Hypertension Flashcards
essential hypertension definition BP + risk factors
-Systolic BP > 140 mmHg OR diastolic BP > 90mmHg with no underlying or specific identifiable cause
Risk factors:
-increasing age
-men + post menopause women
- African Americans
What drugs have an association due to similar effects on cell membrane alteration?
CCBs + Thiazide Dieuretics
Thiazides:
- alter Na+ influx into smooth muscle cells too decrease PVR -> decrease BP
CCBs:
- block CC in plasma membrane of smooth muscles -> relaxes smooth muscles/vasodilates -> decrease PVR -> decrease BP
In the African American population what contributes to higher incidence of htn. Treat with what?
Low RAAS system
- Due to their generally low renin levels + high aldosterone levels = increased sodium-water retention = HTN
First line Tx: calcium channel blockers + dieuretic*
Secondary Hypertension
Definition:
- HTN caused by an underlying or primary disease
Causes:
- Renal ds
- Endocrine (thyroid, pheochromocytoma, hyperaldosteronism, Cushing’s syndrome)
-Sleep Apnea
-Drug-Induced HTN: NSAIDs, COX-2 inhibitors, OCs, steroids, sympathomimetics; antidepressants, erythropoietin; cyclosporine; tacrolimus; licorice, herbal preps, Illicit drugs (cocaine)
-Social factors: Increased sodium intake, alcohol
Blood pressure equation
BP = Cardiac Output x Peripheral vascular resistance
CO = SV x HR
physiological control of BP: what 3 factors
- Cardiac Output
- Peripheral Vascular Resistance
- Baroreceptor Reflex - fast, short-term regulation controlled by SNS
baroreceptor reflex
- fast, short-term regulation controlled by SNS
-ACE- angiotensin 1
-ARB- angiotensin 2
non-pharmacological tx: when is it indicated and what treatment options
First line tx: is always LIFESTYLE modifications!!!!!
- prehypertensive
- Stage 1 HTN
LIFESTYLE modifications:
- weight reduction
- diet: ↑ K+, ↑ Ca2+, ↓ Na+ (DASH DIET)
- exercise
- moderation of alcohol intake
When should drug therapy be initiated?
-Immediate tx if diastolic BP >90mmHg*
- stage 2 htn
-If BP > 150/90mmHg after 3-6 months of lifestyle modifications with stage 1 HTN
- DM and CKD pts with BP >140/90
-if ASCVD risk > 10% with stage 1 HTN
goal BP: < 130/80 is goal
First line drug treatment for hypertension?
thiazide diuretics = first line!!
- absolute CI: CKD
Other 1st line agents include:
- ACE inhibitors/ARBs
- CCBs
JNC 8 report – guidelines, tx must be individualized based on pt factors
BP management chart
-dont memorize charts
-important to know when to start tx
-130/80 is goal
diuretics notes
-hydrochlorothiazide -> no real change from 25 to 50 dose -> better off switching to chlorthalidone
CCB
-non-DHP for HTN and arrythmia
What is the MOA of diuretics? indications for diuretics
MOA:
- increase renal sodium EXCRETION: aka natriuresis
- decrease blood volume causes decrease in SV -> decrease CO -> decrease BP
- thiazides: alters cell membrane to lower sodium influx into smooth muscle cells -> lowers PVR -> lowers BP
Indications:
- first line tx for mild HTN
- treat EDEMA associated w/ CHF and renal disease
Diuretics pregnancy categories
Thiazide: Category B/D (first line)
Loop: Category C (second line)
Potassium sparring: B/D (second line)
thiazide diuretics (pregnancy B/D) MOA and description
1st line tx!!!* (pregnancy category B/D)
- association in response b/w thiazide diuretics and CCBs – mainly due to similar effects on cell membrane alteration
MOA at distal convoluted tubule:
-blocks reabsorption of NaCl -> more Na and water excreted
- decreases Ca excretion in urine (GOOD to increase bone density/osteoporosis)
-cell-membrane alteration: lowers PVR in smooth muscles
thiazide diuretics: indications
Indications:
- monotherapy of mild HTN ESPECIALLY IN AFRICAN AMERICANS
- Useful for isolated systolic hypertension (ISH) in the elderly
- tx of EDEMA in CHF and nephrotic syndrome
thiazide precautions and CI
Precautions:
- ineffective in severe renal disease
Contraindications:
- CKD
- hypreuricemia
- gout
- sulfa allergy (sulfonamide-like structure)
-Hx of severe hyponatremia
thiazide diuretics: ADRs
Electrolyte abnormalities:
- hyponatremia
-hypokalemia
- hypomagnesaemia
Metabolic effects:
- hyperglycemia* (early on): K+ is associated with insulin so ↓ K+ = ↓ Insulin = ↑ Blood Glucose
- hyperuricemia
- Hypercholesterolemia & Hypertriglyceridemia
Sexual dysfunction: ED = MC reason for non-compliance
thiazide: DDIs and drug names
DDIs:
- decreased effect of diuretic: NSAIDS
- increased lithium levels
- anti-HTN effects increase with ACEi
Drug names:
- hydrochlorothiazide (HCTZ) *
- chlorthalidone *
- chlorthiazide
- indapamide
- metolazone
loop diuretics (pregnancy cat C)
MOA, indications
MOA: Loop of HENLE!!
