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PHAR152 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Which component of the heart is responsible for initiating contraction?

A

SA node

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2
Q

At what rate does the SA node depolarize?

A

every second OR 70 times per minute

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3
Q

What is sick sinus syndrome?

A

SA node not firing at regular pace
SA node no longer driving depolarization
fairly common problem among elderly

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4
Q

What is the solution to sick sinus syndrome?

A

pacemakers
-little electrode inserted in chest wall
-pumps 60-70 times per minute
-no longer have to rely on SA node

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5
Q

What is the role of the AV node?

A

gateway for electrical impulses into ventricles
-delays ventricular contraction=allows time for ventricle to
fill
located between atrium and ventricles, allows impulses to pass between the two
only way for an impulse to trigger ventricles in a healthy heart

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6
Q

Describe what is happening to cardiac cells prior to conduction.

A

cardiac cells are polarized
-80-90mV negative compared to outside the cell
ion pumps work to maintain this resting membrane potential
Na+ atoms sitting outside the polarized cell wanting to get inside due to the negative charge

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7
Q

Describe each phase of cardiac action potential.

A

prior to AP, cardiac cells are polarized at -80-90mV and some
Na+ will start to leak into the cell and reach a point (-75mV)
where Na voltage-dependent channels open
Phase 0:
-increase in permeability to Na+ influx
-Ca channels open at around -60mV
=depolarization has been coupled with contraction
Phase 1:
-brief re-polarization from K+ escaping cell
Phase 2:
-Ca continues to enter center (started in phase 0)
-Ca enters through L type calcium channels
-Ca movement initiates muscle contraction
Phase 3:
-membrane remains permeable
-Na and K ejected to repolarize the cell
Phase 4:
-Na+ is cleared from the cell and K+ loss slows
-eventually, an abrupt increase in Na+ permeability will occur
when a certain threshold potential is reached

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8
Q

Which part of the heart will have the steepest slope in phase 4 of an action potential?

A

SA node
depolarizes once every second

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9
Q

True or false: muscle cannot contract again until repolarization occurs

A

true

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10
Q

What is an ECG?

A

graph of electrical activity in heart
detected by electrodes (i.e. leads) attached to the patient
the location of the leads allows different angles of the heart to be examined
6-12 leads are often used

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11
Q

What does each lead of an ECG measure?

A

2, 3, and aVF=inferior region
1 and aVL=lateral activity
aVR=rightward
V1, V2=septal activity (wall between atria and ventricle)
V3, V4=apical activity
V5, V6=lateral regions

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12
Q

What is the most sensitive and effective way to detect a heart attack?

A

ECG

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13
Q

What does the P-wave represent?

A

depolarization (contraction) of atria
normal duration=0.12 seconds

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14
Q

What does the QRS complex represent?

A

depolarization (contraction) of the ventricles
normal duration=0.12 seconds

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15
Q

What does a normal QRS complex look like on an ECG?

A

narrow
should happen in a short period of time
ventricle is wired via Purkinje fibers and Bundle of His, thus allowing for ventricle to contract all at one time

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16
Q

What does the QT interval represent?

A

time from Q to T
=time it takes from ventricular contraction to ventricular repolarization (full cycle)

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17
Q

What could a wide QRS complex be a sign of?

A

sign that ventricular impulse did not originate from the AV node
could be okay, but eventually can lead to ventricular fibrillation

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18
Q

What does does a prolonged QT interval represent?

A

prolonging means it takes longer to repolarize and some cells dont depolarize at the right time
=takes longer to recharge between beats

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19
Q

What does the T-wave represent?

A

ventricular repolarization

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20
Q

What does the PR interval represent?

A

AV node conduction
long PR=AV node block

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21
Q

True or false: Canadian guidelines recognizes pharmacy blood pressure machines

A

false

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22
Q

What approach to assess blood pressure is considered the gold standard?

A

ambulatory blood pressure monitor
-wearing a cuff for 24hrs
-takes bp every 30 mins
-shows a full 24 hour series of measurements

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23
Q

List off each approach to assess blood pressure and the values that are considered high with each approach.

