Jan15 M1,2-Hypertension Flashcards
htn is the leading risk factor for __ and __
cardiac disease and strok
lifetime risk of developing htn
90%
determinants of BP
SV, HR, TPR and hormones that modulate all that + SS
in perfect kidney, why does htn not occur
pressure natriuresis of Na and water
consequence of repeated exposure to high BP in patients with chronic htn
- pressure natriuresis is blunted
- bad RAAS response (is activated)
chronic htn consequence on the kidney
microvascular and tubulointerstitial damage
ctly high BP consequence on heart+circulation
- increased afterload
- damage to arterial system from mechanical shear stress
name for complications from htn
target organ damange
target organ damage in brain, eye, circulation, kidneys, heart
brain: TIA, stroke
eye: retinopathy
vessels: peripheral vascular disease
kidneys: hypertensive nephrosclerosis and renal failure
heart: LVH, CHD, HF
how BP affects CV risk
every increase in 20/10 above 120 doubles CV death risk
how target organ damage risk varies with BP
higher BP = higher risk
other risk factors that htn clusters with (4)
hyperlipidemia
diabetes
obesity
smoking
2 types of htn and %
essential (95%)
secondary (5%)
cause of essential htn
complex and multifactorial (genetics, RAAS dysfct, SS response, etc.)
what proportion of patients with htn have essential + what proportion require secondary htn workup
majority have essential
majority doesn’t require 2ndary htn workup
causes of secondary htn with main one
primary hyperaldo*, CKD, RAS, thyroid disease, sleep apnea, meds, cushing, coarctation of the aorta
primary hyperaldo cause
adenoma or hyperplasia of adrenals
primary hyperaldo: renin level, K level, Na level, H+ level
renin is low (suppressed)
Na is high
K is low
H is low (alkalosis)
why alkalosis in hyperaldo
aldo revs up the Na-H exchanger in the PCT
2 factors that contribute to htn in CKD
- rise in AT2 happens, causing vasoconstriction
- retention of Na and water
RAS causes (2)
ats or fibromuscular dysplasia
RAS: why causes htn
kidney senses low flow and activates RAAS
how htn due to RAS detected
- abdominal bruit
- hypoK (bc of high aldo)
- AKI happens after giving an ACEi or an ARB
ACEi/ARBs in bilateral vs unilateral RAS
- NO in bilateral bc precipitates renal failure: even lower flow to kidneys
- YES in unilateral bc inactivate AT2 (RAAS) and other kidney can compensate
2 hormones causing htn in RAS
AT2 and aldo
thyroid diseases that can cause htn
hypo and hyperthyroidism
how hypothyroidism causes htn
cardiac hyperactivity occurs (CO = SV x HR is now greater)
how hyperthyroidism causes htn
increase in peripheral resistance occurs
how to check for thyroid disease if suspect it as cause of htn (in 2ndary htn workup)
other symptoms + blood test (easy to check)
sleep apnea def
intermittent hypoxia during sleep
3 abnormal things in sleep apnea
- SS overactivity
- oxidative stress
- lack of nocturnal declne in BP
how to check for sleep apnea
snoring, daytime sleepiness, obesity
why meds can cause htn (what meds)
NSAIDs, glucocorticoids, RBC stimulating agents (increase blood viscosity), alcohol, cocaine, licorice root, calineurin inhibitors (anti rejection agent)
pheochromocytoma as cause of htn: def
adrenal tumor where high catecholamine (E, NE) secretion
symptoms of pheochromocytoma as cause of htn
high SS activity: htn, tachy, headache, anxiety, sweating
pheochromocytoma as cause of htn: labs
high catecholamines in the blood
coarctation of the aorta as cause of htn def
narrowing distal to subclavian artery: higher BP in upper extremities
hormones activated in coarctation of the aorta
RAAS bc low flow to the kidneys
how to check for coarctation of the aorta on physical exam and name for that
radial femoral delay (check BPs diff)
criteria for 2ndary htn screening (5)
- extremes of age (-20 and +50)
- sudden onset of htn
- resistant htn
- family history
- specific labs/physical
what labs/physical exam hints lead us to testing for 2ndary htn
hypoK, abdominal bruit, radial femoral delay, OSA, drop in GFR after starting ACEi/ARB
hypertensive crisis def