- blocks reabsorption of Na+ at loop of henle
- more potent -> good for CHF
Indications:
- EDEMA associated with CHF (first line tx), hepatic, or renal disease
- HTN 2nd line tx
Loop diuretics drug names
Furosemide (Lasix)*
Torsemide
Bumetanide
Ethacrynic Acid: If severe sulfa allergy
category C
LOOP C (“oopsie”): we BE FT (“we be facetiming in a LOOP”)
If sulfa allergy, which loop diuretic can you use?
Ethacrynic Acid - Edecrin
Loop diuretic Precaution and CI
Precautions:
- Causes profound diuresis -> monitor fluid status, renal function and electrolyte status closely -> Adjust doses to avoid dehydration
Contraindications:
- sulfa allergy
note: its preferred over thiazides for pts with CKD (thats why its not a CI)
Loop diuretics ADRs and DDis
ADRs:
- Electrolyte imbalance: Hypocalcemia, Hypokalemia
- Hyperglycemia, Hyperuricemia
- Sexual Dysfunction
- Renal Effects: ↑ BUN/Cr, Oliguria, Azotemia
- GI effects: Pancreatitis, Hepatic damage
- Ototoxicity: More likely if IV or IM route***
DDI:
- decreased effect of diuretics: NSAIDS
- increased lithium levels
- AMG interaction
- anti-HTN effects increase with ACEi
“same as thiazides + renal effects, GI effects, and ototoxicity”
potassium sparing diuretics MOA and indication
MOA: COLLECTING DUCT
- block reabsorption of Na+ in Na+ channels in collecting duct
-reduces K+ secretion into urine (maintains blood K+ levels)
Indications:
- edema due to CHF
- HTN (last line tx)
potassium sparing diuretics contraindication + precaution
Precautions:
- can cause HYPERKALEMIA especially in combination w/ ACE inhibitors and K+ supplements
CI:
- hyperkalemia (K+ > 5 mEq/L prior to treatment)
potassium sparing diuretics ADRs and DDIs
ADRs:
- Hyponatremia
- Increased BUN/Creatinine
- GI effects: Jaundice, nausea/vomiting, diarrhea
- headache
DDIs:
- causes hyperkalemia w/ ACEi and K+ supplements**
- NSAIDs (lowers)
- Lithium (increases)
potassium sparring diuretics pregnancy class + drug names
pregnancy: category B/D
“ATES POTASSIUM”
- Amiloride
- Triamterene
- Eplerenone
- Spironolactone*
Spironolactone (+ eplerenone)
MOA, uses, ADRs
DUAL MOA:
- K+ sparing diuretic and aldosterone antagonist
Uses:
- HTN
- CHF
- primary hyperaldosteronism
- polycystic ovary disease
- hirsuitism
ADRs: **
- gynecomastica
-ED
-amenorrhea*
Association of two drugs mainly due to similar effects on RAAS?