A

automated office blood pressure:
-mean SBP>135mmHg or DBP>85mmHg is high
office blood pressure monitoring:
-mean SBP 130-139mmHg or mean DBP 85-89 mmHg is high-
normal
-mean SBP >140mmHg or DBP>90mmHg is high
ambulatory blood pressure monitor:
-mean awake SBP>135mmHg or DBP>85mmHg or mean 24-
hour SBP>130mmHg or DBP>80mmHg are high
home blood pressure monitor:
-mean SBP>135mmHg or DBP>85mmHg are high and
associated with an increased overall mortality risk

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24
Q

What is the role of pharmacy blood pressure monitors?

A

they should serve as screening tools only
they have not been evaluated for their association with clinical outcomes

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25
Q

Which approach to blood pressure monitoring is more highly correlated with BP-related risk?

A

out-of-office BP measurements
-HBPM or ABPM
-ambulatory wins in predicting damage
in doc offices bp can be elevated

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26
Q

Describe good posture while taking blood pressure.

A

sitting position with back supported
arm bare and supported
cuff size appropriate for your arm
middle of the cuff at heart level
lower edge of cuff 3cm above elbow crease
do not talk or move before or during the measurement
legs uncrossed
feet flat on floor

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27
Q

What are the proper conditions for taking home blood pressure?

A

resting
low stimulation/stimulants/irritants
-avoid exercise, caffeine or full bladder prior to taking bp
(30min)
not a bright room
take duplicate measures
-2nd could be lower than 1st

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28
Q

What is a good rule for when to be measuring blood pressure at home?

A

one week blocks during times of interest
do not have to measure every day for extended periods if stable

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29
Q

Which cuffs are preferred for taking blood pressure?

A

brachial cuffs

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30
Q

When can validated wrist devices be used for BP estimation?

A

patients with large arm circumference when standard methods cannot be used

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31
Q

How prevalent is hypertension in Canada?

A

approximately 23% of Canadian adults have hypertension
more prescriptions for hypertension than any other disorder
-4 million Rx’s every month in Canada
cost of hypertension approaches 10% of all health care spending

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32
Q

What is the benefit of high blood pressure during activity?

A

increased blood flow=increased oxygen and glucose delivered to muscle
regular activity (with rest) will trigger cellular changes such as increased protein and increased mitochondria

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33
Q

What is the issue with high blood pressure during rest (long term)?

A

increased afterload=increased energy to pump blood
-wastes energy
-fatigues tissues/cells–>adverse changes over long term
damages specific tissues/cells

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34
Q

Describe the damage the results from hypertension. (flow chart)

A

increased afterload:
-systolic dysfunction, LVH, increased myocardial oxygen
demand
-LVH–>diastolic dysfunction–>heart failure
-systolic dysfunction–>heart failure
-increased myocardial oxygen demand–>ischemia and
infarction
arterial damage:
-accelerated atherosclerosis, weakened vessel walls
-accelerated atherosclerosis can hit coronary vessels
(myocardial ischemia or infarction), cerebral
vessels (ischemic stroke), or the aorta (aneurysm)
-weakened vessel walls–>hemorrhagic stroke, renal failure,
retinopathy

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35
Q

True or false: hypertension risk increases with age

A

true
lose 1ml/min of GFR every year after age 18

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36
Q

What are the origins of hypertension?

A

fluid an electrolyte imbalances
-RAAS, natriuretic hormone, electrolyte imbalance, renal
dysfunction/poor renal perfusion
sympathetic nervous system/baroreceptor function
-increased SNS activity
metabolic syndrome
-hyperinsulinemia/insulin resistance, abdominal obesity, low
HDL, high BP, high TG
vascular endothelial function
-prostacyclin, NO production
HYPERTENSION IS MULTI-FACTORIAL

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37
Q

What is essential (primary) hypertension?

A

chronically increased bp resulting from multiple factors, no single factor predominates
most commonly diagnosed form of hypertension

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38
Q

Will single antihypertensive drug regimens have great success in control of primary hypertension?

