Hypertension Flashcards
Hypertension: what is it
- risk factors
- how we get the readings
high blood pressure – either primary (we dont know why) or secondary (we have a patho. understanding of an underlying cause)
we care because increased BP can increased risk DRAMATICALLY for a ASCVD
risk factors (so many!!)
- genetics, diet, exercise, family history, lifestyle, smoking, diabetes, sleep apnea
how we get the reading
- 2+ seperate readings within 5 minutes at 2 different occasions & take averages of last 2
what are some non-pharmacologic interventions for hypertension
- weight loss (dec. 1 kg –> bring down BP by 1)
- healthy diet (DASH diet) & reduce sodium intake
- intake more potassium
- increase physical activity
- reduce alcohol consumption
blood pressure categories
normal
elevated
stage 1
stage 2
HTN emergency v urgency
white coat HTN
masked HTN
normal: anything < 120/ < 80
elevated: 120-129 / < 80
stage 1: 130- 139 / 80-89
stage 2: 140+ / 90+
** always put them in the higer category if one of their readings falls in a different category**
emergency/urgency : > 180 / > 120
emergency: target organ damage (symptoms!! like MI or stroke)
urgency: no TOD (no symptoms)
white coat: they’re htn is higher in the office than at home ( usually < 130/80 at home
masked: higher at home than in the office (usually > 130/80 at home)
what is the thresholds for therapy for HTN? what are our goal BPs
what is our flow-chart of decision making??
goal BP: normally < 130/ 80
if acute post-stroke they can have < 140/ 90
FLOW CHART
1. first identify their BP (via elevated, stage 1, 2)
if elevated….
- intervene with non-pharm management
- reassess in 3-6 months
if Stage 1 HTN…
- get a clincal ASCVD risk score % from the calculator
score < 10%? –> non-pharm therapy & reassess in 3-6 months
score > 10% (or have CKD or DM) —> start on a BP med & promopt non-pharm & reassess in 1 month
1 month post meds –> not met goal? consider adding theapry or increasing dose
if Stage 2 HTN…
- no need to get the score –> BP is high and we need thearpy initiate pharm BP meds and promote non-pharm
- can consider starting with 2 BP meds off the bat
what is secondary HTN?
- some examples of disease processes which might cause it
- questions you need to ask/things to consider if you suspect secondary HTN
- drugs which may cause HTN
examples of dz. to cause secondary HTN
- renal parenchymal disease
- renovascular disease
- primary aldosteronsim (increased aldosterone)
- OSA
- drug or alcohol induced HTN
Consider secondary if….
- treatment resistant HTN
- abrupt onset
- the HTN occurring < 30 years old
- exacerbations of once controlled HTN
- too much end organ damange for controlled HTN
- malignant HTN
- unprovoked hypokalemia
Drugs which can cause HTN
- illicit drugs
- ADHD meds (appetite suppressants becuase theyre stimulators)
- decongestants
- MOAIs, TCAS, buproprion, venlafaxine
- HERBALS!
- NSAIDS (inc. uptake of NA and H2O nephrotoxic)
- steroids ( increase fluid retention)
- estrogen & OCPs
- cylosporines
- triptans
what are our primary HTN drugs? Secondary?
primary agents: used in the absence of compelling indications (like heart failure with rEF, CKD, DM)
- Diuertics: Thiazides
- RAAs agents: ACE & ARBs
- Calcium Channel Blockers: dihydropyridine
secondary agents: used in compelling indications & once you have EXHUSTED the primary liste (use all drugs in the list together and still not luck) – add-on these
- diueritics: loops, potassium sparing, aldosterone antagonists
- RAAS: direct renin inhibitor
- Beta- Blocker: cardio-selective (B-1) , non-cardioselective (beta1&2), combined alpha1 & beta)
- centrally acting alpha 2 agonists
- direct vasodilation
- direct alpha 1 blockers
Thiazides
- indications for use
- MOA
- names of drugs
- toxicities
- a diuretic used as primary treatment of HTN
MOA: acts at the proximal tubule to block reabsorbtion of sodium and chloride thus, blocking reabsorbtion of water –> increasing output of water and therefore decreased blood pressure
- may not be indicated for those with eGFR < 30 (because not enought sodium getting to proximal tubule anyway so ineffective med)
names
- Chlorthalidone
- Hydrochlorothiazide (HCTZ)
- Indapamide
- Metolazone
Toxicities
- electrolyte imbalances: decreases Na, Mg, Cl, K
- INCREASES calcium
- hyperuricemia (onlt a big deal if pt. has gout)
(less common)
- increase blood glucose
- increased BUN/creatitine ratio (dehydration)
- cholesterol elevations
- thrombocytopenia, panceratitis (if they have this, stop immediately)
Loops (diuretics)
- MOA
- indications
- names
- side effects & toxicites
MOA: block the reabsorbtion of Na+, Cl- in the thick ascending Loop of Henle – therefore it blocks the reabsorbtion of water