ACE inhibitors and beta-blockers
ACE:
- blocks conversion to Ang II
BBs:
- blocks release of renin in kidney cells
ACEi MOA
MOA:
- Acts on RAAS to block conversion of Angiotensin I to Angiotensin II (potent vasoconstrictor -> lowers SV)
- Blocks degradation of BRADYKININ (potent vasodilator) = more vasodilation = ↓↓↓ PVR = ↓ BP
note: Block of bradykinin degradation is what causes all of the noticeable ADRs
ACEi Indication
Indications:
- HTN: first line tx
- CHF: stage A or B
- post MI: reduces mortality
- DM/CKD: drug modifications
ACEi precaution, contraindications
Precautions:
- Can cause renal failure in pts w/ bilateral renal artery stenosis
Contraindications:
-angioedema
-bilateral renal artery stenosis*
- pregnancy
“These pts are dependent on blood flow so we want a higher blood flow not a lower one or else kidneys wont get enough perfusion”
angiotensin receptor blockers (ARB) MOA
MOA
-block the binding of angiotensin II to its receptors in vascular smooth muscle -> increases vasodilation -> decrease PVR -> decrease BP
-blocks the binding of angiotensin II to its receptors in the adrenal cortex -> decrease aldosterone secretion -> decrease blood volume -> decrease stroke volume -> decrease CO -> decrease BP
Which two drug class have association and similar effects on RAAS?
ACE Inhibitors + beta-blockers
beta blockers MOA + what is ISA
MOA:
-blocks beta receptors in heart and other tissues -> decrease HR and contractility -> decrease CO -> decrease BP
-Inhibits RENIN secretion from renal juxtaglomerular cells -> decrease formation of angiotensin II -> decrease aldosterone secretion -> decrease blood volume -> decrease SV -> decrease CO -> decrease BP
-Reduce sympathetic outflow from CNS: lowers HR -> lowers BP
Some BBs have Intrinsic sympathomimetic activity (ISA)
- weak agonist activity on beta receptors (smaller reduction in heart rate)
- cause less bradycardia
- less ADR on lipid profile
alpha 1 blockers MOA
MOA:
-block vasoconstriction of peripheral vascular smooth muscle -> vasodilation -> decrease PVR -> decrease BP
- some activation of SNS -> increase HR and contractility
-activates RENIN system: may cause fluid retention -> often combined with diuretics
“Oh Stressful RED NEckers”
- think alpha 1 male that cannot stand up for himself is also a stressful RED NEcker with positve effects on lipids”
direct vasodilator MOA and indication
MOA
-directly dilates arteriolar smooth muscle -> decreases PVD -> decrease BP
Indications:
-refractory HTN after other agents
direct vasodilator
direct renin inhibitors: MOA, indication, ADR
MOA:
- inhibits renin-angiotensin-aldosterone system earlier in cascade than ACE inhibitors or ARBs
Indications
–approved for HTN
- currently studied for heart failure and nephropathy tx
ADRs: “Ren should join CAD”
- cough
- angioedema
- diarrhea
combination products examples
Combining drugs from different classes to achieve a synergistic effect is a common practice in the management of hypertension!!
Examples
-ACEi + CCBs (AC combo)
- ACEi + diuretic (AD combo)
-Beta blockers and diuretics (BD combo)
“AC AD”
“BD”
dosing of HTN drugs
-Initial doses: start at lowest dose
-Titration: Increase after several weeks of therapy
Assessment of blood pressure control: regular monitoring
-Is patient at goal BP?
-Poor response: reassess and adjust meds
hypertensive crisis, emergency, urgency
Hypertensive crisis:
- SBP > 180mmHg OR
- DBP > 120 mmHg
Hypertensive emergency:
- Severe increase in BP WITH EVIDENCE of target organ damage
-Treatment should be over minutes to hours
-Treat inpatient with IV meds*
-GOAL: Reduce pressure by < 25% within first hour (less for HTN associated w/ stroke)
Hypertensive urgency:
- Severe increase in BP WITHOUT evidence of target organ damage.
-Tx should be over several hours to days
-May be treated as an outpatient with follow-up with PO meds*
-GOAL: Reduce DBP < 100 over 24-48 hours