A

limited success in control (-10/-5)

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39
Q

What is primary hypertension commonly associated with?

A

metabolic syndrome

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40
Q

What is secondary hypertension?

A

hypertension caused by significant dysfunction of a single system
often not recognized until patients show resistance to conventional treatment
much less common

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41
Q

90-100% of heart attacks occur in people with at least 1 of: ____,____,____,____.

A

HTN
dyslipidemia
diabetes
smoking

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42
Q

True or false: most CV risk factors are silent

A

true

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43
Q

Why is early screening for hypertension important?

A

earlier in life is the greatest opportunity to reverse/slow impact of hypertension

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44
Q

What are the diseases that hypertension is a risk factor for?

A

atherosclerosis
diabetes
cardiac dysfunction
atrial fibrillation

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45
Q

What are the modifiable risk factors for developing hypertension?

A

obesity
poor dietary habits
high sodium intake
sedentary lifestyle
high alcohol consumption
high-normal blood pressure
diabetes or metabolic syndrome (pre-diabetes)

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46
Q

What are the goals of therapy for hypertensives?

A

ultimate goal: prevent CV complications
control blood pressure
reduce/prevent myocardial cell dysfunction
reduce/stabilize atherosclerosis burden and endothelial cell dysfunction
reduce/prevent weakened vessel walls

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47
Q

What are the values for the following categories of hypertension: optimal, normal, high-normal, grade 1 (mild htn), grade 2 (moderate htn), grade 3 (severe htn), isolated systolic hypertension

A

optimal: <120 and or <80
normal: <130 and or <85
high-normal: 130-139 and/or 85-89
grade 1: 140-159 and/or 90-99
grade 2: 160-179 and/or 100-109
grade 3: >180 and/or >110
ISH: >140 and/or <90

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48
Q

What would be a scenario where a patient would be diagnosed immediately with hypertension at the doctors?

A

extremely high bp (>180/110)

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49
Q

What would be the presentation of hypertension in the following in a healthcare setting compared to at home?
normotensive
sustained hypertension
masked hypertension
white coat hypertension

A

normotensive:
-healthcare setting: no HTN
-home: no HTN
sustained hypertension:
-healthcare setting: HTN
-home: HTN
masked hypertension
-healthcare setting: no HTN
-home: HTN
white coat hypertension:
-healthcare setting: HTN
-home: no HTN

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50
Q

What are the key cardiovascular risk factors that are non-modifiable?

A

age >55 years
male
family history of premature CV disease (age <55 in men and <65 in women doubles FRS)

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51
Q

What are the key cardiovascular risk factors that are modifiable?

A

sedentary lifestyle
poor dietary habits
abdominal obesity
dysglycemia (or diabetes)
smoking (even 2nd hand)
dyslipidemia
stress
hypertension

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52
Q

True or false: two people with the same blood pressure (ex: 151/96) can have different CV risk

A

true
one person can have clear, relatively healthy vessels
the other person can have atherosclerosis, therefore they are higher risk even though they have the same bp as the first person

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53
Q

What is target organ damage?

A

damage that occurs from long-standing hypertension
sign that damage has already been done

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54
Q

What are some examples of target organ damage?

A

cerebrovascular disease
-transient ischemic attack
-ischemic or hemorrhagic stroke
-vascular dementia
hypertensive retinopathy
left ventricular dysfunction
left ventricular hypertrophy
coronary artery disease
-myocardial infarction
-angina pectoris
-congestive heart failure
chronic kidney disease
-hypertensive nephropathy (GFR <60ml/min/1.73m2)
-albuminuria
peripheral artery disease
-intermittent claudication
-ankle brachial index <0.9

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55
Q

What is a Framingham risk calculator?

A

a widely used tool to assess overall CV risk in Canada
a simple algorithm estimates an individuals 10-year risk of experiencing a major CV event (MI, stroke, etc) or death

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56
Q

What are the limitations of the Framingham risk calculator?