here (at the loop) its responsible for approx. 25% water reasorbtion – therefore the loops work better than thiazides & all other diuretics in their ability to decrease HTN
indication
- loops are used in seondary treatment – once youve’ exhusted all of the primary agents (thiazides, CCBs, ACE/ARB)
Names
- Bumetanide
- Furosemide
- Toresemide
Side Effects
- Decrease electrolytes K, Na, Mg & Cl
- DECREASED CALCIUM
- ** think this becuase LOOP has a LOWWW– all the electrolytes go low**
- Hyperuricemia (watch with gout)
- increased BUN/creatitine ratio (dehydration)
- cholesterol
- thrombocytopenia, pancreatitis
loops can be used in those with a eGFR < 30 since they work at a different part of the kidney
Potassium-Sparing Diuretics
- MOA
- indications
- Names
- Side Effects
MOA
- potassium-sparing diuretics work at the most distal (late distal) covoluted tubule – *therefore have the least dieuretic effect and BP effect *
- therefore at distal end –> limited sodium reabsorbtion effect
- can be used in combination with thiazide or loop to counteract their potassium and magnesum effects (good for those who cannot tolerate a potassium supplement)
Indications
- CANNOT BE USED AS STAND ALONE BP MEDS
- for those who need more than just primary treatment – add-on therapy
Names
- amiloride
- triamterene
Side Effects
- avoid in those with eGFR < 45
Aldosterone Antagonists (diuretics)
MOA
indications
Names
Side Efffects
MOA: blocks aldosterone –> which normally helps to reabsorb K+ –> blocks that therefore –> increase excretion of K+ & H20 –> decrease BP
- Aldosterone normally also can increase resistnace so the antagonist can also modulate vasular tone of the vessel walls to vasodialate and reduce resistance
Indications
- for pts. with RESISTANT HYPERTENSION this can be add-on tp their other priamry treatment drugs
- for those with secondary hypertension and a primary aldosteronism
Names
- spironlactone
- eplerenone
Side Effects
- can increase serum potassium (k+)!!!! with use of ACE/ARB,DRIs
- monitor: serum K+ for 3-7 days after starting meds
- spironlactone: gynocomastia
- eplerenone: rare gynecomastia
RAAS: ACE Inhibitors
MOA
Indications
names
Side Effects
MOA: ACE inhibitros block the conversion of angiotensin I to angiotensin II –> therefore decreasing the ability to vasoconstrict vessels, decrease the ADH release and dereases aldosterone effect —> decrease BP
Indications
- primary treatment for hypertension
Names - all end in -PRIL !!!
- enalapril
- lisinopril
- ramipril
Side Effects
- HYPERKALEMIA – becuase it prevents aldosterone synthesis
- DRY COUGH (later onset)
- orthostatic hypotension
-angioedema (RARE but LIFE THERATENING)
** AVOID IN PREGNANCY**
RAAS: ARBs
MOA
Indications
Names
Side Effects
MOA
- atagonist at the angiotensin II receptor –> block angiotension II from doing its thing (similar to ACE effects) therefore decreased BP
Indications
- primary hypertension management
- works simialr to an ARB – so never using those two together
Names - -sartan
- candesartan
- irbesartan
- losartan
- telmisartan
- valsartan
Side Effects
- HYPERKALEMIA!!!
- angioedema!! less of a risk here but can switch from ACE to this
- NO COUGH – since AGII is still being produced
- AVOID IN PREGNANCY
potassium levels when starting and treating with an ACE or ARB
- dont initiate at what level
- dont increase dose at what level
- decrease or d/c if at what level
what about SCr?
true hyperkalemia is 6+ – but we dont want to get there soooo
1. dont INITIATE tx. if k+ = GREATER than 5
2. dont increase rx. if k+ = 5-5.5
3. discontinue or decrease if k+ = GREATER than 5.5
SCr should be stable prior to initiated therapy
a 10-30% increase is expected from baseline – anything higher – stop
ACE/ ARB & SCr
ACE/ARB can INCREASE serum creatatine levels
- can be good or bad
SCr –> allows us to understand the PRESSURe inside the glomerelus
HIGH p in glom: triggers protein to be pushed out into urine – SCr LOW
LOW p in glom: triggers protein to stay in circulation – SCr HIGH
ACE/ARB decrease P in gol: therefore holding onto SCr more –> increase in SCr this is the good effect
ACE/ARB dilate efferent arteriole of glom: will lower pressure in glom. may cause a slight inc. in SCr (not as much forced out)
- but this relies on a properly working afferent arteriole
- this could cause a BIG increase in SCr – a probelm!!!! if theres a bad wokring afferent arteriole
increase SCr – dec. eGFR and vis versa
RAAS: Direct Renin Inhibitor
MOA
indications
Names
Side Effects
MOA: directly inhibit renin, therefore decreasing the ability to conver angiotensinogen to angiotenisn (upstream effects to eventaully decrease HTN)
- not great effects : rarely used & not any better than an ACE/ARB
Name
- aliskirin
Side Effects
- hyperkalemia
- diarrhea
- cough (less than ACE)
- angioedema (more rare)
- do not use in pregnant
