1st Line In Essential Hypertension Treatment Resistant HTN or Pts w.

Co-morbid conditions
Diuretics RAAS Targeting Drugs Ca2+ Channel Blockers (CCBs) Sympatholytics Direct Vasodilators
Class Thiazide Diuretics Angiotensis Angiotensin Direct Renin Dihydropyridines Nondihydropyridines ɑ1 Blockers ɑ2 Antagonist B1-β2 B1-β2 β1 β1 β1, β2, &ɑ1 K+ Channel Openers Nitric Oxide (NO) Prostacyclin Endothelin Antagonists PDE-5 Inh
Converting Enzyme Receptor Inhibitor Cardioselective Non-selective Non-selective Selective Selective Releasers Pathway
Inhibitors Blocker (ISA) (No-ISA) (ISA) (No-ISA) Agonists
(ACEIs) (ARBs)
Name Hydrochlorothiazide Catopril Losartan Aliskiren Nifedipine* Varapamil Prazosin Methyl-Dopa* Pindolol Propanolol Acebutolol Aatenolol Labetalol* Minoxidil Hydralazine* Epoprostenol Bosentan Riociguat Sildenafil
Chlorothiazide Benazepril, Enalapril Candesartan Amlodipine Diltiazem Doxazosin Clonidine Carteolol Nadol Metropolol Carvedilol Treprostinil Ambrisentan Tadalafil
Chlorthalidone Fosinopril, Lisinopril Ibersartan Isradipine Terazosin Guanfacine Penbutolol Timolol Esmolol Iloprost Macitentan
Indapamide Quinapril, Ramipril Telmisartan Nicardipine Guanabenz Selexipag
Valsartan Nismodipine
Nisoldipine
Mechanism of Blocks Na+/CL- Inhibits ACE-> Blocks AT1 Blocks conversion Bind to ɑ1 subunit of membrane & storage ɑ1 Blockers-> Presynaptic ɑ-2 R.-> Competitive antagonist of adrenergic receptors ɑ and/or β) K+ Channel Opener Direct vasodilator NO release Prostaglandin It sensitizes Increases
Action Symporter in in DTC ↓ATII-> ↓GFR by receptor (step of site L-type calcium channels ↓Vascular tone-> inhibition of NE release-> ↓HR & CO-> Eventually ↓Left Ventricular Mass Agonist guanylyl cGMP levels
-↓Ca2+ excretion preventing afferent before Angiotensinogen -Block Ca2+ influx into cytosol-> ↓ Mucle smooth muscle SNS effect -↓Renin & Aldosterone-> ↓TPR cyclase to
constriction of Aldosterone) to Angiotensin-I contractility. relaxation, (G-protein gated K+ -Vasocontriction (Non-selective β-Blockers) make cGMP
efferent arterioles -Dilate arteries- -Verapamil & Diltiazem: Act on Heart vasodilation, channel-> (similar to
-↑Renin >↓A. P- Others on Vascular Smooth Muscle ↓Peripheral R. Hyperpolarization) endogenous
-↑Bradykinin >↓Afterload (mainly dilates arteries) NO)
-Dilate Veins-
>↓V.P->
↓Preload
-↓Sympathetic
Activity
-↑Renal
Indications DOC: Hypertension excretion
1st Line Drugs in DM of Na+
or Renal Hypertension HTN, Angina DOC: Benign DOC: HTN in pregnancy HTN MI Pulmonary Pulmonary Eractile
-Osteoporosis Insufficiency -Paroxysmal Supraventricular Tachycardia Prostetic (Methyl-Dopa) HTN, MI, CHF -Severe refractory Angina HTN HTN Dysfunction
-Severe edema +loop Adjunctive therapy in HF (PSVT) Hypertrophy Hyperthyroidism & Migraine PPX (Propranolol) Hypertension -Pulmonary
diuretics (DOC: PPX, 2nd Choice for treatment) (BPH) -Pheochromocytoma (Labetalol) -Male Pattern Baldness HTN
-Nephrogenic Diabetes -Vasospastic & Effort-Associated Angina (PPX, -2nd line HTN -HTN + HF (Carvedilol) (Rogaine)
Insipidus (lack of ADH 2nd line) -Post MI-Protective
effect) -Ventricular control-Afib -HTN in Pregnancy (Labetalol)
-Migraned PEP *CI: Bronchospasmic Disease (asthma, COPD, emphysema)