A

just an estimate
poor performance in extremes of age (young, old)
10-year risk may not always correlate to lifetime risk

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57
Q

If a patient comes into your pharmacy and takes their blood pressure on the pharmacy blood pressure machine and the results are very high, what should you do?

A

not necessarily an emergency
check technique and re-take bp
ask patient if they are experiencing symptoms
if no signs/symptoms of danger, ask patient to make an appointment within a day or two, might have to go to a walk in clinic

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58
Q

What are the symptoms of concern if a person just had a high blood pressure reading?

A

neurologic:
-severe headache, numbness, weakness, slurred speech
-vision problems
cardio-respiratory:
-chest pain, difficulty breathing

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59
Q

What is the difference between hypertensive urgency and hypertensive emergency?

A

hypertensive urgency: situation where bp should be reduced within hours
-bp >180/130 AND
-papilledema or other target organ changes
hypertensive emergency: situations that require immediate bp reduction
-ex: hypertensive encephalopathy, intracranial bleed, unstable
angina/MI, acute heart failure

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60
Q

What are the physical assessments commonly documented in medical charts?

A

jugular venous pressure (JVP):
-indirect assessment of right atrial pressure
edema:
-may represent ‘volume’ or tissue-specific fluid
pulse:
-heart rate
-pressure/circulation (feet)
heart sounds:
-normal: S1=systole (lub); S2=diastole (dub)
-not normal: murmur, S3 or S4 (may indicate disease)
blood pressure
point of maximal impulse (PMI):
-normal=4-5 ICS, mid clavicular line
-assessment of LVH
bruit:
-carotid and renal

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61
Q

What is edema?

A

swelling or accumulation of fluid in a tissue
-extracellular or interstitial fluid

62
Q

Is edema always detrimental to cardiac function?

A

no
could be due to a local cause such as a sprained ankle

63
Q

What is often assessed to gauge volume/preload?

A

jugular venous pressure

64
Q

What is a normal JVP?

A

<2cm above sternal angle

65
Q

Where are peripheral pulses taken? What does a diminished peripheral pulse mean?

A

legs and arms
diminished may mean reduced stroke volume or PAD

66
Q

What is the ankle-brachial index? What is the ideal ABI?

A

bp in ankle divided by bp in arm
ideally they are the same (ABI of 1)
less than 0.9 means PAD

67
Q

Describe the heart sounds.

A

S1 (lub):
-first heart sound, start of ventricular contraction
-due to closure of mitral and tricuspid valves
S2 (dub):
-2nd heart sound, closure of aortic and pulmonic valves during
ventricular relaxation
S3 and S4 are not normal heart sounds and may indicate presence of problem

68
Q

What are murmurs?

A

result from turbulent flow through the heart
mid systolic murmurs may indicate pulmonic stenosis, aortic stenosis, hypertrophic obstructive cardiomyopathy

69
Q

What are bruits?

A

represent turbulent flow (maybe sign of atherosclerosis)
stethoscope can pick up bruits in some arteries such as carotid or renal artery
flow through a healthy vessel should be silent

70
Q

What are the baseline laboratory tests recommended for hypertension patients?

A

urinalysis:
-protein, glucose, RBC, WBC, bacteria, etc
electrolytes:
-K and Na
creatinine:
-renal function (creatinine clearance)
glucose:
-screening for diabetes
cholesterol:
-screening for dyslipidemia
urinary albumin excretion:
-urine protein is a possible sign of kidney dysfunction

71
Q

What are some drugs that can induce blood pressure elevations?

A

NSAIDs
corticosteroids (and anabolic steroids)
oral contraceptives and sex hormones
decongestants (stimulants)
certain antidepressants (MAOIs, SNRIs, SSRIs)
stimulants (e.g., methylphenidate, dextroamphetamine)
excessive alcohol

72
Q

How do NSAIDs elevate blood pressure?

A

inhibition of renal prostaglandin perfusion
lowers renal perfusion

73
Q

How do corticosteroids elevate blood pressure?

A

mineralocorticoid effect (acts like aldosterone)

74
Q

How do hormonal contraceptives elevate blood pressure?

