential HTN?

A

HTN with no known etiology - idiopathic

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10
Q

how is HTN related to the cardiac system?

A

directly to the systemic vascular resistance and cardiac output

BP = cardiac output x systemic vascular resistance
cardiac output = stroke volume x heart rate
stroke volume = end diastolic volume - end systolic volume

Overall, there is an increased total peripheral resistance and increased afterload on the heart

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10
Q

what is more common, primary HTN or secondary HTN?

A

primary! it’s the most common chronic medical condition worldwide

prevalence rises with age

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11
Q

what are “A BOSS FR” risk factors for essential htn?

A

A - Age

B - Biological male
O - obesity, DM, diet (sodium/alcohol), cholesterol, OSA
S - stress/social/smoking
S - sedentary lifestyle

F - FH of HTN
R - Race: African > White European > Asian

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12
Q

what are the numbers for stage 1 HTN?

A

130-139/80-89

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13
Q

what are the numbers for stage 2 HTN?

A

> 140/>90

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14
Q

what are the numbers for stage 3 (hypertensive crisis) HTN?

A

> 180/>120

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15
Q

how can salt absorption lead to HTN?

A

more salt ➔ more water ➔ volume expansion ➔ increased diastolic volume ➔ increased stroke volume which increases CO which increases BP

BP = CO x systemic vascular resistance
CO = stroke volume x HR

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16
Q

how does an impaired RAAS response lead to HTN?

A

impaired RAAS response ➔ overactive ➔ increased salt and water reabsorption ➔ increased stroke volume which increases CO which increases BP

BP = CO x systemic vascular resistance
CO = stroke volume x HR

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17
Q

how does increased activation of the SNS lead to HTN?

A

increases SNS ➔ vasoconstriction ➔ increased systemic vascular resistance ➔ increased BP

BP = CO x systemic vascular resistance
CO = stroke volume x HR

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18
Q

what are the s/s of primary and secondary HTN?

A

there normally are NONE until it’s too late! referred to as the “silent killer”

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19
Q

what are some end organ damage that can occur due to HTN?

A

Cardiac: end-stage finding, S4 heart sound bc stiff and non-compliant LV
- may hear a S3 bc increased diastolic volume and fluid however S3 can be NORMAL in a young fit, thin person
- chest discomfort and palpitations

Lungs: rales or peripheral edema or dyspnea ➔ steming from CHF

Other
- headaches, dizziness, blurred vision, tinnitus, epistaxis, fatigue and sleep disturbances

20
Q

what ix would you do besides BP measurements to work up a HTN pt?

A
  1. cardiac w/u ➔ ECG: look for LVH pattern
  2. eye w/u ➔ fundoscopy: look for retinal hemorrhage
  3. renal function tests ➔ creatinine/eGFR, urea, electrolytes
  4. CVD risk w/u ➔ FRS
    - lipid panel, fasting plasma glucose/HbA1c
21
Q

what cx are we concerned about for HTN?

A

uncontrolled HTN can result in target-organ damage
1. hypertensive retinopathy ➔ damaged retinal vessels from elevated BP (copper wiring, hemorrhage, exudates, cotten-wool spots)
2. cardiomyopathy (LVH)
3. stroke ➔ high pressure vs small vessels in brain
4. hypertensive nephropathy: high pressure vs all small blood vessels/capillary networks in kidney ➔ scarring and progressive kidney damage
5. hypertensive encephalopathy ➔ intracerebral elevated BP ➔ vasular fluid breaches the blood-brain barrier bc chronic HTN changes the normal brain BP autoregulation thresholds

22
Q

What tx options do you have for HTN, list classes

A
  1. ACEi/ARBs
  2. CCB/BB
  3. Diuretics - thiazides and loop diuretics (K+ wasting)
23
Q

MoA of ACEi and ARBs

A

stops RAAS!

ACEi ➔ inhibits the ACE enzyme so no conversion of angiotensin I into angiotensin II

ARBS ➔ angiotensin II receptor blocker ➔ stops angiotensin II from stimulating aldosterone, ADH, and salt/water retention and vasoconstrction

24
Q

MoA of BB

A

decreases renin output and reduces cardiac output

25
Q

MoA of thiazide diuretics

A

blocks Na/Cl channels and impairs Na/K pump ➔ Net: decreased Na and water reabsorption into circulation

26
Q

MoA of loop diuretics

A

competitive with Cl- ➔ inhibits reabsorption of Na and Cl ➔ net: increased free water excretion

27
Q

what are the two types of CCB? and their MoA

A

cardiac-selective - non-dihydropyridines
- slows cardiac conduction and contractility resulting in less cardiac output
non-selective - dihydropyridines
- peripheral dilators

28
Q

Why would someone use a thiazide diuretic instead of a loop?