Adverse Effects Hypercalcemia, Hyperkalemia (ACEIs>>>ARBs) Hypotension SA nodal arrest (↑w. β-blockers) Postural Sedation Impotence Hirtuism Headache, Dizziness Flushing CI: Nitrate Pts
Hyperglycemia, -Cough (ACEIs-Catopril) -Stroke -Negative Ionotropic Affects (↑w. β-blockers) Hypotension -Orthostatic Hypotension -Bradycardia -Dizziness -Tachycardia Jaw Pain (Nitroglycerin)
Hypouricemia (↑gout) -Angiogenic Edema (ACEIs) -Angioedema -GI reflux/Constipation (Verapamil) (Prazosin, less -Fatigue -Tachycardia -Anxiety (severe
Hypokalemia, -Rash -Hyperkalemia -Reflex tachy & Perpheral Edema likely for reflex -Exercise Intolerance -Headache -GI upset (NVD) Hypotension)
Hyponatremia, -Itching -↓GFR-> Renal (Dehydropyridines) Tachy) -Orthostatic Hypertension (Labetalol/Carvedilol) -Act. of RAAS -Anemia
Hypotension, -Bloody dyscrasias (neutropenia, failure -Gingival Hyperplasia (NonDihydros) -Dyspnea
Hypovolemia agranulocytosis) -CI: w. ACE & ARBs -HTN in Pregnancy (Nifedipine) -Edema
-Impotenxe CI: Pregnancy (teratogenic), BiLat & Pregnancy -Nasal Congestion
-Sulfonamide toxicity renal stenosis -Act. of RAAS
-Lupus Like Syndrome**
(Antihistones)
-HTN in Pregnancy

Other *Not affective if GFR Often used w. a diuretic ↓PVR *Administered w. β- Short acting
<30 ml/min ↓Renin release from blockers to prevent reflex (Epoprostenol)
*↓Effectivenes if used Kidneys Tachy
w. NSAIDs (G: afferent
vasoconstriction)

Hypertensive Urgencies:
SBP ≥180 &/or DBP≥120 Better Cardiac Mortality
1. Nicardipine, Clevidipine Bisprolol, Carvidolol, Metropolol
2. Labetalol
3. Esmolol
4. Nitroglycerine
5. NB: Sodium Nitroprusside
 Heart Failure Drugs
Positive Ionotropic Drugs Potassium-Sparing Diuretics
Class Cardiac Glycosides β1>β2, ɑ PDE -3 HCN Channel Loop (high-ceiling) Diuretics Aldosterone Na+ Channel Blockers
Inhibitors Blocker Receptor
Antagonists
Name Digoxin Dobutamine Milrinone Ivabradine Furosemide Ethacrynic acid Spironolactone Amiloride
Digitoxin Bumetanide Eplerenone Triamterene
Torsemide
Mechanism of Direct Inhibition of BP, ↑HR, ↑CO Phosphodiestera Prolongs slow Sulfonamide inhibitor Nonsulfonamide Aldosterone Block Na+ channels in
Action Na+/K+-ATPase se inhipitor depol by of Na/K/2CL co- inhibitor of receptor cortical collecting tubule
-Indirect Inhibition of ↑cAMP-> selectively transporter in thick Na/K/2Cl Antagonist in
Na+/Ca2+ exchanger ↑Ca2+ influx-> inhibiting "funny" ascending limn loop of cotransporter of cortical
-↑Ca2+-> +Ionotropy ↑Ionotropy & sodium channels Henle. thick ascending limp collecting tubule
↓HR chronotropy in (If) -Ass. w. ↑PGE of loop of Henle Androgen R. & 17ɑ-
Hydroxylase/17,20-lyase
-↓AV conduction vascular smooth (pacemaker cells) -↑Excretion of Ca2+
inhibitor
muscle: ⭐

↑cAMP-> MLCK
↑Mortality ⭐
inhibition ->
vasodilation ->
↓Preload &
afterload
Indications HF (↑contractility) Unstable Acute Chronic Stable Hypercalcemia Diuresis in patients CHF
-Atrial Fibrillation bradycardia decompensated Angina (if pts can't -Hyperkalemia allergic to sulfa drugs -Essential HTN
(↓Conduction at AV -Shock HF w. take β-blockers) -Edematous states <----- -PCOS
node & depression of SA -Inotropic & Cardiogenic -Chronic HFrEF (CHF, cirrhosis, -
node) Chronotropic shock (inotrope) nephrotic syndrome, 1°Hyperaldostero
effects at lower pulmonary edema) nism In Addition
doses via β effects -Inhibited by NSAIDs -Hirtuism to:
-Vasoconstriction at -Edematous β-blockers
high doses via ɑ cond.
affects -Hepatic Ascietes ACEI's
-Hypokalemia ARB
CI: Thiazide
Hyperkalemia,
Diuretics
Kidney Dx
Nitrates
Adverse Effects Cholinergic effects Tachycardia Luminous Ototoxicity Similar Hyperkalemia Kidney Stones (in other
(nausea, vomiting, -Ventricular Phenomena Hypokalemia** <--- -Gynecomastia, chart above)
diarrhea) arrhythmias (visual brightness) Hypomagnesemia More Ototoxic antiandrogen
-Bradycardia -Hypotension -Hypertension Dehydration effects, metabolic
-Gynecomastia -Brasycardia Allergy (sulfa) acidosis
-Blurry yellow/Green Alkalosis (metabolic) -Impotence
vision "halos around Nephritis (int) -Benign Prostatic
light" Gout Hyperplasia (very
-Arrhythmias rare)
(Lidocaine used to
treat)
-↓AV block
-Hyperkalemia
-Toxicity -Antidote:
Digibind /Anti-digoxin
Immune Fab
-CI: Vtach, Heart Block,
Hypokalemia,
Hypercalcemia, kidney
dx, RHF