A

triggers angiotensinogen production from liver

75
Q

How do decongestants/certain antidepressants/stimulants elevate blood pressure?

A

SNS activity (vasoconstriction +/- increased CO)

76
Q

How does alcohol elevate blood pressure?

A

in excess only
impairs ADH + other mechanisms likely important

77
Q

What is the criteria for a Hypertension Canada High-Risk Patient?

A

individuals >50yrs old AND SBP 130-180mmHg AND one or more of the following CV risk factors should be considered for intensive bp management:
-clinical or sub-clinical CV disease
OR
-chronic kidney disease (non-diabetic nephropathy,
proteinuria <1g/d, eGFR 20-59 mL/min/1.73m2)
OR
-estimated 10-year global CV risk >15%
OR
-age >75yrs

78
Q

Name each patient population and their bp threshold for initiation of antihypertensive therapy and their bp treatment target.

A

hypertension Canada high-risk patient:
-threshold: SBP>130, DBP N/A
-target: SBP<120, DBP N/A
diabetes mellitus:
-threshold: SBP>130, DBP>80
-target: SBP<130, DBP<80
moderate-to-high risk (TOD or CV risk factors):
-threshold: SBP>140, DBP>90
-target: SBP<140, DBP<90
low risk (no TOD or CV risk factors):
-threshold: SBP>160, DBP>100
-target: SBP<140, DBP<90

79
Q

What are the indications for drug therapy in stage 1 hypertension?

A

stage 1 hypertension: 140-159/90-99
lifestyle modification ALONE can be considered in LOW risk patients if bp <160/100
use medications without delay if target organ damage OR if bp>160/100

80
Q

What are the 1st line treatments for uncomplicated hypertension?

A

HEALTH BEHAVIOUR MANAGEMENT
thiazide diuretic
ACE inhibitor
ARB
CCB
beta-blocker
single pill combination (ACEI+CCB, ARB+CCB, or ACEI/ARB+diuretic)

81
Q

When are beta-blockers not indicated as first line therapy for uncomplicated hypertension?

A

for those age 60 and older

82
Q

Which CCB should not be used for the management of hypertension?

A

short-acting nifedipine

83
Q

What are contraindication of ACE inhibitors and ARBs?

A

pregnancy
caution in prescribing to women of child bearing potential
bilateral renal artery stenosis
hyperkalemia

84
Q

What is the most common form of hypertension?

A

essential (primary) hypertension

85
Q

What are the non-pharmacological treatments for hypertension?

A

being more physically active
weight reduction
moderation in alcohol intake
eating healthier
relaxation therapies
smoking cessation

86
Q

By how much mmHg do most bp drugs lower bp?

A

-10/-5

87
Q

What is the time to maximal effect of antihypertensives?

A

> 1 month

88
Q

True or false: adding therapy for hypertension is preferred over switching therapy

A

true

89
Q

What is the strategy for adding on therapy for hypertension?

A

AB-CD rule: add non-renin drug to renin active drug
non-renin drugs: thiazides, CCB
renin-active drugs: beta-blockers, ACEI, ARB

90
Q

Which drug combinations should be avoided for hypertension therapy?

A

DHP-CCB with a beta-blocker
ACEI/ARB combos

91
Q

True or false: in most cases of hypertension, ACEI or ARBs will be chosen 2nd line over BB for bp control

A

true
BB not used not run of the mill HTN

92
Q

What is the biggest difference between ACEI and ARBs?

A

frequency of cough with ACEI

93
Q

If we have progressed to triple therapy for hypertension, what must be included in the regimen?

A

triple therapy should contain a diuretic

94
Q

When would you start with two antihypertensives?

A

if >20/10 drop is required
-use single pill combination if possible

95
Q

What is treatment resistance in hypertension?

A

poor bp response despite:
-3 antihypertensive drugs used in combination
-one of the drugs is a diuretic
-non adherence is ruled out
REFER FOR ADDITIONAL INVESTIGATIONS

96
Q

What are the usual alternatives for treatment resistance?