severe elevation of BP (over 200/120) with acute or chronic end organ damage
causes of hypertensive crisis (2)
untreated htn
acute illness superimposed on htn
treatment of hypertensive crisis
rapid lowering of BP
normal circulatory changes in pregnancy
higher: blood volume, SV, HR, CO, lower TPR due to increased resistance to AT2 and NE and increased vasodilators
how BP changes in pregnancy from trimester to trimester
drops. 1st trimester drop 2nd trimester: peak low 3rd trimester: back to nromal slowly
4 htn disorders in pregnancy
- pre-existing chronic htn
- transient htn in pregnancy
- preeclampsia-eclampsia
- preeclampsia superimposed on chronic htn
if pregnancy is before 20 weeks (first half), what’s the cause
had chronic htn before
ddx if htn after 20 weeks of pregnancy (3)
- preeclampsia
2. gestational htn (transient htn or will lead to preeclampsia)
most serious pregnancy associated htn disorder
preeclampsia
preeclampsia def
presence of htn + proteinuria/other organ damage in the mother
preeclampsia cause
abnormal placental vasculature dev so substances circulating lead to endoth damage and vasoconstriction
transient htn treatment
resolves by itself. BP meds if BP too high (prevent stroke)
preeclampsia effect on the mother
hemolytic anemia, thrombocytopenia, high liver enzymes, renal failure, pulm edema
preeclampsia effect on the baby
growth restriction, premature delivery, maybe death
risk factors for preeclampsia
-primigravidy or primipaternity (first baby)
-extremes of maternal age (18- 35+)
-chronic htn
-diabetes
etc.
preeclampsia treatment
delivery of the baby
BP meds
pregnancy htn approach
- rule out preeclampsia (check organ damage)
2. dx is chronic htn, transient htn or ealy stage of preeclampsia
Canadian guidelines htn def (when to initiate therapy)
140/90 most pts
130/80 diabetics
130 for certain pts
160/100 in low risk pts
target BP with OBPM (office BP measurement: manual)
below 120 for high risk
below 130/80 for diabetics
below 140/90 for others
target BP with AOBP (automated office BP)=BP true
135/85
pregnancy htn: treat over what
150/100
pregnancy htn treatment target no comorbidities patient vs comorbidities
no comorb: aim 130/80
comorb: aim 140/90
key things for pregnancy htn
history, physical exam (some things can show previous htn so chronic. like foot ulceR), labs, ECG, risk factors
2 home BP measurements
ABPM (24 hrs): ambulatory monitor
HBPM: home monitor
key thing for using the BP guidelines and numbers
must do proper technique
best method for office BP measuremnet
AOBP
key point on htn dx
not made on first visit
- need out of office repeated measurements
- need to check white coat htn and masked htn
3 kinds of htn
masked, true, white coat (false htn)
only way you would dx htn on first measurement
BP over 180/110
why out of office BPM is better
correlates better with end organ damage
types of htn : worst to best
masked, uncontrolled, white coat
2 steps in htn treatment
lifestyle changes
meds
lifestyle changes to treat BP and main one
reduce salt* (less 2g a day) weight loss physical activity stop smoking less 2 drinks a day
major Na source in our diet
processed foods
5 first line BP meds
thiazide ACEi ARB CCB (long-acting) single pill combination (ACE or ARB + CCB or diuretic)
key point on BP meds
monotherapy is often not enough
what determines first line BP med chosen (2)
- special indications
- side effects
main side effect of ACEi and of CCB
ACEi: cough
CCB: edema (but otherwise it’s a very good med)
what meds to use in pregnancy and main one
- CCB (nifepidine**)
- methyldopa (alpha 2 agonist so less SS)
- hydralazine (vasodilator)
- labetalol (beta blocker)
what meds not to use in pregnancy
ACEi/ARB (associated with fetal renal abnormalities)
after treating BP, important thing to remember
must act on other risk factors
how to choose if non pharma or pharma treatment
non pharma if only 1 risk factor + no evidence of end organ damage: then give 6 months max for change
important thing to consider in choosing BP med
electrolyte abnormalities. can’t give diuretic if hypoK patient