Other *Levels↑by "OHH DAANG" Add in Stage II/III

amiodarone, -retain activity even
quinidine, verapamil, when GFR is low
erythromycin

Total Cholesterol=HDL + TG/5 + LDL

 Dyslipidimia Drugs
Class Statins Niacin Bile Acid Resins Fibrates PCSK9 Inhibitors
Name Atorvastatin Niacin/B3 Colestipol Gemfibrozil Ezetimibe Alirocumab
Simvastatin Cholestyramine Fenofibrate Evolocumab
Bezafibrate
Mechanism of Block *RL enzyme: HMG Blocks Hormone Insoluble Agonists of PRAR- Dietary cholesterol Inhibits LDLr
Action CoA Reductase (1st Sensitive Lipasa polymeric a (Peroxisome proliferator- absorption inhibitor Breakdown
step in sterol synthesis) (HSL) in adipose cation exchange activated nuclear receptor) -> -Inhibits Niemann-Pick (PCSK9 protein binds
& stimulate Hepatic tissue-> resins (bind to ↑β-oxidation in C1-like-1 (NPC1L1) the LDL receptrs and
LDL & ↓ Hepatic VLDL ↓breakdown of TGs bile acids)-> the liver (C- protein brakes it down the
Synthesis into FAs (↓VLDL & Stop absorption >ketones) -↑regulation of LDLr LDLr)
-↓ Mortality in Pts with LDL production) & ↑excretion -↑ LPL-↑TG in liver -Humanised Abs ($$$)
CAD -↓C & Lp(a) up to 10X clearance -↓LDL up to 70%
-↑HDL -HDL may ↑ -↓TGs, ApoB-100,
Lp(a) levels by ~25%
-↓incidence of new
coronary events
Indications DOC: In Dyslipidemias Hypertriglyceridemia
Inflammatory Action..?
(Lupus, MS, Alzheimer's)
-Adult CHD
-Pediatric Familial
Hypercholesterolemia

Adverse Effects Toxicity (rare) Flushing & Itching Constipation Rash, GI distress, GIT disturbances Myalgias
-Hepatotoxicity (give Aspirin with) -Bloating -Myopathy (↑risk w. -Hepatitis -Delirium
-Myositis & -Heart Palpitations (relieved by fiber) Statins) -Myopathy (rare) -Dementia
Rhabdomyolysis -GI distress -↓Absorption of -Arrhythmias -Neurocognitive
-CNS effects: -Hyperglycemia other drugs and -Hypokalemia Effects
Sleepinessm -Hyperuricemia Fat soluble -Gallstone ↑Risk
depression, memory -(drug not tolerated vitamins (inh. Of 7ɑhydroxylase)

deficits (Simvastatin) in 50% of pts) -CI: Kidney or

Other May be combined w.
Niacin &/or Bile acid
biding resins
-*Given at night (when
C synthesis is at it's max)
Liver disease, Co-
morbid
hyperlipidemia
*Most effective *~20% ↓LDL, w. ↑Risk of May be combined w.
agent at ↑HDL functional LDLR Rhabdomyolysis statins w. bile acid
(Exercise is most -May be (Gemfibrozil)*Risk resins
important) combined w. ↑ when given w.
-May be combined statins statins
w. Statins or resins
 ANTITHROMBOTIC DRUGS
Anticuagulants Antiplatelet Drugs Fibrinolytics (Thrombolytics)
Class Indirect Thrombin Inh. Direct Thombin Inh. (IIa) Vit K. Red. Inh. Direct Xa Inh. Cox inhibitors Glycoprotein Iib/IIIa Inh ADP Inh. Plasminogen Act.
Name Heparin* Enoxaparin Dabigatran Lepirudin Warfarin Apixaban Aspirin Abciximab Clopidogrel Cilostazol Streptokinase Reteplase (rPA) Tenecteplase(TNK-
Dalteparin, Tinzaparin Agatroban Hirudin Endoxaban Eptifibatide Ticlopidine Dipyridamole Altaplase (tPA) tPA)
Fondaparinux
Bivalirudin Rivaroxiban Tirofiban Prasugrel
Ticagrelor