A

spironolactone (MRA)
-most success is usually achieved
clonidine/methyldopa (a2 agonists)
hydralazine/minoxidil + beta-blocker
-need the BB to prevent reflex tachycardia

97
Q

What are the causes of treatment resistance?

A

hyperaldosteronism
-unregulated aldosterone release
pheochromocytoma
-unregulated SNS activity
chronic kidney disease
-fluid/electrolyte imbalance
renovascular disease
-insufficient blood flow to kidney
obstructive sleep apnea
-insufficient oxygen concentrations
hyper/hypothyroidism
-metabolic dysfunction

98
Q

What are the specific therapies for each cause of treatment resistance?

A

hyperaldosteronism: MRA or K-sparing diuretic (amiloride)
pheochromocytoma: alpha-blockers +/- beta blockers (surgery needed)
chronic kidney disease: manage as recommended
renovascular disease: caution with ACE/ARBs
obstructive sleep apnea: correct underlying problem
hyper/hypothyroidism: correct underylying problem

99
Q

What is isolated systolic hypertension?

A

persistently high SBP yet normal DBP
there is evidence that a lower diastole makes worse outcomes for systole

100
Q

Which group is ISH commonly seen in? What is a likely reason for this?

A

common in elderly
as you get older, arteries lose pliability (become more stiff) and they cannot accommodate systolic pressure

101
Q

What does ISH create?

A

high pulse pressure
pulse pressure is the difference between SBP and DBP

102
Q

What are the treatments for ISH?

A

thiazide
ARB (not ACEI)
DHP CCB
can eventually move into dual combination or triple/quadruple therapy

103
Q

What is the diastolic pressure that we must be very cautious with for ISH?

A

DBP<60mmHg
especially in patients with coronary atherosclerosis because the coronary artery is the only arteries filled during diastole

104
Q

Describe thiazides based on the following: efficacy, safety, drug interactions, convenience, contraindications, and cost. (table from slid deck 2)

A

efficacy:
-excellent effectiveness from RCTs
-added benefit of decreased edema, fluid overload
-reduced effectiveness if CrCl <30ml/min (switch to loop)
safety:
-decreased K and Na most common electrolyte disturbances
-decreased Mg and Cl also possible
-may increase Ca (loops decrease Ca)
-may increase blood sugar slightly (does not cause risk)
-may increase uric acid (caution in ppl with gout)
-may increase urinary frequency (likely minimal with TZD)
drug interactions:
-other bp reducing drugs
-electrolyte interactions (K and Na)
convenience:
-once daily dosing (dose in AM to reduce nocturia)
contraindications:
-consider other options in people with low K or Na
-“sulfa” allergy, ABX sulfa allergies usually do not cross react,
avoid if reaction was severe (SJS, etc)
-caution if hypercalcemia is present
cost:
-one of the cheapest classes of bp drugs available

105
Q

What are the following diuretics best for: thiazides, loop, K sparing

A

thiazides: best for bp reduction
-gentle effects on diuresis=less RAAS activation
loops: best for fluid excretion (short term)
K sparing: K supplement (great if you wanna keep thiazide)

106
Q

What are the thiazides listed in the formulary?

A

chlorthalidone
hydrochlorothiazide
-both ineffective if GFR<30-40ml/min
indapamide
metolazone
-both possibly more effective in reduce renal function

107
Q

What are the reference levels for Na, K, and SCr?

A

Na: 133-146mmol/L
K: 3.5-5.3mmol/L
SCr: 50-98mmol/L

108
Q

How does hypokalemia occur from diuretics?

A
  1. diuretic-induced sodium/water loss
  2. reduce blood volume
  3. body attempts to re-establish blood volume (RAAS)
  4. aldosterone production
  5. sodium reabsorption (distal tubule)
  6. body must replace loss of positive ions in urine
  7. potassium loss
109
Q

What are some other causes of hypokalemia aside from diuretics?