A

thiazide is first line bc cheap and outcomes research has shown decreased cardiovascular mortality and morbidity for both systolic and diastolic htn.

thiazide diuretics produce a lot of initial fluid loss, then its ability to remove water decreases as it’s main function is stopping reabsorption

vs loop, it’s net effect is continuous free water excretion

29
Q

when do we give htn pts a diuretic?

A

when there is a high diastolic pressure, bc they have an overfilling issue and we want to remove fluid from circulation

30
Q

in what pt population would we want to put on an ACEi or ARB for htn?

A

those with chronic kidney disease or diabetes

ACEi is renal protective

31
Q

when would we put a patient on BB instead of CCB for HTN?

A

when they have CVD or an MI history

32
Q

what is the benefit of using CCB instead of BB for HTN?

A

CCB can be non-selective - dihydropyridine where it does NOT act on the heart

whereas the BB will always work on the heart

33
Q

what are some non-pharmacological therapies for HTN?

A
  1. wt loss and exercise
  2. sodium restriction or DASH diet (diet approach to stop HTN)
  3. smoking cessation
  4. alcohol restriction
  5. reduce stress
34
Q

what is the target BP range for controlled HTN?

A

depends on the pt background

normally <140/90

in DM <130/80

35
Q

how would we select medications for htn pts?

A

two strategies
- one medication, get to max dose before adding another
- use more than one medication, not on max doses

36
Q

what is uncontrolled HTN? define

A

> =140/90 mmHg

37
Q

what is resistant HTN?

A

pt has BP > target/goal, taking at least 3 antihypertensive drug classes, and pt adherent → start thinking 2ndary causes

38
Q

what is secondary HTN?

A

HTN secondary to an identifiable cause

39
Q

common causes of secondary HTN

A
  • renal artery stenosis (from atherosclerosis, fibromuscular dysplasia (CTD), congenital) ➔ reduced renal perfusion ➔ RAAS activated
  • primary hyperaldosteronism ➔ increased blood volume ➔ increased BP
  • NSAIDs ➔ vasoconstriction of afferent arterioles ➔ decreased excretion of sodium/water ➔ increased volume ➔ increased BP
  • Cardiac: coarctation, aortic dissection ➔ reduces renal perfusion ➔ RAAS activated
  • oral contraceptive: increases angiotensin II ➔ increases BP
  • OSA: hypoxic vasoconstriction ➔ reduced renal perfusion ➔ RAAS activated
  • recreational drug use ➔ Stimulants cause SNS activation
40
Q

whats the RAAS pathway for HTN?

A

the kidneys have decreased perfusion, so they think that systemically there is low BP

it releases renin and activates the RAAS pathway resulting in increased salt and water retention even tho systemic BP is normal or high

41
Q

what is the difference between a hypertensive emergency and urgency?

A

both have BP >180/120 mmHg

emergency has evidence of target-organ damage

urgency has no evidence of target-organ damage

42
Q

what are 2 common triggers for hypertensive emergency?

A
  1. non-compliance with medications
  2. use of other stimulants that activate SNS (e.g., dobutamine, dopamine, norepi)
43
Q

what is the goal of tx for hypertensive emergency?

A

aggressive lowering of BP esp if there is acute worsening of MOF

44
Q

what target-organ damage cx should we be concerned about for hypertensive emergency?

A
  1. Neuro: altered mental status, stroke, vision loss, headaches
  2. Lungs: flash pulmonary edema
  3. Cardio: cardiac ischemia/MI
  4. Renal: acute renal failure, renal artery bruit
  5. Gyne: eclampsia (seizure in preg pts)
  6. Vascular: aortic dissection
45
Q

T/F: a pt with hypertensive urgency is most likely a primary uncontrolled htn pt

A

true!
would only start thinking a 2ndary HTN when they have resistant HTN: BP>target goal and taking at least 3 antihypertensive drug classes and pt is adherent

46
Q

How do you ix a pt with a hypertensive emergency?

A
  1. serial BP - via arterial line to get continuous BP monitoring
  2. labwork to understand the level of organ damage
    - CBC, lytes, creatinine and BUN, urinalysis, ECG with troponin
    - consider toxicology screen, pheochromocytoma
  3. consider imaging to work up presenting s/s ➔ head CT, CXR, U/S with doppler re: kidney, abdo CT, angiography
  4. consider targeting physical exam tests
47
Q

how would you approach a htn urgency pt?

A
  1. repeated BP measurements, put pt in a calm space (potentially a dark room)
  2. if they are on htn medications, confirm the last time they took their medications and give meds if appropriate
  3. if they are not showing signs of MOF or end-target damage, then send them home with pt education on return instructions and to f/u for more aggressive htn management from family doc
48
Q

how would you treat an htn emergency?

A
  1. IV antihypertensives ➔ most commonly used it Labetalol which is both an alpha and beta blocker
  2. goal is to lover BP by 20% over 24 hours if end-organ damage is worsening
  3. arterial line for continous BP monitoring
  4. tx the underlying cause and secondary cx from organ damage

PAEP Renal (11 decks)

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