Mechanism of Activates antithrombin Catalyze inhibition Monovalent, Bivalent-> binds Inhibits Vitamin K Directly Inhibit Nonselective, Block GP IIb/IIIa Block ADP Block Directly or indirectly aid conversion of plasminogen to
Action III, which ↓ action of of Factor Xa by AT- small molecules, at two sites epoxide Reductase - Factor Xa Irreversible Cox- Fibrinogen receptors on (P2Y12) R. - Phosphodiesterase plasmin, which cleaves thrombin and fibrin clots.
factors IIa (thrombin) III, less able to only bind at the (catalytic site of synthesis of Factors II, 1 Inhibitor-> activated platelets >↓ADP-induced -> ↓cAMP ↑PT, ↑PTT, no change in Platelet Count.
and Xa. Short half-life. inactivate thrombin thrombin active trhombin & at VII, IX, & X ↓Thromboxane expression of hydrolysis
III site substrate --Has no effect on A2 synthesis (Abciximab-monoclonal GpIIb/IIIa -> ↑cAMP in
(low molecular -Directly bind to recognition)- previously formed Ab Fab fragments) platelets
weight heparins) active site of >Directly inhibit thrombin
thrombin-> throbin (Factor IIa)
inhibit -Parental
downstream
effects of
thrombin

Indications Immediate anticoag for Venous MI + PPX PPX for DVT & PE PEP of arterial Percutaneous Same as Aspirin Intermittent Short term emergency management
PE, ACS, MI, DVTs Thrombolism -DVT -PPX for Stroke in pts thrombosis in pts Transluminal Coronary -Dual antiplatelet Caludication -Coronary Thromboses in MI, DVT, Acute MI, PE
Given IV -Atrial -PE w. Atrial Fibrillation w. IHD & Stroke Angiography therapy -Stroke PPX -Acute Ischemic Stroke, d/ thrombosis
Fibrillation -Atrial fibrillation -PEP in Angina, -Angioplasty (PCI) -Post MI -Cardiac Stress -Most effective within 3 hrs of symptomatic onset of
-Used in HIT -Valvular stenosis MI, Tas, & Atrial -Post Angioplasty, ACS -Unstable Angina testing MI**
Arrhythmias -Unstable Angina -Coronary Stent (may still be useful 12 hrs after onset)
restenosis PPX
Adverse Effects HSR-Hep-Induced Not easily reversible Bleeding Teratogenic Bleeding Gastric Ulcers Bleeding Neutropenia Nausea Bleeding
Thrombocytopenia (HIT -Renal insufficiency (Antidote: -↑Risk of Bleeding (Antidote: -Tinnitus -Thrombocytopenia (ticlopidine) -Headache CI: Past Stroke. Peptic Ulcer, Healing wounds, recent
Type 1 & 2) patients needing an idarucizumab -Warfarin Skin necrosis Andexanet Alfa) -Allergic (Abciximab) -TTP may be seen -Facial Flushing surgery, H/O cerebrovascular accidents, Pregnancy,
-Excessive bleeding & anticoag (Praxbind)- for -CI: Pregnancy, Peptic (APCC in real life) Reactions -Hypotension Metastatic Cancer
complications Dabigatran) ulcers, Intracranial -Renal Injury -Abdominal Pain Antidote of Fibrinolytic-Induced Bleeding:
(antidote: Protamine Bleeding, Liver Dx w. Aminocaproic acid & Tranexamic Acid, Platelet infusion,
Sulfate) defective CF def. Factor Corrections
-Thrombosis &
Osteoporosis in chronic
use
-DOC: In Pregnancy

Other Heparin monitoring Half life 4.5 hrs *not as potent as Antidote: Vitamin K, 🎶 "ABC - 2b3a"🎶 *Can be Inhibited *Urokinase-
aPTT heparin Fresh Frozen Plasma by Omeprazole Synthesized by
-HIT 2: Immune -Only oral agent (FFP), Prothrombin- the kidney
mediated IgG against in class: no complex concentrates Prasugrel & -Enzyme
PF4 in 4-14 days post monitoring (PCC) Ticagrelor: Used obtained from
adm. *Narrow theraputic synergestically w. Group C beta-
-Bovine UFH>Porcine index: INR needs to be aspirin in ACS and hemolytic
UFH> LMWH monitores (Theraputic maintanence post- strep-
-Half life 60-90 min 2-3) MI