A

inadequate K intake (elderly)
high dietary Na intake
hypomagnesemia
prolonged diarrhea (laxatives)/vomiting
hyperaldosteronism (ie secondary HTN)
heart failure (HF)
catecholamines
insulin

110
Q

What are the thresholds for treatment of low K?

A

<3.0mmol–>always undesirable
3.0-3.5–>usually treated
3.5-4.0–>action may be taken

111
Q

What are the thresholds for treatment of low K?

A

<3.0mmol–>always undesirable
3.0-3.5–>usually treated
3.5-4.0–>action may be taken

112
Q

What are the alternatives for low K from a diuretic?

A

general measures
-reduce Na intake
-increase K intake (dietary)
lower diuretic dose
discontinue diuretic if K seriously low
add K sparing drugs (ACEI, ARB, K-diuretics, BB)
add K supplement

113
Q

What can hyperkalemia cause?

A

ventricular arrythmia (widening QRS)

114
Q

What are the drugs that increase K?

A

RAAS drugs (BB, ARBs, ACEI)
NSAIDs
vitamins/supps
K sparing diuretics
TMP/SMX

115
Q

What are patient factors associated with hyperkalemia?

A

CrCl<60ml/min (healthy kidneys excrete 90% of daily K intake)
baseline K>4.5mmol/L

116
Q

True or false: dietary repletion is often successful to correct hypokalemia

A

false
but its okay for K maintenance

117
Q

What are compelling indications for hypertension?

A

diabetes with nephropathy
diabetes without nephropathy
non-diabetic kidney disease
coronary heart disease
heart failure
left ventricular hypertrophy
stroke or TIA

118
Q

If someone has hypertension and diabetes, what should be the first thing you look at to determine drug therapy for bp control?

A

renal function

119
Q

True or false: urinalysis is very sensitive for protein in the urine and should be reviewed before deciding if nephropathy is present

A

false
albumin-excretion ratio is more sensitive and should be reviewed before deciding is nephropathy is present

120
Q

What is the urinary albumin to creatinine ratio indicative of diabetes with nephropathy?

A

> 2.0mg/mmol in men
2.8g/mmol in women
or chronic kidney disease

121
Q

What are the treatments for hypertension for the following:
diabetes mellitus with microalbuminuria, renal disease, CVD or CV risk factors
diabetes mellitus without above risk factors

A

DM with risk factors: ACEI or ARB, addition of DHP CCB is
preferred over thiazide
DM without risk factors: ACEI, ARB, DHP CCB or thiazide, if
combination of ACEI is being
considered then DHP CCB is
preferable over thiazide

122
Q

What are the treatments for hypertension for non-diabetic chronic kidney disease with proteinuria?

A

ACEI (ARBs if ACEI intolerant) if there is proteinuria
diuretics as additive therapy

123
Q

What does long-standing hypertension and diabetes increase the risk for?

A

chronic kidney disease (increased pressure can damage glomerulus)
-filtering function is damaged (protein escapes)

124
Q

What happens as kidney function declines?

A

decreased rate of glomerular filtration
increased serum creatinine (easily excreted in healthy state)
difficulties excreting fluid and toxins
leakage of proteins, large molecules

125
Q

Provide a quick review of RAAS.

A

renin secreted via reduced renal artery pressure/blood flow or increased sympathetic stimulation
renin converts angiotensinogen to ANG I
ANG I converted to ANG II via ACE
ANG II actions:
-increased contractility
-vasoconstriction (especially on efferent renal artery)
-aldosterone secretion

126
Q

How do ACEI and ARBs provide renal protection?

A

ANG II vasoconstricts the efferent vessel, ACEI and ARBs block the effect of ANG II, thus allowing for decreased glomerular pressure

127
Q

What is pre-eclampsia?

A

high bp with proteinuria
onset after 20 weeks of pregnancy
associated with poor outcomes for baby and mother
can progress to seizures (eclampsia)

128
Q

What is gestational hypertension?

A

high bp without proteinuria after 20 weeks

129
Q

What are first and second line treatments for hypertension in pregnancy?

A

first line:
-labetalol
-methyldopa
-long-acting nifedipine
-other B blockers (acebutolol, metoprolol, pindolol,
propranolol)
second line:
-clonidine
-hydralazine
-thiazides

130
Q

What are first and second line treatments for hypertension in lactation?

A

1st line:
-labetalol
-methyldopa
-long-acting nifedipine
-enalapril or captopril
2nd line: combination of 1st line agents

131
Q

How do alpha-2 agonists work?

A

stimulate alpha-2 receptors in the brain
-a2 receptor located on pre-synaptic terminal
-stimulating a2 receptor shuts down further release of
messengers into the SNS nerve fiber
-decreased NE and SNS nerve transmission

132
Q

What is the outcome of alpha-2 agonists?

A

lowered blood pressure and heart rate

133
Q

What are the frequent side effects of alpha-2 agonists?

A

sedation
dry mouth

134
Q

What are examples of beta-1 selective blockers?

A

atenolol
bisoprolol
metoprolol
-the above three are the most commonly used
acebutolol
esmolol

135
Q

What are examples of non-selective beta blockers?

A

nadolol
pindolol
propranolol
timolol
carvedilol is a non-selective BB that also blocks a-1 receptors

136
Q

What is carvedilol indicated for?

A

heart failure with LVSD
not typically considered for hypertension management

137
Q

What is the conclusion about beta-blockers in uncomplicated hypertension?

A

minimal role in uncomplicated patients even if <60
might consider in individual presents with high heart rate
important to note that BB are extremely protective in certain complicated cases (HF, afib, ACVD)

138
Q

What are examples of alpha-1 blockers?

A

doxasozin
prazosin
terazosin

139
Q

Why arent alpha-1 blockers recommended as first line for hypertension?

A

shown less effective than others
can be used for add-on therapy
used frequently for BPH

140
Q

True or false: DHP CCB are the only vasodilators used first line in uncomplicated hypertension

A

true

141
Q

True or false: you will see ACEI recommended in most patients at “high-risk” for CV events, even if their bp is normal

A

true
HOPE trial showed ACEI lower risk of MI, stroke, and death

142
Q

True or false: you will see ACEI recommended in most patients at “high-risk” for CV events, even if their bp is normal

A

true
HOPE trial showed ACEI lower risk of MI, stroke, and death

143
Q

What is the favoured combination in high risk patients who havent met their target?

A

ACEI + DHP CCB

144
Q

What can DHP CCB exacerbate?

A

ankle edema

145
Q

What is the bottom line with ACEI/ARBs in CKD?

A

benefit to kidneys increase in people with more severe disease
in lower risk people (lower SCr/higher GFR) other drugs appear to provide similar protection
these studies have influenced the use of ACEI/ARBs as first line in patients with diabetes/nephropathy

146
Q

How is renal harm possible from ACEI and ARBs?

A

dilating the efferent vessel too much will reduce GFR
excessive drops in glomerular pressure can:
-decrease GFR
-decreased GFR lowers ability to excrete fluid (edema,
increased bp)
if not reversed–>acute renal failure can result
-nephron collapse due to lack of pressure
-urine production halted
-toxins and fluids accumulate over short term

147
Q

How do we monitor ACEI and ARBs for renal safety?

A

obtain SCr and K within 1-2 weeks of starting drug (or increasing dose)
SCr is expected to increased from baseline but must be less than 20-25%
bp and edema should get better

148
Q

What are side effects to monitor for all bp drugs?

A

dizziness/headache/hypotension
-especially on standing
orthostatic hypotension
-reduction >20/>10 on standing
-signal to start with lower doses and titrate carefully
erectile dysfunction

149
Q

What are specific monitoring examples for classes of bp agents?

A

ACEI/ARB: SCr, K, cough (with ACEI)
diuretics: gout, electrolytes, SCr, urination
DHP CCB: edema
BB and non-DHP CCB: HR
alpha-2 agonists: fatigue
vasodilators: tachycardia

150
Q

What is the benefit of anti-hypertensives in low-risk people based on?

A

bp acheived

PHAR152 (21 decks)

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